Complete Textbook of Anaesthesia and Intensive Care PDF

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complete textbook of Anaesthesia
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Anaesthesia
and intensive care medicine
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Anatomy
Anaesthesia
on CD-ROM
The Abdominal Wall and
Inguinal Region
John Craven
John Craven was formerly Consultant Surgeon at York District Hospital, York, UK.
He trained in Manchester, Uganda and Cardiff. He is past chairman of the primary
examiners of the Royal College of Surgeons of England.
Abdominal wall
There is only superficial fascia over the anterior abdominal wall. It is generally fatty
but in the lower abdomen there is a deeper membranous layer (Scarpas fascia) which
blends inferiorly with the fascia lata of the upper thigh, invests the penis and scrotum (or
labia), before gaining attachment to the ischiopubic rami and the perineal membrane.
These attachments define the clinical picture that develops after injury to the posterior
urethra when blood and/or urine may extravasate deep to this membranous layer into
the perineum and lower abdomen but not into the thigh.
Laterally the anterior abdominal wall consists of three sheet-like muscles in layers, an
outer external oblique, a middle internal oblique and an inner transversus abdominis.
Each becomes aponeurotic anteriorly and these aponeuroses fuse to form a sheath
around the rectus abdominis.
These four muscles form an elastic wall supporting the abdominal viscera. They assist
in expiration and expulsive efforts such as defecation, micturition and parturition. They
are supplied by the lower five intercostal nerves, the subcostal nerve and the first
lumbar nerve. Deep to the muscles lie the transversalis fascia and the peritoneum. The
skin of the abdominal wall is supplied by the sixth thoracic to the first lumbar nerves. T6
supplies the epigastric region, T10 the umbilical region and L1 the groin.
Rectus abdominis
These are paired vertical muscles lying in the midline anteriorly enclosed in fibrous
sheaths. They extend from the 5th, 6th and 7th costal cartilages and the xiphoid to the
pubic crests.
External oblique
From the outer surfaces of the lower eight ribs the fibres descend obliquely downwards
to the iliac crest, with a free posterior border. Anteriorly it becomes aponeurotic to form
the anterior layer of the rectus sheath and thereby gain attachment to the linea alba,
a midline condensation of fibrous tissue, and through it to the body of the pubis. The
pubic crest forms the base of a triangular defect in the aponeurosis, the superficial
inguinal ring. Between the pubic tubercle and the iliac crest the lower aponeurotic
border is thickened to form the inguinal ligament. To the ligaments inner surface is
attached laterally the internal oblique and, deep to that, the transverse abdominis.
Internal oblique
Laterally, the internal oblique is attached to the thoracolumbar fascia, the anterior part
of the iliac crest and the lateral part of the inguinal ligament. Posteriorly the muscle
gains attachment to the costal margin but most fibres pass medially, become
aponeurotic and this aponeurosis splits to enclose the upper two-thirds of the rectus
abdominis. Inferiorly, the aponeurosis passes anterior to the rectus. Those fibres arising
from the inguinal ligament pass medially and arch over the spermatic cord to unite
with the transverse abdominis aponeurosis to form the conjoint tendon which gains
attachment to the upper surface of the pubis.
Transversus abdominis
Laterally, the transversus abdominis is attached to the inner surface of the lower six
costal cartilages, the thoracolumbar fascia, the anterior iliac crest and the lateral part of
the inguinal ligament. Medially, the fibres become aponeurotic and form
the posterior part of the rectus sheath. Inferiorly, the aponeurosis blends with that of the
internal oblique to form the conjoint tendon.
The inguinal region

The inguinal canal (Figures 1 and 2) is an oblique path through the lowest part of the
anterior abdominal wall. It extends from the deep inguinal ring, a deficiency in the
transversalis fascia just above the midpoint of the inguinal ligament, to the superficial
inguinal ring, a deficiency in the external oblique aponeurosis, lying above and medial
to the pubic tubercle.
Horizontal section through the inguinal canal
Inferior epigastric vessels Deep inguinal ring

Transversalis fascia Transversus
abdominis
Conjoint
tendon Internal
oblique
External
oblique Red arrow indicates the path of
an indirect inguinal hernia. It
enters the deep inguinal ring and
Superficial exits via the external ring
inguinal ring alongside the spermatic cord.
Blue arrow indicates the path of a
direct inguinal hernia.
Inguinal canal showing anterior wall
External oblique aponeurosis
External ring
Ilioinguinal nerve
Spermatic cord
Femoral artery
Femoral vein
Femoral canal
It is covered anteriorly by the external oblique aponeurosis which is reinforced laterally

by the muscle fibres of internal oblique.
Its posterior wall is formed by transversalis fascia throughout but this is reinforced by
the conjoint tendon medially.
Its floor is the re-curved edge of the inguinal ligament and its roof the lowest fibres of
internal oblique (Figure 3).
Inguinal canal with external oblique removed
Internal oblique
Internal ring
Conjoint
tendon
It contains the ilioinguinal nerve and the spermatic cord in the male and the round
ligament of the uterus in the female.
The femoral artery lies deep to the inguinal ligament which separates it from the deep
inguinal ring and its pulsation can be found at the midinguinal point, half-way between
the anterior superior iliac spine and the symphysis pubis. Medial to the artery is the
femoral vein. Both vessels are invested in a fascial sheath, the femoral sheath which
also contains, medial to the vein, the femoral canal (Figure 4).
Structures lying deep to the inguinal ligament
Femoral nerve Anterior

Femoral artery superior
Femoral vein iliac spine
Femoral sheath
Femoral canal
Lacunar ligament
Inguinal ligament Iliopsoas
muscle
Pubic tubercle
Symphysis pubis
Hernias
Hernias are common in the inguinal region. Congenital inguinal hernias, present from
birth, are caused by the persistence of a patent peritoneal sac within the spermatic
cord. The hernial sac pursues an oblique course through the length of the inguinal
canal and is known as an indirect inguinal hernia. From middle age onwards the direct
inguinal hernia is common. It results from weakness in the posterior wall of the inguinal
canal. It presents as a forward protrusion of the peritoneal sac. Femoral hernias are
less common. They occur via the femoral sheath through the narrow unyielding femoral
ring immediately below the inguinal ligament. u
Anatomy of Tracheostomy and
Laryngotomy
Anil Patel
Anil Patel is Consultant Anaesthetist at the Royal National Throat, Nose and Ear
Hospital, London. He qualified from University College, London, and trained in
anaesthesia at Guy's Hospital, London.
Knowledge of the anatomy of the upper respiratory pathway is essential for the safe
practice of tracheostomy, in which a hole is made in the anterior tracheal wall, and
laryngotomy or cricothyroidotomy, in which a hole is made through the cricothyroid
membrane.
The larynx consists of articulating cartilages linked together by ligaments. It lies

opposite the 4th, 5th and 6th cervical vertebrae. The thyroid notch of the thyroid
cartilage can be palpated anteriorly and the cricoid cartilage below this (Figure 1). The
cricothyroid ligament lies between the thyroid and cricoid cartilage.
Anatomy of the trachea
Hyoid bone
Thyrohyoid membrane
Thyroid cartilage
Arytenoid cartilage
Cricothyroid membrane
Cricoid cartilage
First tracheal ring
The trachea starts at the lower end of the cricoid cartilage at the level of the 6th
cervical vertebrae and descends through the superior mediastinum to terminate at the
bifurcation at the 4th thoracic vertebrae (Figure 2).
Features of the throat

Anterior relations anteriorly in the neck the trachea is covered by skin, superficial
fascia, deep fascia, thyroid isthmus overlying 2nd, 3rd and 4th tracheal rings and lower
in the neck strap muscles (sternohyoid and sternothyroid).
The blood supply of the larynx is from the superior and inferior laryngeal artery
branches of the superior and inferior thyroid artery, respectively. Venous drainage is
into superior and inferior thyroid veins.
Laryngotomy or cricothyroidotomy (Figure 3) an incision is made through the

skin, fascia and avascular cricothyroid membrane to enter the upper airway.
Position for cricothyroidotomy and tracheostomy
Tongue base
Epiglottis
Hyoid bone
Arytenoid cartilage
Cricoid cartilage
False vocal fold
True vocal fold
Thyroid cartilage
Cricothyroidotomy
Cricoid cartilage
First tracheal ring
Tracheostomy tube
(cuffed)
Tracheostomy (Figure 3) an incision is made midway between the cricoid ring

and suprasternal notch, the strap muscles are separated in the midline and retracted
laterally, the thyroid isthmus is retracted upwards or divided and a circular window
created between 2nd and 3rd or 3rd and 4th tracheal rings. u
Copyright 2003 The Medicine Publishing Company Ltd

The Autonomic Nervous
System
John Craven
examiners of the Royal College of Surgeons of England. His particular interest is gastric
cancer.
The autonomic nervous system supplies viscera, glands and smooth and cardiac
muscle. Its fibres arise in the lateral columns of the spinal cord, synapsing
with peripheral ganglion cells before supplying these structures (Figure 1). The
two complementary parts of the autonomic nervous system (sympathetic and
parasympathetic) leave the CNS at different sites and usually have opposing effects
on the structure they supply through endings that are mainly adrenergic or cholinergic.
The sympathetic system prepares the body for fight or flight and the parasympathetic
system controls its vegetative function.
Sympathetic reflex arc

1
Sympathetic system
In the sympathetic system preganglionic fibres arise from the lateral columns in
segments T1L2, passing for a short distance in the anterior roots of the corresponding
spinal nerves before leaving as white, myelinated, rami communicantes to join the
sympathetic trunk.
The paired sympathetic trunks consist of ganglia and nerve fibres, and extend from
the base of the skull to the coccyx. There are three cervical, eleven thoracic, four
lumbar and four sacral ganglia and from each pass somatic and visceral fibres (Figure
2).
The autonomic nervous system

Somatic fibres are distributed as grey, non-myelinated, postganglionic rami

communicantes to each of the 31 spinal nerves supplying vasoconstrictor fibres to
arterioles, secretory fibres to sweat glands and pilomotor fibres to the skin. Grey fibres,
unlike the white preganglionic fibres, do not run up or down the sympathetic trunk.
Visceral fibres pass to the:
thoracic viscera and synapse in the cervical and upper thoracic ganglia; their
postganglionic fibres pass to the viscera via the cardiac, oesophageal and pulmonary
plexuses
abdominal viscera and pass through the ganglia without synapsing, to enter one
of the splanchnic nerves before synapsing in one of the prevertebral plexuses in the
abdomen
adrenal medulla and through the trunk without synapsing, travelling in the greater
splanchnic nerve through the coeliac plexus to synapse with ganglion cells in the
medulla
cranial and facial structures (e.g. dilator pupillae, salivary glands) that accompany
the carotid vessels; the larynx and pharynx are supplied by postganglionic fibres from
the middle cervical ganglion which accompany the inferior thyroid artery.
The cervical sympathetic trunk and the stellate ganglion: see ANATOMY.
The thoracic sympathetic trunk comprises 1113 ganglia and gives branches to all
the corresponding spinal nerves; the first is usually fused with the lower cervical to
form the stellate ganglion. Visceral branches pass from the upper six ganglia to the
pulmonary and cardiac plexuses and three splanchnic nerves. The greater splanchnic
nerve (T510) ends in the coeliac plexus, the lesser (T9 and 10 or T10 and 11) in
the aortic plexus and the lowest in the renal plexus. The coeliac plexus lies around
the origin of the coeliac artery and is formed from the greater splanchnic nerve and
postganglionic fibres of L1. It is continuous with the network of sympathetic nerves
on the aorta, the aortic plexus, the branches of which accompany the branches of
the aorta.
The lumbar sympathetic trunk usually comprises four ganglia in each trunk. Its
branches pass to the coeliac and hypogastric plexuses, and to each of the lumbar
spinal nerves.
The hypogastric plexuses supply the pelvic viscera. The superior plexus receives
branches from the coeliac plexus and the sympathetic trunks and its efferent fibres
mainly travel in two hypogastric nerves descending on each side of the rectum
supplying the rectum, bladder and genitalia. The plexus receives autonomic sensory
fibres of pain and bladder and rectaldistension, from the pelvic viscera. The inferior
plexus also receive parasympathetic branches from the nervi erigentes (S24).
Parasympathetic system
The parasympathetic system is much smaller and comprises a cranial and sacral
component on each side. Its actions contrast with those of the sympathetic system
constriction of the pupils, decrease in the rate and conduction of the heart, broncho-
constriction, an increase in peristalsis, sphincter relaxation and an increase in glandular
secretion. Its pelvic component inhibits the bladders internal sphincter and it is
stimulatory to the bladders detrusor muscle. Its medulated preganglionic fibres are
much longer than those of the sympathetic system and synapse with postganglionic
cells close to or in the walls of the viscera they supply. The cranial outflow is conveyed
in the oculomotor, facial, glossopharyngeal and vagus nerves (Figure 2). The latter
is the largest component and most widely distributed. The parasympathetic nerves
of the oculomotor, facial and glossopharyngeal nerves are transmitted via four gan-
glia through which also pass sympathetic and somatic fibres.
The ciliary, lateral to the optic nerve, from which passes postganglionic fibres to
sphincter pupillae and ciliary muscles.
The sphenopalatine in the pterygopalatine fossa is supplied by fibres from the
greater petrosal branch of the facial nerve; postganglionic fibres supply the lacrimal
gland, nasal and pharyngeal glands.
The submandibular ganglion receives fibres from the facial nerve through the
chorda tympani branch and via the lingual nerve which lies on the hyoglossus
muscle. Preganglionic fibres pass in the lingual nerve to supply the submandibular and
sublingual salivary glands, and oral and pharyngeal glands.
The otic ganglion receives fibres from the glossopharyngeal nerve via the tympanic
plexus and the lesser petrosal nerve; postganglionic fibres pass in the auriculotemporal
nerve to the parotid gland.
The parasympathetic supply of the abdomen and pelvis is derived from the vagi and
the pelvic splanchnics. The anterior and posterior vagal trunks are distributed through
the coeliac plexus along the branches of the aorta to the alimentary tract and its
derivatives as far as the splenic flexure. The pelvic splanchnic nerves (S2,3,4) pass to
the hypogastric and pelvic plexuses. From the former, branches pass along the inferior
mesenteric artery to supply the gut distal to the splenic flexure; from the latter are
supplied the pelvic viscera. Their action helps in micturition and defecation by producing
relaxation of bladder and bowel sphincters.
2002 The Medicine Publishing Company Ltd

The Axilla
John Craven
The axilla is a fat-filled space, the shape of a truncated cone, lying between the lateral
thoracic wall and the arm. At its apex it is bound by the upper border of the scapula,
the outer border of the first rib and the middle third of the clavicle and it is through
this that structures pass from the posterior triangle of the neck to the upper limb. The
base of the axilla is formed by skin and subcutaneous tissue. It is bounded anteriorly
by the pectoralis major and, deep to that, pectoralis minor. The posterior wall extends
lower than the anterior wall and is formed, from above downwards by subscapularis,
latissimus dorsi and teres major muscles. The axilla is limited medially by the upper
ribs and intercostal spaces, which are here covered by slips of the serratus anterior
muscle. The lateral wall is thin and is represented by the narrow intertubercular groove
of the humerus, into the lips of which the muscles of the anterior and posterior walls
are inserted. It contains the axillary artery and vein, cords and branches of the brachial
plexus, coracobrachialis and biceps, axillary lymph nodes and vessels, and fat.
The axillary artery begins as the continuation of the subclavian artery at the outer
border of the first rib below the middle of the clavicle. It passes through the axilla to
become the brachial artery as it leaves at the lower border of teres major. Throughout
its course it lies on the muscles of the posterior wall of the axilla and is surrounded
by the cords and branches of the brachial plexus. The axillary vein lies medial to this
neurovascular bundle; coracobrachialis and the short head of biceps are lateral.
Anteriorly, the vessels and nerves are crossed by the pectoralis minor. It supplies
branches to the upper thoracic wall, the muscles of the axilla and the shoulder joint. Its
largest branch, the subscapular artery, gives an important contribution to the scapular
anastomosis, which provides a collateral circulation to the upper limb in the event of
obstruction of the axillary artery by virtue of its communication with branches of the
thyrocervical trunk, which arises from the subclavian artery.
The axillary vein is a continuation of the brachial vein and ascends through the
axilla, medial to its artery, before leaving it to become the subclavian vein at the outer
border of the first rib. Its branches correspond to those of the artery, apart from the
cephalic vein which drains the superficial tissues of the upper limb. It ascends in the
groove between pectoralis major and deltoid muscles before piercing the deep fascia
just below the clavicle. Obstruction of the axillary vein by a thrombus, though not
as common as that of the leg veins, occasionally occurs after prolonged infusion of
hyperosmotic fluids and/or intravenous nutrition. It results in acute swelling of the arm
and the possibility of pulmonary embolus.
The brachial plexus is described elsewhere. The three cords of the plexus (lateral,
medial, posterior) are named according to their position around the axillary artery.
Lymph system
Lymph vessels are superficial or deep. The superficial group drains the skin; medially
the vessels accompany the basilic vein and terminate in the axillary nodes; laterally the
vessels accompany the cephalic vein and drain via infraclavicular nodes into the axillary
nodes.
The axillary lymph nodes are of considerable clinical importance because they drain
the arm, the upper abdominal wall and the pectoral region and also receive most of the
lymphatic drainage of the breast. They are arranged in five groups (Figure 1).
The anterior group lie deep to pectoralis major draining
the lateral and anterior chest wall, the breast and the upper abdominal wall.
The lateral group lie on the lateral wall of the axilla and receive the efferent vessels
from the upper limb.
The central group are arranged around the axillary vessels in the axillary fat.
The posterior group lie to the lateral edge of the subscapularis muscle on the
posterior wall of the axilla.
The apical group lies at the apex of the axilla immediately behind the clavicle; they
are continuous with the inferior deep cervical nodes and receive drainage from all the
preceding groups.
Lymph nodes of the axilla
Axillary vein
Central
axillary
nodes
Apical
axillary
Lateral nodes
axillary
nodes Anterior
axillary
nodes
Posterior
Pectoralis
axillary nodes
minor
Subscapular vein
1
A subclavian lymph trunk conveys the lymph from the apical group to the right jugular
trunk or the thoracic duct. Lymphoedema, an excessive accumulation of tissue fluid,
occurs when the lymph trunk becomes disrupted or obstructed. In the developed world,
the most common cause of this occurring in the arm is a combination of radiotherapy
and surgical excision of the axillary lymph nodes in the treatment of advanced breast
cancer. u

Central Nervous System
John S P Lumley
John S P Lumley is Professor of Surgery and Honorary Consultant at St

Bartholomew's Hospital, London, UK. He is past World President of the International
College of Surgeons. His main clinical and research interests relate to the surgery of
cerebrovascular diseases and microvascular surgery.
The brain and spinal cord develop from a longitudinal dorsal tube of neural plate
ectoderm. The walls of the tube become greatly expanded by the cell bodies, dendrites
and axons of the developing neurons, and peripheral neural extensions from the paired
12 cranial and 31 spinal (8 cervical, 12 thoracic, 5 lumbar, 5 sacral, 1 coccygeal) nerves
making up the peripheral nervous system. The spinal nerves carry somatic sensory
fibres and innervate skeletal muscle. In addition, the cranial nerves carry special
sensory fibres from the head and neck and supply branchial arch musculature.
The autonomic nervous system overlaps the central and peripheral nervous
systems. It innervates smooth and cardiac muscle, and glands, and carries visceral
sensory fibres. The complementary sympathetic and parasympathetic parts of the
autonomic system are carried, respectively, in the thoracolumbar (T1L2) and
craniosacral (cranial nerves 3, 7, 9, 10 and S2, 3, 4) outflow.
Spinal cord
The spinal cord retains its longitudinal cylindrical form. Its fine central canal is
surrounded by cellular grey matter. The dorsal horns have a predominantly sensory
function and the ventral horns contain motor neurons. The fibres in the peripherally
placed white matter are organized into tracts (Figure 1).
1
Brain stem
The brain stem is made up of the medulla and pons of the hindbrain, and the midbrain.
It is in continuity with the spinal cord below and the diencephalon of the forebrain
above. Posteriorly the cerebellum is united to it by three paired cerebellar peduncles.
The brain stem and cerebellum lie within the posterior cranial fossa, the midbrain
passing through the anterior midline opening of the dural roof of the fossa the
tentorium cerebelli. The brain stem gives attachment to, and contains the nuclei of, the
312 cranial nerves. It gives passage to the ascending and descending fibres from
forebrain to the spinal cord, and the afferent and efferent fibres to the cerebellum.
The crossed and uncrossed corticospinal pathways form the prominent pyramids
of the anterior medulla. These bundles are broken up in their passage through the
pons but form part of the cerebral peduncles in the midbrain. The olivary nuclei
produce anterolateral oval longitudinal swellings in the upper medulla before forming
the ipsilateral inferior cerebellar peduncles. The pons forms the prominent anterior
convexity between the medulla and midbrain, and is formed of transversely running
fibres passing posterolaterally to become the middle cerebellar peduncle.
The midbrain is formed anteriorly by the cerebral peduncles, containing
frontoparietal and frontotemporal, as well as pyramidal fibres. Posteriorly are the paired
inferior and superior colliculi concerned with the integration of auditory and visual
sensation, respectively. The intervening tegmentum contains the prominent decussation
of the superior cerebellar peduncles, passing to the red nuclei.
The cerebellum is attached by the inferior, middle and superior cerebellar peduncles,
respectively, to the medulla, pons and midbrain. It comprises a central, midline vermis
and a hemisphere on each side. A deep primary transverse fissure divides anterior
and posterior lobes and the posterolateral fissure, across the caudal surface of the
cerebellum, separates the posterior and flocculonodular lobes. The ridges (folia) of the
greatly convoluted surface represent only one-sixth of this area, the remainder lining
the deep sulci.
Most afferent fibres to the cerebellar cortex end in the middle granular and outer
molecular layers, where a profuse dendritic network of flask-shaped, Purkinje fibres
is situated. The complex circuitry of the cortical neuronal units and the profuse
connections of the cerebellum uniting all major motor regions throughout the CNS,
provide an integrative control of motor function, not only in locomotion but also in
posture, tone and equilibrium.
The reticular formation is an extensive collection of nuclear masses in the brain stem,
partly organized into median, medial and lateral columns. It forms an isodendritic core
traversing the entire brain stem. The reticular formation has extensive connections, both
crossed and uncrossed, with input and back projection to and from all parts of the CNS,
including the spinal cord, diencephalon, limbic system and the neocortex. It influences
somatic and visceral neural activity. Investigation has shown a complex facilitatory and
inhibitory synaptic transmission. The diffuse nonspecific activity is linked with arousal,
levels of consciousness, sleep patterns and biorhythms, together with providing an
ascending sensory gating mechanism that influences all forms of behaviour.
Fourth ventricle: the central canal of the spinal cord is retained as the aqueduct in
the midbrain, but in the hindbrain it is widened from side to side into a diamond-shaped
cavity, the fourth ventricle, posterior to the medulla and pons. On either side, the
fourth ventricle is enclosed by the inferior, middle and superior cerebellar peduncles.
Posteriorly the cavity is tented into the overlying cerebellum. The ependyma lining of the
ventricle and the covering pia matter are invaginated by numerous vessels to form the
choroid plexus of the fourth ventricle.
Diencephalon
Thalamus: the midbrain tegmentum merges rostrally with the inferior surface of the
egg-shaped thalami (Figure 2). These two nuclear masses, sitting on either side of a
flattened cavity, the third ventricle, also overlie the subthalamus and the hypothalamus,
and are united posterosuperiorly by the epithalamus. The various thalamic structures
form the diencephalon: the diencephalon, limbic system and cerebral hemispheres
make up the forebrain. The narrower anterior pole of each thalamus is near the midline
and borders the interventricular foramen (the communication between the third and
lateral ventricles). The lateral surface of the thalamus is applied to the posterior limb
of the internal capsule, while the arched exposed dorsal and medial surfaces are in
continuity, related in turn from lateral to medial to the body of the caudate nucleus,
the lateral ventricle, the stria terminalis, and thalamostriate vein, the stria medularis
and the third ventricle.
Pain reaches consciousness at the thalamic level, though it is poorly localized,
while thalamic injury alters the discrimination of all sensation. The thalamus serves to
integrate somatic and visceral function. This has a powerful influence on emotional and
endocrine activity, and profound effects on the arousal reaction.
Coronal section through the brain showing relations

of thalamus and striatum

Subthalamus is that part of the diencephalon merging inferiorly with the red nucleus
and substantia nigra of the midbrain; superiorly with the lateral thalamic nuclei; and
anteriorly it lies adjacent to the hypothalamus. Anterolateral to the subthalamus the
cerebral peduncles of the midbrain become the posterior limbs of the internal capsule.
The area contains the discrete subthalamic nucleus on each side and a grey lamina,
the zonar inserrata, passes rostrally in front of the thalamus.
The subthalamus is the site of integration of motor centres, particularly the
midbrain tegmentum, the corpus striatum and dorsal thalamic nuclei. Prominent
bands of fibres, the funiculus and ansa lenticularis, traverse the internal capsule,
uniting the corpus striatum and dorsal thalamic regions. Lesions of the subthalamus
produce hemibalismus, with disabling and violent uncontrolled choreiform movements,
predominantly of the limbs, suggesting loss of corpus striatal control over the motor
cortex.
Hypothalamus lies in the midline in the floor of the third ventricle anterior to the
subthalamus and below the two thalami. Anteroinferior to the hypothalamus is the
optic chiasm, and behind this an elevation (the tuber cinereum) gives rise to the stalk
(infundibulum) of the pituitary. Two small elevations (the mamillary bodies) lie behind
the tuber cinereum, and separate it from the posterior perforated substance and the
cerebral peduncles of the midbrain.
The medial parts of the hypothalamus have a number of named nuclear masses,
the more obvious being the preoptic, supraoptic, paraventricular, dorsomedial, ventral,
ventro-medial, infundibular and posterior. Afferent fibres pass to the hypothalamus from
the orbital surface of the frontal cortex, the septal nuclei, the hippocampus (through the
fornix) and the amygdaloid nucleus (through the stria terminalis). Afferent fibres pass
in the median forebrain bundle and dorsal longitudinal bundle to the midbrain reticular
nuclei. Fibres from the mamillary bodies pass to the anterior nucleus of the thalamus
(mamillothalamic tracts) and the midbrain (mamillotegmental tracts).
The hypothalamus has powerful influences on anterior and posterior lobe hormone
production of the pituitary, but the associated behavioural changes, particularly those
of an emotional nature, are closely linked to its connections with the limbic system.
The area is concerned with temperature regulation and control of circadian rhythms.
A rigid hypothalamic division of the autonomic regulation of the parasympathetic and
sympathetic nervous systems is no longer supported, but the region has profound
influence on the cardiovascular, respiratory and alimentary systems.
Epithalamus: the midline epithalamus is situated in the posterior wall of the third
ventricle between the posterior ends of the thalami. It comprises the habenular nuclei
and commissure, the posterior commissure and the pineal body. The habenular nuclei
receive the stria medullaris, a narrow bundle of fibres passing backwards over the
thalamus from the septal nuclei. Its efferents pass through the habenular commissure to
the interpeduncular nucleus of the subthalamus. The habenular nuclei and connections
contain a large number of neuromed-iators and these influence, particularly through
hypothalamic connections, gastrointestinal function, metabolism and thermal regulation.
The posterior commissure unites the two superior colliculi and the medial longitudinal
bundles of the two sides. It is a focus of interaction of olfactory, visual and somatic
afferent pathways.
The pineal body develops as an outgrowth from the third ventricle. It is an oval
mass lying between the superior colliculi. It has a powerful inhibitory effect on the
hypothalamus, releasing factors influencing thyroid, adrenal and gonadal hormone
secretion. Serotonin secretion and melanin production are reduced by photic stimulation
and the organ probably influences circadian rhythmicity.
Cerebral hemispheres
The dorsolateral aspect of each side of the primitive forebrain undergoes extensive
expansion, at first backwards and then anteroinferiorly to form the hemisphere. The two
limbs of this expanded hemisphere overlap a submerged area of cortex known as the
insula. The line of contact is termed the lateral fissure. The areas of the hemisphere
are named after the bones that overlie them. The anterior and posterior extremities are
respectively the frontal and occipital poles of the frontal and occipital lobes, with the
parietal lobe in between. The anteroinferior extension of the hemisphere is the temporal
lobe, housed within the middle cranial fossa, its apex being the temporal pole.
The rostral end of the primitive forebrain persists as a thin glial sheet, the lamina
terminalis, passing from the optic chiasm to the anterior commissure and corpus
callosum. The adjacent area on the inferior surface of each hemisphere houses the
olfactory bulb, tract and medial and lateral olfactory striae.
The surface of the hemisphere is convoluted, the exposed gyri being only one-third
of the surface area, the rest being hidden from view in the sulci. The sulci and gyri have
characteristic patterns (Figure 3). The central and calcarine sulci provide the anterior
and posterior limits of the parietal lobe. The surface is covered by a cellular outer layer
of grey matter the cortex, or pallium. The human neocortex is a highly organized
neuronal hemispheric covering with a great deal of functional localization. Conflicting
literature on these subjects is partly a result of the evidence being predominantly
derived from non-human studies. For example, Brodmanns mapping of 52 cortical
areas in 1909, while providing a useful reference grid, was based on comparative
studies of simian brains and did not include the human cortex.
Left hemisphere functional localization
Pre central motor

Motor association areas
Brocas area (motor speech)
Associated speech
Vision
Associated visual area
Auditory area
Wernickes area
Post central sensory
Sensory association area
3
Cortical cells are predominantly of two types: pyramidal (agranular) and stellate
(granular). Pyramidal cells vary from small (10 ) to very large (70 ), the latter
including the Betz cells characteristic of the human motor cortex. They have a large
apical dendrite and each forms the core of a columnar unit extending through the
cortex, having numerous horizontal communications, and many inter-hemispheric
and projection fibres. This unit has enormous potential for intercommunication and
interconnections, each column having more than a thousand interconnecting neurons.
Stellate cells are 68 in diameter with a short axon and an extensive dendritic field:
they are of various shapes (e.g. the basket cell). Different workers have used the
dispersion of these cell types to identify major cortical areas. The most favoured system
identifies six cortical layers: Brodmanns mapping was based on this template.
In spite of the variable phylogical patterns throughout the pallium, with the exception
of the striate cortex, there is remarkable homogenicity of cellular numbers and ratios
of the two prime cell types: independent of the thickness (1.54.5 mm). Two-thirds
of neurons in any area are pyramidal and one-third stellate. The striate cortex, while
representing only 3% of the surface, contains 10% of cortical neurons.
Anatomical localization based on single projections to an area is oversimplistic,
because all areas of the pallium receive and project extensively by association and
commissural fibres, to the dorsal and reticular thalamic nuclei, the corpus striatum and
pons, and other areas throughout the CNS.
Initial focal pathology and anatomical localization of cortical somatomotor and
sensory pathways were supported in humans by operative recording and stimulation, by
Penfield and Rasmussen in the 1950s. However, stimulation of the motor cortex never
produced a co-ordinated movement, emphasizing that functional localization is linked
to association and efferent pathways, being more a mosaic than a clear body image.
The trend has thus been to label the first or leading area (e.g. Brodmann 4 as MsI) and
adjacent associated areas as secondary or tertiary fields (Brodmann 6, 8 as MsII, III).
Secondary areas in motor and sensory localization are involved with coordination and
discriminative interpretation, and generally linked with behavioural activity.
Asymmetrical localization was recognized by early workers undertaking cortical
mapping, but Brocas classical studies linked speech with the left hemisphere. It
became fashionable to attribute speech and linguistic comprehension to a dominant
hemisphere and although this was supported by pathological studies, other functions
such as spatial comprehension and musicology can be attributed to the non-dominant
counterpart. In the intact brain, the complementary nature of the two hemispheres
ensures appropriate concise complex bilateral responses to multifactorial stimuli.
Hemisphere white matter is organized into commissural fibres, uniting the two
hemispheres across the midline; association fibres joining adjacent or widely separated
gyri of the same hemisphere: and projection fibres to or from lower-lying parts of the
CNS.
The largest commissural band is the corpus callosum in which 200 million fibres
unite corresponding areas on the two sides. The callosum develops with the enlarging
hemispheres extending in hook-like fashion from the lamina terminalis, at first forwards
and then horizontally backwards over the diencephalon, the space between them being
the transverse fissure. The point of continuation with the lamina terminalis is termed
the rostrum, the anterior bend the genu, and the main bulk the body. The posterior
thickest portion of the corpus callosum, overhanging the posterior thalami, epithalamus
and midbrain colliculi, is termed the splenium. Despite this extensive point-to-point
communication, the rare congenital absence of the structure in the human may go
unnoticed.
Cortical projection fibres pass predominantly in the internal capsule, a broad
V-shaped band lying between the caudate nucleus and thalamus medially, and the
lentiform nucleus laterally. It fans out within the hemisphere as the corona radiata,
interdigitating with the transverse fibres of the corpus callosum. The anterior limb
of the capsule lies between the head of the caudate nucleus and globus pallidus,
and is crossed by extensive intercommunicating pathways between these structures.
It contains frontopontine fibres, from the frontal lobe to the nuclei of the pons, and
thalamic and hypothalamic cortical pathways.
The genu, between the anterior and posterior limbs of the internal capsule, contains
the corticonuclear fibres passing to the cranial nerve nuclei, while the adjacent part of
the posterior limb carries corticospinal fibres from the motor cortex.
Corpus striatum is a group of large nuclear masses situated in the substance of the
cerebral hemispheres adjacent to the internal capsule. The caudate nucleus has an
expanded head bulging into the anteral horn of the lateral ventricle. It then tapers into a
body and tail, curving around the lateral aspect of the thalamus in the wall of the lateral
ventricle, at first in the lateral wall and then in the roof of its inferior horn.
The corpus striatum receives fibres from all areas of the neocortex, and also from
the thalamus and brain stem. It has dense reciprocal connections with the subthalamus
and substantia nigra. Its principal outflow is to the thalamus, particularly the ventral
nuclei, the motor and pre-motor cortex, and to the reticular nuclei and thence to the
reticulospinal and rubrospinal tracts.
It is involved in motor coordination and damage to the structure increases tone,
producing resistance to stretch or rigidity. There is also loss of associated movement
and sometimes accessory, choreiform, athetoid and ballistic movements and tremor,
these being purposeless and uncontrolled. Ablation of the striatum produces poverty
of movement and manipulative skills. It has also been used to reduce the tremor and
rhythmicity of Parkinsonian movements, although the link with dopamine transmission
is unconfirmed.
Limbic system: the median area of anterior fusion of the two hemispheres, together
with their medial aspect, are drawn with the developing hemisphere into a C-shape
round the thalamus and are developed into a number of distinct nuclear tracts (Figure
4). This region was originally termed the olfactory brain or rhinencephalon. However,
the development of this area in the human renders this term meaningless, and the
functional name of limbic system is more appropriate.
The system encompasses the bulb, tract, and medial and lateral olfactory striae,
the anterior perforated substance between the striae, the adjacent inferior frontal (pre-
piriform) cortex on each side, and the anterior commissure linking these structures.
Three nuclear masses the hippocampus, amygdala and septal nuclei, and their
projections and commissural fibres, also contribute to the system.
The hippocampus lies in the floor of the inferior horn of the lateral ventricle,
three grooves in its distal enlargement giving it a paw-like shape and the name pes
hippocampus. Its afferent fibres are from adjacent cortical areas but the sole efferent
channel forms on its surface as the alveus, and passes backwards as the fimbria: the
two fimbria meet in the midline to form the body of the fornix which projects to the
anterior thalamic nuclei.
The amygdala is a composite nuclear mass situated in the roof of the inferior limit
of the inferior horn of the lateral ventricle. It connects with its fellow on the opposite
side via the anterior commissure and its main efferent pathway is the stria terminalis.
This follows the curve of the caudate nucleus and passes anterior to the interventricular
foramen and thence to the hypothalamus and septal nuclei. Some fibres then pass
backwards within the striae medullaris to the epithalamus. Other fibres pass to the
dorsal thalamus.
The septal nuclei are most prominent in humans and lie adjacent to the lamina
terminalis. The anterior commissure is embedded within the lamina and carries fibres
from the stria terminalis and commissural linkages between the medial olfactory tracts,
the anterior perforated substance, the pre-piriform cortex and the amygdala. There are
also extensive temporal neocortical connections of ill-defined function.
The complex network of nuclei, fibres and cortical areas in the limbic system is
concerned with the interaction of olfactory, visceral and somatic information and is
particularly concerned with emotional behaviour.
Limbic system

The third and lateral ventricles: the cavity of the forebrain is made up of the
midline third ventricle, communicating through two interventricular foramina with
the lateral ventricle on each side. The third ventricle lies between the two thalami.
Posteroinferiorly, it communicates with the aqueduct of the midbrain and above this is
related to the epithalamus, the cavity being recessed into the base of the pineal body.
Anteriorly, the third ventricle is limited by the midline lamina terminalis, the original
anterior limit of the primitive forebrain.
The lateral ventricle comprises a body and anterior, posterior and inferior horns. The
cavity extends backwards from the interventricular foramen over the thalamus and then
downwards in a C-shaped curve within the medial aspect of the hemisphere. It is limited
laterally by the reciprocally curved body and tail of the caudate nucleus. The ventricle
is overlain superiorly by the corpus callosum, as it curves into the temporal lobe; the
inferior horn has the hippocampus and overlying fimbria in its floor and is overlain by
the amygdala.
The body of the lateral ventricle is completed medially by the fused pial and
ependymal layers, the tela choroidea, passing from the undersurface of the fornix to
the upper border of the thalamus. In the third and lateral ventricles, the tela choroidea is
greatly expanded and infolded into the ventricles to form the choroid plexus which has
an extensive capillary network within it. It produces CSF, partly by filtration and partly
by secretion from the blood stream. The fluid passes through the midbrain aqueduct
into the fourth ventricle, and is added to by the choroid plexus invaginating the roof of
the fourth ventricle. It then circulates into the subarachnoid space through pores in the
tela choroidea of the fourth ventricle, known as the median foramen of Magendi and
lateral foramina of Luschka, between the superior and inferior cerebellar peduncles on
each side. The subarachnoid CSF is reabsorbed into the blood stream through venous
sinuses and spinal veins, through areas termed arachnoid granulations.

Cervical and Brachial
Plexuses
John Craven
cancer.
There are two plexuses of nerves in the neck:

the cervical plexus supplies the diaphragm and the skin and muscles of the neck
the brachial plexus supplies the upper limb.
Each lies on scalenus medius and is formed by the anterior divisions of spinal nerves.
The cervical plexus
The cervical plexus is formed by the upper four cervical nerves, which each receive
rami communicantes from the superior cervical ganglion. Its most important cutaneous
branches are the lesser occipital nerve (C2) and the great auricular nerve (C2, 3). They
emerge from the middle of the posterior border of the sternocleidomastoid muscle to
supply the neck and scalp posterior to the ear. The muscular branches of the cervical
plexus supply the rhomboids, neighbouring prevertebral muscles and the diaphragm via
the phrenic nerve (C4 with contributions from C3 and C5). The phrenic nerves contain
motor, sensory and sympathetic fibres, which provide the sole motor supply to the
diaphragm and sensation to its central portion and the mediastinal pleura. They travel
down the neck behind the jugular vein on scalenus anterior and pass anterior to the root
of the lung under the mediastinal pleura to reach the diaphragm
The brachial plexus
The brachial plexus lies in the posterior triangle of the neck along a line from the
middle of the posterior border of the sternocleidomastoid to the middle of the clavicle
(Figure 1). Knowledge of the anatomy of the brachial plexus and its branches is of great
practical importance to the anaesthetist who may use it to induce regional anaesthesia
in the upper limb.
The brachial plexus is formed from the anterior primary rami of the lower four
cervical and the first thoracic nerves. These five roots of the plexus emerge between
the middle and anterior scalene muscles and unite to form three trunks. The upper two
roots (C5, 6) form the upper trunk, the middle root (C7) the middle trunk and the lower
two roots (C8, T1) the lower trunk.
Behind the middle of the clavicle, at the apex of the axilla, each trunk divides into
anterior and posterior divisions. The three posterior divisions join to form the posterior
cord, the anterior divisions of the upper and middle trunks form the lateral cord and the
anterior division of the lower trunk continues as the medial cord. The cords lie around
the axillary artery related to it as their names imply (Figure 2) and are enclosed with
the artery in a neurovascular sheath the axillary sheath. The posterior cord and its
branches supply structures on the dorsal surface of the limb and end by dividing into
axillary and radial nerves.
The medial and lateral cords and their branches supply structures on the flexor
surface of the limb; the lateral cord ends by dividing into the musculocutaneous nerve
and the lateral head of the median nerve, the medial cord ends as the ulnar nerve and
the medial head of the median nerve (Figure 3).
Surface anatomy of the brachial plexus emphasizing

the approaches for brachial plexus block
Neck First rib

Supraclavicular
Cricoid approach
Clavicle
Humerus
Axillary
sheath
Axillary Arm
approach
Relationship of the brachial plexus to the axillary

artery
Ventral rami (roots) C5
Trunk C6 Cervical
C7 nerves
Divisions
Lateral cord C8
Coracoid process
T1 Thoracic nerve
Posterior cord
Axillary artery
Medial cord
Pectoralis minor
Axillary nerve
Musculocutaneous nerve
Ulnar nerve
Median nerve
Radial nerve
Branches of the brachial plexus C5

1
Middle trunk 1 Dorsal scapular nerve
Superior trunk C6 2 Suprascapular nerve
2 3 Nerve to subclavius
4 Long thoracic nerve
Lateral cord C7 5 Lateral pectoral nerve
3
6 Medial pectoral nerve
Axillary nerve 7 Medial brachial
5 C8 cutaneous nerve
Radial nerve
8 Medial antebrachial
Musculocutaneous cutaneous nerve
9
nerve 10 T1
11 4 9 Upper subscapular
6 nerve
Inferior trunk 10 Thoracodorsal nerve
Median nerve 8 Medial cord 11 Lower subscapular
7
Posterior cord nerve
Ulnar nerve
3
Branches of the plexus
From the roots: there are small branches to the back muscles, C5 contributes to the
phrenic nerve, the long thoracic nerve passes posteriorly to the medial wall of the axilla
to supply serratus anterior.
From the trunks: from the upper trunk arises the suprascapular nerve, which crosses
the root of the neck to supply supraspinatus and infraspinatus.
From the lateral cord branches the lateral pectoral nerve, which supplies pectoralis
major, the musculocutaneous nerve, which supplies coracobrachialis, biceps and
brachialis, before becoming the lateral cutaneous nerve of the arm, and the lateral
head of median nerve.
From the medial cord: the medial pectoral nerve supplies pectoralis major and minor,
the ulnar nerve supplies flexor muscles in the forearm, small muscles in the hand and
the skin of the medial side of the hand. Also branching from the medial cord are the
medial head of the median nerve, the medial cutaneous nerves of the arm which supply
skin on the medial side of the arm, and the medial cutaneous nerve of the forearm
which supplies the skin of the medial side of the forearm.
From the posterior cord the subscapular nerves descend the posterior axillary wall
to supply subscapularis and teres major. The thoracodorsal nerve supplies latissimus
dorsi by entering its upper border. The axillary nerve descends on subscapularis and
turns posteriorly around the surgical neck of the humerus supplying deltoid, teres minor
and the shoulder joint before ending as the upper lateral cutaneous nerve of the arm,
which supplies a small patch of skin over the insertion of deltoid muscle. The radial
nerve is a terminal branch of the posterior cord and descends through the posterior
compartment of the arm supplying triceps, brachioradialis and extensor carpi radialis
longus and brevis and sensory branches to the skin on the posterior and medial sides of
the limb and the posterior surface of the lateral three and a half fingers.
Brachial plexus block

The two techniques most commonly used are described here (Figure 1).
Axillary approach: the patient lies supine, arm abducted to a right angle with the
humerus externally rotated. A weal of local anaesthetic is raised over the palpable
axillary artery and the needle advanced until the neurovascular sheath is felt to be
entered. Anaesthetic solution can then be injected. Finger pressure over the artery
distal to the point of injection will prevent the downward spread of the analgesic. There
are few complications following this technique and the anatomical landmark is easy to
find, but the shoulder joint, supplied by the suprascapular nerve is not anaesthetized.
Supraclavicular approach: the patient lies supine, head rotated away from the
side of injection. A weal is raised 1 cm above the midpoint of the clavicle just
lateral to the palpable pulsation of the subclavian artery. The needle is advanced
downwards, inwards and backwards towards the spine of T4 until a motor jerk or
sensation indicates that the needle has pierced the neurovascular sheath. The local
anaesthetic solution can then be injected. A cough would suggest that the pleura has
been touched or pierced by the needle. This is a more difficult approach to perform
safely. Pneumothorax and haematomas due to vessel trauma are well-recognized
complications.

Cervical, Thoracic and Lumbar
Vertebrae
John Craven
The 33 vertebrae of the vertebral column have a basic form though they show regional
differences. They each have a body, neural arch and a vertebral canal. The body is
short and cylindrical, with flat upper and lower articular surfaces. The neural arch is
made up of paired pedicles that arise from the posterior surface of the body and paired
flattened laminae that fuse in the midline posteriorly to form a spinous process. Each
arch bears lateral paired transverse processes that arise close to the junction of the
laminae and the pedicles, and paired upper and lower articular processes. Each pedicle
is notched superiorly and inferiorly and these, with those of their neighbour, form a
intervertebral foramen which transmits a spinal nerve. Cervical, thoracic and lumbar
vertebrae are recognizable by characteristics that are most marked in their central
members, while those at either end of the group tend to resemble in part those of the
adjacent group.
A typical cervical vertebra (Figure 1) has an oval small body. Its superior articular
surface has lateral lips that articulate by synovial joints with the articular surface of the
vertebra above. The vertebral foramen is large. The short wide transverse processes
enclose a foramen transversarium, containing the vertebral vessels, and end laterally in
anterior and posterior tubercles. The articular processes on the junction of the lamina
and the transverse process are large, the superior faces backwards and upwards and
the inferior in the opposite direction. The spine is bifid and gives attachment to the neck
extensor muscles. The 1st, 2nd and 7th cervical vertebrae vary from this pattern.
A typical cervical vertebra: superior aspect
The 1st cervical vertebra, the atlas, allows free movement of the head and is modified
to comprise a ring of bone with neither body nor spine (Figure 2). Two bulky articular
lateral masses are united by a short anterior and a longer posterior arch. The superior
articular facets are large and oval and articulate with the occiput, the lower facets
are smaller. The posterior surface of the anterior arch has a small midline facet for
articulation with the dens of the axis, and lateral to this there are two tubercles on the
medial surface of the lateral mass for attachment of the transverse ligament of the
atlas. The superior surface of the posterior arch is grooved laterally on each side by
the vertebral artery. The transverse processes are long and wide and the tip of each is
palpable behind the angle of the mandible.
Atlas: superior aspect

The 2nd cervical vertebra (Figure 3), the axis, bears a conical projection, the dens
on its upper surface which articulates with the anterior arch of the atlas and is held
in position by the transverse ligament of the atlas. Lateral to the dens are two large
circular upward-facing articular facets.
Axis: superior aspect

The 7th cervical vertebra is also known as the vertebra prominens because it has
a long spine, easily palpable on the back of the neck at the lower end of the nuchal
furrow.
A typical thoracic vertebra (Figure 4) has a wedge-shaped body that is shallower

anteriorly. Each side of each body articulates with a rib at superior and inferior costal
facets towards the back of its upper and lower borders. The transverse processes point
backwards and laterally, and bear articular facets for articulation with the tubercle of
the corresponding rib. The broad laminae and the downward-projecting spines overlap
with those of the vertebra below. The bodies of the upper thoracic vertebrae are smaller
and narrower; the spines of the lower vertebrae are more horizontal. The transverse
processes of the lower two thoracic vertebrae do not bear costal facets. The costal facets
on the bodies of the 10th, 11th and 12th vertebrae are normally single and complete.
A typical thoracic vertebra: lateral and

superior aspects

A typical lumbar vertebra (Figure 5) has a larger kidney-shaped body that is wider
from side to side. The transverse processes are bulky and project directly laterally. The
superior articular facets face backwards and medially, and each spinous process is
broad and projects horizontally backwards. The 5th lumbar vertebra is untypical its
body is wedge-shaped, being thicker anteriorly and its transverse process is small and
conical.
A typical lumbar vertebra: superior aspect
Joints and ligaments

Hyaline cartilage covers the articular surfaces of the vertebral bodies, which are
united by a thick fibrocartilaginous inter-vertebral disc. The peripheral fibrous part,
the anulus fibrosus surrounds a gelatinous centre, the nucleus pulposus. The discs
are, in part, shock absorbers and contribute about 25% of the length of the vertebral
column. They are thicker in the cervical and lumbar regions. The vertebral bodies are
united by anterior and posterior longitudinal ligaments, which are also attached to each
intervertebral disc and extend the length of the vertebral column. The ligamenta flava
are formed of elastic tissue and play a part in maintaining the shape of the spine. They
unite adjacent laminae. There are also supraspinous, interspinous and intertransverse
joints.
Adjacent vertebrae also articulate by plane synovial joints between the paired articular
processes. The atlanto-occipital joints are synovial joints with only weak capsular
ligaments and the accessory anterior and posterior atlanto-occipital membranes. There
are three atlanto-axial joints; two lateral synovial joints between the lateral masses of
the two vertebrae and a median joint between the dens of the axis and the ring formed
by the transverse ligament of the atlas and its anterior arch. u

Cranial Nerves: Part I
John S P Lumley
John S P Lumley is Professor of Surgery and Honorary Consultant at St

Bartholomew's Hospital, London, UK. He is past World President of the International
College of Surgeons. His main clinical and research interests relate to the surgery of
cerebrovascular diseases and microvascular surgery.
The twelve pairs of cranial nerves originate from the forebrain (III), midbrain (IIIIV)
and hindbrain (VXII), and leave the skull through foramina in the anterior (I), middle
(IIVI) and posterior cranial fossae (VIIXII). Collectively, the cranial nerves carry
general somatic motor and sensory fibres; general visceral motor and sensory fibres;
special somatic sensory fibres; and special visceral motor and sensory fibres. The
general somatic motor fibres, passing to somatic mesoderm, are carried in the IIIrd,
IVth, XIth and XIIth cranial nerves. The general somatic sensory fibres passing to the
skin of the face are carried by the Vth cranial nerve. The general visceral motor and
sensory fibres making up the cranial component of the parasympathetic (craniosacral
outflow) nervous system, are carried in the IIIrd, VIIth, IXth and Xth cranial nerves.
The special somatic sensory fibres comprise the organs of vision (II), and hearing and
balance (VIII). The special visceral motor fibres innervate mesoderm derived from the
branchial arches, and are carried in the Vth, VIIth, IXth and Xth cranial nerves. The
special visceral sensory fibres carry smell (I) and taste (VII and IX).
Damage to cranial nerves may be the first indication of an intracranial lesion and nerve
damage is characteristic of various types of head injuries. The identification of cranial
nerve lesions and a knowledge of their anatomy are thus an essential part of clinical
practice. Cranial nerves IVI are described in this article, the other cranial nerves will
be described in Anaesthesia and Intensive Care Medicine 3:5.
Olfactory nerve (I)

The olfactory mucosa is situated on the upper nasal septum, the roof and the superior
concha on the lateral wall of the nose. The 1520 olfactory nerves innervating this area
on each side pass through the sieve-like cribiform plates of the ethmoid bone to the
olfactory bulbs. The nerves may be sheared off in anteroposterior impact head injuries,
and this may be accompanied by a CSF leak through the nerve channels or through an
associated fracture of the cribiform plate.
Optic nerve (II)

The optic nerve passes from the back of the eyeball through the orbit and enters the
middle cranial fossa through the optic canal. In the middle cranial fossa the nerves from
each side meet in the midline and their medial (nasal) halves decussate at the optic
chiasm, before reforming as the right and left optic tracts that pass to, and synapse in,
the lateral geniculate body. Each lateral geniculate body projects ipsilaterally through
the optic radiation to the visual cortex. (Other fibres from the lateral geniculate body
pass to the adjacent ipsilateral superior colliculus of the midbrain; these are concerned
with optic reflexes.)
The optic nerve is purely sensory. Its cell bodies form the ganglion layer of the retina
and its fibres converge posteriorly at the optic disc. The disc is sited medial to the
axis of the eyeball and has no retinal rods or cones; it thus produces the blind spot
on visual field mapping. The nerve pierces the sclera to lie within a meningeal sheath
that extends from the middle cranial fossa through the optic canal to the back of the
eyeball. The sheath is embedded in orbital fat and lies within the cone of extraocular
muscles. The ciliary ganglion and the ophthalmic artery lie on its lateral side, the artery
is also a lateral relation within the optic canal. Its retinal branch pierces the meningeal
sheath about 1 cm behind the globe and for a short distance lies within the CSF, before
entering the nerve to become the central artery of the retina.
The optic chiasm lies in the floor of the third ventricle above the hypophysis cerebri
and anterior to its stalk. The chiasm lies medial to the termination of the internal carotid
artery above the cavernous sinuses. The optic radiation passes distally in the posterior
limb of the internal capsule, grooving the floor of the posterior horn of the lateral
ventricle. The fibres converge on to the superior and inferior margins of the calcarine
sulcus along the medial aspect of the occipital lobe.
Spatial orientation is preserved through the length of the visual pathways. Fibres from
the nasal half of each retina (receiving light from the temporal field) cross in the optic
chiasm;thus the optic tract, lateral geniculate body, optic radiation and visual cortex of
each side receive visual information from the contralateral side. Fibres from the lower
retina pass through the temporal lobe to the inferior margin of the calcarine sulcus.
Upper quadrant fibres pass through the parietal aspect of the optic radiation and to
the upper margin of the calcarine sulcus. The macula is the most sensitive part of the
retina, and makes up about 25% of the visual cortex.
Assessment
Assessment of vision is carried out by history, and tests of acuity, visual fields and
ophthalmoscopy. The history in-corporates questions on near and distant vision,
visual loss, visual phenomena (e.g. blurring, flashes, double vision), ocular pain and
headache. Tests of visual acuity and of the visual fields are undertaken in each eye
separately (the other eye being covered with a hand or card) and then together.
Abnormalities of acuity are predominantly refractory, and patients are assessed with
and without their spectacles. Near vision is assessed with varying sized text, distant
vision with Snellen charts, and colour with Ishihara cards. Further tests of acuity are
carried out by an optician using an appropriate series of lenses.
Clinical assessment of the visual fields is by confrontation of the examiner and subject,
each covering in turn an opposing eye, the examiners other hand is brought in from
each quadrant. A red-topped hatpin is used to identify the blind spot and any central
defect (scotoma). Both the examiners hands are used to determine visual preference or
suppression of an image on one side. Normal pupils react to light and accommodation.
Ophthalmoscopy is used to examine the anterior aspect of the eye, the cornea, the
anterior chamber, iris and lens, and then the posterior chamber and retina.
Abnormalities of vision
Vision is affected by abnormalities of the eye and the neural pathways: these may
co-exist. The former include abnormalities of the lens (e.g. refractory errors, cataract)
or retina (e.g. detachment, ischaemia, hypertension, diabetic eye disorders); macular
degeneration; inflammation; or trauma to the globe. Lesions of the various parts of the
visual pathway produce characteristic visual field defects (Figure 1).
Oculomotor (III), trochlear (IV) and abducent (VI) nerves

The oculomotor, trochlear and abducent nerves carry somatic motor fibres to the
extraocular muscles. In addition, the oculomotor nerve carries parasympathetic fibres
that synapse in the ciliary ganglion and supply the pupillary and ciliary muscles. The
nuclei of the three nerves are in the periaqueductal grey matter of the upper (III) and
lower (IV) midbrain, and in the lower pons (VI).
The oculomotor nerve passes anteriorly through the midbrain, and emerges between
the cerebral peduncles; it passes through the posterior and middle cranial fossae
to divide into superficial and inferior branches near the supraorbital fissure. In the
posterior cranial fossa the nerve passes near the edge of the tentorium cerebelli. In
the middle cranial fossa the nerve pierces the cerebral layer of dura to pass forwards
on the lateral wall of the cavernous sinus. The superior division passes through
the superior orbital fissure and supplies the superior rectus and levator palpebrae
superioris. The inferior division supplies the medial and inferior recti, and inferior
oblique muscles. The nerve to inferior oblique gives the parasympathetic branch to the
ciliary ganglion.
The trochlear nerve is the thinnest cranial nerve. It passes posteriorly and undergoes
a dorsal decussation with its fellow of the opposite side caudal to the inferior colliculus.
The nerve then passes through the posterior and middle cranial fossae and enters the
orbit through the superior orbital fissure to supply the superior oblique muscle. In the
posterior cranial fossa, the nerve passes forward around the midbrain. In the middle
cranial fossa, it pierces the cerebral layer of dura, and lies between the oculomotor
and ophthalmic nerves in the lateral wall of the cavernous sinus. It passes through the
superior orbital fissure outside the tendinous ring and passes medially between levator
palpebrae superioris and the roof of the orbit, to reach and supply the superior oblique
muscle.
The abducent nerve leaves the inferior border of the pons near the midline, passing
forwards through the posterior and middle cranial fossae, the cavernous sinus and
the orbit to reach and supply the lateral rectus muscle. In the posterior cranial fossa
the nerve lies between the pons and the basilar part of the occipital bone and passes
over the apex of the petrous temporal bone, through the cavernous sinus lateral to the
internal carotid artery. It enters the orbit through the superior orbital fissure within the
tendinous ring.
Assessment
When examining the IIIrd, IVth and VIth cranial nerves, first check the extraocular
movements (LR6, SO4 provides a way of remembering the muscles supplied by the IVth
and VIth nerves). In addition, the IIIrd nerve is responsible for the pupillary responses
to light and accommodation, and eyelid elevation by the levator palpebrae superioris
(PERLA pupils react to light and accommodation). Note any squint or nystagmus.
Horizontal movements are brought about specifically by the lateral and medial recti
muscles, but other movements are more complex: upward and downward gaze should
be assessed in extremes of abduction and adduction (i.e. in H fashion). The eyes are
examined together but when abnormalities of conjugate gaze are present, or the patient
complains of diplopia, the eyes are examined independently.
With abnormalities of the IIIrd nerve, there is:

weakness of elevation and adduction (i.e. a divergent strabismus is present, the eye
looking downwards and outwards on forward gaze)
ptosis the patient is unable to elevate the eyelid (compared with retention of
voluntary lid-raising in Horners syndrome)
a dilated pupil non-reactive to light or accommodation, though the consensual light
reflex is retained
proptosis, as a result of muscular relaxation
diplopia.
In IVth nerve paralysis, there is torsion of the globe on downward gaze. The head may
be tilted to the opposite shoulder, so the patient can achieve binocular vision. Although
the superior oblique muscle directs the eye downwards and outwards, adduction is also
produced by the inferior rectus and the prime defect is that of intorsion (i.e. the patient
cannot look at the tip of their nose). Damage to the VIth nerve produces a convergent
strabismus, the patient is unable to abduct the eye and diplopia is a prominent feature.
The three nerves can be damaged by tumours within the orbit and the nasopharynx.
In lesions of the superior orbital fissure (Tolosa-Hunt syndrome) there is additional
damage to the ophthalmic division of the trigeminal nerve, producing pain. In the middle
cranial fossa, caroticocavernous fistulae and aneurysms of the internal carotid artery
may produce nerve damage, and in the posterior fossa, aneurysms, particularly of
the posterior communicating artery. The three nerves commonly provide important
signs in head injuries; in tentorial coning, the IIIrd nerve is first stimulated and then
progressively paralysed, the pupil becoming fixed and dilated. The IVth nerve is
damaged in reversed coning from expanding lesions in the posterior fossa. The effect
can be the result of direct nerve pressure on the lateral edge of the tentorium, or
posterior shift of the brainstem with pressure of the tentorium on the third and fourth
nerve nuclei in the midbrain. The VIth nerve can produce false localizing signs owing to
its long intracranial course.
Trigeminal nerve (V)
The trigeminal nerve is the largest cranial nerve. It emerges from the cerebellopontine
angle as a large sensory (general somatic) and a smaller motor (special visceral) root.
The roots pass over the apex of the petrous temporal bone to the trigeminal ganglion,
pushing a pouch of dura (Meckels cave) into the middle cranial fossa. The semilunar
(Gasserian) ganglion lies lateral to the cavernous sinus in the middle cranial fossa.
The ophthalmic, maxillary and mandibular divisions arise from the anteroinferior aspect
of the ganglion. The motor root, passing medial to the ganglion, joins the mandibular
division.
The ophthalmic division is the smallest. It lies in the lateral wall of the cavernous
sinus below the oculomotor and trochlear nerves. Near the superior orbital fissure, it
divides into lacrimal, frontal and nasociliary branches that pass through the fissure into
the orbit. The lacrimal nerve supplies the lacrimal gland (conveying parasympathetic
fibres from the zygomaticotemporal branch of the pterygopalatine ganglion), the upper
eyelid and the lateral conjunctiva. The frontal nerve divides into supraorbital and
supratrochlear branches, supplying the upper eyelid, medial forehead and the scalp
as far as the vertex. Only the nasociliary branch passes through the tendinous ring. It
divides into anterior ethmoidal and infratrochlear nerves, supplying the ethmoidal and
sphenoidal air sinuses, the upper eyelid and the adjacent nose. Long ciliary branches
carry sympathetic dilator pupillae fibres that pass through the ciliary ganglion.
The maxillary division passes forward, lateral to the cavernous sinus in the middle
cranial fossa to the pterygopalatine fossa to enter the inferior orbital fissure and
become the infraorbital nerve. The pterygopalatine ganglion is suspended from it in the
pterygopalatine fossa where it is also related to the terminal branches of the maxillary
artery. Through the ganglion, the maxillary nerve supplies sensory fibres to the lateral
nose and nasopharynx. The zygomatic nerves supply skin over the cheek and temple.
Posterior superior alveolar nerves supply the maxilla, and upper molar and premolar
teeth. The infraorbital nerve emerges through the infraorbital foramen on the face
to supply the lower eyelid and conjunctival side of the nose and upper lip. Its middle
and anterior superior alveolar branches, given off in the infraorbital canal, supply the
premolar, canine and incisor teeth, and the lateral wall of the nose and maxillary air
sinus.
The mandibular division leaves the middle cranial fossa through the foramen ovale to
lie between tensor palati and the lateral pterygoid muscles, with the otic ganglion on its
medial side. The surface marking of this opening is 4 cm medial and just anterior to the
neck of the mandible, the nerve may be anaesthetized using these relationships. The
motor branches supply the muscles of mastication, tensor tympani and tensor palati.
The sensory branches have a wide distribution to the meninges of the middle cranial
fossa, the skin and mucous membrane in the cheek, through the buccal nerve, the
temporal region of the scalp, tympanic membrane, external auditory meatus and
the anterior auricle through the auriculotemporal nerve. This nerve also carries
parasympathetic fibres from the otic ganglion, and sympathetic fibres from the plexus
around the middle meningeal artery, to the parotid gland. The inferior alveolar branch of
the mandibular nerve enters the mandibular foramen and passes along the mandibular
canal to supply the gums and teeth. The mental nerve emerges through the mental
foramen, and supplies the skin and mucous membrane of the lower lip, and gum. The
inferior alveolar nerve also carries motor fibres, that pass to the mylohyoid and anterior
belly of the digastric muscles, before the nerve enters the mandibular canal.
The largest branch of the mandibular nerve is the lingual, which is formed between
the tensor palati and lateral pterygoid muscles. It passes forward between the medial
pterygoid and ramus of the mandible, and under the mucous membrane, over the root
of the third lower molar tooth (an important relation for dental anaesthesia) and then
between hyoglossus and mylohyoid. On the hyoglossus, the lingual nerve is overlapped
by the submandibular gland and has the submandibular ganglion suspended from it.
The nerve supplies sensory branches to the anterior two-thirds of the tongue, the floor
of the mouth and the lingual gums. 3 cm below the base of the skull, the nerve is joined
by the chorda tympani branch of the facial nerve, carrying parasympathetic fibres;
these synapse in the submandibular ganglion and pass to the submandibular and
sublingual salivary glands, and taste fibres for the anterior two-thirds of the tongue.
Assessment
Examination of the three divisions is by assessment of sensation over the forehead,
cheek and lower jaw, together with the corneal reflex. Motor fibres are assessed by
palpation of the masseter and temporalis, on jaw-clenching, protrusion of the jaw by
the pterygoid muscles and the jaw jerk. The proximal divisions may be damaged by
caroticocavernous fistulas and aneurysms in the middle cranial fossa, and by fractures,
aneurysms, meningiomas, acoustic neuromas and other intracranial tumours in the
middle and posterior cranial fossa. Brainstem lesions such as vascular, tumours
and syringobulbia produce a bulbar palsy, and bilateral cortical lesions produce a
pseudobulbar palsy, affecting the motor component, and the nerve is subject to
trigeminal neuralgia. u

Cranial Nerves: Part II
John S P Lumley
John S P Lumley is Emeritus Professor of Vascular Surgery and Honorary Consultant

at St Bartholomew's Hospital, London, UK. He is past World President of the
International College of Surgeons. His main clinical and research interests relate to the
surgery of cerebrovascular diseases and microvascular surgery.
This article describes cranial nerves VIIXII. Cranial nerves IVI are described in
Anaesthesia and Intensive Care Medicine 3:3: 116.
Facial nerve (VII)

The facial nerve carries special visceral, and autonomic, motor and sensory fibres.
The special visceral motor fibres supply the muscles of the second pharyngeal
arch mesoderm, which are primarily those of facial expression, while the special
visceral sensory fibres carry taste from the anterior two-thirds of the tongue to the
tractus solitarius, they pass through the chorda tympani branch to the lingual nerve.
Parasympathetic fibres are secretomotor to the submandibular, sublingual and lacrimal
glands, and glands of the mucous membrane of the nose, pharynx and mouth,
branches passing via the pterygopalatine and submandibular ganglia.
Sensory (nervus intermedius) and motor roots leave the lower lateral surface of the
pons and enter the internal auditory meatus, passing to the geniculate (facial) ganglia.
The nervus intermedius also carries the parasympathetic fibres. The nerve turns
sharply posteriorly through a bony canal medial to the middle ear and then downwards,
related to the posterior aspect of the middle ear, through the temporal bone to emerge
at the stylomastoid foramen. The nerve then turns forwards into the parotid gland
where it divides into temporal, zygomatic, buccal, mandibular and cervical motor
branches, to supply facial muscles, buccinator and platysma.
The greater petrosal branch

The greater petrosal branch leaves the geniculate ganglion to pass through the petrous
temporal bone and middle cranial fossa to join the deep petrosal nerve (sympathetic
branches from the internal carotid plexus) and pass through the pterygoid canal to the
pterygopalatine ganglion.
The chorda tympani branch

The chorda tympani branch arises from the nerve in the temporal bone, just above
the stylomastoid foramen, and passes forward through the middle ear between the
tympanic membrane and the handle of the maleus. It passes forward through the
temporal bone to emerge from the petrotympanic fissure, to join the lingual nerve 3 cm
below the base of the skull.
Assessment
Motor function is assessed by facial symmetry (forehead wrinkles, nasolabial fold,
corner of mouth) and expression, and power of eye closure, whistling and blowing out
the cheeks actively and against resistance. Lower motor neuron damage produces
paralysis of the ipsilateral face, whereas in upper neuron damage, only the contralateral
lower face is paralysed, sparing the muscles of the forehead and eyebrow, which are
bilaterally innervated. Sensory examination is of taste over the anterior two-thirds of the
tongue.
The most common lower motor neuron lesion is Bells palsy, but the nerve may be
damaged by lesions and surgery of the parotid gland, basal skull fractures, Hunt's
syndrome, otitis media and tumours of the posterior cranial fossa, particularly acoustic
neuromas. Nuclear lesions include vascular, tumours, syringobulbia and multiple
sclerosis. Supranuclear lesions are primarily vascular or tumours. Bilateral facial
weakness may be part of a pseudobulbar palsy of vascular origin, Guillain-Barr
syndrome, bilateral parotid disease and skull fractures. The onset following a
skull fracture may be delayed owing to oedema, this has a better prognosis than
primary nerve damage. Isolated loss of taste is unusual, but may be related to middle
ear infection, damaging the chorda tympani.
Vestibulocochlear nerve (VIII)

This special somatic sensory nerve consists of vestibular fibres, concerned with
balance, and cochlear fibres, concerned with hearing. The latter originate in the organ
of Corti and pass in the bipolar cells of the spiral ganglia within the modiolus. Vestibular
fibres pass from the semicircular ducts, saccule and utricle to the bipolar cells in the
vestibular ganglion in the internal auditory meatus. The two components of the nerve
unite in the internal auditory meatus and pass medially to enter the cerebellomedullary
angle of the brainstem, to reach the nuclei in the floor of the fourth ventricle.
Assessment
Assessment of hearing includes examination of the external auditory meatus to identify
disease of the canal or eardrum, and the appreciation of soft noises, such as a watch
tick or a whisper. Rinnes test assesses whether air conduction of the sound of a clinical
512 Hz tuning fork is better than bony conduction of the base of the fork placed over
the mastoid process (the normal pattern). In Webers test sound transmission from the
base of the tuning fork placed in the centre of the forehead is transmitted equally to the
two ears (normal).
Deafness may be related to:
wax
infective and other diseases of the external auditory meatus, tympanic membrane
and middle ear
tumours, particularly acoustic neuromas and those of the skull base
toxicity (e.g. streptomycin and alcohol) and degenerative disease such as excess
environmental exposure
otosclerosis and bony abnormality (e.g. Pagets disease).
Abnormalities of balance are usually detected by the patients history and they may
be associated with nystagmus and vertigo. They may be caused by acute labyrinthitis,
Menires disease, drug toxicity and motion sickness, as well as trauma, and lesions of
the skull base and brainstem.
Glossopharyngeal nerve (IX)

General visceral sensory fibres arise from the pharynx, posterior third of the tongue,
the carotid sinus and carotid body, taste from the posterior third of the tongue and
parasympathetic fibres synapsing in the otic ganglia supplying the parotid and
pharyngeal glands.
The glossopharyngeal nerve carries special visceral motor fibres to the tylopharyngeus
muscle. The nerve rootlets leave the medulla lateral to the olive and the nerve passes
through the jugular foramen medial to the vagus and accessory nerves, descending
between the internal and external carotid arteries to enter the pharyngeal wall, between
the superior and middle constrictor muscles.
The tympanic branch of the nerve passes through the petrotympanic fissure to the
tympanic plexus in the middle ear, from whence lesser petrosal nerve fibres pass to
the otic ganglion, carrying parasympathetic fibres to the parotid gland. The sinus nerve
descends between the internal and external carotid arteries to supply the carotid body
and carotid sinus.
Isolated nerve damage is uncommon, but produces loss of sensation over the anterior
pillar of the fauces (gag reflex) and loss of taste from the posterior third of the tongue,
including the circumvalate papillae, and impairment of carotid sinus and carotid body
reflexes. The gag reflex is reduced with age. Lesions resemble those of the Xth nerve,
to which it is closely related intracerebrally.
Vagus nerve (X)

The vagus nerve has a more extensive distribution than any other cranial nerve. It
carries:
visceral motor fibres to the striatal muscle of the palate, pharynx and larynx
parasympathetic visceral motor and sensory fibres to the mucosa of the palate,
pharynx and larynx and to the heart, lungs and alimentary tract as far as the splenic
flexure
somatic sensory fibres to the posterior aspect of the external auditory meatus and
tympanic membrane, via its auricular branch
a few taste fibres.
The nerve is formed from a number of rootlets emerging lateral to the olive and leaves
the posterior cranial fossa through the internal jugular foramen, between the IXth
nerve medially and the XIth laterally. It has swellings within and just below the jugular
foramen; these ganglia are somatic and visceral sensory in nature. It lies posteriorly
in the carotid sheath as it descends through the neck and in the thorax, the two vagal
nerves pass posteriorly to each bronchus to form the pulmonary plexus and then
converge on the oesophagus to form the oesophageal plexus, and thence the anterior
and posterior vagal nerves (the left and right vagal trunks, respectively) for distribution
to the alimentary tract.
The various branches include pharyngeal, cardiac and pulmonary, together with two
constant branches to the larynx. The superior laryngeal nerve descends between the
pharynx medially and the internal carotid artery laterally. It divides below the hyoid bone
into the internal laryngeal nerve that pierces the hyoid membrane to supply the mucous
membrane of the larynx above the vocal folds, and the external laryngeal nerve, that
descends on the larynx to supply the cricothyroid muscle. The recurrent laryngeal
nerves hook round the subclavian on the right and the aortic arch on the left, to ascend
in the groove between the trachea and oesophagus, closely related to the thyroid
gland, entering the larynx deep to the inferior constrictor muscle to supply the mucous
membrane below the vocal folds and all the intrinsic muscles except the cricothyroid.
Assessment
The muscles of the palate are assessed by watching:
the uvula and palate rise when saying aah
the pharynx for evidence of regurgitation when swallowing a cup of water
the larynx by coughing and saying a high ee.
Clinically demonstrably abnormal signs are limited to the pharynx and larynx. Pareses
produces lateral displacement of the uvula, coughing and spluttering on swallowing,
implying fluid regurgitating into the larynx rather than passing down the oesophagus,
and a bovine cough because the vocal cords are not fully approximated. Bilateral
recurrent laryngeal nerve injuries may produce stridor and respiration obstruction.
The vagal nuclei lie on the medulla and are the dorsal motor and sensory
(parasympathetic) and the nucleus ambiguous (special visceral motor), taste fibres
pass to the nucleus of the tractus solitarius.
Lower motor neuron lesions are produced by tumours of the posterior fossa and around
the skull base, aneurysms, chronic meningitis and Guillain-Barr syndrome. Nuclear
abnormalities are produced by tumours, syringobulbia and motor neuron disease. The
bilateral pyramidal innervation requires bilateral lesions to produce a pseudobulbar
palsy, this is usually secondary to cerebrovascular disease.
Accessory nerve (XI)

This somatic motor nerve supplies sternomastoid and trapezius muscles, the fibres
having their nuclei in the upper five cervical segments of the cervical cord. The fibres
ascend through the foramen magnum to the posterior fossa, and the nerve leaves the
fossa through the jugular foramen, lateral to the IXth and Xth nerves. It then passes
laterally, anterior to the internal jugular vein and the transverse process of the atlas into
the substance of the sternomastoid, crossing the posterior triangle of the neck, over
levator scapulae, to reach the deep surface of the trapezius. Inside the posterior fossa,
the cranial root of the accessory nerve, carrying fibres from the nucleus ambiguus,
joins the accessory, but those fibres ultimately return to the vagus.
Examination of the nerve is by assessing the bulk of the trapezius and sternomastoid
muscles, asking the subject to turn the head to the opposite side against resistance,
and watching shoulder shrugging.
Lesions occur through trauma of the base of the skull, tumours of the posterior cranial
fossa and skull base, poliomyelitis, syringomyelia, motor neuron disease and Guillain-
Barr syndrome. The nerve may be damaged by trauma or surgery in the neck. These
muscles may also be involved in muscular dystrophies.
Hypoglossal nerve (XII)

The hypoglossal nerve provides the somatic motor supply to all the intrinsic and
extrinsic muscles of the tongue except palatoglossus. Its nucleus is situated in the
medulla in the floor of the fourth ventricle. The nerve emerges from the medulla
between the pyramid and the olive and leaves the posterior cranial fossa through the
hypoglossal canal, above the occipital condyle. It descends behind the carotid sheath,
then passes forwards round the pharynx between the internal carotid artery and the
internal jugular vein to cross in turn the internal and external carotid arteries, the
loop of the lingual artery on the middle constrictor, and the hyoglossus muscle. It is
covered laterally by the posterior belly of the digastric, the submandibular gland and the
mylohyoid muscle. The hypoglossal nerve also receives branches from the first cervical
nerve near the base of the skull and conveys these fibres to the geniohyoid and
thyrohyoid muscles, they then form the descendens hypoglossi nerve which supplies
the infrahyoid muscles through the ansa hypoglossi.
In lower motor neuron lesions, the tongue is observed for wasting, weakness, and
fasciculation and dysarthria: the tongue is protruded towards the side of a lesion.
Upper motor neuron defects are unusual in view of the bilateral innervation, but may
occur in vascular diseases. Nuclear lesions are seen in motor neuron disease, tumours,
thrombosis of the vertebral artery, syringobulbia and lower motor neuron lesions due
to tumours and aneurysms of the posterior cranial fossa, trauma, chronic meningitis,
Arnold-Chiari malformation, poliomyelitis and the Guillain-Barr syndrome.
Parasympathetic cranial ganglia
Whereas the sympathetic nerve fibres relay in a proximally placed series of ganglia
in the sympathetic chain (T1L2), the ganglia of the parasympathetic system
(craniosacral) are sited near the organs they innervate. There are four well-defined
cranial ganglia: the ciliary, pterygopalatine, submandibular and otic (Figure 1).
Parasympathetic ganglia related to the trigeminal nerve

Ciliary ganglion
The ciliary ganglion is the smallest and the size of a pin head; it is situated between
the optic sheath and the lateral rectus muscle, near the apex of the orbital cavity. It is
usually lateral to the ophthalmic artery.
The parasympathetic fibres arise in the EdingerWestphal nucleus in the midbrain and
are carried by the short ciliary nerves to the back of the eyeball to supply the sphincter
pupillae and ciliary muscles.
Sympathetic fibres from the superior cervical ganglion reach the ciliary ganglia via the
plexus on the ophthalmic artery and pass without synapse to the blood vessels and
smooth muscle of the eyeball.
Sensory fibres pass without relay through the ganglia to the eyeball, reaching the ciliary
ganglion through the long ciliary branches of the nasociliary nerve.
Pterygopalatine (sphenopalatine) ganglion

The pterygopalatine (sphenopalatine) ganglion is the largest of the peripheral
parasympathetic ganglia. It is situated in the pterygopalatine fossa suspended from the
maxillary nerve receiving afferent and efferent branches from it.
Parasympathetic fibres originate in the VIIth nerve nuclei, leaving the nerve in the
temporal bone as the greater petrosal nerve. This receives sympathetic fibres from
around the internal carotid artery as the deep petrosal nerve, to form the nerve of the
pterygoid canal that passes to the ganglion. The numerous branches of the ganglion,
including nasal, nasopalatine and pharyngeal, are primarily derived from the maxillary
nerve but carry postsynaptic secretomotor fibres to the palate, pharynx and nasal
glands, and also via the connection to the zygomatic frontal nerve to the lacrimal gland.
Sympathetic fibres are similarly distributed to the smooth muscle of the blood vessels of
the palate, pharynx and nose.
Submandibular ganglion
The submandibular ganglion lies on the hyoglossus muscle, suspended from the lingual
nerve by afferent and efferent branches, and above the deep part of the submandibular
gland. Its parasympathetic fibres originate in the seventh nerve, and pass with the
taste fibres via the chorda tympani nerve. Parasympathetic fibres originate in the
superior salivary nucleus in the midbrain and the taste fibres in the tractus solitarius.
Postsynaptic parasympathetic fibres pass via the lingual nerve and direct branches
to the submandibular, sublingual and other oral glands, accompanied by sympathetic
fibres derived from the superior cervical ganglion and reaching the submandibular
ganglion via the facial artery.
Otic ganglion
The otic ganglion lies between the tensor palati muscle laterally and the auditory tube
medially, with the middle meningeal artery posteriorly. It is closely related to the nerve
to the medial pterygoid muscle.
Parasympathetic fibres are derived from the inferior salivary nucleus of the IXth nerve,
passing through the foramen ovale to the otic ganglion. Efferent fibres pass via the
auriculotemporal nerve to the parotid gland.
Sympathetic fibres derived from the superior cervical ganglion pass via the plexus
on the middle meningeal artery and through the otic ganglion without synapse, to be
distributed to the blood vessels of the parotid gland. u

The Cubital Fossa
John Craven
cancer.
The cubital fossa is a triangular hollow area that lies in front of the elbow joint. It is
bounded (Figure 1):
superiorly by an imaginary line connecting the medial and lateral epicondyles
medially by the pronator teres muscle
laterally by the brachioradialis muscle.
Cubital fossa with superficial veins and deep

fascia removed
1
Its floor is formed of the brachialis and supinator muscles overlying the capsule of the
elbow joint. The deep fascia of the forearm forms its roof, which is strengthened by
fibres of the bicipital aponeurosis. Lying on the roof in the superficial fascia are the
anterior branches of the medial and lateral cutaneous nerves of the forearm and the
median cubital vein which joins the cephalic and basilic veins.
The cephalic, basilic and median cubital veins are usually easily seen and palpated
in the roof of the fossa, and this is therefore a common site for venepuncture. It is worth
noting that variations in venous anatomy at this site are common (Figure 2). The use of
the cubital fossa for intravenous fluid therapy is not recommended because movement
of the elbow joint disturbs the cannula and irritates the vein wall with the consequence
that thrombosis of the vein quickly occurs.
The contents of the fossa from medial to lateral are:
median nerve
brachial artery and its terminal branches, the radial and ulnar arteries
biceps tendon and bicipital aponeurosis (which separates the median cubital vein
from the brachial artery)
radial and posterior interosseous nerves, which are often overlapped by the fibres
of brachioradialis.
The brachial artery is palpated here when the arterial pressure is being taken by a
sphygmomanometer but, because of the bicipital aponeurosis, the elbow should be
fully extended so that the artery is pressed back on to the elbow joint, which renders
palpation a little easier. The brachial artery is in close relation to the medial nerve,
which lies on its medial side. Awareness of this relationship should minimize the
incidence of nerve trauma during arterial puncture for blood sampling or the insertion
of arterial catheters for cardiac or other investigations. Rarely, the cubital fossa is used
for distal nerve blocks.
The median nerve can be anaesthetized by injecting 5 ml of local anaesthetic
solution through a weal raised midway between the outer side of the tendon of biceps
and the medial epicondyle. This anaesthetizes the lateral half of the palm and fingers.

The Diaphragm, its Action and
Innervation
John Craven
cancer.
The diaphragm is a musculotendinous septum that separates the abdominal and

thoracic cavities. It has a peripheral muscular portion, which attaches to its central
tendon. It is attached peripherally to:
the sternum by two muscular slips from the back of the xiphoid process
the ribs from the inner surfaces of the lower six ribs and costal cartilage where its
fibres interdigitate with fibres of transversus abdominis
the upper lumbar vertebrae.
It is attached to the sides of the upper lumbar vertebrae by two crura and from the
medial and lateral arcuate ligaments on each side. The right crus attaches to the first
three vertebral bodies and the left crus to the first two. The right crus is the larger and
passes forwards and to the left, surrounding the oesophageal opening.
The medial arcuate ligament, the thickened upper edge of the psoas fascia extends
in front of the psoas from the body of the first lumbar vertebra to its transverse
process. The lateral arcuate ligament lies anterior to the quadratus lumborum attached
between the transverse process of the first lumbar vertebra and the 12th rib. The central
attachment of the diaphragm is to the margins of a trilobed central tendon.
Nerve supply
The right and left phrenic nerves (C3,4,5) supply the corresponding halves of the
diaphragm.
The right phrenic nerve descends on the lateral wall of the right brachiocephalic vein
then on the pericardium over the superior vena cava, the right atrium and the inferior
vena cava before passing through the caval opening of the diaphragm. It is covered
throughout its course by the mediastinal pleura.
The left phrenic nerve enters the thorax between the left subclavian artery and the
left brachiocephalic vein and descends to cross the aortic arch and the pericardium
over the left ventricle. It too is covered laterally by the mediastinal pleura.
Both nerves also supply sensory fibres to the central part of the diaphragm,
the mediastinal and diaphragmatic pleura, the pericardium and the diaphragmatic
peritoneum. The peripheral part of the diaphragm receives sensory fibres from the
lower intercostal nerves.
Pain from inflammation of the diaphragmatic pleura or peritoneum may be referred
to the ipsilateral shoulder tip, the cutaneous area which is innervated by the
supraclavicular nerves, mainly originating like the phrenic nerve, from the C4 segment
of the spinal cord.
Openings in the diaphragm
There are three openings in the diaphragm (Figures 1 and 2). From the posterior, they
are for the aorta, oesophagus and inferior vena cava.
The opening for the aorta lies between the crura of the diaphragm in front of the 12th
thoracic vertebra, which also transmits the thoracic duct and the azygos vein.
The opening for the oesophagus lies within the right crus at the level of the 10th
thoracic vertebra, which also transmits the anterior and posterior gastric branches of
the vagus nerves and the oesophageal branches of the left gastric vessels.
The opening for the inferior vena cava lies to the right of the midline within the
central tendon, which also transmits the right phrenic nerve.
Inferior view of the diaphragm
Level of the diaphragmatic openings
2
Relationships
The heart and lungs lie within the pericardial and pleural sacs, respectively, on the
upper surface of the diaphragm. The pericardium is adherent to the central tendon.
Below the diaphragm on the right side are the liver, the right kidney and suprarenal
gland and, on the left, the fundus of the stomach, spleen, left kidney and suprarenal
gland.
Respiration
Inspiration and expiration are produced by increasing or decreasing the volume of the
thoracic cavity. Quiet respiration is produced by diaphragmatic action alone.
Inspiration
The diaphragm contracts and descends, the first rib is fixed by the scalene muscles
and the external intercostals elevate and evert the succeeding ribs which increases
the anteroposterior diameter of the upper chest and, by elevating the costal margin,
increases the transverse diameter of the lower chest. Forced inspiration is achieved
by fixing the shoulder girdle, which allows serratus anterior and the pectoral muscles
to raise the ribs.
Expiration
Expiration is produced mainly by recoil of the lung tissue and the costal cartilages but
simultaneous contraction of the abdominal wall muscles forces the diaphragm upwards,
an action that is exaggerated in forced expiration.

Eye and Orbit
Hari Jayaram
Hari Jayaram is a Basic Surgical Trainee in Ophthalmology. He qualified from the

Universities of Cambridge and Oxford and is currently working in the Department of
Neurosurgery at the National Hospital, Queen Square, London.
Anatomy
Orbit: each orbit is pyramidal in shape with its base anteriorly and its apex
posteromedially directed towards the optic canal. The average dimensions are 40
mm wide, 35 mm high and 25 mm deep. The angle between both lateral walls is 90
and between lateral and medial walls of the same side is 45 (Figure 1). The medial
walls are almost parallel to the sagittal plane. Needles introduced in this plane travel
a greater distance towards the orbital apex and can potentially cause more damage,
compared with those inserted laterally along the orbital wall.
Angular relationships of medial and lateral

orbital walls

Globe: the globe is located anteriorly within the orbit in a superolateral position; its
dimensions vary. Myopic eyes are longer with thin sclera, and are at greater risk of
needle perforation. An axial length over 26 mm should hazard caution. A socket is
formed by Tenons capsule, which extends from the optic nerve meninges posteriorly
to within millimetres of the corneoscleral limbus anteriorly. This layer is pierced by the
extraocular muscle tendons, which pass to insert into the sclera. The globe itself has
three layers. The outermost fibrous sclera which envelops the globe except the anterior
transparent cornea, the vascular pigmented layer (choroid, iris and ciliary body) and the
innermost sensory retina. The conjunctival mucosa lines the inner surface of the eyelids
and the anterior aspect of the eyeball.
Orbital apex: the four recti muscles arise from a common tendinous ring formed from
periosteum at the orbital apex, which lies medial to the globe. This ring encloses the
optic canal and the medial portion of the superior orbital fissure. The cone formed by
the recti muscles passing towards the globe, helps define an incomplete extraconal
(peribulbar) and intraconal (retrobulbar) space (Figure 2). The relationship of the
important anatomical structures to this muscular cone is shown in Figure 3.
Conal space and fibrous septa
Orbital apex

Fibrous septa: there is no strict anatomical separation of the extraconal and intraconal
spaces. A matrix of connective tissue gives support, allows dynamic function and
controls the spread of injectate within fibro-adipose compartments (Figure 2).
Blood vessels: the main supply is from the ophthalmic artery. This is a branch of
the internal carotid after it emerges from the cavernous sinus. It initially lies within the
subarachnoid space, but pierces the optic nerve sheath meninges after leaving the
optic canal. It first runs inferiolateral to the nerve, but then moves above and towards
the superomedial orbit with a tortuous course. Behind the medial upper lid, the facial
and supraorbital veins pass posterolaterally as the superior ophthalmic vein. The
venous plexus on the anterior orbital floor contributes to the inferior ophthalmic vein.
Nerves: the abducent nerve supplies lateral rectus, trochlear nerve supplies superior
oblique and the other muscles are supplied by the oculomotor nerve, which also gives
a branch to the upper lid levator. The skin and conjunctiva of the upper lid are supplied
by the lacrimal and frontal branches of V1 (extraconal), and those of the lower lid by the
infraorbital nerve (terminal branch of V2). The nasociliary division of V1 gives branches
to the ciliary ganglion, medial aspect of eyelid skin and conjunctiva, ciliary body and
cornea.
Lacrimal gland is located in the superolateral orbit. Drainage is via superior and
inferior puncta near the medial lid margins. Each punctum leads to the respective
canaliculus, which passes medially to the lacrimal sac. This drains via the nasolacrimal
duct to the inferior meatus of the nose. Injection between the caruncle and canthal
fold will avoid these structures, and anaesthetize the medial aspect of the eyelids and
cornea.
Anaesthesia
Injection into avascular regions such as the medial or preferably inferolateral
compartment, can provide adequate regional anaesthesia while minimizing
complications. The superomedial compartment must be avoided, because of the risk
of damaging the vasculature, muscles and optic nerve at the orbital apex. Current
guidelines suggest the use of fine, short needles (25 mm or less), though the issue of
blunt versus sharp is still being debated. u
FURTHER READING
Rubin A P. Complications of Local Anaesthesia for Ophthalmic Surgery. Br J Anaesth
1995; 75: 936.
Snell R S, Lemp M A. Clinical Anatomy of the Eye. 2nd ed. Oxford: Blackwell Science,
1998.
The Royal College of Anaesthetists and The Royal College of Ophthalmologists. Local
Anaesthesia for Intraocular Surgery, 2001.

The Great Vessels of the
Thorax, Abdomen and Neck
John Craven
cancer.
Aorta
The aorta arises from the left ventricle and ascends for a short distance before arching
backwards to descend through the thorax and abdomen.
The ascending aorta ascends to the right from the aortic orifice to the sternal angle.
It is about 5 cm long and lies within the fibrous pericardium in a sheath of serous
pericardium directly behind the sternum. Above each of the semilunar valvules of the
aortic valve is an aortic sinus the right and left coronary arteries arise from the
anterior and left posterior sinuses.
The arch of the aorta ascends from the sternal angle and arches backwards and
leftwards over the root of the left lung before descending to the left side of the fourth
lumbar vertebra. On its left side lie the phrenic and left vagus nerves under the
mediastinal pleura and on its right side, from front to back lie the superior vena cava,
right phrenic nerve, trachea, oesophagus, thoracic duct and the body of the fourth
thoracic vertebra. It has the following branches.
The brachiocephalic artery ascends to behind the sternoclavicular joint to divide into
the right subclavian artery and right carotid artery.
The left common carotid artery ascends the neck to divide into the internal and
external carotid arteries at the upper border of the thyroid cartilage.
The left subclavian artery ascends to the neck, lateral to the oesophagus and
trachea and medial to the left pleura.
The descending aorta descends in the posterior mediastinum inclining medially from
the left side of the fourth thoracic vertebra behind the root of the left lung to the front of
the twelfth thoracic vertebra where it passes through the diaphragm. It is in contact with
the left pleura throughout its course. It has the following branches:
third to eleventh posterior intercostal arteries and the subcostal artery
small bronchial branches
small oesophageal branches.
Severe deceleration trauma, for example, in a car crash, can cause injury to the aorta.
The arch of the aorta is relatively fixed by its branches but the more mobile descending
part continues to travel forwards during severe deceleration, producing a shearing force
and tearing at the junction. lf the adventitia remains intact, a false aneurysm is caused,
resulting in mediastinal widening which is visible on radiography. Urgent surgical attention
must be sought.
The abdominal aorta enters the abdomen between the two crura of the diaphragm
in front of the twelfth thoracic vertebra and descends on the posterior abdominal wall
slightly to the left of the midline. On its left side is the inferior vena cava. It is surrounded
by networks of autonomic nerves and ganglia, lymph vessels and nodes. Anteriorly it
is covered by the lesser sac, pancreas, duodenum and small intestine. It ends on the
body of the fourth lumbar vertebra by dividing into two common iliac arteries. It has
the following branches.
The coeliac trunk arises above the pancreas. Its three branches (the left gastric,
common hepatic and right gastric arteries) supply the lower oesophagus, stomach,
duodenum, liver, pancreas and gallbladder.
Superior mesenteric.
Inferior mesenteric.
Paired branches: the suprarenal, renal and gonadal arteries supply their respective
organs.
Parietal branches: the four pairs of lumbar arteries supply the posterior abdominal
wall and spinal cord.
Terminal branches: the two common iliac arteries each descend without branches
away from the midline to divide into internal and external iliac arteries anterior to the
sacroiliac joint. The external iliac artery continues to descend and passes below the
midpoint of the inguinal ligament to form the femoral artery. The internal iliac artery
passes backwards, anterior to the internal iliac vein, to provide branches to the pelvic
viscera, perineum and buttock.
Vena cava
The superior vena cava is a wide vessel about 7 cm long formed by the union of
the two brachiocephalic veins at the right border of the manubrium. It descends behind
the sternum to enter the right atrium at the level of the third right costal cartilage. It
has no valves. Its lower half is covered by fibrous and serous pericardium and on its
lateral side lies the right pleura and phrenic nerve. The azygos vein is its only tributary,
entering it posteriorly (Figure 1).
Structures seen in a cross-section of the

mediastinum at the level of the fourth thoracic
vertebra

The brachiocephalic veins are formed behind the sternoclavicular joints by the union
of the corresponding internal jugular and subclavian veins. The right brachiocephalic
vein is 3 cm long and descends behind the right border of the manubrium. The right
phrenic nerve lies on its lateral surface. The left brachiocephalic vein, about 6 cm long,
descends obliquely behind the manubrium above the arch of the aorta and anterior to
its branches.
Tributaries from the neck muscles, the thyroid and the anterior chest wall enter both
veins and the thoracic duct enters the origin of the left brachiocephalic vein.
The internal jugular vein arises at the jugular foramen on the base of the skull and
descends the neck within the carotid sheath lateral to the internal carotid artery. The
deep cervical lymph glands lie closely applied to the vein. It receives tributaries from the
pharynx, larynx and thyroid and the common facial vein (Figure 2).
The veins of the neck
Superficial temporal
Maxillary vein
Posterior auricular
Retromandibular
Facial
Common facial
Internal jugular
External jugular
Anterior jugular
2
The subclavian vein is the continuation of the axillary vein, beginning at the outer
border of the first rib. It joins the internal jugular vein behind the sternoclavicular
joint. Central venous catheterization is an important clinical technique widely used to
measure central venous pressure, to administer rapid fluid replacement and for long-
term administration of chemotherapy and intravenous feeding (Figure 3).
3
The inferior vena cava formed in front of the body of the fifth lumbar vertebra by the
union of the two common iliac veins ascends the posterior abdominal wall, to the right
of the midline through the caval opening of the diaphragm. It has a short intrathoracic
course before it opens into the right atrium. The right sympathetic trunk lies behind
it. Anteriorly it is covered by the parietal peritoneum below and is crossed by the
pancreas and duodenum. Superiorly it lies behind the right lobe of the liver in which it is
embedded. The aorta is in contact with its left side.
Right and left common iliac veins are formed anterior to the sacroiliac joints by
the union of the internal and external iliac veins. They each ascend obliquely to join
their fellow to the right of the body of the fifth lumbar vertebra.
The internal iliac vein is formed by tributaries draining the venous plexuses which
drain the pelvic viscera. Both veins lie behind their arteries.
The external iliac vein is the proximal continuation of the common femoral vein
which enters the abdomen under the inguinal ligament medial to its artery.
In the case of total occlusion of the inferior vena cava by thrombus or tumour,
extensive oedema of the lower body follows. A collateral circulation develops between
tributaries of the inferior vena cava which include the superficial and inferior epigastric
veins. These convey the blood to the thoraco-epigastric and superior epigastric veins
and thence to the superior vena cava. This collateral flow is evident as tense and
tortuous veins visible over the trunk
Great vessels of the neck
Arterial blood supply

The head, neck and upper limbs are supplied by the three large branches of the
aortic arch: the innominate, and the left carotid and subclavian arteries (Figure 4). The
innominate artery divides into the right common carotid and right subclavian arteries:
the common carotid arterial supply to the head and neck is supplemented by the
vertebral branch of each subclavian artery, arising as this vessel passes over the apex
of the lung.
Each common carotid artery ascends through the neck from behind the
sternoclavicular joint and divides into its terminal (and only) branches, the internal and
external carotid arteries, lateral to the upper border of the thyroid cartilage (fourth
cervical vertebra). The artery lies within the fascial carotid sheath, accompanied by and
medial to the internal jugular vein, with the vagus lying between and posterior to both.
The left common carotid artery in the thorax lies between the innominate,
anteromedially, and the left subclavian artery, posterolaterally; the trachea, oesophagus
and recurrent laryngeal nerve lie posteromedially. Anterolaterally, the common carotid
is covered by the pleura, the left lung and the thymic remnant. The left phrenic and
left vagus nerves descend anterior to the artery, and the vessel is crossed by the left
brachiocephalic vein.
Each common carotid artery in the neck lies on the transverse processes of the
fourth to the sixth cervical vertebrae, separated by the prevertebral muscles and the
sympathetic chain. Medially are the trachea and larynx and behind this, the oesophagus
and pharynx, with the recurrent laryngeal nerve descending in the groove between
these structures. The lateral lobe of the thyroid gland overlaps the proximal common
carotid artery in the neck. The artery is overlain by the sternomastoid muscle with
its deep fascial coverings: the platysma and skin become direct relations of the distal
common carotid above the medial border of the sternomastoid. The common carotid
artery is crossed anteriorly by the superior belly or the intermediate tendon of the
omohyoid muscle, and the inferior thyroid and common facial veins.
Great vessels

The internal carotid artery of each side continues distally from the carotid bifurcation
to the base of the skull. It passes through the latter within the carotid canal of the
petrous temporal bone and within the dural coverings of the cavernous sinus, before
piercing the dural roof and dividing into its middle and anterior cerebral terminal
branches. It gives off the ophthalmic artery in its intracavernous portion.
In the neck, the posterior relations are similar to those of the common carotid artery
with the transverse process of the upper three cervical vertebrae, the prevertebral
muscles and the sympathetic chain posteriorly, the internal jugular vein laterally, with
the vagus posteriorly between them, and the pharynx medially. The proximal internal
carotid artery is covered with deep investing fascia, platysma muscle and skin, but it is
crossed by the hypoglossal nerve and then the posterior belly of the digastric, with the
occipital artery below and the posterior auricular artery above the muscle.
As the internal carotid artery approaches the skull base, the styloid process and
the attached muscles lie anterolaterally. The stylopharyngeus, accompanied by the
glossopharyngeal nerve, pass between the internal and external carotid arteries.
The external carotid artery is at first medial to the internal, but then becomes anterior
and lateral, and also crossed by the hypoglossal nerve, the posterior belly of the
digastric muscle and adjacent arteries. As it ascends laterally it reaches and passes
through the carotid sheath and thence through the substance of the parotid gland,
anterior to the facial nerve, dividing within the gland into terminal, superficial, temporal
and maxillary branches, respectively passing to the scalp and pterygoid regions. Other
branches are the superior thyroid, passing to the superior pole of the lateral lobe of the
thyroid gland, an inconstant ascending pharyngeal, a lingual branch to the tongue, a
facial branch and the occipital.
The distal end of the common carotid artery is expanded to form the carotid sinus
and this may also include the origin of the internal carotid artery. The adventitia of the
sinus contains stretch receptors, and these pressure-sensitive baroreceptors provide
a rapid mechanism for responding to changes in blood pressure. They are innervated
by the carotid sinus branch of the glossopharyngeal nerve descending medial to
the internal carotid artery. The nerve also supplies to the carotid body, a vascular
chemoreceptor situated posterior to the distal common carotid or external carotid
artery. The receptor is stimulated by hypoxia, hypercapnia or increased hydrogen ion
concentration, producing reflex increase in the rate and volume of ventilation.
The vertebral artery arises from the superoposterior aspect of the first part of the
subclavian artery, as it arches over the apex of the pleura, lung and suprapleural
membrane. It passes between the prevertebral muscles to enter the transverse process
of the sixth cervical vertebra and ascends through the canal in the proximal six
transverse processes, accompanied by its vein. It turns medially over the posterior arch
of the atlas to pierce the cervical dura and enter the posterior fossa, joining its fellow on
the opposite side to form the basilar artery.
The internal jugular vein

The main venous drainage of the head and neck is through the internal jugular vein.
Additional superficial contributions come from the anterior jugular vein over the anterior
aspect of the neck (passing laterally deep to the sternomastoid to enter the internal
jugular) and the external jugular vein passing from the angle of the jaw superficially
over the sternomastoid muscle to pierce the deep fascia and enter the subclavian vein
behind the midpoint of the clavicle.
The internal jugular vein is the continuation of the sigmoid sinus, commencing at the
jugular foramen in the occipital bone, and descending vertically in the neck to terminate
behind the medial end of the clavicle, joining the subclavian vein to form the right or left
innominate vein. A slight dilatation near its termination contains a pair of valves.
The relations of the internal jugular vein in the neck are similar to those of the
common and internal carotid arteries. It lies lateral to them within the carotid sheath,
with the vagus nerve between and posterior to both.
The internal jugular vein is related posteriorly to the tips of the transverse processes
of the first to sixth cervical vertebrae and the attached muscles, their covering
prevertebral fascia and the cervical sympathetic chain. Posteromedially are the rectus
capitus and prevertebral muscles, while posterolaterally are the attachments of levator
scapulae and the scalenus anterior muscles. The latter overlies the scalenus medius
with the roots of the cervical and brachial plexuses between. The phrenic nerve passes
on to the anterior surface of scalenus anterior and descends across the muscle deep
to the internal jugular vein. It is at this site it is approached surgically, and may
be damaged in approaches to the subclavian and common carotid arteries, or the
sympathetic chain.
Inferiorly, the internal jugular vein passes anterior to the first part of the subclavian
artery and its thyrocervical trunk, together with the vertebral vein, and either the right
mediastinal lymph trunk or the thoracic duct.
The internal jugular vein lies lateral to the internal and common carotid arteries, and
at the skull base is related to the last four cranial nerves. The twelfth passes medially,
anterior to the internal carotid artery, the eleventh passes laterally anterior to the
internal jugular vein, the tenth descends in the carotid sheath posterior to those vessels,
and the ninth passes medially between the internal and external carotid arteries.
The sternomastoid muscle overlies the anterior and lateral surfaces of the internal
jugular vein with the superior belly of the omohyoid muscle and the anterior jugular vein
passing between them. The descendens hypoglossi descends over the anterior aspect
of the interior jugular vein before turning laterally to become the ansa hypoglossi. The
deep cervical lymph nodes are grouped around the vessel, the cranial nodes lying more
medially and termed the retropharyngeal nodes, and in the lower neck a more laterally
placed group is termed the supraclavicular nodes.
The tributaries of the internal jugular vein are the inferior petrosal sinus, and the
facial, laryngeal, pharyngeal, and superior and middle thyroid veins, together with the
right mediastinal lymph trunk or, on the left side, the thoracic duct.
The common carotid artery and internal jugular vein provide important sites
of vascular access. The common carotid artery runs distally from behind the
sternoclavicular joint towards the angle of the jaw, and can be palpated or compressed
on the transverse processes of the fourth and sixth cervical vertebrae. This is either
through, or above, the sternomastoid muscle.
The internal jugular vein, lying lateral to the common and internal arteries, runs over
the tips of the transverse processes, the transverse mass of the atlas being palpated
deeply between the angle of the jaw and the mastoid process. If the artery is not
palpable the surface marking of the internal jugular vein is from the earlobe to the
medial end of the clavicle. A constant and useful site of access to the lower internal
jugular vein is between the sternal and clavicular heads of the sternomastoid muscle.
The jugular venous pressure can be observed within the internal jugular vein by
rotating the head to the opposite side and appropriate positioning of the trunk. The level
can be modified by deep breathing and a Valsalva manoeuvre.

Anatomy of the Heart
Anatomy of the Heart
cancer.
The heart is a cone-shaped organ that lies obliquely in the mediastinum within the
pericardial sac, suspended by the large vessels (Figure 1). Its four chambers, the
left and right atria, and the left and right ventricles are demarcated on its surface
by coronary and interventricular sulci. Its square base lies posteriorly and is formed
largely of the left atrium, which receives the four pulmonary veins at each corner. The
inferior vena cava enters the right atrium at its right postero-inferior angle, which rests
on the central tendon of the diaphragm; the superior vena cava enters the upper part
of the atrium.
Position of the heart
The right border lies 2 cm from the sternal edge

between the 3rd and 6th right costal cartilages; the 2 cm
inferior border lies between the latter point and the 5th Pulmonary valve
left interspace in the midclavicular line. A line from this 2 cm
Aortic valve
point to the 2nd left costal cartilage, 2 cm from the A P
sternal edge, defines the left border. The valves Mitral valve
(pulmonary, aortic, mitral and tricuspid) lie obliquely Tricuspid valve
behind the sternum. However, their sounds are best
heard at the auscultatory areas over the chamber or T
X
vessel into which blood is pumped (P, A, M, T,
M
respectively). An intracardiac injection can be made Y
through the medial aspect of the 5th intercostal space
(X). Pericardial aspiration, in cases of effusion or
tamponade, can be achieved by a needle inserted
alongside the xiphisternum (Y), which is directed deep
to the sternum towards the left shoulder
The right atrium is a thin-walled chamber. It forms the right border of the heart and
has a small projection, the right auricle, overlapping the origin of the ascending aorta
(Figure 2). Its posterior wall behind the caval openings is smooth and marked by a
shallow depression, the fossa ovalis, which is the remnant of the fetal opening.
Interior of the right atrium and right ventricle
Aortic arch
Superior vena cava
Pulmonary trunk
Pulmonary
Right auricle orifice
Pulmonary
valve
Fossa ovalis comprising
three
Coronary semilunar
sinus valvules
Opening of
inferior
vena cava
Tricuspid valve
Septal tendinous
cords
Papillary muscles with
tendinous cords
The right ventricle is a thick-walled chamber that projects to the left of the right
atrium forming part of the hearts anterior and inferior surfaces. The interventricular
septum separates the right from the left ventricle and bulges into the right cavity, making
it crescentic in cross-section. The atrioventricular (AV) orifice lies postero-inferiorly
guarded by the tricuspid valve, comprising three cusps each consisting of thin fibrous
tissue covered on both sides by endocardium. The atrial surfaces of the cusps are
smooth and the ventricular surfaces are rough and anchored to the ventricular walls
by tendinous cords arising directly from the septum or from two papillary muscles. The
muscles tighten the cords during ventricular contraction and thereby prevent eversion of
the cusps into the atrial cavity. The pulmonary orifice is a fibrous ring lying at the upper
end of the ventricle, the infundibulum. A valve, comprising three semilunar valvules lies
at the entrance to the orifice.
The left atrium is a thin-walled chamber that lies behind the right ventricle and forms
most of the base of the heart. Superiorly, the left auricle, a small projection, overlies
the origin of the pulmonary trunk. The four pulmonary veins enter each corner of the
posterior wall. Their orifices possess no valves. The left AV orifice lies in the anterior
wall. The posterior wall of the left atrium is separated from the oesophagus and the left
bronchus by the pericardial sac.
The left ventricle extends forwards and to the left from the left atrium, and lies mainly
behind the right ventricle. It forms the apex, the left border and surface, and part of the
anterior and inferior surfaces of the heart. Its walls are thick and surround a conical
cavity with two orifices, the left AV orifice posteriorly and the aortic orifice superiorly.
The left AV orifice is guarded by the mitral (bicuspid) valve, the two cusps of which
are attached to a fibrous ring surrounding the orifice. The free margins of the cusp are
anchored to papillary muscles on the ventricular wall by tendinous cords. The aortic
orifice is a fibrous ring guarded by a valve of three semilunar valvules similar to the
pulmonary valve. The thick interventricular septum is marked on the surface by anterior
and posterior interventricular sulci; the right ventricle lies anterior to the left ventricle.
Blood supply
The right coronary artery arises from the anterior aortic sinus just above the aortic
valve, and descends in the right coronary sulcus on the anterior surface and crosses
the posterior surface of the heart to anastomose with the left coronary artery (Figure 3).
It supplies atrial and ventricular branches, and a larger posterior interventricular artery,
which anastomoses with the anterior interventricular artery.
The left coronary artery arises from the left posterior aortic sinus and, in the left
coronary sulcus supplies atrial, ventricular branches, and the important anastomotic
vessels, the anterior interventricular artery and the circumflex artery. The latter
anastomoses with the right coronary artery. Generally, the right ventricle is supplied
by the right coronary artery, the left ventricle by the left coronary artery and the
interventricular septum by both.
Veins accompany the major arteries and most drain via the coronary sinus, which
is formed at the left border of the heart as a continuation of the great cardiac vein. It
lies in the posterior coronary sulcus and enters the right atrium above and posterior to
the orifice of the inferior vena cava.
Arterial supply of the heart

Circumflex
artery
Left coronary artery
Right coronary
artery
Marginal branch of
the right coronary artery
Posterior interventricular artery
Anterior interventricular artery
Marginal branch of left coronary artery
3
Nerve supply
The nerve supply is by vagus and sympathetic fibres through the cardiac plexus. The
fibres are distributed with the coronary vessels. Parasympathetic ganglion cells are
found in the heart walls. Sensory fibres subserving reflex activity pass in the vagus and
pain fibres in the spinal nerves (T13).
The conducting system of the heart is formed of specialized heart muscle cells.
It comprises the sinoatrial node, the AV node, the AV bundle (of His), its right and
left branches, and a terminal subendocardial plexus of Purkinje fibres. The conducting
system initiates the muscle contractions of the cardiac cycle and controls its regularity.
The sinoatrial node (pacemaker) is a small vascular area of conducting tissue in the
anterior wall of the right atrium to the right of the superior vena caval opening. Impulses
are conducted from it through the atrial wall to the AV node, a similar nodule in the
septal wall of the right atrium above the coronary sinus opening. The AV bundle arises
from the node, descends in the interventricular septum, and divides into right and left
branches to supply their respective ventricles. If the AV bundle is damaged, as it may
be following infarction, total heart block occurs and the ventricles contract slowly at their
own rate, independent of the atria, which continue to contract at the rate determined
by the sinoatrial node.
FURTHER READING
McMinn R M H, Hutchings R T, Pegington J, Abrahams P A. Colour Atlas of Human
Anatomy. 3rd ed. London: Wolfe, 1993: 160176.

Large Veins of the Neck
John Craven
The internal jugular vein drains blood from the intracranial region and the head and
neck. It arises at the jugular foramen on the base of the skull as a continuation of the
sigmoid venous sinus, passes downwards through the neck and, behind the medial end
of the clavicle, is joined by the subclavian vein to form the brachiocephalic vein. The
vein has a dilatation at each end, the superior and inferior jugular venous bulbs and a
fairly constant pair of valves just above the lower bulb.
The vein lies within the carotid sheath with the vagus nerve behind and the internal or
common carotid arteries medially. The deep cervical lymph nodes lie around it. At the
base of the skull it lies lateral to the last four cranial nerves. Posteriorly it lies on the
sympathetic chain, prevertebral fascia and muscles, the phrenic nerve and, inferiorly,
the subclavian artery. It is crossed laterally by the accessory nerve passing downwards
and laterally, then by the posterior belly of digastric and the omohyoid muscles.
Further laterally, from above downwards, are the styloid process and its muscles, the
sternocleidomastoid muscle and the medial end of the clavicle. Its tributaries are the
pharyngeal plexus, facial vein, lingual vein and the superior and inferior thyroid veins.
On the left side, the thoracic duct may enter the vein and on the right the right lymph
duct (Figures 1 and 2).
Veins of the neck
Superficial
temporal
Maxillary vein
Posterior auricular
Retromandibular
Facial
Common facial
Internal jugular
Anterior jugular
External jugular
Termination of the thoracic and right lymphatic ducts

Jugular
trunk Left internal
Right internal jugular vein jugular vein
Bronchomediastinal
trunk
Subclavian
trunk
Subclavian
trunk
Thoracic duct
Right
lymphatic Left subclavian vein
duct
Left brachiocephalic
Right vein
subclavian Bronchomediastinal trunk
vein Superior vena cava
Right
brachiocephalic
vein
Most techniques for cannulating the internal jugular vein depend on identifying the
sternal and clavicular heads of sternocleidomastoid muscle. One preferred technique
is to insert the needle in the triangular gap between the clavicular and sternal heads
of sternomastoid just above the clavicular. The needle is inserted at the apex of the
triangle at an angle of 40 and advanced caudally and slightly medially behind the
clavicle along the posterior border of the sternocleidomastoid cephalic to the point
where the external jugular vein can be seen crossing the posterior border. The needle
is directed towards the sternal notch and aimed about 10 above the coronal plane.
The maxillary vein and superficial temporal vein join below the ear to form the
retromandibular vein in the substance of the parotid gland.
The external jugular vein, a superficial vein, is formed behind the angle of the mandible
by the union of the posterior auricular and a branch of the retromandibular vein. It
descends in the subcutaneous tissues over sternocleidomastoid and pierces the
cervical fascia above the midpoint of the clavicle to enter the subclavian vein.
The anterior jugular vein begins below the hyoid bone near the midline and passes
downwards and laterally, crossing the thyroid isthmus deep to the sternomastoid to
enter the external jugular vein behind the clavicle. u
CROSS REFERENCE
Anaesthesia and Intensive Care Medicine 2:4: 163.

The Larynx
Lynn M Carragher
John Shaw-Dunn
Lynn M Carragher is Specialist Registrar in Anaesthesia at the Royal Infirmary,

Glasgow, UK.
John Shaw-Dunn is Senior Lecturer in Anatomy at the University of Glasgow. His

main research interest is clinical anatomy.
The larynx started life among the lungfish as a simple circular collar of muscle fibres,
which could tighten and prevent water entering the lung buds while the fish was
submerged. In modern humans, the larynx is still needed to protect the air passages,
but has evolved into a complex sphincter with sophisticated control, which is needed for
breathing, coughing, lifting and speaking.
Anaesthetists and Intensive Care Specialists require a thorough knowledge of

the anatomy of the larynx for direct laryngoscopy, tracheal intubation, regional
anaesthesia for awake intubation, cricothyroid puncture for retrograde intubation and
cricothyroidotomy in the cant intubate cant ventilate situation.
Skeleton of the larynx

The larynx lies level with the third to sixth cervical vertebrae in adult men. In women
and children, it is slightly higher.
The laryngeal skeleton (Figure 1) is part of the primitive skeleton of the pharynx derived
from the pharyngeal arches. It is composed of the hyoid bone and nine cartilages
(three single and three paired). The hyoid bone is U-shaped and best felt gently from
the sides. The thyroid cartilage, shaped like the prow of a ship, projects forward at the
laryngeal prominence and is well marked in men, while the cricoid cartilage is like a
signet ring, with the narrower arch in front. It forms most of the posterior wall of the
larynx and the lower part of the anterior and lateral walls. It is the only complete skeletal
ring of the airway and is of relevance in the application of cricoid pressure during rapid
sequence inductions.
Anterolateral view of the larynx with a scheme of the

laryngeal nerves
The epiglottis (Figure 2) is visible from inside the pharynx. It is a large elastic cartilage,
classically leaf-shaped and projecting obliquely up behind the tongue and the hyoid
bone. The paired arytenoid cartilages, pyramidal in shape and sited superolaterally on
the cricoid lamina, are best seen from the back of the larynx. The corniculate cartilages,
over the apices of the arytenoid cartilages and the cuneiform cartilages, complete the
skeleton of the larynx.
The cartilages articulate with each other at tiny synovial joints and are connected by
fibroelastic membranes. The thyrohyoid membrane lies above the thyroid cartilage and
the cricothyroid ligament below. The position of each can be felt with the tips of the
fingers. Knowledge of the relationship of the internal branch of the superior laryngeal
nerve to the thyrohyoid membrane and hyoid bone is important because the nerve
can be blocked at this site. The cricothyroid ligament is the membrane punctured in
cricothyroidotomy and in the infiltration of local anaesthetic, if required, for awake
intubation and bronchoscopy.
Muscles and interior of the larynx

The laryngeal muscles are divided into extrinsic and intrinsic groups. The extrinsic
muscles are attached to the outside of the cartilages and the hyoid bone, whereas the
intrinsic muscles are confined to laryngeal attachments.
The cavity of the larynx extends from the laryngeal inlet to the lower border of the
cricoid cartilage (Figure 2). Mucosa, extending from the tongue to the anterior surface
of the epiglottis, forms the midline-raised fold called the median glosso-epiglottic fold
and on either side, the lateral glosso-epiglottic folds. The depression formed between
the folds is the vallecula, into which the standard Macintosh blade is inserted for
laryngoscopy.
Coronal section of the larynx looking forwards to

the anterior comissure
From the epiglottis, the mucosa sweeps down in the aryepiglottic folds to the vestibular
folds (false cords) and then to the vocal folds (true cords) below. This forms a three-
tier sphincter, bounding a series of compartments the vestibule, the ventricle and
the infraglottic cavity. These structures can be seen, typically foreshortened, at direct
laryngoscopy (Figure 3).
View of the larynx as seen on direct laryngoscopy
The upper sphincter is the laryngeal inlet, with the epiglottis in front and the
aryepiglottic folds at the side, almost in a vertical plane. The vocal folds form the lower
sphincter, surrounding the glottis or rima glottidis. The vocal folds are wedge-shaped
and contain the vocalis muscle. The mucosa is covered by stratified squamous, non-
keratinized epithelium, which, firmly bound to the underlying ligament, gives the typical
pale appearance. In the adult, this is the narrowest part of the larynx. In children, less
than 810 years of age, the cricoid ring is the narrowest part. With the exception of
the vocal folds, the whole interior of the larynx is covered with pseudostratified ciliated
respiratory epithelium.
During quiet respiration the folds swing outwards and inwards with the tidal flow of air.
The folds adduct completely and close off the glottis in speech and in cough, as well as
in effort. The arytenoids probably rock inwards and downwards to close the glottis.
The intrinsic muscles of the larynx, apart from the crico-thyroid, lie between the
mucosa and the laryngeal skeleton. It is easiest to think of a ring of muscles that close
the sphincters (the lateral cricoarytenoids and the transverse and oblique arytenoids)
and a pair of dilator muscles that open them (the posterior cricoarytenoids). Much
of the opening and closing of the sphincters may be biomechanical and depend on
longitudinal compression of the larynx, causing the folds to buckle inwards like the
pleated folds of a jack-in-the-box.
Nerve supply
The larynx develops from the pharyngeal arches and this relationship can be seen
in the nerve supply, which comes from the superior laryngeal nerve, the nerve of the
fourth arch and the recurrent laryngeal nerve, the nerve of the sixth arch. Both are
derived from the vagus nerve.
The superior laryngeal nerve arises below the inferior vagal ganglion and divides,
usually within the carotid sheath, into an internal branch (sensory and autonomic)
and an external branch (motor). The larger internal branch pierces the thyrohyoid
membrane with the superior laryngeal artery and supplies sensory fibres to the
laryngeal mucosa, above the vocal cords (Figure 1). Two methods of nerve blockade
of the internal branch for awake intubation are infiltration of local anaesthetic where the
nerve pierces the thyrohyoid membrane or direct application of cotton pledgets soaked
in local anaesthetic into the piriform recesses, using Krauses forceps. The external
branch runs downwards to reach the cricothyroid and the inferior pharyngeal constrictor
muscles.
The recurrent laryngeal nerve loops around the aortic arch on the left and the
subclavian artery on the right. It ascends on the trachea and passes behind the
cricothyroid joint in the wall of the larynx. It supplies all the intrinsic laryngeal muscles
except the cricothyroid and sensation to all the mucosa below the vocal folds. It is an
important nerve on the afferent limb of the cough reflex. Various reviews and case
reports suggest that there may be some overlap between the different territories of
supply, even across the midline. u
FURTHER READING
Hillel A D. The Study of Laryngeal Muscle Activity in Normal Human Subjects.
Laryngoscope 2001; 111 Supplement 97: 147.
Stavroulaki P, Birchall M. Comparative Study of the Laryngeal Innervation in Humans. J

Laryngol Otol 2001; 115: 25766.

Joints and Ligaments of the
Vertebral Column
John Craven
The articular surfaces of the bodies of adjacent vertebrae are covered by hyaline
cartilage and united by a thick fibrocartilaginous intervertebral disc. The disc centre
(nucleus pulposus) is gelatinous and surrounded by a fibrous part, the annulus fibrosus.
The disc is a shock absorber. Occasionally the semisolid nucleus protrudes through
a defect in the annulus; it may press on the spinal cord or a spinal nerve to produce
symptoms and signs of nerve compression. Adjacent vertebrae articulate by two
synovial joints between the paired articular processes. The vertebral bodies are united
by anterior and posterior longitudinal ligaments.
The anterior ligament extends from the occiput to the sacrum and is attached to each
vertebra. Its deep fibres blend with the intervertebral discs.
The posterior ligament extends from the occipital bone to the sacrum and is attached
to each vertebral body and disc. Its superior part, from the body of C2 to the occiput is
known as the tectorial membrane.
The ligamenta flava unite the adjacent laminae. They contain a large amount of yellow
elastic tissue and are strong. Because of their elasticity they remain taught during
flexion and extension of the spine, maintaining the curvature of the spinal column
and supporting it when it is flexed. The ligaments have no sensory supply and can be
pierced painlessly when a lumbar puncture is performed.
The supraspinous, interspinous and intertransverse ligaments help to unite

adjacent vertebrae. The supraspinous is a strong ligament connecting the tips of the
spinous processes from C7 to the sacrum. Above C7 it forms the ligamentum nuchae
which attaches to the occipital protuberance and provides attachment to neck muscles.
The intertransverse ligaments are weak but best developed in the lumbar region.
The articular ligaments around the joints of the articular facets provide additional
support.
All these ligaments contribute to supporting the spinal column when it is in the flexed
position.
The occipito-atlanto-axial articulation: the atlanto-occipital and atlanto-axial joints

(Figure 1) are modified to allow free movement of the head. Radiographs taken through
the wide open mouth are used to demonstrate these joints.
Median section to show ligaments of axis, atlas and occiput
Membrana tectoria
Anterior atlanto-occipital
Anterior condylar canal
membrane
Apical ligament
Anterior arch of atlas Edge of foramen magnum
Atlanto-axial joint Vertebral artery
Posterior arch of atlas

Transverse ligament of atlas
(transverse part of cruciate) Lamina and spine of axis
Ligamenta flava
Anterior longitudinal ligament
Posterior longitudinal ligament which is
continuous above with the membrana tectoria
The atlanto-occipital joints are condyloid synovial joints between the convex occipital
condyles and the concave upper articular surfaces of the atlas. Flexion and extension
occur at these joints. The joints are supported by the posterior longitudinal ligament,
here known as the membrana tectoria, and the anterior atlanto-occipital membrane,
which connects the anterior margin of the foramen magnum with the anterior atlas.
The atlanto-axial joints comprise two lateral synovial plane joints between the
lateral masses of the two vertebrae and a midline synovial pivot between the dens or
odontoid process, a stout pillar projecting vertically from the body of the vertebra in
the midline, and a ring formed by the anterior arch and the transverse ligament of the
atlas. Rotation occurs at this joint. The joint is strengthened by accessory ligaments;
the apical ligament attaches the apex of the odontoid process to the foramen magnum,
laterally there are two alar ligaments attaching the odontoid process to the margin of
the foramen magnum, the membrana tectoria covers the entire joint and connects the
back of the axis, the occiput and the adjacent cruciate ligament.
Functional aspects
Curvature and mobility in fetal life the vertebral column is flexed its primary
curvature. After birth, two secondary curvatures develop: extension of the cervical
region by the muscles raising the head; and extension of the lumbar region after
adoption of the erect posture. The primary curvature is retained in the thoracic and
sacral regions. These curvatures and the intervertebral discs give some resilience to
the column.
Muscles the extensor muscles of the back and neck extend the head and vertebral
column. They form a large composite mass lying deep to trapezius and girdle muscles
and extend from the sacrum to the occiput. The largest and most powerful are the
erector spinae muscles but these are supported by shorter muscles attached to
adjacent vertebrae and to nearby ribs. These muscles play a large part in maintaining
posture and are in constant action when standing at rest for the centre of gravity lies
anterior to the vertebral column. The muscles attached to the skull produce extension,
lateral flexion and rotation of the head.
Movements only limited movements are possible between adjacent vertebrae but
because these can augment each other it is possible to produce extensive movement
of the whole vertebral column. Flexion is most marked in the cervical region, rotation in
the thoracic, and extension and lateral flexion in the lumbar region (Figure 2).
Muscles causing movement of the vertebral column
Movement Muscles
Trunk
Flexion Rectus abdominis and
prevertebral muscles
Lateral The oblique abdominal muscles

flexion and quadratus lumborum
Neck
Rotation Sternocleidomastoid, trapezius
Flexion Longus capitis and the muscles

depressing
the fixed mandible
Extension Postvertebral muscles
Lateral Sternocleidomastoid and

flexion trapezius
2
Stability depends almost entirely on the pre- and post-vertebral muscles helped by the
ligamenta flava; neither the bones nor ligaments alone could withstand the large forces
occasionally acting on the column. Most vertebral functions do not produce instability
of the vertebral column for the intervertebral ligaments are not easily torn. If, however,
the ligamenta flava and interspinous ligaments are ruptured, the vertebral column is
unstable and subsequent displacement may produce compression of the spinal cord
and irreversible nerve damage. Fracture of the odontoid process allows the forward
displacement of the arch of the atlas together with the skull and fractured part of the
odontoid process; a similar forward displacement follows a rupture of the transverse
ligament of the atlas. Only 15% of such injuries are followed by neurological damage
because the spinal canal is wide at this level.
Vertebral canal a bony ligamentous structure that extends from the foramen
magnum to the sacral hiatus. The spinal cord ends at L2, the dural sac at S2, the
supracristal plane, which lies between the highest points of the iliac crests, crosses the
spine of L4 (Figure 3).
Site of lumbar puncture
Spinal cord
Dura
Subarachnoid space
a The site of choice for lumbar puncture is between L3 and L4.

The spinal cord is out of danger. Cauda equina not shown.
b The usual site for lumbar puncture is shown as the intersection

of the midline (A) with the intercristal plane (B).
3
Lumbar puncture a needle inserted just above the spine of L4 passes through the
interspinous ligament and ligamentum flavum entering the epidural space and then
the dura to enter the spinal canal, from which cerebrospinal fluid can be drawn off for
examination. Local anaesthetic solution can be injected into the extradural (epidural
anaesthesia) or into the spinal (spinal anaesthesia) canal. The dural sac, with its
contents, the spinal cord, the spinal nerves and the cerebrospinal fluid, is separated
from the walls of the spinal canal by the extradural space, in which lie the emerging
spinal nerves and vertebral venous plexus. u

Lumbar, Sacral and Coccygeal
Plexuses
John Craven
cancer.
Lumbar plexus
The lumbar plexus (Figure 1), is formed by the anterior primary rami of L1L4 nerves.
It lies within psoas major on the posterior abdominal wall. All nerves receive grey rami
communicantes from the sympathetic trunk. From the plexus emerge:
the obturator nerve (L24) supplying the thigh adductors
the femoral nerve (L24) supplying iliacus and the knee extensors
the lumbosacral trunk (L45), which descends over the sacrum to contribute to the
sacral plexus
the ilioinguinal (L1), and the iliohypogastric (L1) nerves, which obliquely traverse the
abdominal wall muscles, supplying them and the inguinal and suprapubic skin
the lateral femoral cutaneous nerve (L23) entering the thigh just medial to the
anterior superior iliac spine to supply the skin of the anterolateral surface of the thigh
the genitofemoral nerve, (L12) supplying the skin of the genitalia and the femoral
triangle.
Lumbar plexus
1
Sacral plexus
The sacral plexus is formed by the lumbosacral trunk, a conjunction of the anterior
divisions of the L4 and L5 nerves and the upper four sacral nerves (S1S4). It lies in
front of the sacrum on piriformis deep to the pelvic fascia (Figure 2). Its branches can
be divided into pelvic branches and those leaving the pelvis.
In the pelvis there are muscular branches to the piriformis, levator ani, coccygeus
and the external anal sphincter. Pelvic splanchnic nerves arise from the anterior primary
rami of S24 to supply the pelvic viscera. These have a vasodilator function when
acting on the erectile tissue (nervi erigentes), an inhibitor action on the internal anal
and vesical sphincters and a motor function on the smooth muscle of the rectum and
bladder.
Leaving the pelvis most of these branches pass through the greater sciatic
foramen, above or below piriformis.
Above piriformis the superior gluteal nerve supplies gluteus medius and
minimus.
Below piriformis
The sciatic nerve (L45, S13) descends in the posterior compartment of the
thigh to end by dividing into the tibial and peroneal nerves just above the popliteal
fossa. It supplies the hip and knee joints and the hamstrings, semimembranosus,
semitendinosus and biceps. The sciatic nerve lies midway between the ischial
tuberosity and the greater trochanter and may be injured by a carelessly placed
intramuscular injection. The only safe area in which to place injections is the upper,
outer quadrant.
The pudendal nerve, S23 enters the perineum via the lesser sciatic foramen and
runs forward in the pudendal canal on the medial surface of obturator internus. It
supplies levator ani, the perineal muscles, including the external anal sphincter, and
the perianal and perineal skin. It carries parasympathetic fibres to the corpora of the
penis or clitoris. A pudendal nerve block can be achieved by inserting a finger into the
vagina, to guide the needle to the ischial spine and injecting local anaesthetic there.
An effective nerve block results in relaxation of levator ani, anaesthesia over the vulva
and loss of the anal reflex.
Muscular branches supply gluteus maximus, obturator internus and quadratus
femoris.
Cutaneous branches supply the back of the thigh and the gluteal region.
Major nerves of the leg the sciatic nerve branches at or above the popliteal fossa
into the tibial and common peroneal nerves. The tibial nerve descends vertically in the
popliteal fossa through the flexor compartment of the leg to reach the back of the medial
malleolus where it divides into medial and lateral popliteal nerves. Its branches are:
the sural nerve, which descends on gastrocnemius then passes behind the lateral
malleolus, to supply the skin of the back of the leg and lateral surface of the heel
and foot
muscular branches to gastrocnemius, soleus, tibialis posterior, flexor hallucis longus
and flexor digitorum longus.
The common peroneal nerve descends laterally through the popliteal fossa and
divides in peroneus longus into:
the superficial peroneal nerve, which descends between peroneus longus and
brevis, supplying them, and ends by dividing into cutaneous branches, which supply
the skin of the lower lateral part of the leg and the dorsal surface of the foot and
lateral four toes
the deep peroneal nerve, which lies subcutaneously and winds round the neck of
the fibula, and descends in the extensor compartment of the leg supplying the long
extensor muscles before passing in front of the ankle to divide into medial and lateral
terminal branches to supply the ankle joint, extensor digitorum brevis and the skin of
the first interdigital cleft.
Lateral wall of pelvis showing sacral plexus

Nerve blocks
Lower and upper limb nerve blocks are discussed elsewhere.

The Lungs and their Relations
John Craven
Each lung lies in a pleural sac (see page 315) attached by the pulmonary vessels
to the mediastinum. Each is cone-shaped to conform to the contours of the thoracic
cavity and is spongy and elastic in texture. The right lung is slightly larger (620 g) than
the left (560 g). Each lung has an apex in the root of the neck and a base resting on
the diaphragm. The base is separated by a sharp inferior border from a lateral convex
surface and a medial concave mediastinal surface. In the centre of the mediastinal
surface the structures forming the root of the lung are surrounded by a collar of
reflected pleura. The medial surface of the left lung is concave to accommodate the
left ventricle of the heart and the anterior border of the left lung is indented by the heart
to form the cardiac notch. In both lungs the posterior border is rounded and lies in the
paravertebral sulcus.
Each lung is divided into lobes by fissures that extend deeply into their substance (see
Anaesthesia and Intensive Care Medicine 3:5: 191). An oblique fissure divides the left
lung into an upper and a lower lobe. In the right lung, oblique and horizontal fissures
divide the right lung into upper, middle and lower lobes (Figure 1). In both lungs the
surface marking of the oblique fissure is a line extending round the chest wall from the
spine of the third thoracic vertebra to the sixth costochondral junction. The horizontal
fissure is marked on the surface by a horizontal line passing laterally to the oblique
fissure from the fourth right costochondral junction (Figure 2).
The lower lobes of both lungs lie below and behind the oblique fissure and comprise
most of the posterior and inferior borders and parts of the medial and costal surfaces.
The upper lobe of the left lung lies above and in front of the oblique fissure and
comprises the apex, large parts of the mediastinal and costal surfaces and the whole
of the anterior border. The equivalent part of the right lung is divided by the horizontal
fissure into a large upper lobe and a smaller, wedge-shaped, anteriorly placed middle
lobe. Some variation exists in this lobar pattern. Fissures may be missing or incomplete.
The hilus of each lung contains a main bronchus, pul-monary artery, two pulmonary
veins, the pulmonary nerve plexus and lymph nodes. It is surrounded by the collar of
pleura reflected from the lung onto the mediastinum, the narrow inferior extension of
which is known as the pulmonary ligament.
Parietal relations
The borders of the lungs closely follow the lines of pleural reflection on the chest wall
except where the inferior border of the lung lies about two intercostal spaces above
the inferior limit of the pleura and in front on the left side where the cardiac notch lies
about 3 cm lateral to the pleural refection (Figure 2). The costal surface is related to the
thoracic wall. The base is separated by the diaphragm, on the right side from the right
lobe of the liver, and on the left side from the left lobe of the liver, the stomach and the
spleen. The apex is covered by the dome of the pleura and the suprapleural membrane
and above them arch the subclavian vessels.
Posteriorly the apex is separated from the neck of the first rib by the anterior primary
ramus of the first thoracic nerve, the superior intercostal artery, the sympathetic trunk
and the pleura.
Medial relations
The medial relations of the two lungs differ (Figures 3 and 4). On the left lung there is
a concavity antero-inferiorly for the left ventricle, which is continuous superiorly with
a groove for the aortic arch passing in front of and above the hilum. Above this groove
the surface is in contact with the left brachiocephalic vein, left common carotid and left
subclavian arteries and the oesophagus.
Medial surface of the left lung

Medial surface of the right lung
On the right lung there is a shallow concavity in front of the hilum for the right atrium
which is continuous above and below with shallow grooves for the superior and
inferior vena cavae. Above the superior groove the surface is in contact with the
left brachiocephalic vein, the left common carotid and subclavian arteries and the
oesophagus.
Blood supply
The heart returns mixed venous blood to the lungs by the pulmonary trunk. After
respiratory exchange the blood is then returned by the pulmonary veins.
The pulmonary trunk is a wide vessel, about 5 cm long. It begins at the pulmonary
valve, ascends posteriorly to the left of the aorta and bifurcates under the concavity of
the aortic arch into right and left pulmonary arteries.
The right pulmonary artery passes horizontally to the hilus of the right lung behind
the ascending aorta and in front of the oesophagus and right main bronchus before
dividing into branches that follow the segmental bronchi, ending in a capillary network
within the alveolar walls.
The left pulmonary artery passes to the left lung hilus in front of the left bronchus and
the descending aorta (see Anaesthesia and Intensive Care Medicine 3:2: 76, Figure 1).
It is connected by the ligamentum arteriosum, normally fibrosed shortly after birth, to
the lower surface of the aortic arch. It also divides within the substance of the lung, its
branches following the segmental bronchi.
Bronchial arteries: lung tissue is supplied, not by the pulmonary arteries, but by the
bronchial arteries, which are small branches of the descending thoracic aorta. The
corresponding bronchial veins drain into the azygos or hemiazygos veins. Some of the
bronchial arterial blood drains back to the heart in the pulmonary veins.
The pulmonary veins are short, wide vessels that pass directly horizontally into the
left atrium. There are usually two (upper and lower) from each lung. In the lung hilus
they lie below the pulmonary artery; on the right they lie behind the superior vena cava
and the right atrium and on the left behind the left atrium and in front of the aorta. The
pulmonary veins are formed by the union of smaller veins that drain oxygenated blood
from the capillary bed in the alveolar walls.
Lymphatic drainage
Lymphatic drainage of the lungs is via a superficial subpleural lymph plexus and a deep
plexus of lymph vessels accompany-ing the bronchi. Both groups drain through hilar or
broncho-pulmonary nodes to tracheobronchial nodes and thence to mediastinal lymph
trunks.
The tracheobronchial nodes lie alongside the trachea and bronchi and receive
afferents from the lungs, bronchi, trachea and heart. Their efferents drain to the
bronchomediastinal lymph trunks which ascend alongside the trachea to end in the right
lymph duct and, on the left, the thoracic duct.
Nerve supply
Innervation of the lung is by the pulmonary plexus which conveys both the sympathetic
(bronchodilator) fibres from the upper four thoracic sympathetic ganglia and
parasympathetic (bronchoconstrictor) fibres from the vagus. Sensory fibres pass largely
in the vagus nerves. u
FURTHER READING
Ellis H. Clinical Anatomy. A Revision and Applied Anatomy for Clinical Students.
Oxford: Blackwell Science, 1997.

Anatomy of the Nose, Mouth
and Pharynx
N Woodall
John Shaw-Dunn
N Woodall is Consultant Anaesthetist at the Norfolk and Norwich University Hospital

NHS Trust. He qualified from Liverpool University and trained in anaesthesia in the
North-West, London, and California. His clinical research interests include airway
problems and training in airway management.
John Shaw-Dunn is Senior Lecturer in Anatomy at the University of Glasgow, UK. His
main research interests are in clinical anatomy.
The nose: within the external nose the hair-lined vestibules act as a nasal valve,
causing turbulence to improve air conditioning. Each nasal cavity is about 1014 cm
long in the adult.
The floor of the nasal cavity is the bony palate (Figure 1). The arched roof includes the
delicate cribriform plate of the ethmoid bone, which separates the nasal cavity from the
anterior cranial fossa. The septum contains cartilage anteriorly and the vomer more
posteriorly. The septum is seldom midline, perhaps because of microtrauma during
labour. Three delicate turbinates project from the lateral wall of each cavity. Air sinuses
open on to the lateral wall as do the nasolacrimal ducts. The nasal cavity and sinuses
have a thick mucosa with cilia which warms, moistens and cleans incoming air, an
action lost during intubation.
Sagittal section of mouth, nose and pharynx
Frontal air sinus
Middle turbinate Sphenoid air sinus
Nasopharynx and opening

Bony palate of auditory tube
Dens of axis
Genioglossus Oropharynx
Hyoid bone
Mylohyoid and geniohyoid Vallecula
Epiglottis Ligamentum nuchae
Larynx
1 Laryngopharynx
Oesophagus
Sensation to most of the nasal cavity is provided by branches of the sphenopalatine

Trachea
ganglion, which is accessible to topical anaesthesia behind the middle turbinate.
The mouth: the lips and cheeks contain the orbicularis oris and buccinator muscles
Redrawn fromand form
Forrester J M,the
ed. Aouter wallto of
Companion the Studies.
Medical vestibule.
3rd ed.The
Oxford:mouth
Blackwellcavity
Scientificis limited posteriorly
Publications, by theof the publishers.
1985, by kind permission
fauceal isthmus.
The tongue: the buccal surface of the tongue is separated from the posterior
pharyngeal portion by a V-shaped groove behind a row of large vallate papillae with
taste buds. The pharyngeal portion has multiple lymphoid nodules, which produce an
irregular pebble-like appearance. The intrinsic muscles of the tongue modify its shape
and the extrinsic group alter its position. Genioglossus, which forms the bulk of the
tongue mass, protrudes the tongue. It originates from the mid-line mental spine on the
inner surface of the mandible. During sleep and anaesthesia, reduced muscle tone
may allow the tongue to fall backwards and obstruct the airway. This can sometimes be
relieved by extending the neck with the mouth closed, stretching the extrinsic muscles
like a washing line.
Floor of mouth: the mylohyoid creates a muscular floor for the mouth. On the outside
it is covered by deep fascia, platysma and skin. Infection, swelling or bleeding into the
deep layers may elevate the tongue, or spread backwards into the pharynx leading to
problems with direct laryngoscopy or obstruction of the pharynx.
Salivary glands: the parotid ducts open into the vestibule at the level of the second
upper molar crown. Each submandibular gland duct (Figure 2) opens at the sublingual
papilla lateral to the frenulum linguae, which connects the underside of the tongue to
the floor of mouth. Multiple sublingual glands drain directly into the sublingual folds.
Dissection of constrictor muscles and nerves of

the pharynx from the medial side
Sphenoid bone
Pterygomandibular
raphe
Superior constrictor
Lingual nerve
Submandibular Palatoglossus
duct
Soft palate
Palatopharyngeus
Glossopharyngeal
nerve
Submandibular gland
Hypoglossal nerve
Middle constrictor
Hyoid bone
Sublingual gland
Internal laryngeal
nerve
Epiglottis (cut)
Piriform fossa
Arytenoid cartilage
Cricoid cartilage Cricopharyngeus
Redrawn from Romanes G J. Cunninghams Manual of Practical Anatomy.

Oxford: Oxford University Press, 1986, by kind permission of the publishers. 2
Teeth: the 24 deciduous teeth are replaced by up to 32 permanent teeth. Permanent

teeth are recorded numerically in each quadrant. 1 and 2 correspond to the central
and lateral incisors anteriorly, 3 the canines, 4 and 5 the premolars and 6, 7, and 8, the
molars, posteriorly. Deciduous teeth are recorded alphabetically in the same way.
Nerve supply: the anterior and posterior superior alveolar nerves supply the
upper jaw, while the lower is innervated by the inferior alveolar nerve. Lateral to the
pterygomandibular raphe a needle can be inserted through the buccinator into the
pterygomandibular space to block the inferior alveolar nerve. The anterior two-thirds
of the tongue are supplied by the lingual nerve, though fibres conveying taste pass via
the chorda tympani to the facial nerve. Extrinsic and intrinsic muscles of the tongue are
innervated by the hypoglossal nerve except the palatoglossus muscle, supplied by the
vagus.
The pharynx is a muscular tube lined by mucosa extending from the base of the skull
to the lower border of the cricoid cartilage at the level of C6.
The nasopharynx lies behind the nasal cavity. The lateral wall bears the opening
of the Eustachian tube. This cartilaginous structure, with attachment to the
salpingopharyngeus muscle, produces the tubal elevation that is often visible during
fibre-optic endoscopy. Behind it lies the blind pharyngeal recess. High on the superior
pharyngeal constrictor are the pharyngeal tonsils, which when enlarged become the
adenoids. Deep to the pharyngeal muscle layer are the arch of the atlas, the axis and
the cervical vertebrae. During nasotracheal intubation, contact with the posterior wall
forces the tube tip downwards. Insertion may be impeded by a prominent vertebral
arch, tubercles or osteophytes.
The oropharynx is entered through the nasopharyngeal isthmus, formed by the

soft palate, uvula and the superior pharyngeal constrictor. Anteriorly, the oropharynx
communicates with the mouth via the oropharyngeal or fauceal isthmus, bounded by
palato-
glossus and palatopharyngeus between which lie the tonsils.
The laryngopharynx commences at the upper level of the epiglottis and extends to
the lower level of the cricoid cartilage. The base of the tongue is separated from the
epiglottis by the vallecula, with the median glossoepiglottic fold in the midline. The
larynx bulges posteriorly into the laryngopharynx producing a recess on either side,
the piriform fossa. The internal laryngeal nerve which mainly provides sensation to
the mucosa of the larynx pierces the thyrohyoid membrane and passes beneath the
mucosa of the piriform fossa. At this point it may be anaesthetized, by the application of
swabs soaked in local anaesthetic.
The pharyngeal wall is surprisingly thin and nerves and blood vessels are vulnerable
to penetrating injury. The back and sides of the pharyngeal wall are reinforced by three
flattened constrictor muscles, which overlap. They meet in a raphe, which extends from
the pharyngeal tubercle on the sphenoid bone to merge with the oesophagus. During
swallowing, the bolus is propelled downwards through the cricopharyngeal sphincter
into the oesophagus by peristaltic waves in the constrictors. A pouch can develop
between the sphincter and the thyropharyngeal portion of the inferior constrictor at
Killians dehiscence. Accumulation of undigested material here may be a potential
source for aspiration.
Nerve supply: sensation to the pharynx is supplied by the glossopharyngeal nerve via
the pharyngeal plexus. Sensation to the anterior surface of the epiglottis is therefore
glossopharyngeal in origin but the inferior or posterior surface, which is anatomically part
of the larynx, is supplied by the vagus. Transcranial electrical stimulation shows that one
side of the brain is usually dominant in control of the pharynx, which may explain why
cerebrovascular accidents on one side of the brain often cause dysphagia. u
FURTHER READING
Hiiemae K M, Palmer J B. Food Transport and Bolus Formation during Complete
Feeding Sequences on Foods of Different Initial Consistency. Dysphagia 1999; 14:
3142.

The Pericardium
John Craven
The pericardium is a fibroserous membrane investing the heart and the great
vessels entering and leaving it. It is composed of two distinct layers, the outer fibrous
pericardium and the inner serous pericardium.
The serous pericardium is a closed serous sac invaginated by the heart. It has
visceral and parietal layers, which enclose a potential space, the pericardial cavity.
The visceral pericardium covers the entire outer surface of the heart and is reflected to
become continuous with the parietal pericardium, which lines the inner surface of the
fibrous pericardium. These lines of reflection form:
the oblique sinus behind the left atrium bounded by the four pulmonary veins and
the inferior vena cava
the transverse sinus below the reflection around the superior vena cava and also
behind the left atrium (Figure 1).
Interior of pericardium viewed after removal of

heart and anterior part of pericardium
Transverse sinus
Oblique sinus
Cut edge of
pericardium
The fibrous pericardium forms a strong conical sac around the heart and the
serous pericardium, blending inferiorly with the fibrous tissue of the central tendon of
the diaphragm and the adventitia around the inferior vena cava. Superiorly, it blends
with the adventitia around the aorta, pulmonary trunk and superior vena cava and
posteriorly with that of the pulmonary veins. Anteriorly, the pericardium is closely
related to the posterior surface of the body of the sternum, the 2nd to 6th costal
cartilages and the thin anterior borders of both lungs (Figure 2). Posteriorly, it is related
to the oesophagus, the descending aorta and the vertebral bodies T5T8 and laterally
to the mediastinal pleura. The entire thoracic part of the inferior vena cava, about 2 cm
long, is within the pericardium.
Surface marking of pericardium
Arrow showing route of insertion for pericardiocentesis

2
The pericardial cavity in health contains no more than a thin film of fluid but a
pericardial effusion may occur as the result of heart failure, generalized oedema and
infection. If the effusion is extensive, the excess fluid in the pericardial cavity interferes
with the action of the heart because the fibrous pericardium is inelastic. Similar cardiac
embarrassment may occur as the result of blood accumulating within the pericardium
after stab wounds to the heart. The condition is known as cardiac tamponade; the heart
is compressed and its output falls. The veins of the neck and face become engorged
because of constriction of the superior vena cava as it enters the pericardial sac.
Pericardiocentesis, drainage of fluid from the pericardial sac, is readily achieved using
a large-bore venous cannula inserted into the pericardial sac. It is inserted beneath
the costal margin at its border with the xiphoid process and directed towards the left
shoulder at an angle of 45 to the horizontal. u

The Pleura
John Craven
Each pleural cavity is a closed cavity of serous membrane invaginated by the lung. The
visceral layer covers the lungs and the parietal layer covers the inner surface of the
thoracic cavity. The layers are continuous around the root of the lung and separated by
only a thin layer of serous fluid. Thus, the two layers glide easily over each other but are
prevented from separating by the negative pressure within the thoracic cavity and the
surface tension of the pleural fluid. This ensures that when the thoracic cage expands
so does the lung and air is then drawn in from the trachea.
The pleura is a fibro-elastic membrane lined by squamous mesothelial cells; parietal

pleura line the ribs, costal cartilages and intercostal muscles, the lateral surface of the
mediastinum and the upper surface of the diaphragm. Superiorly it extends, above the
thoracic inlet into the neck forming the cervical dome of the pleura. The apical pleura
is covered by a fascia, the suprapleural membrane (Sibsons fascia) which is attached
to the inner surface of the first rib and prevents the lung expanding too far into the neck
on inspiration. At this point, the pleural cavity is at risk of being entered during surgery
in the root of the neck or during subclavian cannulation. On the left side, anteriorly,
in front of the heart the costal and mediastinal surfaces are in contact, forming the
costomediastinal recess. The mediastinal pleura loosely invests the main bronchi and
pulmonary vessels and continues on to the lung to form the pulmonary (visceral) pleura
which covers the lung and extends into its interlobar fissures.
On both sides of the lung the cervical pleura extends about 3 cm above the middle
of the clavicle (Figure 1). Anteriorly, on both sides, the lines of reflection (where the
parietal pleura meets the visceral layer) descend behind the sternoclavicular joint to
meet in the midline at the level of the second costal cartilage. They descend side by
side to the fourth costal cartilage where the left pleural reflection deviates laterally,
descending along the lateral border of the sternum to the sixth costal cartilage. The
right pleural reflection, however, continues downwards near the midline to the same
level. Thereafter the course of the reflection line is similar on both sides. Each passes
laterally behind the costal margin, reaching the eighth rib in the midclavicular line, the
tenth rib in the midaxillary line and the twelfth rib in the paravertebral line. The lower
limit of the pleura medially is below the twelfth rib and thus at risk during renal or
adrenal surgery. The posterior reflection line ascends, on each side, about 3 cm from
the midline. A pneumothorax is best drained, with a catheter and underwater seal, by
catheter insertion in the second intercostal space in the midclavicular line. A pleural
effusion should usually be drained by insertion of the catheter in the sixth or seventh
space in the midaxillary line.
Surface relationship of the lungs and pleural cavities

The pleura gains its blood supply from adjacent tissues. Though the pulmonary pleura
has no pain fibres the parietal pleura is richly supplied by the nerves in the subjacent
tissues, the intercostal and the phrenic nerves. Therefore, pleurisy may produce pain
referred to the upper abdomen from inflammation of the lower sixth intercostal nerves
or referred to the root of the neck from the phrenic nerve. u

The Ribs and Intercostal
Spaces
John Craven
cancer.
The thoracic contents are contained in an osteocartilaginous cage formed by the

thoracic vertebrae behind, the sternum in front and between them the ribs and costal
cartilage.
Ribs
The ribs (Figure 1) are narrow, curved flat bones. The first seven or eight pairs of
ribs attach the vertebrae to the sternum through their costal cartilage. The eighth to
tenth pairs are known as false ribs because their cartilage articulates with the cartilage
above them and not with the sternum. The eleventh and twelfth pairs of ribs are
known as floating ribs because their cartilage ends in the muscles of the posterior
abdominal wall.
A typical rib (ribs 39) comprises a head bearing two facets. The lower facet
articulates with its corresponding vertebra and the upper facet articulates with the
vertebra above that. Lateral to the head (23 cm) is a tubercle that articulates with
the transverse process of the corresponding vertebra (Figure 2). Close to this, the
costotransverse ligament gains attachment. Beyond the tubercle, the shaft of the rib
becomes flatter and wider and the inner surface of its lower border is grooved (costal
groove) to accommodate the intercostal nerves and vessels.
The first rib is short, wide and flattened. On its upper surface the scalene tubercle
separates an anterior groove for the subclavian vein and a posterior groove for the
subclavian artery and brachial plexus. The heads of ribs 1 and 1012 bear a single
facet.
Anterior view of thoracic cage

Sternal angle (manubriosternal
joint)
1
Sternocostal joint
2
Costal cartilage 3
of third rib
4
Costochondral joint
5
Interchondral joint 6
Xiphoid process 7
8
Interchondral
ligament 12 9
10
Costal margin
11
The ribs are numbered 1 to 12.
Posterior view of the fifth rib

Head
Angle
Articular facets
Neck
Shaft
Articular
Tubercle
Nonarticular
Costal groove
Intercostal spaces
The intercostal spaces are bounded by adjacent ribs and costal cartilage and contain
the intercostal muscles, vessels and nerves. Deep to them lies the pleura. The external
intercostal muscle is the most superficial. Deep to it is the internal intercostal muscle
and deepest of all is the incomplete sheet of the innermost intercostal muscle attached
to the inner surfaces of the sternum, costal cartilage and ribs. The vessels and nerves
lie together in the costal groove between the internal and innermost muscles. The
artery lies between the vein superiorly and the nerve inferiorly in the neurovascular
bundle (Figure 3).
Twelve pairs of thoracic spinal nerves supply the muscles and skin of the thoracic
and abdominal wall. The cutaneous distribution of each nerve is striplike and is known
as a dermatome (Figure 4). Though there is overlapping of the dermatomes, knowledge
of their distribution allows the clinician to determine the extent of sensory deficiencies
and the proximal extent of anaesthesia after, for instance, a spinal block.
The parietal pleura has a similar segmental dermatomal distribution. Thus,
inflammation of the pleura results in pain being referred to the cutaneous distribution
of the nerve affected which, in the case of the lower pleura, is the anterior abdominal
wall.
The intercostal arteries supply the chest wall and its overlying muscles and the
breast. They anastomose with branches of the internal thoracic artery and its terminal
branches.
Intercostal space
External intercostal
Rib
Intercostal vein, artery

and nerve
Internal intercostal
Innermost intercostal
Cutaneous distribution of dermatomes
C2
C2
C3
C3 C4
C5
C6
C4 T1
T2
T2 T3
C5
T4
T3
T5
T4 T6
T7
T3
T5 T8
T9
T2 T6 T2
T10
C5
T7 T11
T12
T8 L1
L2 T1
T9 L3
T10 L4
T1 S1
T11 S2 C8
T12 S3
S4
L1 S5
C6
C7
C6 C8
L2
C7 L5
L3
S1
L4 S2
L3
S3
S4
L5
L4
S1
S1
4
Procedures
Drainage
Fluid (e.g. blood, pus, inflammatory exudate) or air may be drained from the thorax
for diagnostic or therapeutic reasons. This is done by inserting a narrow-bore or wide-
bore needle through an intercostal space previously infiltrated with local anaesthetic.
Radiography determines the level at which the fluid is best aspirated. The needle should
be passed along the superior border of the rib to avoid the neurovascular bundle. There
is a risk of penetrating the diaphragm if aspiration is attempted below the seventh
intercostal space.
Anaesthesia
Local anaesthesia of intercostal nerves has an important role to play in managing the
pain arising from fractured ribs or reducing the pain of a thoracotomy. The appropriate
nerve and the two nerves above and below (because of the overlapping supply) are
infiltrated at or around the rib angle. In each space, the needle is advanced until the rib
is met, then withdrawn and guided under the inferior angle for 0.5 cm. If no blood is then
aspirated, 14 ml of local anaesthetic solution is injected.
FURTHER READING
Rushman G B, Davies N J H, Cashman J N. Lee's Synopsis of Anaesthesia. Oxford:
Butterworth-Heinemann, 1999: 62634.

Sacrum and Sacral Hiatus
John Craven
The sacrum is formed from the five fused sacral vertebrae (Figure 1). It is triangular
and possesses a base superiorly, an apex inferiorly and dorsal (posterior), pelvic
and lateral surfaces. Two rows of foramina on its dorsal and pelvic surfaces divide
it into a median portion, the body, formed from the fused vertebral bodies, and two
lateral masses formed from the fused transverse processes. The paired pelvic and
dorsal sacral foramina communicate by intervertebral foramina with the central sacral
canal and convey the ventral and dorsal rami of the sacral nerves. The base, directed
upwards and forwards is formed from the upper surface of the first sacral vertebra
and contains an oval concavity, the articular facet, for the disc that separates it from
the 5th lumbar vertebra. Lateral to this the lateral masses of the sacrum are at their
widest and form the prominent ala. The anteriorly protruding central part of the superior
surface is known as the promontory. Behind the body, superiorly, is the upper opening
of the sacral canal on each side of which project the superior articular processes for
articulation with the 5th lumbar vertebra. The small apex articulates with the coccyx.
The pelvic surface is concave and the smooth lateral masses give attachment to the
piriformis muscle. Superiorly this surface is related to the peritoneum and inferiorly
to the rectum. The posterior surface is convex and rough, and in the midline where
it roofs the sacral canal it bears a median sacral crest, which is subcutaneous and
palpable, and two less prominent intermediate sacral crests more laterally. Each row of
dorsal sacral foramina lie lateral to the intermediate sacral crests. The posterior wall of
the sacral canal is deficient posteriorly, forming the sacral hiatus which is covered by
fibrous tissue. The hiatus is bounded on each side by the palpebral sacral cornua with
which the coccyx articulates.
The sacral canal is triangular in transverse section and contains the cauda equina and
CSF with the meninges. The dural sac ends at the 2nd sacral vertebra on a line joining
the posterior superior iliac spines. Extradurally lie the spinal nerves and the internal
vertebral venous plexus, the bulk of which lies anteriorly in the canal. The dorsal
surface gives attachment to erector spinae, gluteus maximus and the thoracolumbar
fascia.
The lateral surface is the roughened articular surface forming part of the sacroiliac joint.
Strong interosseous ligaments connect the sacrum and ilium.
Spinal and caudal anaesthesia techniques are so commonly used that it is important to be
aware of the anatomical abnormal-ities that may be encountered:
the sacral hiatus may be displaced upwards or downwards
the sacral canal may be narrowed or obliterated
the fibrous sheet covering the hiatus may be ossified
the dural sac may extend distally as far as S3 or, occasionally, S4. u

Segmental Bronchi and
Structure of the Lung
John Craven
cancer.
The segmental structure of the lungs is significant because infection and neoplastic
processes are often localized to one or more adjacent segments. Knowledge of the
anatomy of the intrapulmonary bronchial tree is important for:
understanding lung radiology
interpreting diagnostic bronchoscopy
therapeutic application of bronchoscopy to sputum retention
effective application of postural drainage for sputum retention
the surgical resection of diseased segments of the lungs.
Although the lung appears to be a homogeneous entity, each lung consists of ten
bronchopulmonary segments, which are in continuity. The parenchyma of each
segment is distinct from that of its neighbours and there is little vascular anastomosis
between them. Each segment has its own bronchus and is supplied by one or more
pulmonary arteries and drained by its own veins. The arteries and bronchus have
a central position in the segment, but the veins tend to lie peripherally along the
intersegmental planes. Segmental resection along intersegmental lines is possible
with little bleeding or leakage of air.
Each bronchopulmonary segment has a constant position, is wedge-shaped with its

apex at the hilum, and its base extending on to the pleural surface of the lung (Figure 1).
The differences in the anatomical arrangement of each side are slight; the arrangement
on the two sides would be similar but for the fact that the lingular bronchus branches
from the lef t upper lobe bronchus.
The right lung

The upper lobe the three segments are anterior, posterior and apical (which forms
the dome of the lung). The posterior segment of the right upper lobe is often the site of
infective processes, especially aspiration pneumonitis. The most common lesion of the
anterior segment of the upper lobes is neoplastic.
The middle lobe is divided vertically into a lateral and medial segment. The middle lobe
bronchus is long and surrounded by hilar lymph nodes and therefore is subject to pressure
and external compression by their enlargement. Thus, viral infections, bronchiectasis and
tuberculosis may be the cause of middle lobe collapse.
The lower lobe is the largest. There is an apical or superior lobe and four basal lobes
(medial, lateral, anterior, posterior) that are related to the diaphragm.
The left lung

The upper lobe consists of five segments. The lower two comprise the superior and
inferior lingual segments. The remaining segments of the upper lobe are arranged in
the same way as those on the right side apical, anterior and posterior.
The bronchial tree (Figure 2)

The right main bronchus is wider, shorter and more vertical than the left and therefore
more subject to accidentally inhaled foreign bodies. The upper lobe bronchus passes
laterally for l cm before branching into its three divisions (apical, anterior, posterior). The
pulmonary artery lies anteriorly to it and below this the middle lobe bronchus arises
anteriorly to divide into medial and lateral branches. Beyond the origin of the middle
lobe bronchus all other branches are destined for the segments of the lower lobe.
Segmental bronchi

The left main bronchus is longer than the right and about 5 cm from its origin it divides
into a lateral branch (the left upper lobe stem bronchus) and the bronchus to the lower
lobe. Just beyond the bifurcation, the upper lobe stem bronchus bifurcates into the
bronchus to the lingular segment, which divides into two segmental branches, the
anterior and posterior lingual branches. The stem bronchus to the upper lobe divides
to give the anterior and then the apical and posterior branches. The left lower lobe
bronchus usually gives off a posterior branch to the apical (superior) segment of the
lower lobe and branches to the remaining segments arise distal to that.
The structure of the bronchi

The bronchi are strengthened by horseshoe-shaped rings of cartilage, similar to
those of the trachea, and divide as they continue into the substance of the lungs into
progressively smaller structures until they are reduced to a diameter of less than l mm
when they lose their cartilaginous support. The bronchial tree is lined throughout by
mucous, submucous and connective tissue coats that become progressively thinner
in their distant ramifications. Plain muscle fibres bridge the intervals between the
cartilaginous rings or plates and replace them in the bronchioles. The submucous coat
contains mucous glands and the mucous coat consists of an elastic lamina on which
lies the respiratory epithelium as far as the respiratory bronchioles where the abundant
goblet cells and the cilia disappear. Each bronchiole ends in an alveolar sac. Fine
elastic cells continue into the alveolar walls. The alveolar walls are invested in a dense
capillary network.
Bronchial vessels
The bronchial vessels arise, one on each side, from the aorta or, sometimes from
the intercostal vessels to supply the lung parenchyma. The bronchial and pulmonary
vessels communicate freely on both the arterial and venous sides. These anastomoses
are of significance in chronic inflammatory lung disease when the bronchial arterial
system enlarges considerably. The bronchial circulation is an arteriovenous shunt; the
artery arises from the systemic circulation, but the veins enter the pulmonary system.
Nerve supply
The pulmonary plexuses lie anterior to the hilum of the lung and derive fibres from
both the vagi and the sympathetic trunk. Their efferent fibres pass to the bronchial
musculature and they receive afferents from the mucous membranes of the alveoli and
the bronchioles. u

Spinal Nerves and Dermatomes
John Craven
There are 31 pairs of spinal nerves, each attached to its appro-priate segment of
the spinal cord, by anterior and posterior nerve roots which unite just beyond the
posterior root ganglion (Figure 1). The nerves leave the vertebral column through
the intervertebral foramina (Figure 2). They are numbered after their corresponding
vertebra except the 8th cervical nerves, which pass out below the 7th cervical
vertebrae, because there are only seven cervical vertebrae. The remaining spinal
nerves take the name of the vertebra below which they emerge, there are
12 thoracic, five lumbar, five sacral and one coccygeal nerve. The segment of the spinal
cord from which each pair of spinal nerves arises takes the same name and number as
its nerves.
Spinal cord
Dura mater
Dorsal root
Arachnoid mater
Posterior root
Posterior root
ganglion
Spinal nerve
Posterior primary ramus Anterior root
Anterior primary ramus
1
Intervertebral foramen and spinal nerve
Spinal nerve
Intervertebral
disc
Vein
The anterior and posterior nerve roots emerge separately through the cords meninges.
Each posterior root ganglion lies without the dural sac and, apart from the first two and
the last two spinal nerves each lies in its intervertebral foramen. The adult spinal cord
is shorter than the vertebral column and thus there is a progressive obliquity of the
spinal nerve roots and the length of the nerve roots increases as the lower end of the
vertebral column is approached (Figure 3). The lumbar and sacral nerve roots are the
longest and most of these contribute to the bundle of nerve roots in the subarachnoid
space caudal to the end of the spinal cord (the cauda equina).

C1
Meninges
C2
C1
C3 2
C4 3
4
C5 5
Cervical segments
C6 6
C7 7
T1
C8 2
T1
Thoracic segments
3
T2
T3 4
T4 5
T5
T6 6
T7
7
T8
8
T9 Dura mater
9
T10
T11 10
Lumbar segments
11
T12
Sacral segments
12
L1
L1
Coccygeal segments
L2 2
Cauda equina
3
L3
4
L4 5
L5
S1
S2
S3
S4
S5

Co1
3
The dorsal roots contain afferent or sensory fibres from the skin, subcutaneous and
deeper tissues and often from viscera. The ventral roots contain efferent or motor fibres
to skeletal muscles and most contain preganglionic autonomic fibres. The cell bodies of
axons contributing to the ventral roots lie in the ventral grey horns of the spinal cord, but
the cell bodies of axons contributing to the dorsal roots lie outside the cord in the dorsal
root ganglion. Once the nerve lies outside the intervertebral foramen it is connected to
the sympathetic nervous system by rami communicantes. The 12 thoracic and first two
lumbar nerves each send a white ramus communicans to the sympathetic trunk and
each receives back a grey ramus communicans, the fibres of which are then distributed
with the branches of the spinal nerve. The spinal nerve then divides into anterior and
posterior primary rami (Figure 1). The posterior primary rami supply the skin and the
muscles of the back, the anterior primary rami supply the skin and muscles of the
lateral and anterior parts of the trunks and both upper and lower limbs. It is the anterior
primary rami that form the cervical, brachial and lumbosacral plexuses.
Dermatomes
The body skin is innervated in simple continuous strips, from behind forwards by
branches of the posterior and anterior primary rami. Although there is great complexity
of the several plexuses of the anterior roots, the nerve fibres of each spinal segment,
irrespective of their differing courses, are distributed to one strip (dermatome) of
skin. The dermatomes overlap each other so that on the trunk, for example, alternate
dermatomes meet each other. Segments whose nerves are primarily concerned with
limb innervation are absent or restricted from any innervation of the trunk. Muscles,
which are derived from myotomes, are also segmentally innervated.
Clinical importance
The relationships of the nerves, nerve roots and spinal cord segments to the vertebral
bodies and spines is of the greatest
clinical importance. Some useful surface markings include:
the spine of C7 (vertebra prominens) is easily palpable
the spine of T3 is opposite the medial portion of the spine of the scapula
the spine of T7 is opposite the inferior angle of the scapula (with the arms to the
sides)
a line drawn between the summits of the iliac crests intersects L4 or the L4/5
interspace
the dimples overlying the posterior superior iliac spines are on a line crossing the
second posterior sacral foramen; the dural sac in the adult usually ends at this point.
Figure 3 summarizes the relationship of the spinal cord and the meninges to the
vertebrae and their spines. u

The Sympathetic Trunk and
Stellate Ganglion
John Craven
examiners of the Royal College of Surgeons of England. His particular interest is in
gastric cancer.
The sympathetic nervous system has motor and sensory functions. The important
motor functions are the vasoconstriction of blood vessels and pilomotor and sudomotor
control to the skin; they are conveyed by efferent fibres, which pass in the white
(medullated) rami communicantes to synapse in a ganglion of the sympathetic trunk
(Figure 1). The medullated, preganglionic fibres arise only from cells in the lateral
horns of T1L2 and are conveyed within their anterior primary rami to enter the
sympathetic trunk. Within the trunk, fibres destined for the head and neck, arising
from the uppermost thoracic segments, ascend to one of the three cervical ganglia
(upper, middle or lower). In the ganglion, the fibres synapse with postganglionic,
non-medullated nerves.
The afferent (sensory) fibres reach the sympathetic trunk travelling on blood vessels,
within somatic nerves or within sympathetic nerves supplying sympathetic plexuses.
They pass from the sympathetic ganglia in the white rami communicantes to the
posterior root ganglion conveying visceral sensations such as colic or visceral pain.
Each sympathetic ganglion has a somatic and a visceral branch; the somatic branches
of the three cervical ganglia accompany the cervical nerves, the inferior cervical
ganglion giving branches to C7 and C8. The three cervical ganglia each supply vascular
branches, which allows wide distribution to the skin of the head and neck; each also
has a cardiac branch passing to the cardiac plexus. Visceral branches of the superior
cervical ganglion supply the dilator pupillae muscle and levator palpebrae superioris
muscle. The paired sympathetic trunks are formed of ganglia connected by nerve fibres.
They extend from the base of the occiput to the coccyx lying on the prevertebral fascia.
Developmentally there are ganglia for each spinal nerve but their number has been
reduced by fusion, producing three cervical, 11 thoracic, four lumbar and four sacral
ganglia.
A sympathetic ganglion Grey ramus

communicans
Spinal nerve (postganglionic)
White ramus Cardiac

communicans (postganglionic)
(efferent)
Visceral branches
Splanchnic (preganglionic)
1
The stellate ganglion
In 80% of the population, the inferior cervical ganglion is fused with the first thoracic
ganglion to form the large stellate ganglion, which lies on the neck of the first rib
behind the cervical pleura. Its branches are conveyed by grey (non-medullated) rami
communicantes to the C7, C8 and T1 spinal nerves and, via a plexus, to the subclavian
artery and its branches, from where they are distributed to the upper limb. It is of
clinical significance that the sympathetic nerve supply of the pupil and levator palpebrae
superioris joins the sympathetic trunk from the grey rami of the first thoracic segment
at the stellate ganglion.
Cervical sympathectomy: removal of the second and third thoracic ganglia is required
occasionally to abolish the excessive sweating of hyperhidrosis, the vasospasm of
Raynauds disease and, more controversially, to relieve the pain of causalgia (complex
regional pain syndrome type 2) after trauma to the upper limb. The aim of the operation
is to obtain sympathetic denervation of the upper limb without dividing the oculopupillary
fibres and thus producing the complications of ptosis, constriction of the pupil and loss
of sweating on the affected side of the face (Horners syndrome).
Sympathetic ganglion block with local anaesthetic solution (0.5% lidocaine

(lignocaine)) can be attempted to establish whether benefit can be expected from
sympathectomy (Figure 2). The patient lies supine, head and neck extended. A 6 cm
needle is directed posteriorly, 1.5 cm superior and 1.5 cm lateral, to the suprasternal
notch between the trachea and the carotid sheath alongside the body of the VIIth
cervical vertebra until it strikes its transverse process. The needle is then withdrawn
0.5 cm, suction applied to ensure it is extravascular and 10 ml of anaesthetic is injected.
A temporary Horners syndrome results if the block is successful.
Stellate ganglion block

Trachea
Common carotid
Sternomastoid
Jugular vein
C7
Subclavian artery
Vagus nerve
Stellate ganglion

The Thoracic Inlet and First Rib
John Craven
cancer.
The thoracic inlet, small and kidney-shaped, is about 10 cm wide and 5 cm

anteroposteriorly. It slopes forward and is bounded by the first thoracic vertebra
posteriorly, the upper border of the manubrium anteriorly and the first rib and costal
cartilage laterally. It transmits the oesophagus, the trachea, and the large vessels
comprising the right and left subclavian arteries, and the right and left brachiocephalic
veins, which unite behind the lower border of the right first costal cartilage to form the
superior vena cava. Lying on the neck of the first rib posteriorly is the sympathetic trunk.
On each side is the apex of the lung, some 3 cm above the medial third of the clavicle,
covered by the dome of the pleura (Figure 1).
The subclavian arteries commence behind the sternoclavicular joint and curve
laterally in front of the apex of the lung before passing on to the upper surface of the
first rib. Both subclavian veins lie anterior to their respective arteries curving medially
from the middle third of the clavicle to form the brachiocephalic vein by joining their
internal jugular vein behind the sterno-clavicular joint.
The first rib (Figure 2) is short, wide, flattened and lies in an oblique plane, sloping
forwards and downwards. It possesses a head that articulates with the body of the
first thoracic vertebra, a rounded neck, a posterior tubercle and a body. The anterior
end of the body bears the costal cartilage, which articulates with the manubrium. Its
head bears a single facet for articulation with the first thoracic vertebra and posteriorly
it bears a small tubercle posteriorly on its angle. The lower surface of the body is
smooth and lies on the pleura. A small scalene tubercle on its medial border marks the
attachment of the scalenus anterior muscle and this tubercle, on the upper surface of
the body, separates an anterior groove for the subclavian vein from a posterior groove
for the subclavian artery and the lower trunk of the brachial plexus which lies behind the
artery. Scalenus medius is attached to the upper surface of the body behind the groove
for the artery. Anterior to the neck of the rib and behind the pleura lie, from medial to
lateral, the sympathetic trunk and the large branch of the first thoracic nerve to the
brachial plexus.
The proximity to the surface and the constancy of their surface anatomy allows
percutaneous access to the large veins in this region; the subclavian vein can
be catheterized for intravenous feeding or monitoring central venous pressure. The
infraclavicular approach is preferred because there is less chance of accidental
puncture of the pleura by this route (Figure 3). The needle is inserted one fingers
width below the midpoint of the clavicle and directed medially and as far anteriorly as
possible (to ensure that neither the pleura nor the subclavian artery is pierced) towards
the jugular notch of the manubrium. The subclavian vein should be entered as it curves
over the body of the first rib.
The thoracic inlet
Infraclavicular access to the large veins

The Trachea and
Extrapulmonary Bronchi
John Craven
cancer.
The trachea, beginning at the level of the 6th cervical vertebra, descends from the
larynx through the neck and thorax to its bifurcation into the two bronchi at the sternal
angle, at the level of the 4th thoracic vertebra. In the adult, it is about 10 cm long and 2
cm in diameter. It is covered by the pretracheal fascia, which is attached superiorly to
the hyoid bone and the thyroid cartilage. The fascia splits to enclose the thyroid gland,
below which it blends into the carotid sheaths (Figure 1).
Trachea

The wall of the trachea is formed of fibrous tissue reinforced by 1520 cartilaginous
rings. These are incomplete posteriorly where the trachea rests on the oesophagus
and are there united by fibroelastic and smooth muscle tissue. The trachea is lined
interiorly by respiratory epithelium. It lengthens and widens slightly during inspiration
and recovers during expiration because of the elastic tissue within its walls.
Relations in the neck (Figure 2): the trachea lies anterior to the oesophagus with
the recurrent laryngeal nerve lying laterally in the groove between them. Anteriorly it is
covered by the cervical fascia and the infrahyoid muscles and is crossed by the isthmus
of the thyroid gland and the left brachiocephalic vein. To its lateral aspect lies the lateral
lobe of the thyroid gland, the inferior thyroid artery and the carotid sheath.
Carotid
sheath
Vertebral
body
Oesophagus
Prevertebral
fascia
Vagus nerve
Common
carotid artery
Internal
jugular vein
Left recurrent
nerve
Thyroid gland

Trachea
2
Relations in the thorax (Figure 3): the brachiocephalic artery and, below it, the arch
of the aorta separate the trachea from the manubrium. The oesophagus descends
behind the trachea. On its left lie the common carotid and subclavian arteries above
and the aortic arch below, to the right lie the mediastinal pleura, the right vagus nerve
and the azygos vein.
The tracheal bifurcation, the carina, lies anterior to the oesophagus and to its left lies
the bifurcation of the pulmonary trunk. Tracheobronchial lymph nodes lie on either side.
The extrapulmonary bronchi: each arises at the carina and descends laterally to
enter the hilum of the lung where it divides to form the intrapulmonary bronchial tree.
Their structure is similar to that of the trachea.
The right bronchus is about 3 cm long. It is wider and more vertical than the left
bronchus, which is why inhaled foreign bodies tend to enter it more often. The right
upper lobe bronchus arises from it just before it enters the hilum of the lung. Anteriorly,
the right pulmonary artery separates it from the pericardium and the superior vena
cava. The arch of the azygos vein is above it and the bronchial vessels lie posteriorly.
The left bronchus is about 5 cm long. Anteriorly, the left pulmonary artery separates
it from the left atrium. The arch of the aorta is above it and posteriorly the bronchial
vessels separate it from the oesophagus and the thoracic aorta. u

The Veins of the Lower Limb
John Craven
The veins of the lower limb are classified as superficial, deep or communicating
(perforating) veins. Valves are present in all the larger vessels including the
communicating veins.
Superficial veins
The superficial veins drain the subcutaneous tissue and terminate in the two large
longitudinal channels, the great and the small saphenous veins.
Great (or long) saphenous vein

The great (or long) saphenous vein originates from the medial side of the dorsal venous
arch beginning just in front of the medial malleolus. It ascends the medial side of the
calf and thigh (accompanied in the calf by the saphenous nerve) and passes through
the saphenous opening of the deep fascia 1.5 cm below the inguinal ligament to enter
the femoral vein. Its tributaries drain the leg, thigh, inguinal region and the pubic region
but its most clinically important branches are the several communicating branches (or
perforating veins) that drain from it into the deep veins of the calf and thigh, perforating
the deep fascia generally on the medial side of the leg (Figure 1).
The long saphenous vein and calf perforators
Perforator below knee
Posterior
Great saphenous arch vein
Perforator
Perforator
Perforator
Small (or short) saphenous vein

The small (or short) saphenous vein originates from the lateral end of the dorsal
venous arch. It ascends behind the lateral malleolus along the back of the calf to end
by piercing the deep fascia a variable distance below the popliteal fossa to end in the
popliteal vein. In its lower course it is accompanied by the sural nerve. It has tributaries
communicating with the deep veins of the calf and one or more that join with the great
saphenous nerve (Figure 2).
Short saphenous vein entering popliteal vein

(deep fascia has been incised)
Deep fascia
Popliteal fossa Popliteal vein
Posterior
arch vein
Short saphenous
vein
Lateral malleolus
Deep veins
The deep veins comprise the soleal plexus, the popliteal and the femoral veins.
They communicate with the superficial veins by perforators, veins that perforate the
deep fascia (Figure 1), the valves of which are arranged to allow blood to flow only
towards the deep veins. The soleal plexus, which lies within the muscles of the calf,
drains into the popliteal vein, which drains into the femoral vein and both accompany
their corresponding artery deep to the deep fascia. The soleal plexus has a large
volume and it is the pressure of the contracting calf muscles (the soleal pump) that
is an important factor in ensuring venous return from the lower limb to the heart. The
soleal pump is dependent for its efficiency on the competence of the valves in the
communicating veins.
The soleal plexus is the most common site of origin of a deep vein thrombosis.
Immobility as a result of bed rest or anaesthesia increases the stagnation of blood in
the lower limb especially in the soleal plexus. The thrombus may extend from the soleal
plexus to the popliteal and femoral veins, if so the risk of pulmonary embolism becomes
significant. Thrombosis in the soleal plexus may also extend into the perforating veins;
subsequently, after spontaneous recanalization, the protective valves in those vessels
are destroyed, which allows venous blood to travel retrogradely, from the deep veins to
the superficial resulting in obvious varicose veins. This results in venous hypertension
in the superficial tissues of the leg as shown by soft tissue fibrosis, hyperpigmentation
and, in severe cases, chronic skin ulceration. It is thought that the primary cause
of varicose veins is the incompetence of the valves in the perforating veins and the
retrograde flow that follows produces distension of the superficial veins. This distends
the saphenous veins and renders their valves incompetent. u

Cardiac
Anaesthesia
on CD-ROM
Anaesthesia for Off-pump
Coronary Artery Bypass
Surgery
Virin S Sidhu
Sri Varaday
Virin S Sidhu is Consultant in Anaesthesia and Intensive Care at St Marys Hospital,

London, UK. He qualified from the University Hospital of Wales, Cardiff.
Sri Varaday is Specialist Registrar at the Imperial College School of Anaesthesia,

London. He graduated from Andhra University, India.
Off-pump coronary artery bypass (OPCAB) surgery is performed on a beating

heart without the use of cardiopulmonary bypass. The first work relating to coronary
artery bypass graft on a beating heart was carried out in 1910 by Carrel, and the first
successful surgery using cardiopulmonary bypass was performed in 1953 by Gibbon.
The initial morbidity and mortality on cardiopulmonary bypass was high, allowing
the development of coronary artery surgery without it. In 1967, Kolessov reported a
series of six cases in which the internal mammary artery was anastomosed to the
left anterior descending artery on the beating heart. With the development of bubble
oxygenators and cardioplegia in the late 1960s, coronary artery surgery performed
on cardiopulmonary bypass became the technique of choice, though cardiopulmonary
bypass is still associated with deleterious effects.
In 1996, Calafiore introduced minimally invasive direct coronary artery surgery through
a left anterior short thoracotomy incision or mini-sternotomy, which renewed interest in
off-pump surgery. This technique was improved by the use of stabilizers designed to
imobilise a target area of the heart. However, its main limitation was that access was
limited to the left anterior descending and proximal right coronary arteries. The main
potential benefit of minimally invasive direct coronary artery surgery was the avoidance
of cardiopulmonary bypass. This has resulted in an increase in popularity of OPCAB
through a median sternotomy, allowing access to multiple vessels, and the avoidance
of one-lung ventilation (mandatory for minimally invasive direct coronary artery surgery)
while retaining rapid access to cardiopulmonary bypass in difficult or failed procedures.
OPCAB presents new challenges for the surgeon and anaesthetist.
Exposure and stabilization of coronary arteries

Complete revascularization of the heart by accessing all coronary territories requires
adequate exposure and stabilization of target coronary arteries. The left anterior
descending and proximal right coronary arteries are exposed with minimal cardiac
displacement and haemodynamic compromise using surgical packs. The circumflex,
diagonal, posterior descending artery and distal right coronary artery are more difficult
to expose. The application of slings, pericardial sutures and the placement of surgical
packs help to displace and elevate the heart anteriorly providing adequate exposure.
A Trendelenburg tilt with rotation of the operating table to the right and opening the
right pleura reduces haemodynamic compromise due to compression of the heart
against the right pleura, while performing anastomosis on the posterior and lateral
walls. Exposure of the posterior descending artery may require a steep Trendelenburg
tilt, such that the apex of the heart is almost pointing towards the ceiling! In order to
prevent bleeding from the open coronary artery during anastomosis, the target vessel
is occluded with slings or microvascular clamps. A humidified carbon dioxide blower is
used to prevent blood obscuring the arteriotomy site. Intracoronary shunts may be used
to maintain perfusion, display the suture line and reduce back-bleeding.
Mechanical stabilizers have greatly contributed to the feasibility of beating heart

surgery, allowing good quality anastomotic suturing. Stabilization of the target site is
accomplished by using stabilizers such as the Octopus Systems (Medtronic) (Figure
1a), which offer secure, stable access to all coronary arteries. Using gentle suction, the
Star-Fish (Figure 1b) gently lifts, positions and holds the beating heart. Stabilization
of the tissue at the grafting site is achieved by the smaller, more flexible arm and
turret-mounted design of the Octopus device. The malleable suction pods assure easy
application, such that the site is lifted and not depressed, thus avoiding impairment of
ventricular filling.

Vacuum tubing Swivel head link
Flexible arm
Turret
mount Flexible arm
Vacuum tubing
Suction pods
Anaesthetic technique
The most important anaesthetic considerations are the prevention of haemodynamic
instability and ischaemia. The technique lends itself to early extubation and ambulation.
Preoperative assessment should include a review of the angiogram and a discussion
with the surgeon of the order of grafting. Adequate premedication is required and
tachycardia avoided.
Operating room set up

Early extubation requires the maintenance of normothermia. The operating room is kept
warm to avoid radiant heat loss. The head should be covered with drapes. A warming
mattress and fluid warmer are used. A forced-air warming blanket is used over the
lower half of the body once the saphenous vein has been harvested. The heartlung
machine and perfusionist should be available immediately, but it is usually unnecessary
to have the machine primed. Facilities for defibrillation, cardiac pacing and intra-aortic
balloon pump counterpulsation should also be available immediately. For multiple
vessel OPCAB a cell saver reduces homologous blood transfusion.
Monitoring
Standard cardiac monitoring is used. The ECG may be distorted during cardiac
displacement; in particular, the amplitude and ST segment changes may be
reduced. ST segment trending is useful. Pulmonary artery pressure monitoring and
transoesophageal echocardiography (TOE) may be used in high-risk patients with
severe left ventricular dysfunction. TOE is useful in the detection of regional wall
motion abnormalities and thus early ischaemic changes. During OPCAB, the heart is
displaced or lifted and standard TOE views are lost. Furthermore, the stabilizers used
may produce artefacts of regional wall motion abnormalities. However, a baseline
TOE allows their assessment with particular attention to the areas supplied by the
vessel to be grafted. A TOE examination following the completion of the anastomosis
allows regional wall motion abnormalities to be re-checked. Continuous cardiac output
monitoring is considered insensitive for routine use. The response time is too slow
to detect sudden changes following manipulation and tilting of the heart; it is more
useful as a trend monitor. Continuous monitoring of mixed venous oxygenation usefully
detects abrupt changes in cardiac output.
Anaesthesia
Induction and maintenance of anaesthesia are determined by local extubation
protocols. A balanced anaesthetic technique using limited doses of opioids, volatile
agents and propofol is popular. A thoracic epidural technique provides cardiac
sympathectomy, attenuates the stress response, reduces anaesthetic requirements and
thus promotes early extubation and provides excellent postoperative analgesia. The
risk of spinal haematoma formation can be reduced by siting the epidural catheter well
before surgery. The advent of stabilizers has made the induction of pharmacological
bradycardia, originally used to provide the surgeon with a relatively immobile area,
less important, but tachycardia should be avoided. The serum potassium should be
maintained at about 4.5 mmol/litre. Magnesium sulphate prevents and treats atrial and
ventricular arrhythmias during OPCAB surgery and can be infused following induction
of anaesthesia. Partial heparinization (1 mg/kg) maintaining an activated clotting time of
250300 s and complete reversal with an appropriate dose of protamine is advocated.
During proximal coronary anastomosis, arterial pressure should be reduced to 90 mm
Hg to reduce the risk of aortic dissection on application of aortic side-biting clamps.
Diuretics, in small doses, may be required to correct fluid balance.
Management of haemodynamic instability

The main causes of haemodynamic instability during OPCAB surgery are the
impairment of venous return due to chamber compression and abnormal positioning,
and pump failure due to direct ventricular compression or ischaemia during occlusion of
the target arteries. Mitral valve distortion can contribute significantly to haemodynamic
instability, and cardiac displacement increases the risk of intraoperative arrhythmia.
The extent of the haemodynamic compromise depends on the coronary artery being
anastomosed, the greatest being the circumflex artery and its branches on the posterior
aspect of the heart, and the diagonal vessels on the lateral aspect. It may therefore
be prudent to revascularize vessels on the anterior aspect of the heart, before any
lifting or rotation occurs. Changes in arterial pressure and cardiac output may occur
rapidly with cardiac manipulation and the anaesthetist must pre-empt these to maintain
haemodynamic stability. The use of the Trendelenburg position, optimizing preload, the
use of vasoconstrictors, inotropes, or repositioning of the heart may improve cardiac
output. Occlusion of the target coronary arteries during anastomosis of grafts may
result in ischaemia and arrhythmias, including ventricular fibrillation. Occlusion of the
proximal right coronary artery may lead to ischaemia of the atrioventricular node and
complete heart block. The application of pacing wires may be necessary before arterial
occlusion. If adequate haemodynamic parameters cannot be maintained it may be
necessary to convert to an on-pump technique. Good communication with the surgeon
is mandatory.
Advantages and disadvantages of OPCAB

Advantages: off-pump surgery avoids the complexity and may avoid some of the
deleterious effects of cardiopulmonary bypass. This includes derangements in
coagulation, and multiple-organ dysfunction occurring through a combination of the
systemic inflammatory response syndrome, flow abnormalities and emboli. The specific
advantages of the technique are shown in Figure 2; the most important is the possible
reduction of subtle neurological deficit and cognitive dysfunction. By avoiding cardio-
pulmonary bypass the potential for emboli originating from the aorta and the bypass
circuit is reduced, though the need for aortic manipulation is not eliminated. The renal
impairment and respiratory dysfunction that may occur following cardiopulmonary
bypass, have not been universally demonstrated to be reduced with an off-pump
technique. The results of large randomized prospective trials are awaited.
Advantages of OPCAB
Reduced systemic inflammatory response syndrome

Reduced blood loss and transfusion requirements
Short operating, intubation and ventilation times
Possible reduced neurological and neuropsychological effects
Shorter ICU and hospital stay
Potential cost saving
Disadvantages: OPCAB surgery demands a high level of vigilance on the part of the
anaesthetist and is technically demanding for the surgeon. Cardiovascular collapse or
ventricular fibrillation may occur rapidly. The ability to respond quickly to such changes
is essential, including conversion to an on-pump technique. Patients with severe left
ventricular dysfunction requiring multiple grafts may be unsuitable for an off-pump
technique as may patients with certain patterns of coronary artery disease. The long-
term patency of grafts is unknown. u
FURTHER READING
Alston P R. Off-pump Coronary Artery Surgery and the Brain. Br J Anaesth 2000; 84:
54952.
George S J. Mitral Annulus Distortion during Beating Heart Surgery: A Potential

Cause for Haemodynamic Disturbances A Three Dimensional Echocardiography
Reconstruction. Ann Thorac Surg 2002; 73: 142430.
Heames R M, Gill R S, Ohri S K et al. Off-pump Coronary Artery Surgery. Anaesthesia

2002; 57: 67685.
Mehta Y, Juneja R. Off-pump Coronary Artery Bypass Grafting: New Developments but
a Better Outcome? Curr Opin Anesthesiol 2002; 15: 918.
Ramsay J. Anaesthesia for Off-pump Coronary Bypass Grafting. In: Clement F,

Shanewise J, eds. Minimally Invasive Cardiac and Vascular Techniques. Baltimore:
Lippincott, Williams & Wilkins, 2001; 1328.

Anaesthesia for Patients with
Cardiac Disease Undergoing
Non-cardiac Surgery
K Moyna Bill
K Moyna Bill is Consultant in Cardiac Anaesthesia and Intensive Care at the Royal
Hospitals Trust, Belfast, UK. She qualified from the University of Edinburgh and trained
in anaesthesia in Northern Ireland, and Leiden, The Netherlands.
The number of patients with cardiac disease presenting for anaesthesia to facilitate
non-cardiac surgery is increasing. They present some of the greatest anaesthetic
challenges because their cardiac lesions will still exist after the operation, unlike
patients undergoing cardiac surgery. Perioperative cardiac morbidity (myocardial
ischaemia, infarction, arrhythmias) is the most common cause of death following
anaesthesia and surgery. Despite improvements in anaesthetic technique, the mortality
associated with a perioperative myocardial infarction is 4070%. The prevalence of
coronary artery disease increases with increasing age and it is estimated that about
33% of patients undergoing non-cardiac surgery are at risk of having cardiovascular
disease. In many patients this will not have been diagnosed, therefore preoperative
assessment is important to identify it and its attendant risks. Other forms of cardiac
disease (valvular and congenital heart disease or heart transplant patients) should also
be considered.
Preoperative assessment
Preoperative assessment is important to:
assess the risk to the patient
optimize the patients condition
form a plan for perioperative management to minimize the risk of an adverse
outcome.
Assessment of risk
The best known scoring system for estimating the risk of surgery for patients with
cardiac disease was developed by Goldman in 1977, and modified by Detsky in 1986.
It is a multifactorial risk analysis that combines clinical and investigation parameters
and allows patients to be grouped into four risk categories, for major complications
or cardiac death. The most widely used index of perioperative risk remains the ASA
(American Association of Anesthesiologists) physical status system even though it is
somewhat subjective and lacks specificity.
In 1996, the American College of Cardiology and American Heart Association (ACC/
AHA) produced guidelines for peri-operative evaluation for non-cardiac surgery; they
were updated in 2002. These guidelines differentiate clinical predictors of increased
perioperative cardiac risk into three categories (major, intermediate and minor; Figure
1). Recognition of these factors, the functional capacity and the type of surgery are
then used to inform the anaesthetist as to the need for further cardiac investigation.
Clinical predictors for perioperative cardiac risk
Major risk factors

Unstable coronary syndromes
Acute myocardial infarction (< 6 weeks)
Myocardial infarction > 6 weeks or < 6 months but with
myocardium at risk
Unstable or severe angina (CCS Class III or IV) 1
Decompensated congestive heart failure
Symptomatic arrhythmias
Severe valvular disease
Coronary artery bypass grafting (CABG) or percutaneous
transluminal coronary angioplasty (PTCA) stent < 6 weeks
Intermediate risk factors

Stable angina (CCS Class I or II)
Previous myocardial infarction by history or ECG
Compensated or previous congestive heart failure
Diabetes mellitus
Minor risk factors

Age (physiological) > 70 years
Abnormal ECG (left ventricular hypertrophy, left bundle branch block,
ST abnormalities)
Rhythm other than sinus (e.g. atrial fibrillation)
Systemic hypertension
History of stroke
Hyperlipidaemia
Low functional capacity
Smoking
Renal insufficiency
1
CCS, Canadian Cardiovascular Society
1
The history, physical examination, basic haematological tests, 12-lead ECG, and chest
radiograph should be carried out to identify the:
presence of heart disease
severity, stability and previous treatment of the disease
functional capacity of the patient
presence of co-morbid conditions.
More detailed cardiac investigations may be appropriate in patients who are awaiting
elective or, on occasions, urgent surgery. In the emergency situation, patients with
cardiac risk factors and reduced functional capacity have a high perioperative risk, but
delaying surgery for detailed investigation does not benefit the patient.
Patient risk factors

Previous coronary revascularization patients who have undergone coronary artery
bypass grafting (CABG) or percutaneous transluminal coronary angioplasty (PTCA)
with or without stent insertion in the previous 5 years and who have had no recurrence
of symptoms with return to an active lifestyle do not need further testing. Those who
have had a recent stent placement should have their surgery postponed for 6 (or
preferably 12) weeks, if possible, because of the bleeding risks associated with the anti-
platelet drugs (aspirin, clopidogrel) that they are obliged to take to prevent re-stenosis
of the vessel and stent.
Previous coronary evaluation those who have had cardiac evaluation in the
previous 2 years should need no further investigation providing their symptoms have
not changed and their activity levels have not deteriorated.
Myocardial infarction and ischaemia advances in the treatment of myocardial

infarction (thrombolysis, PTCA with or without stent) have meant that the traditional
high-risk period following infarction of 6 months may be reduced, providing there is
evidence that no further myocardium is at risk. This is assessed by stress testing (see
later). The heart takes 46 weeks to remodel and heal following infarction, during which
time it is more vulnerable to arrhythmias and myocardial stunning. The haemodynamic
stresses and hypercoagulability associated with surgery may also lead to extension
of the infarct. Patients who have unstable or severe angina (Canadian Cardiovascular
Society (CCS) Class III or IV) also have a high probability of continuing plaque rupture
and thrombosis. Although it is common practice to postpone truly elective surgery until
6 months after a myocardial infarction, patients who have had a myocardial infarction
over 6 weeks previously and show no evidence that further myocardium is at risk
can proceed with urgent surgery with perioperative cardiac risk reduction strategies.
When at least 6 months have elapsed, those who have resumed normal daily activity
and have no post-infarction angina should not need further testing, unless the risk of
surgery or the functional capacity warrants it.
Arrhythmias the cause should be identified and treatment instituted, especially for
those that are symptomatic and cause hypotension. Indications for antiarrhythmic drugs
and cardiac pacing are the same as in the nonsurgical patient.
Decompensated congestive heart failure these patients should have their medical
therapy optimized to minimize the risk of worsening their pulmonary oedema. If
ischaemia is the cause, they are also at risk of developing a perioperative myocardial
infarction.
Compensated congestive heart failure patients with a left ventricular ejection

fraction less than 35% are at particular risk for perioperative complications.
Diabetes mellitus there is a high incidence of silent ischaemia associated with

diabetic neuropathy, making the lack of angina with exercise a less reliable symptom.
Dyspnoea, especially with minimal exertion, may be a more important symptom.
Hypertension inclusion of hypertension as an intermediate or minor risk factor

remains controversial. There is some evidence that if left ventricular hypertrophy
is present and the blood pressure is not well controlled, the risk is more significant
because the increase in left ventricular mass makes it more susceptible to changes in
oxygen delivery and demand. Severe hypertension should be controlled before surgery
if possible.
Minor risk factors cerebrovascular disease and renal insufficiency are possibly not
direct risk factors but markers of end organ damage from the same factors that cause
coronary artery disease. The greater the number of minor and intermediate risk factors
the greater the risk of the patient having coronary artery disease.
Functional capacity: exercise tolerance is assessed by history and is expressed

as metabolic equivalents (1 MET = 3.5 ml O2/kg/min) on a scale defined by the Duke
Activity Status Index in order to estimate their maximal oxygen consumption capacity
(Figure 2). Patients with moderate or excellent functional capacity and low clinical
predictors of risk do not need further cardiac investigation. The functional capacity of
some patients may be limited by other conditions (e.g. respiratory, peripheral vascular
or joint disease). These patients and those with poor functional capacity should
undergo detailed cardiac assessment.
Estimated energy requirements for various activities
Poor functional capacity (14 MET)

Light housework
Shower or dress without stopping
Walk at 2.5 mph on level ground
Moderate functional capacity (57 MET)

Climb a flight of stairs without stopping
Walk briskly (> 4 mph) on flat
Light gardening
Excellent functional capacity (> 7 MET)

Digging in garden
Carrying shopping upstairs
More strenuous sports (e.g. cycling uphill, jogging)
Surgical risk factors: the type of surgery and the resultant degree of haemodynamic
stress influences the risk to the patient (Figure 3). Some procedures previously counted
as high risk are now categorized as intermediate risk, owing to improved perioperative
management. Account must also be taken of the risk of not performing the surgery, and
the experience and skill of the surgeon and anaesthetist. Peripheral vascular surgery
may also be counted as high risk because the extent of the cardiac disability can be
masked by the limits imposed by intermittent claudication.
Further cardiac investigations: all cardiovascular tests have limitations and risks and
should be carried out only if the results will change the patients management.
Coronary angiography and revascularization the indications for these are the
same as for those not having surgery (e.g. unstable angina unresponsive to medical
treatment, deteriorating severity of symptoms).
Ambulatory ECG monitoring has been used to assess silent ischaemia, but in
a significant number of patients (up to 50%) resting ECG abnormalities make the
interpretation difficult.
Stress tests (e.g. exercise ECG, dipyridamole-thallium scinti-graphy (DTS) or

dobutamine stress echocardiography (DSE)) are dynamic investigations that elucidate
the possibility of threatened myocardium and the maximal tolerated heart rate. DSE and
DTS are the only non-invasive tests that improve preoperative risk stratification.
Echocardiography and technetium-99 scanning assess myocardial function but

cannot predict ischaemic events. Echocardiography is also used to assess the nature
and severity of valvular heart disease.
Surgical risk factors
High risk (complication rate > 5%)

Emergency, intermediate and major procedures
Aortic and major vascular procedures
Prolonged procedures
Procedures with large fluid shifts, blood loss or which produce
haemodynamic instability
Intermediate risk (complication rate 15%)

Minor vascular procedures (including carotid endarterectomy)
Prostatic surgery
Orthopaedic surgery
Head and neck surgery
Intraperitoneal surgery
Intrathoracic surgery
Low risk (complication rate < 1%)

Endoscopic procedures
Superficial surgery
Breast surgery
Ophthalmic surgery
Plastic and reconstructive surgery
Other systems (e.g. respiratory, renal, endocrine, skeletal, airway) need assessment
and possible further investigation. The results may affect the anaesthetic plan.
Preoperative therapy
The patients condition and medication should be optimized. Most cardiac medication
should be continued peroperatively. There is evidence that continuation of ACE
inhibitors may increase the incidence of hypotension and some physicians have
recommended withholding them for 24 hours preoperatively.
Two specific strategies have been suggested to reduce postoperative morbidity and
mortality.
In goal-directed optimization, patients with high risk factors for major surgery
are admitted preoperatively to a high dependency or intensive care unit for invasive
monitoring (including pulmonary artery catheter) and manipulation of fluid and inotropic
therapy in order to achieve the optimal cardiac index, oxygen delivery and consumption.
In selected patients, -blockade has reduced perioperative cardiac events and
improved 6-month survival. The optimum time from surgery for commencing and
discontinuing -blockers is less clear and it seems that achieving a target heart rate is
more important.
Other studies with 2-agonists are not so convincing. There is insufficient evidence
about the effects of preoperative and intraoperative nitroglycerine.
CABG and PTCA are appropriate only in patients who would require them even if they
were not awaiting surgery. The combined risk of both procedures may be greater than
that of non-cardiac surgery with perioperative risk-reduction strategies.
Premedication should be adequate to allay anxiety, and oxygen therapy preoperatively

may be advantageous. Warfarin therapy should be replaced with heparin and
antiplatelet drugs (aspirin, clopidogrel) should be stopped at the appropriate time. This
depends on the severity of the coronary artery disease and the surgical procedure.
Intraoperative management
Principles: the oxygen supply:demand ratio must be maintained to avoid ischaemia
(Figure 4). In coronary artery disease, the pressure gradient across the fixed stenoses
is important because the coronary arteries cannot dilate in response to increased
oxygen demand. Maintenance of arterial blood pressure and reduction of heart rate
should reduce the risk of ischaemia. This is also important in patients with aortic
stenosis. It has been suggested that in cardiac patients, a haemoglobin level of 10 g/dl
or more is needed to optimize the oxygen supply.
Factors affecting myocardial oxygen supply and demand
Supply
Coronary perfusion pressure (aortic diastolic perfusion left
ventricular end-diastolic pressure)
Blood oxygen content
Partial pressure of oxygen in arterial blood (PaO2)
Haemoglobin concentration
Coronary vascular resistance
Coronary artery stenosis
Heart rate and left ventricular end-diastolic pressure
Autoregulation
Demand
Heart rate
Contractility
Wall tension
Left ventricular end-diastolic pressure
Arterial pressure
Contractility
In the preoperative plan, it is important to decide which values of preload, heart

rate, systemic vascular resistance, pulmonary vascular resistance and rhythm are
acceptable and to anticipate the times when the maintenance of these values will
be most difficult (e.g. induction, intubation, blood loss). Strategies to deal with these
situations should be considered preoperatively.
Anaesthetic agents: the choice of anaesthetic agents and techniques does not
significantly affect the risks of perioperative complications, providing hypertension,
tachycardia and hypotension are avoided. It should be governed by the experience
and skill of the anaesthetist and their familiarity with the techniques and drugs.
Etomidate has the fewest cardiovascular effects but most people are more familiar
with thiopental (thiopentone) or propofol, both of which should be titrated carefully to
effect. Pretreatment with a dose of opioid reduces the required dose of induction agent
and may attenuate the haemodynamic response to intubation. Remifentanil is a new,
potent, ultra-short-acting opioid, which has great ability to produce haemodynamic
stability and suppress the stress response. It is administered by infusion and transfer to
other methods for postoperative analgesia needs careful consideration. Concerns were
previously raised that isoflurane might cause a coronary steal situation but these have
subsided. It should be remembered that N2O is also a myocardial depressant. The role
of regional blockade is keenly debated. It has many advantages, not least in reduction
of the stress response and in effective analgesia. Preservation of an adequate
perfusion pressure is vital and the vasodilatation produced may be better avoided in
some patients. However, incomplete anaesthesia can lead to increased stress response
and myocardial ischaemia.
Monitoring: a 5-lead ECG gives better detection of myocardial ischaemia. Recent

studies have shown that V5 is the most sensitive single lead. ST segments should
be monitored in high-risk patients. Invasive monitoring by arterial and pulmonary
artery catheters may be useful in those at high risk, especially if they have had a
recent myocardial infarction with cardiac failure, providing the anaesthetist has the
experience to insert them and interpret the data. The pulmonary artery catheter is
most useful in monitoring volume status and cardiac performance, such as cardiac
output/index, mixed venous oxygen saturation, systemic and pulmonary vascular
resistances. Transoesophageal echocardiography may be used to assess volume
status and valvular disease and is the best way to detect ischaemia early (segmental
wall motion abnormalities), but requires expertise to interpret it. Information received
from the monitors (e.g. hypotension, ischaemic changes, left ventricular dysfunction,
arrhythmias) needs to be acted on urgently, especially in those with severe disease.
Temperature control: there is a higher incidence of cardiac morbidity in patients who

become hypothermic, therefore active warming measures are often required.
Blood glucose control: it has been shown that tighter blood glucose control (4.46.1
mmol/litre) leads to reduced morbidity and mortality.
Postoperative management
The period after surgery is associated with increased levels of catecholamines and
hypercoagulability. Most perioperative infarcts occur in the first 3 days, therefore the
preoperative plan should include the most appropriate place for postoperative care and
the same management goals should be adhered to in this period. All patients should
receive humidified oxygen, for at least 72 hours after major surgery. Postoperative
analgesia should be adequate. Anaemia should be treated and thromboprophylaxis
continued. The patients normal cardiac medication should be restarted as soon as
possible.
Specific conditions
Valvular heart disease: stenotic lesions lead to a low, fixed cardiac output, which
tolerates poorly any changes in rhythm, tachycardia and decrease in preload and
vascular resistance. Replacement of the valve before non-cardiac surgery may need to
be considered in severe symptomatic disease, especially aortic stenosis. Patients with
regurgitant valves benefit from afterload reduction, faster heart rates and maintenance
of preload. Antibiotic prophylaxis is necessary for all cases and should be governed by
the type of surgery and local regimens.
Congenital heart disease: anaesthesia for these patients is discussed elsewhere. It is

vital to understand the pathophysiology of the particular lesion.
Cardiac transplant: all electrical stimulation in the heart is initiated from the donor
sino-atrial node. The resting heart rate is generally 90120 beats/min and there is no
response to carotid sinus massage, changes in body position, light anaes-thesia or
hypotension. An adequate preload should be maintained. Cardiac drugs that act directly
on the myocardium or peripheral vasculature are necessary because those acting on
the autonomic system have no effect on the denervated heart. Invasive monitoring
should be avoided where possible and strict asepsis used at all times. Antibiotic
prophylaxis depends on the type of surgery and should include anti-staphylococcal
cover. It is imperative that immunosuppressive therapy is continued. u
FURTHER READING
ACC/AHA Task Force. Guidelines for Perioperative Cardiovascular Evaluation for Non-
cardiac Surgery. Circulation 1996; 93: 1278317. (Review. Anesth Analg 2002; 94:
105264.)
Aitkenhead A R, Rowbotham D J, Smith G. Textbook of Anaesthesia. 4th ed.

Edinburgh: Churchill Livingstone, 2001.
Chassot P-G, Delabays A, Spahn D R. Preoperative Evaluation of Patients with, or at

Risk of, Coronary Artery Disease Undergoing Non-cardiac Surgery. Br J Anaesth 2002;
89: 74759.
Shaw A, Boscoe M J. Anaesthetic Assessment and Management of Cardiac Patients

for Non-Cardiac Surgery. Part 1. Int J Clin Practice 1999; 53(4): 2816. (Part 2. Int J
Clin Practice 1999; 53(5): 3538.)

Management of
Cardiopulmonary Bypass
Judith Hall
Brian F Keogh
Judith Hall is Head of Perfusion at the Royal Brompton Hospital, London.
Brian F Keogh is Consultant in Cardiothoracic Anaesthesia at the Royal Brompton

Hospital, London. His special interests include modes of respiratory support,
particularly in acute severe pulmonary failure.
The driver for the development of cardiopulmonary bypass (CPB) was the desire to
operate on a still heart in a blood-free surgical field. The concept was first applied in
the animal laboratory by Gibbon in 1935. Research continued until the first clinical
application of CPB by Dennis in 1951, in which the patient died due to surgical
complications. In 1953, Gibbon successfully closed an atrial septal defect, using his
design of heartlung machine, and triggered the evolution of present day cardiac
surgery.
The CPB circuit

The three basic functions of the CPB circuit are gas exchange, heat exchange and
blood flow. The structural components of the circuit are outlined in Figure 1 and are
connected with PVC tubing. The circuit requires a priming volume (usually a mixture of
crystalloid and colloid) of 1.52 litres.
Cardiopulmonary bypass circuit
Venous blood drains by gravity from a single cannula placed in the right atrium when
the atria are not opened, for example in coronary artery bypass graft (CABG) and
aortic valve replacements, or by direct cannulation of the inferior and superior vena
cava in more complex procedures. Venous blood is collected in the venous reservoir,
which can be separate from, or more commonly (as in Figure 1) integrated with the
cardiotomy reservoir. The blood is pumped from the reservoir through the oxygenator
by a roller or centrifugal pump. The pump flow rate, reflecting oxygen delivery
requirements at rest, is 2.4 litres/min/m2. The range is 1.63.0 litres/min/m2, depending
on body core temperature, mean arterial pressure and mixed venous saturation. For
each 1oC decrease in temperature, the required cardiac output is 7% less, and the flow
can be reduced by an equivalent factor. The prolonged use of high pump flow rates is
associated with destruction of red cells. In prolonged procedures, even with reduced
flows, haemolysis and haemoglobinuria are common.
The oxygenator system

The oxygenator system usually includes an integrated venous reservoir, heat exchanger
and oxygenator. The heat exchanger regulates blood temperature by altering the water
temperature flowing through its tubing. The heat exchanger is situated proximal to the
oxygenator because alterations in the temperature of blood that is 100% saturated can
cause nitrogen, in the form of gaseous microemboli, to be released. The oxygenator
is a series of hollow fibres bundled together and encased in a polycarbonate shell.
Venous blood flows around the fibres and the inlet gas (oxygen/air) passes though
the centre. Gas exchange takes place by diffusion across the oxygenator membrane.
The inlet fraction of oxygen in inspired air (FiO2) controls the resultant partial pressure
of oxygen in arterial blood (PaO2) and the PaCO2 is controlled by the sweep rate of
the inlet gas. Carbon dioxide is exhausted to the atmosphere and can be monitored
by a capnograph attached to the gas outlet to reflect membrane gas transfer function.
An anaesthetic vaporizer can be placed in the circuit before the gas inlet to provide
anaesthesia during CPB.
The oxygenated blood returns to the patient via an arterial cannula, usually placed in
the ascending aorta. A 40 m filter is placed distal to the oxygenator to remove any
aggregated platelets, debris from the circuit materials or large microbubbles. This filter
can be coated to remove leucocytes that are activated by the non-biological surfaces of
the circuit.
Heparinized blood from the pericardium and intracardiac chambers is removed through
the cardiotomy suckers and filtered before it is returned to the circulation.
Conduct of perfusion
In UK practice, the perfusionist is responsible to the surgeon for the provision of safe
and effective CPB. The anaesthetists position is less formally defined, in terms of
accountability, but excellent communication between the three disciplines is vital.
The training and professional conduct of perfusionists is regulated by the Society of
Perfusionists of Great Britain and Ireland. Perfusionists have completed a structured 2-
year postgraduate training period in perfusion. Perfusionists are licensed to administer
heparin and the vasoactive agents, metaraminol and phentolamine. They regularly
administer volatile anaesthetic agents via the CPB circuit, corticosteroids, mannitol and
potassium supplementation.
Haemofiltration in association with CPB has become commonplace and is provided and
regulated by the perfusionist. This is an efficient process, the combination of a large
surface area filter and an extracorporeal pump allowing rapid manipulation of body
water, control of haematocrit and correction of electrolyte and metabolic abnormalities.
Perfusionists have also assumed responsibility for cell salvage technology, now
routinely used for cardiac surgery in many centres and which results in a substantial
reduction in the number of patients requiring homologous red cell transfusion.
Anticoagulation for CPB

Heparin is used almost universally as the anticoagulant for CPB. It potentiates the activity
of antithrombin III, which inhibits the activity of thrombin and other clotting factors, thus
inhibiting clot formation. The elimination kinetics of heparin are variable, dose-dependent
and temperature-related. Near patient testing of anticoagulation in CPB is performed
with the activated clotting time (ACT), which provides an indication of heparinization, but
correlates poorly with measured heparin levels. ACT levels are usually maintained above
480 seconds with supplemental heparin doses.
Monitoring of anticoagulation may be much more difficult in complex, prolonged

procedures and particularly if heparinization has been reversed and re-heparinization
for a further period of CPB is required. In these circumstances, heparin level assays
against residual factor Xa activity, can be provided with a laboratory turn-around time of
20 minutes. Heparin levels are usually over 3 units/ml for CPB.
The introduction of the antifibrinolytic agent, aprotinin, in cardiac surgery has

complicated near patient testing. In the presence of aprotinin, celite-activated ACT
tubes underestimate the ACT and should be maintained at over 700 seconds. Kaolin-
activated ACT tubes are much less affected by aprotinin, and should display ACT over
480 seconds.
In adults, the initial heparin dose is usually 300500 IU/kg (100 IU = 1 mg) with a pump
priming dose of 510,000 IU. Supplemental doses of 510,000 IU are administered
according to ACT values. The typical heparin dose has increased in the last 510 years
with the recognition of higher thrombin and aggregate formation with lower heparin
doses, and with more sophisticated measurements of clotting activation. Baseline levels
of ACT should be checked before heparin administration and prolongation of ACT must
be confirmed before institution of CPB.
Reversal of heparinization
Heparin is highly charged and is reversed by the administration of protamine, which
binds ionically to form a stable precipitate. Various empirical reversal regimens are
used, most commonly 11.5 mg per 100 IU heparin administered. Heparin management
systems that employ dose-response curves usually indicate lower doses are required.
Protamine, derived from salmon sperm, is associated with a range of adverse
effects, including direct myocardial depression. Transient systemic hypotension is
often observed due to release of nitric oxide and histamine in vascular endothelium.
Pulmonary vascular resistance increases, and may be catastrophic in existing
pulmonary hypertension. Anaphylactoid responses, mediated by IgG or complement
activation, include bronchoconstriction and acute lung injury, and are in part associated
with the heparinprotamine complex. True anaphylaxis (probably IgE mediated) seldom
occurs, but the consequences are catastrophic. Patients at risk include those with fish
allergy and diabetics exposed to protamine-containing insulin. Many of the adverse
effects relate to the rate of infusion. Large bolus doses should be avoided; the dose
is usually administered over 510 minutes, and over longer periods and preferably by
controlled infusion to patients at risk of de-stabilization (e.g. poor ventricular function,
pulmonary hypertension).
Control of parameters during CBP

The different approaches to the conduct of perfusion are influenced by the nature of
the planned surgery, the individual surgeons requirements and local practice. Arterial
blood pressure is controlled by a combination of flow or vasopressors or vasodilators;
the normal range is 6080 mm Hg. Venous pressure should be low, often negative.
High venous pressure often indicates poor venous return or venous obstruction. If
SVC pressure is high and systemic pressure is low, cerebral perfusion is impaired. The
temperature range is 1537oC depending on the operation (3235oC for coronary artery
surgery). The acidbase balance should be maintained within normal limits throughout.
The optimum haematocrit level is 2025% owing to viscosity effects at low temperature;
the transfusion trigger is usually a level of haemoglobin below 6 g/dl.
Patient characteristics also influence perfusion conduct. For example, it is usual to

maintain a higher mean arterial pressure in elderly patients and those with known
cerebrovascular disease.
Myocardial preservation
Effective myocardial preservation is one of the main determinants of outcome in cardiac
surgery. There are various methods and delivery of protection.
Electrically induced ventricular fibrillation is used for short (1520 minutes

maximum) surgery. It is used mainly in CABG surgery for distal anastomosis and the
heart is re-perfused during proximal anastomosis.
Cardioplegia: potassium causes electromechanical arrest and is the main ingredient

of cardioplegic solutions (concentration of 20 mmol/litre), along with magnesium and
procaine. Cardioplegia is delivered either anterograde through the aortic root or by
direct cannulation of the coronary ostia, or retrograde via the coronary sinus.
Crystalloid cardioplegia uses ice-cold Ringers solution plus cardioplegia solution, at

a temperature of less than 4C. It is commercially available in 1-litre bags.
Blood cardioplegia is a combined blood and crystalloid solution, usually administered

via the CPB machine, at a volume ratio from 1:1 to 8:1. The potassium concentration in
crystalloid solution is adjusted to maintain a delivered concentration of 20 mmol/litre.
In some instances, substrates such as tham, glucose, glutamate and aspartate may be
added. Blood cardioplegia reduces the amount of fluid given to the patient and delivers
an oxygenated solution, which is theoretically attractive because although the heart is
quiescent, oxygen utilization still occurs.
Monitoring on CPB
Standards of monitoring during CPB have been agreed by specialist societies. In
addition to basic monitoring and invasive systemic arterial and venous pressures,
continuous monitoring of CPB arterial and venous oxygen saturation (or PaO2), the
integrity of gas supply to the oxygenator and CPB arterial line pressure and blood
temperature is mandatory.
Anaesthesia for CPB
During CPB, ventilation is usually discontinued to allow surgical access. If pulmonary
blood flow persists, and is reflected by continuing left ventricular ejection, ventilation
(albeit at low tidal volume and frequency) should be continued to prevent pulmonary
blood flow through collapsed lungs contributing, as true shunt, to deoxygenation of
arterial blood on CPB. Ventilation is not necessary when ejection on CPB is due to
aortic regurgitation (i.e. ejected blood is fully oxygenated blood regurgitated through a
leaking aortic valve).
Provision of anaesthesia on CPB relates strongly to the technique used before or

after CPB and to the conduct of CPB. Anaesthetic requirements are reduced with
hypothermia, but drug pharmacokinetics also alter owing to haemodilution and
altered clearance. Supplemental doses of muscle relaxants and/or opiates are often
administered at re-warming.
Several different approaches are used. Commonly in the UK, moderate dose opiates
(usually fentanyl) are supplemented by volatile administration into the CPB inlet gas
(typically 0.51% isoflurane). Although experience indicates that this is not strictly
necessary, this technique is commonly supplemented by low dose propofol infusion
(100200 mg/hour), particularly during re-warming when the risk of awareness
is thought to be higher. The efficiency of volatile transfer across the oxygenator
membrane is inferior to native pulmonary function so steady-state blood levels of
volatile achieved are lower, and wash-in and wash-out times are prolonged compared
with transpulmonary transfer. An advantage of this approach is that delivery of
anaesthetic agent can be confirmed by oxygenator exhaust gas analysis
(i.e. connection of the capnograph tubing to exhaust port confirms isoflurane delivery).
Total intravenous techniques are also common, combining propofol infusions with
incremental fentanyl, alfentil or remifentanil infusions. Benzodiazepines may be used
with either technique to guarantee amnesia. A disadvantage of a total intravenous
technique is that the effective delivery of anaesthetic agents by infusion is difficult to
monitor, a problem recently highlighted by unreliable delivery from syringe pumps of
propofol in defective pre-filled syringes.
Separation from CPB

The following general principles are applicable to most patients. Cardiac function
should be judged acceptable, either by direct visualization or transoesophageal
echocardiography (TOE) assessment and an acceptable re-perfusion time should be
completed to allow recovery of ventricular function. In intracardiac procedures, effective
de-airing must be ensured and can be facilitated by TOE. Arrhythmias should be
controlled and epicardial pacing instituted for bradycardia, with sequential av pacing
for nodal rhythm or heart block. Electrolytes and acidbase status should be within
normal limits. Core temperature should approach normothermia, skin temperature (e.g.
shoulder tip) should be warm and should reflect a core-peripheral temperature gradient
not more than 57oC. Ensure the lungs have been fully re-inflated (the left lung may be
difficult to see) and are ventilated effectively.
In coronary surgery, separation is often achieved with low filling pressures (RA or
LA 25 mm Hg), to avoid ventricular distension and functional mitral regurgitation,
hence low systolic arterial pressures (e.g. 6070 mm Hg) may be accepted initially
and the heart subsequently filled slowly to achieve more normal systemic pressures.
In such patients, with good or moderate ventricular function, separation is commonly
achieved without inotropic support or with low doses only (dopamine, 57 g/kg/min,
dobutamine, 510 g/kg/min).
In patients with poor ventricular function or who have had prolonged or complex
surgery, more potent inotropic regimens are generally required and are usually
predetermined, somewhat empirically by surgeon and anaesthetist, before separation
is performed. In such patients, adrenaline (epinephrine), usual range 0.1 0.3 g/kg/
min, is commonly used and in recent years the phosphodiesterase inhibitors milrinone,
0.30.7 g/kg/min, and enoximone, 512 g/kg/min, have been used increasingly.
These agents, particularly milrinone, have considerable vasodilator properties and
are commonly combined with noradrenaline (norepinephrine), 0.080.15 g/kg/min,
which, in addition to modest direct cardiac effects, modulates the reduction in systemic
vascular resistance. Much higher filling pressures may be required (LA 1518 mm Hg)
in these patients and a mild degree of mitral regurgitation may need to be tolerated.
If haemodynamics remain unsatisfactory, a further period of support CPB may be
beneficial and inotrope regimens should be further refined. Insertion of an intra-aortic
balloon pump should be considered and temporary assistance with a ventricular assist
device may be appropriate in a small number of patients. Mechanical support of the
failing heart is considered elsewhere. u

Anaesthesia for Cardiothoracic
Transplantation and
Ventricular Assist Devices
Andy Gaunt
Andy Gaunt is Locum Consultant Anaesthetist at Harefield Hospital, Middlesex, UK.

He qualified from the University of London and trained in anaesthesia on the Imperial
Rotation, West London. His main research interest is pain following cardiothoracic
surgery.
The International Society for Heart/Lung Transplantation (ISHLT) maintains a database

of transplants carried out worldwide. The database includes information up to 2001 of
61,533 heart transplants, 2935 heartlung transplants and 14,588 lung transplants.
In 2000, in the UK, 286 cardiothoracic transplant procedures were carried out across
eight centres.
Figure 1 shows the pathologies for which patients typically receive cardiothoracic
transplantation. All these conditions have implications for the conduct of general
anaesthesia.
Pathologies for which patients typically receive cardiothoracic

transplantation
Transplant Patients (%)

Heart transplants
End-stage coronary artery disease 24
Cardiomyopathies 24
Congenital heart disease 48
Single lung transplants

Emphysema 54
Idiopathic pulmonary fibrosis 24
1-antitrypsin deficiency 9
Sarcoidosis 3
Primary pulmonary hypertension 1
Double lung transplants

Cystic fibrosis 35
Emphysema 24
Idiopathic pulmonary fibrosis 10
1-antitrypsin deficiency 10
Primary pulmonary hypertension 9
Bronchiectasis 5
Sarcoidosis 3
1
The preoperative evaluation of transplant patients involves a variety of tests (Figure

2). Patients are evaluated for signs and symptoms of dysfunction of all major organ
systems. Additional tests may be required depending on the patient and the type of
transplantation proposed.
Routine tests before transplantation
Height/weight
Blood pressure
Bacteriology status (swabs/samples)
24-hour urine collection
Chest radiograph
ECG and 24-hour Holter monitor
Echocardiogram
Full blood count, urea and electrolytes, liver function tests, thyroid
function tests, viral screen, clotting profile, tissue typing, blood group
HIV test
Left and right heart catheter
Lung function, VQ scan
Arterial blood gas
Exercise test
Anaesthesia
Pre-induction: anaesthesia for cardiothoracic transplant patients is hazardous. All
patients are ASA III or above. Monitoring is instituted before induction of anaesthesia
and includes multi-lead ECG, oxygen saturation (SpO2) and arterial blood pressure
measurement. Large-bore venous access is mandatory for all transplant patients
because haemorrhage can be significant and life threatening. Central venous access to
allow intraoperative and postoperative infusion of drugs is usually sited via the internal
jugular or subclavian veins. In cardiac transplant patients, this is usually via the left side,
because this preserves the right internal jugular, which is required for endomyocardial
biopsies following the transplant. It is not mandatory to site central venous access
before induction but it is the policy in many institutions.
Additionally, external adhesive defibrillator pads are attached to those undergoing a

re-do sternotomy because episodes of atrial fibrillation and VT/VF may occur before
cardiopulmonary bypass. Also, defibrillation via internal pads may not be possible until
the adhesed heart is fully dissected. Additional ECG electrodes are often attached
before induction to allow synchronization of an intra-aortic balloon pump. Pulmonary
artery flotation catheters are often used to determine cardiac output, left ventricular
end-diastolic pressure and pulmonary artery pressure. The position of the catheter may
have to be changed several times when re-anastomosis of the right heart or pulmonary
artery occurs. Left atrial pressure lines can be sited intraoperatively to facilitate more
accurate estimation of left ventricle end-diastolic pressure (filling pressure).
Pre-oxygenation of the patient before induction is mandatory, particularly if using

moderate doses of opiates. Chest wall rigidity can interfere with bag/mask ventilation
before the onset of muscle relaxation. Hypoxaemia, of even short duration, can lead to
exacerbation of pre-existing pulmonary hypertension or myocardial ischaemia.
Induction: etomidate, ketamine, propofol and thiopental (thiopentone) have all been
used successfully as induction agents in transplant patients. The choice of agent
depends on the experience of the anaesthetist, but may be dictated by the pre-
transplant condition of the patient. For example, in patients with severely impaired
left ventricular function, etomidate may be preferred to propofol because of its
increased cardiostability. Thiopental (thiopentone) is not a good choice for the severely
emphysematous patient undergoing lung transplantation because of its histamine-
releasing properties. In these patients, the exacerbation of pre-existing airway
obstruction can cause ventilation problems. Air trapping during the early stages of
ventilation can prove rapidly fatal.
Moderate doses of opiates (e.g. fentanyl, 5 g/kg) are often used in transplantation
because they can obtund the hypertensive response to intubation and are cardiostable.
Intraoperatively they also decrease the sympathetic stimulation caused by painful
procedures. Sufentanil is commonly used in cardiac anaesthesia in the USA, but is not
licensed in the UK.
Muscle relaxation is commonly achieved by pancuronium. The tachycardia it produces

can offset the loss of sympathetic tone at induction. Most muscle relaxants have been
used in transplant patients, but those known to exacerbate bradycardia (vecuronium)
may be hazardous in patients with severely impaired ventricular function. Tachycardia is
a compensatory mechanism in heart failure and the increased ventricular filling time in
bradycardia can allow overdistension of the failing myocardium and lead to catastrophic
cardiovascular collapse.
Maintenance of anaesthesia can be achieved by a variety of techniques. A balance

of inhalational agents and opiates is often used and total intravenous anaesthesia
techniques are also suitable. Isoflurane and sevoflurane are both suitable volatile
agents for maintenance of anaesthesia. Nitrous oxide is often avoided because
of its sympathomimetic properties, which can exacerbate pre-existing pulmonary
hypertension.
Thoracic epidural analgesia can be used in lung transplant patients to limit

sympathetic stimulation intraoperatively, to provide postoperative analgesia, and to
facilitate early extubation. Their use is controversial because of the theoretical risk of
epidural haematoma following a bloody tap. In the literature, bloody taps and epidural
haematomas are uncommon. In 6000 epidurals for routine cardiac surgery, no clinically
apparent epidural haematomas occurred. The incidence of bloody tap is 1.54.5%.
Patient management
Patient positioning of the transplant patient requires care because procedures can be
prolonged. Pressure areas should be well padded to avoid nerve compression.
Maintenance of normal body temperature in single lung transplantation, and

following cardiopulmonary bypass in double lung, heartlung or heart transplantation,
makes early post-operative extubation feasible. Warming mattresses, forced-air
blankets and blood warmers can be used.
Haemorrhage is often significant in transplant surgery and prior planning of transfusion

requirements is mandatory. Patients who have had previous surgery and required blood
transfusion may have developed antibodies to non-ABO red cell antigens. The routine
use of cell salvage techniques is advised and the use of antifibrinolytic agents (e.g.
aprotinin) can reduce the need for blood transfusion.
Inotropic support is usually instituted during re-warming, if it is not already in place.

The choice of inotropes to facilitate weaning from cardiopulmonary bypass varies
according to the anaesthetists experience. Adrenaline (epinephrine), dobutamine
and dopamine have all been used successfully. Phosphodiesterase type III inhibitors
(milrinone, enoximone) may offer significant advantages over more conventional
inotropic support because of their beneficial effects on the pulmonary circulation,
reducing right ventricular afterload and helping to offset acute right ventricular failure.
Lung transplantation can be single or double. Both procedures can be carried out
without the use of cardiopulmonary bypass if the patient is able to tolerate one lung
ventilation. In single lung transplantation, conventional one lung ventilation allows the
procedure to be carried out through a thoracotomy.
Donor lungs have no lymphatic drainage and following reperfusion injury, interstitial
pulmonary oedema may develop. It is conventional to restrict the fluids given to lung
transplant recipients in the perioperative period, and this may require the use of
inotropic support to maintain the circulation.
Sequential double lung transplantation, is usually carried out through a clamshell

incision. One lung ventilation can be used to allow the first lung to be transplanted,
before switching ventilation to the new lung to allow the second lung to be transplanted.
This can be a problem because the newly transplanted lung can manifest reperfusion
injury and make one lung ventilation un-feasible. Many authorities recommend carrying
out the second lung transplant on cardiopulmonary bypass to avoid exposing the newly
transplanted lung to the whole cardiac output, and ex-acerbating reperfusion injury. It
is now becoming commonplace to transplant both lungs on cardiopulmonary bypass,
thus negating the need for one lung ventilation. The use of cardiopulmonary bypass
is not thought to be associated with an adverse outcome compared with off-pump
transplantation.
Emergence true fast-track transplantation anaesthesia with extubation on the

operating table has proved elusive or undesirable. Most patients require at least a short
period of intensive care before weaning and extubation. Early postoperative problems
such as bleeding, hypothermia and organ dysfunction requiring significant inotropic
support are contraindications to rapid extubation. Patients requiring inhaled nitric oxide
therapy for pulmonary hypertension or right ventricular dysfunction require continuing
ventilation to control the undesirable effects of hypercarbia.
Following an uncomplicated transplantation, extubation may be feasible within 2 hours,

particularly in lung transplant patients with functioning epidural analgesia.
Rejection indicates an immune response to the transplanted organ. All organ recipients
experience episodes of rejection. Prompt diagnosis and treatment of rejection is crucial
to ensure graft survival and patient longevity. Early fulminant rejection is rapidly fatal,
and can occur in the first hours following transplantation. Accurate ABO typing can
avoid this. Chronic rejection refers to the changes that take place in a transplanted
organ over time.
Ventricular assist devices

Ventricular assist devices (VADs) are becoming more widespread as newer devices,
designed for long-term support, become available. They are used as bridge to
recovery support, in patients with acute cardiomyopathy (e.g. Coxsackie endocarditis),
as a bridge to transplantation in those with severe decompensating cardiac failure and
as destination therapy in those who are unsuitable for transplantation.
VADs are divided into extracorporeal and implantable types. External devices, such
as the Abiomed VAD and the Thoratec pneumatic external VAD, are designed for
relatively short-term support of a heart that has failed (e.g. owing to inadequate
myocardial preservation during cardiopulmonary bypass). Both involve implanting
pipes, to establish an extracorporeal circulation, and involve bulky machinery to drive
the pumping mechanism. A portable drive apparatus for external devices is available
to allow movement outside the hospital environment. Some devices (e.g. BiVAD) can
support left and right hearts simultaneously.
Internal devices include the Thoratec HeartMate (Figure 3) and HeartMate II. Both are
implanted under the skin but require a drive line that connects the device to its power
source.
HeartMate ventricular assist device

Left side battery
External omitted for clarity
battery pack
Aorta
Heart
HeartMate
SNAP-VE LVAD
Y-connector
Air vent with vent filter inserted

System controller
Reprinted with permission from Thoratec Corporation.
3
Newer devices such as the Thoratec HeartMate II and the Jarvik 2000 are implantable
impeller devices. They are pumps connected between the apex of the left ventricle
and the aorta. They are designed for longer term use, require less anticoagulation and
have smaller drive units, making them more portable. The newest devices (e.g. Arrow
Lionheart LVAD, Thoratec HeartMate III LVAD) are completely implanted into the body
and power is provided by transcutaneous induction. The absence of drive lines or pipes
penetrating the skin should lead to lower infection rates.
Anaesthesia for VAD implantation is technically challenging. Patients for elective VAD
procedures are often in severe heart failure on maximal medical treatment; typically
ASA IV. Careful induction, judicious fluid management and inotropic support are
required until cardiopulmonary bypass is instituted, exactly as in transplant patients.
Inotropic support is often required following the procedure, to support the parts of the
heart not being supported by the VAD. The interplay between the native circulation and
the VAD can be complicated.
Transoesophageal echocardiography (TOE) in VAD implantation: following

implantation of the devices, TOE is a useful guide to the filling status of the heart. VADs
require adequate inflow in order to function, and inadequate filling can lead to collapse
of the left ventricle caused by the devices drawing too much blood. It may also be
desirable to have the heart ejecting slightly, rather than all the circulation being provided
by the VAD. For example, one device is implanted between the left ventricular apex and
the descending aorta. The machine is programmed to decrease impeller speed, and
hence flow through the VAD, for 10 seconds in every 60 seconds. The idea of this is to
allow the native left ventricle to fill and eject through the aortic valve, in order to flush
the arch of the aorta to discourage clot formation. When these devices are implanted
as a bridge to recovery, weaning of the support provided by the VAD may require
the institution, or modification, of inotropic therapy. The use of TOE allows real-time
estimation and measurement of heart function.
Complications of VAD therapy
Haemorrhage at the time of VAD insertion can be catastrophic and blood conservation
techniques are mandatory. Use of shed red cell salvage and the routine use of
antifibrinolytic agents can help to avoid excessive transfusion.
Heart failure sudden improvements in cardiac output following VAD implantation

can compromise the unsupported ventricle. For example, following left VAD support,
the increase in cardiac output can cause the right ventricle to become overloaded and
to fail. Not infrequently, patients with left VAD require a period of right VAD support to
allow the right heart to adapt to the improved cardiac output.
Anticoagulation the newer VAD devices require less anticoagulation (HeartMate

II patients require aspirin only), but thrombosis and embolization remain potential
problems. This can cause failure of a device or systemic embolization to a limb or
organ. Careful surveillance can avoid potentially fatal problems, especially with the
older devices.
Mechanism failure can be fatal, but the reliability of these devices continues to
improve. Off-loading the heart can achieve significant improvements in left ventricular
function. If pump failure occurs, the native heart function may have improved sufficiently
to allow the patient to get to hospital to remedy the situation. u
FURTHER READING
DeMeo D L, Ginns L C. Clinical Status of Lung Transplantation. Transplantation 2001;
72: 171324.
Westerlind A. Anaesthesia for Heart Transplantation. Curr Anaesth Crit Care 1999; 10:
299304.
Westerlind A. Anaesthesia for Lung Transplantation. Curr Anaesth Crit Care 1999; 10:
30511.
www.chfpatients.com/implants/lvads.htm
www.ishlt.org

Echocardiography in Cardiac
Anaesthesia and Intensive
Care
Marta Bird
Shane J George
Marta Bird is Clinical Fellow at Harefield Hospital. She qualified from Charles
University, Czech Republic, and trained in anaesthesia in Prague and Harefield,
London. Her interests lie in transoesophageal echocardiography and cardiothoracic
anaesthesia.
Shane J George is Consultant in Anaesthesia and Intensive Care at Harefield Hospital,

Middlesex. He qualified from St Bartholomew's Hospital, London. His research interests
include transoesophageal echocardiography, 3D echocardiography and epidural
anaesthesia for cardiac surgery.
Echocardiography has become an essential part of cardiac anaesthesia and intensive

care. The ability to perform echocardiography via the transoesophageal route allows
accurate visualization of the heart, despite the presence of drains and positive-pressure
ventilation, without interfering with the surgical procedure.
Basics of ultrasound
Figure 1 shows an echocardiography machine with a transoesophageal probe.
Ultrasound (sound of frequencies above 20 kHz) represents a valuable and relatively
safe tool for imaging soft tissues. The frequencies can travel through tissues, but when
they meet interfaces of different echodensity they reflect (echo) as well as transmit
through the tissue. This echo is picked up by receiving transducers and translated into
an image. Ultrasound transducers use a piezoelectric crystal to generate and to receive
ultrasound waves. A piezoelectric crystal is a material (e.g. quartz or a titanate ceramic)
that changes its size with electric current application. Conversely, when an ultrasound
wave strikes the piezoelectric crystal, an electric current is generated. The transducer
emits a brief burst of ultrasound and then switches to the receiver mode to await the
reflected ultrasound signals from the intracardiac acoustic interfaces. This cycle is
repeated temporally and spatially to generate ultrasound images. Image formation is
based on the time delay between ultrasound transmission and return of the reflected
signal. Ultrasound information may be displayed in a number of ways to represent an
image of the structures being examined. The most common representation is a two-
dimensional image that represents a slice through the heart. The transducer emitting
the ultrasound may be outside the thorax (transthoracic), directly on the surface of the
heart during surgery (epicardial), or within the oesophagus (transoesophageal).
e
a
b
c
1 The echocardiography machine with a

transoesophageal probe. a Echo display screen,
b Touch screen control panel, c Data input track
ball and control panel, d Transducer scan head,
f e Dial control for rotational probe, f Scan head.
The Doppler principle is used to understand the movement of blood and tissues
in the body. The Doppler effect is a change in observed frequency of a signal when
the signal source is moving. Moving blood or tissue causes the transducer to hear a
different frequency from the one generated and the processor can use this information
to describe the direction and speed of the tissue. By representing colours for changes
in frequency and mapping this onto the two-dimensional image, intuitive representation
of flows is achieved. Colours are usually adjusted so that flow towards the probe is red,
while flow away is blue.
Understanding the two-dimensional image

The image is represented as a segment of a circle, the centre of which represents the
position of the transducer while the periphery represents the depth that the ultrasound
interrogated. With transoesophageal imaging, the transducer is always behind the heart
and therefore the top of the image represents the posterior aspect of the heart and the
bottom of the image represents the more anterior structures. When the slice through
the heart is horizontal (0 plane), the left of the image represents the right of the patient.
When the slice is longitudinal (90 plane), the left of the image represents inferior
structures and the right the superior structures.
The more two-dimensional images we have the better we can understand the three-
dimensional heart. A current recommendation is for 20 cross-sectional views to
complete a routine examination. More recently, the two-dimensional images have been
used to reconstruct a three-dimensional model. It is impossible to cover all the views in
this article; we focus on three main cross-sectional views, to serve as an introduction to
the main structural features of the heart, and then give examples to illustrate their utility.
The four-chamber view (Figure 2) is excellent for comparing the right and left sides
of the heart. The interatrial and interventricular septa, and mitral and tricuspid valves
are easily viewed and the left ventricle assessed. It is obtained by positioning the
transducer in mid-oesophagus about 35 cm from the mouth. The probe is located
posterior to the left atrium, so the left atrium is the structure closest to the transducer.
The long axis of the left ventricle with the lateral wall, apex and inferior septum are seen
in this tomographic plane. The mitral valve is well visualized, with the mitral annulus in
its major dimension, the anterior mitral valve leaflet (located adjacent to the septum),
and the posterior mitral valve leaflet (adjacent to the lateral wall), along with chordae
and attachments to the anterolateral papillary muscle. The tricuspid annulus lies slightly
closer to the apex than the mitral annulus. The septal and posterior tricuspid leaflets,
which are thin and uniformly echogenic, are seen in this view with a wide diastolic
opening.
Four-chamber view
Right atrium
Left atrium
Right ventricle
Left ventricle
Plane of view
Long-axis view (mid-oesophageal view): (Figure 3) the angle of interrogation can

be rotated electronically between 0 and 180 . A long-axis view of the heart may be
obtained by rotating to 130 from the four-chamber view. Different aspects of the heart
can be seen by physically rotating the probe to the left and right. The aortic valve, left
ventricular outflow tract, mitral valve, and part of the right ventricle outflow tract anterior
to the aortic valve are seen in the long-axis view.
Long-axis view

The transgastric midpapillary short-axis view (Figure 4) is seen by passing the

probe into the stomach with anterior flexion of the probe in the 0 plane. This classical
doughnut view of the left ventricle allows evaluation of global left ventricular systolic
function, left ventricular dimensions, wall thickness and regional left ventricular function.
This view is particularly valuable for intraoperative monitoring because all three major
coronary arteries are represented. Regional wall motion abnormalities are a sensitive
indicator of myocardial ischaemia. This view also allows a good assessment of the
systolic function of the heart and the volume status of the patient.
Utility of echocardiography
In the assessment of the heart and cardiovascular status, basic physiological
parameters should be considered (Figure 5). The ECG assesses heart rhythm, while
central venous pressure or pulmonary pressures provide pressure measurements.
Echocardiography provides volume assessment, structural assessment and diastolic
function assessment.
Intraoperative echocardiography is essential for mitral and aortic valve repair because
of its ability to assess the results of surgery. In addition, new wall motion abnormalities
can suggest areas of poor revascularization. A number of reports show the utility of
echocardiography assessment for congenital heart surgery, ventricular assist device
management and the management of ventricular dysfunction.
Diastolic function: there is increasing appreciation of the role of diastole in myocardial

function. Diastole is not a passive process and requires energy for relaxation of
the myocardial cells. Poor diastolic function of the left ventricle leads to higher left
ventricular filling pressures to maintain end-diastolic volumes, with an accompanying
propensity to shortness of breath and pulmonary oedema. An assessment of the
compliance of the left ventricle may be made by measuring the thickness of the
ventricle and comparing the peak mitral flow velocity of the early rapid filling wave (E)
with the peak velocity of the late filling wave of atrial contraction (A) (the E:A ratio).
Pericardial disease: echocardiography is valuable for diagnosing pericardial

effusions and cardiac tamponade and as an aid to pericardiocentesis. Two-
dimensional echocardiography is especially accurate in estimating effusion size.
Signs of tamponade include diastolic compression or collapse of the right atrium and
right ventricle. Leftward displacement of the ventricular septum and an exaggerated
increase in right ventricular size with a reciprocal decrease in left ventricular size
during inspiration are also useful. Echocardiography also identifies the thick ventricle
associated with aortic stenosis (Figure 6).
Transgastric midpapillary view

Assessment of hypotension
Blood Cardiac Peripheral

pressure output resistance
Heart rate
(ECG)
Stroke volume
Preload Contractility Afterload Structure

(echo and (echo) (central (echo)
central pressure and
pressure) cardiac output)
6 Thick ventricle (> 2 cm)

(arrowed) associated with
aortic stenosis, suggesting
poor diastolic compliance.
Right ventricular failure is not easy to diagnose, particularly if it presents in a patient

already in the ICU with organ dysfunction. Echocardiography helps to diagnose acute
right ventricular failure (Figure 7), especially in an ischaemic setting, and to evaluate
its severity and its response to implemented therapy. Echocardiography signs include
volume and geometry of the right ventricle, the function of the free wall of the right
ventricle and septum, the absence or presence of tricuspid insufficiency, and the
distension and size of the inferior vena cava.
7 This transgastric image

shows the normally circular
left ventricle compressed on
the right giving rise to a D-
shaped ventricle (arrowed).
This is the result of right
ventricular pressures being
greater than left ventricular
pressures as a result of
pulmonary hypertension or right
ventricular failure. Hypotension
management in this case may
include the use of nitric oxide,
phosphodiesterase inhibitors
and would be different from
management of left ventricular
failure.
Other structures: rotating the probe to interrogate posteriorly can show the
descending aorta (Figure 8). This can be useful for assessing the atheromatous state
of the aorta, diagnosing dissection and confirming adequate placement of intra-aortic
balloon catheters. With experience, a number of other structures can be seen, including
pleural spaces, hepatic veins and renal arteries. Newer technology may allow better
imaging (harmonics) or presentation in a new way (e.g. three-dimensional).
Short-axis view of the descending aorta
An intra-aortic balloon had been placed for hypotension following

cardiopulmonary bypass. The catheter is seen to have created a
false lumen with dissection of the aorta. The catheter was
removed and the patient was eventually discharged having
suffered nothing more than minor digital ischaemia
Descending
aorta
Intimal
flap
Aorta
Plane of
view Balloon
catheter
Risks and benefits of echocardiography

There is risk associated with oesophageal intubation, but no risk has been ascribed
to the use of ultrasound alone. Many studies have looked at the risk arising from
routine use of intraoperative echocardiography. The largest series to date showed
a complication rate of 0.14%. Although no deaths were reported in this series,
others have reported deaths at a rate of 1/10,000, mainly secondary to oesophageal
perforation.
The benefits of routine use have also been quantified in specific circumstances
including coronary artery surgery, mitral valve surgery, aortic valve surgery and
paediatric cardiac surgery. In general, a benefit in haemodynamic or other management
decisions is expected in about 20% of patients, and a major benefit resulting in a
change of surgical management or return to cardiopulmonary bypass of 5%. u
FURTHER READING
American Society of Echocardiography Council for Intraoperative Echocardiography
and the Society of Cardiovascular Anesthesiologists Task Force for Certification
of Perioperative Transesophageal Echocardiograhy. The Safety of Intraoperative
Transesophageal Echocardiography. Anesth Analg 1999; 89: 87084.
Click R L, Abel M, Schaff H V. Intraoperative Transesophageal Echocardiography: 5-

year Prospective Review of Impact on Surgical Management. Mayo Clin Proc 2000; 75:
2417.
Kallmeyer I J, Collard C D, Fox J A et al. The Safety of Intraoperative Transesophageal

Echocardiography. Anesth Analg 2001; 92: 112630.
Poelaert J, Skarvan K. Transoesophageal Echocardiography in Anaesthesia. London:

BMJ Publications, 2000.
Acknowledgement
All the illustrations in this article have been modified with permission from: Calahan M.
Intraoperative Transoesophageal Echocardiography. Interactive Text and Atlas (CD).

Intra-aortic Balloon
Counterpulsation
Ruediger Stenz
Ruediger Stenz is Consultant Anaesthetist at the Royal Brompton Hospital, London.

He qualified from the University of Freiburg, Germany, and trained in Germany, and in
Boston, USA. His special interests are paediatric and adult cardiac anaesthesia.
Intra-aortic balloon counterpulsation is a simple and affordable method of mechanical

circulatory support using a balloon placed in the proximal descending aorta (Figure 1).
This balloon (volume 3050 ml) is inflated during cardiac relaxation and deflated during
cardiac contraction. The intra-aortic balloon pump (IABP) was first used clinically
in 1968, to support patients in cardiogenic shock after acute myocardial infarction.
Initially, surgical exposure of the femoral artery and a vascular prosthesis were required
for insertion but percutaneous insertion techniques have encouraged a wider use of
the IABP, including postoperative support and aiding weaning from cardiopulmonary
bypass. The IABP is now the most commonly used mechanical cardiac assist device
and about 100,000 are inserted annually worldwide.
Intra-aortic balloon in situ
Theory and application

The IABP has two main effects (Figure 2):
inflation during diastole increases coronary blood flow and thereby myocardial
oxygen supply (and also generates a modest increase in aortic forward blood flow)
deflation at the onset of systole decreases left ventricular workload and thus
myocardial oxygen consumption via afterload reduction.
The clinical effects of IABP include improved ejection fraction and cardiac output in
conjunction with a lower left ventricular end-diastolic pressure as well as alleviating
myocardial ischaemia and reducing the frequency of atrial and ventricular arrhythmias.
The increase in cardiac output can be as high as 25% depending on several factors,
including patient and balloon size, aortic compliance, cardiac rhythm and balloon
timing.
The IABP is connected to a mobile electropneumatic console, which controls its

operation. The console provides an ECG, an arterial waveform transduced from the tip
of the balloon and a numeric display of heart rate and aortic blood pressure. It allows
manual adjustment of timing of balloon inflation and deflation and incorporates controls
for trigger selection, balloon volume and ratio of support (generally between 1:1 and 1:4
augmented beats). The balloon gas delivery system (usually using the inert gas helium)
and a battery back-up power supply are also integrated in the console. Portable models
for patient transfer by ground or air are available.
Indications and contraindications

Indications for the use of the IABP have expanded rapidly (Figure 3) and there has
been a shift from the treatment of haemodynamic decompensation to the control of
myocardial ischaemia. IABP support can be used on its own, but is often instituted in
conjunction with moderate doses of vasoactive drugs and/or mechanical ventilation.
In routine use, the IABP remains in situ for a limited period (2472 hours) but it has
been used for several weeks in heart-transplant candidates. A system for permanent
implantation has also been developed. Experience with IABP treatment in children is
limited, but it appears to be most effective in older children with isolated left ventricular
failure.
Indications and contraindications for the use of intra-aortic

balloon pumps
Indications
Unstable angina refractory to medical treatment
Acute ischaemia associated with coronary angioplasty
Perioperative low cardiac output
Cardiogenic shock after myocardial infarction
Congestive heart failure
Ischaemic ventricular septal defect
Acute mitral regurgitation
Ischaemia-related ventricular arrhythmias
Bridge to heart transplant
Contraindications
Severe aortic regurgitation
Aortic dissection
Aortic aneurysm
Severe calcific aorto-iliac or peripheral vascular disease
Insertion and removal

Most IABP are inserted percutaneously via the femoral artery using a Seldinger
technique under aseptic conditions. This is often done outside the operating theatre in
the catheter laboratory or in the intensive care or high dependency unit. If percutaneous
access proves difficult, or in cases of known anatomical problems, surgical exploration
should be considered early in order to minimize vascular damage. Sheathless
insertion is possible if the diameter of the artery is expected to be small. The balloon
is advanced into the proximal descending aorta until the tip of the balloon is positioned
25 cm below the left subclavian artery (Figure 1). Correct balloon positioning must
be confirmed and documented by fluoroscopy, radiography or transoesophageal
echocardiography. If the femoral artery is not available for balloon insertion (in about
5% of patients) alternative routes are the axillary and subclavian arteries or the
transthoracic approach via the ascending aorta, in the operating theatre.
A surgically inserted IABP must also be removed surgically and embolectomy catheters
may be used proximally and distally to clear any clot or atheromatous debris. After
percutaneous insertion, closed or open removal can be performed. In the case of
closed removal, the artery should be allowed to bleed for several seconds while the
vessel is compressed distally in order to flush out any embolic material.
Timing and weaning

Accurate timing of balloon inflation and deflation in relation to the cardiac cycle is
crucial to optimal function. Balloon inflation should occur immediately after closure of
the aortic valve, represented in the arterial waveform by the dicrotic notch. Balloon
deflation must happen just before the onset of systole. Late inflation and early deflation
lead to suboptimal augmentation of coronary blood flow. Early inflation and late
deflation obstruct anterograde blood flow in the aorta and increase afterload.
In order to synchronize balloon operation with cardiac contraction, the ECG or the
arterial pressure waveform can be used to trigger the IABP. Although the IABP is most
effective with a regular intrinsic rhythm, continuing progress in technology has made
triggering from paced rhythms and compensation for irregular rhythms, such as atrial
fibrillation, more reliable.
IABP support usually begins with a ratio of 1:1 (every cardiac contraction is followed
by a balloon inflation/deflation), however, an initial short period of a 1:2 support ratio
(every other contraction triggers the balloon) allows for a more accurate evaluation and
adjustment of balloon timing. Also, in case of heart rates beyond 100/min an assistance
ratio of 1:2 may be more effective. Balloon operation must be checked and adjusted
regularly throughout the course of treatment.
IABP therapy should be gradually withdrawn rather than stopped abruptly. However,
it is unclear whether reduction of the assistance ratio (most common approach) or
decreasing the balloon volume is superior because both approaches have advantages
and disadvantages. The indication for weaning of IABP support is mainly guided by the
improvement in the patients condition and protocols will help to establish appropriate
criteria (i.e. cessation of ischaemia, adequate cardiac output or arterial blood pressure)
for the weaning process.
Complications
Complications can be broadly divided into vascular injuries, balloon malfunction and
infection. The overall reported incidence of all complications ranges from 11% to 42%
with limb ischaemia being the most common adverse event. Consistent risk factors for
vascular complications are female gender, history of peripheral vascular disease and
diabetes. Most complications can be controlled by balloon removal or repositioning
and antibiotic cover, although surgical intervention may become necessary. Potentially
life-threatening complications of IABP insertion, such as aortic or iliac dissection or
perforation, occur in about 1% of cases.
Trends and outlook

A clear trend towards the early commencement of IABP therapy and the superior
outcomes in ischaemic patients have led to increased use in the perioperative period.
There is little evidence or consensus regarding the optimum use of IABP in this setting,
but data from smaller trials indicate a survival benefit and an advantage of preoperative
over intra- and postoperative insertion. The substantial variation of practice between
centres reflects the lack of widely accepted guidelines as well as differing resources
and attitudes towards specific indications and patient selection. There is a trend toward
prophylactic use to avoid, rather than treat, ischaemia and cardiogenic shock. The use
of the IABP in high-risk angioplasty and off-pump cardiac surgery is likely to increase
and smaller catheter sizes will help to reduce vascular complications. A beneficial effect
on right ventricular failure, particularly in the transplant population, has been suggested.
The role of the IABP in relation to other cardiac support strategies still needs to be
better defined. u
FURTHER READING
Baskett R J F et al. The Intra-aortic Balloon Pump in Cardiac Surgery. Ann Thorac Surg
2002; 74: 127687.
Kaplan J A. Cardiac Anesthesia. 4th ed. London: W B Saunders, 1998.
Torchiana D F et al. Intra-aortic Balloon Pumping for Cardiac Support: Trends in

Practice and Outcome, 1968 to 1995. J Thorac Cardiovasc Surg 1997; 113(4): 75869.

Rational Use of Inotropes
Peter Elliott
Peter Elliott is Consultant Cardiac Anaesthetist at the Royal Hospitals Trust, Belfast,
UK. He qualified from Queens University, Belfast, and trained in Northern Ireland, and
Dallas, Texas. He is also Clinical Director of Anaesthetics, Theatres and Intensive Care
Services at the Royal Hospitals Trust, Belfast.
Inotropes are pharmacological agents that affect the force or energy of ventricular
muscle contraction, and which often have effects on other variables such as heart
rate, preload and afterload, and peripheral vascular tone. The use of such agents is
commonplace in the perioperative or critical care setting, and the indications for their
use are multiple, and not confined to their inotropic actions. No inotrope exerts its
effect purely by altering myocardial contractility, therefore the potentially useful effects
on heart rate, systemic and pulmonary vascular tone and the side-effects of these
agents must be taken into account when choosing an appropriate agent. The choice of
inotrope is influenced by the therapeutic goal, which is seldom an elevation in systemic
blood pressure alone. The purpose of manipulating a patients haemodynamics in the
acute situation is to ensure the adequate delivery of oxygen to vital tissues (to avoid or
treat shock). The causes of inadequate oxygen delivery are:
a cardiac output insufficient to meet the demands of the body or organ
low perfusion pressure despite an adequate cardiac output.
Determinants of cardiac output

Cardiac output is determined by heart rate and stroke volume, the latter being
influenced by preloading and ventricular function. Reduced preloading may be
due to hypovolaemia (relative or absolute) or increased extracardiac pressure (e.g.
raised intrathoracic pressure, or direct pressure on the cardiac chambers as in
tamponade). Ventricular function depends on the interrelated factors of heart rate,
preload, myocardial contractility and afterload, any of which can be manipulated
pharmacologically. Ventricular dysfunction (systolic or diastolic, and left or right) may be
caused by reduced coronary blood flow (coronary artery disease or severe systemic
hypotension), myocardial infarction, drug effects, metabolic disturbances or post-
cardiopulmonary bypass stunning. These factors usually relate to the left ventricle,
but apply to both ventricles, and there has been recent interest in the pathophysiology
and treatment of right ventricular dysfunction. Left ventricular diastolic dysfunction is
a separate pathophysiological entity caused by alterations in ventricular compliance
and may be due to mechanical causes, left ventricular hypertrophy, ischaemia and
hypertrophic cardiomyopathies. Drugs that have an effect on diastolic function (an
active process) have lusitropic properties (enhanced active relaxation and improved
filling characteristics in diastole resulting in a lower end-diastolic pressure for a given
circulating volume). A decreased myocardial oxygen supply tends to cause systolic
dysfunction, while increased demand tends to cause diastolic dysfunction.
In some instances, the cardiac output may be adequate, but the perfusion pressure,
either globally (as measured by systemic blood pressure) or locally, to vital organs
is low. Generally, organs attempt to maintain adequate blood flow in response to an
inflammatory process by altering vasomotor tone, but at a particular minimum pressure,
flow becomes proportional to perfusion pressure and the organ becomes at risk.
Some organs (e.g. heart, brain) have few -adrenergic receptors, and the flow to these
organs is more closely related to the perfusion pressure. In some systemic diseases
(e.g. septic shock) there may be a generalized low perfusion pressure and a normal or
increased cardiac output, due to vasodilatation (mediated by nitric oxide). This type of
hypotension is known as distributive shock.
Increasing the heart rate, within certain limits, increases myocardial contractility
and cardiac output, although in patients with ischaemic heart disease it is important
to control heart rate to minimize oxygen demand and maximize oxygen supply
(longer diastole). However, in the presence of regurgitant valve lesions, ventricular
overdistension (and therefore dysfunction) should be averted by avoiding bradycardia.
Afterload, determined by systemic vascular resistance for the left ventricle and
pulmonary vascular resistance for the right ventricle is closely related to ventricular
function. Raised systemic vascular resistance increases myocardial oxygen demand by
increasing wall tension (Laplaces law) but may improve coronary artery perfusion and
oxygen supply by raising the diastolic blood pressure. The right ventricle is exquisitely
sensitive to variations in pulmonary vascular resistance, which has an inverse
relationship with right ventricular output.
Management of impaired haemodynamics

Managing hypotension depends on diagnosing its cause and understanding the
haemodynamic effects of the available drugs. To make informed decisions, adequate
monitoring data should be available, including the standard measurement and analysis
of the ECG and ST segments, invasive blood pressure and central venous pressure.
Also useful are cardiac output and pulmonary artery pressure measurements with the
derived parameters of systemic vascular resistance and pulmonary vascular resistance
and, increasingly, transoesophageal echocardiography.
Often, combination therapy, using more than one inotrope, in addition to vasodilators, is
indicated. Inotropes have many side-effects and Figure 1 shows the characteristics of
an ideal agent.
Characteristics of an ideal inotrope
Causes increased velocity and force of myofibril fibre shortening

Lacks tolerance
Does not cause vasoconstriction
Does not cause changes in heart rate or rhythm
Predictable and easily titratable
Raises perfusion pressure by increasing cardiac output rather than
systemic vascular resistance
Redistributes blood flow to vital organs
Direct acting (does not rely on release of endogenous amines)
Compatible with other vasoactive substances
Demonstrates lusitropy (see text)
1
Classification of inotropes
Inotropes may be classified according to Figure 2. Most of the inotropes in common
use belong to Class I, but much research is being carried out into drugs of Classes II
and III. Some drugs (e.g. vesnarinone, the -adrenergic agonists) have multiple modes
of action and belong to more than one class. The most commonly used drugs and
drugs that are coming into routine clinical practice are described below (Figure 3). The
general rules that apply to the use of inotropic agents are listed in Figure 4.
Classification of inotropes
Class I Drugs that increase intracellular calcium

Calcium ion
Calcium channel agonists (openers)
Drugs that increase cardiac cAMP
-agonists (adrenaline (epinephrine), noradrenaline
(norepinephrine), dopamine, dobutamine, dopexamine,
isoprenaline, ephedrine, xamoterol)
Phosphodiesterase inhibitors (milrinone, enoximone)
Glucagon
Drugs that inhibit the Na-K pump (digitalis compounds)
Drugs that prolong action potential duration (-adrenergic agonists,
vesnarinone)
Class II Drugs that increase sensitivity of actomyosin to calcium

ions
adrenergic agonists, vesnarinone, pimobendan, endothelin
Class III Drugs that act through metabolic or endocrine pathways

Triiodothyronine, dichloroacetate
Adapted from Feldman (1993) and Merin (1995), see Further Reading.
Doses and effects of commonly used inotropes
Drug Dose/range Predominant Effects1

(g/kg/min) receptor
Adrenaline 0.010.02 2 Lowered SVR, BP

(epinephrine) 0.030.2 1 Increased contractility, HR, CO
0.2-0.3 Increased SVR, BP
Noradrenaline 0.010.4 1 2 2 Raised SVR, BP, possible reflex fall in HR,
(norepinephrine) possible fall in CO
Dopamine 0.013 Dopaminergic Renal and splanchnic vasodilatation

37 1 Increased contractility, HR, CO
>7 Increased SVR, BP
Dobutamine 320 1 (plus some 2, ) Increased contractility, decreased SVR,
increased CO, ?increased HR
Dopexamine 0.56 2 (plus some 1, , Increased contractility, decreased SVR,
and dopaminergic) increased CO,
increased HR, increased renal and
?splanchnic blood flow at low dose
Isoprenaline 0.010.03 1, 2 Decreased SVR, increased HR
Milrinone Bolus 50 g/kg Increased cAMP
0.350.75 Increased contractility, coronary blood flow
Decreased SVR, PVR. Arrhythmias
Phenylephrine 0.11.0 -agonist, prolongs action potential,
increased sensitivity of actinomysin to Ca
Increased SVR, inotropy
1
Abbreviations: BP, blood pressure; CO, cardiac output; HR, heart rate; PVR, pulmonary vascular
resistance; SVR, systemic vascular resistance.
Administration of inotropes
Inotropic therapy should not be instituted until ventricular filling has

been optimized this may be difficult to assess and depends on the
clinical circumstances
Inotropic infusions must be administered through accurate infusion
devices designed for the purpose
Dedicated central line intravascular access must be used for infusions
Accurate and continuous patient monitoring should be carried out by
trained staff using appropriate monitoring equipment in an appropriate
setting (high dependency unit or ICU)
The effects of inotropic therapy should be regularly and frequently
reviewed by appropriate staff
Inotropic therapy should be used for short-term circulatory support
Calcium
The pathophysiology of heart failure includes decreased intracellular calcium,
therefore it seems appropriate to treat it with calcium ions. However, there is little
experimental evidence to support its routine use, and though it briefly causes a rise
in arterial pressure, it does not raise cardiac output. Calcium is recommended as an
inotrope in patients who have a low blood ionized calcium level, and may be of value
in counteracting the effects of raised potassium (including potassium cardioplegia
following cardiopulmonary bypass). It is usually administered as 10% CaCl2 in a bolus
dose of 510 mg/kg.
-adrenoceptor agonists
Adrenaline (epinephrine) is an endogenous catecholamine that stimulates - and
-receptors, with 1 and 2 effects being predominant at lower doses. Positive inotropy
is the main effect and, like all inotropes, there is a possibility of myocardial ischaemia in
patients with coronary artery disease as the oxygen demand increases. This is mainly
a theoretical problem, and the secretion of endogenous adrenaline (epinephrine) is
vital to maintaining contractility, vascular tone and modulating the stress response.
Stroke volume and cardiac index increase in a dose-related manner at the lower end
of the normal dose range, while effects become significant as the dose increases.
Adrenaline (epinephrine) may also cause pulmonary vasoconstriction. An increase
in heart rate is apparent, but not usually clinically significant at lower doses, and
adrenaline (epinephrine) causes less tachycardia than dopamine or dobutamine at
equivalent inotropic doses. Side-effects include arrhythmias, but this is usually not a
problem at lower infusion rates provided the patient is not hypercarbic or receiving other
arrhythmogenic substances. Metabolic effects include glycolysis, causing lactic acidosis
and hyperglycaemia. Most patients receiving adrenaline (epinephrine) infusions require
strict control of blood sugars using insulin infusions.
The normal infusion rate is 0.020.3 g/kg/min, but higher doses may be used for short
periods. Its predictability, lack of serious side-effects and low cost make it a common
and useful first-choice inotrope in the perioperative period and in the ICU, though
chronic use (greater than 24 hours) may lead to down-regulation of the -receptors.
Noradrenaline (norepinephrine) is an endogenous catecholamine. There has

been a resurgence of interest in its use recently. It has powerful -agonist activity,
and 1 activity similar to adrenaline (epinephrine) but with little 2 activity. Low-dose
infusions produce inotropy and an increase in heart rate, while higher doses cause
vasoconstriction, a consequent rise in arterial pressure and a reflex decrease in heart
rate. The increased afterload increases the myocardial oxygen demand (partially
compensated for by a rise in aortic root pressure increasing coronary artery flow) and,
in combination with the lowered heart rate, causes a fall in cardiac output. Mesenteric
and renal arteries may be constricted, but renal blood flow may increase owing to the
increased arterial pressure. It raises pulmonary vascular resistance.
Clinically, noradrenaline (norepinephrine) is used to raise the systemic vascular

resistance in patients who have severe vasodilatation (e.g. in severe septicaemia,
systemic inflammatory response syndrome, or following cardiac surgery). The dose,
in the range 0.010.4 g/kg/min is titrated in response to the desired effect; a rise in
systemic vascular resistance with a concomitant rise in arterial pressure and a possible
decrease in cardiac output.
Dopamine is an endogenous catecholamine, a precursor of adrenaline (epinephrine)

and noradrenaline (norepinephrine), and its actions are mediated via , and
specific postjunctional dopaminergic receptors in the renal, mesenteric and coronary
arterial systems. Its effects on the circulation depend on the dose; low doses
have a predominant effect on the dopaminergic receptors, intermediate doses on
the myocardial -receptors (inotropic effects) and higher doses on -receptors
(vasoconstrictor, noradrenaline-like effects). These dose-dependent effects are not
highly specific and are altered by many factors including the regulation of adrenergic
receptors (e.g. down-regulation in chronic congestive heart failure), the use of other
inotropes or vasodilators and inter-patient and intra-patient variation in response.
Dopaminergic effects may occur at higher doses, and vasoconstrictor effects at lower
doses.
The pharmacodynamic effects of dopamine include inotropy, chronotropy,

vasoconstriction and renal and splanchnic vasodilatation. At higher doses, arrhythmias
may become a problem. Dopamine increases renal arterial blood flow by 2040% by
direct vasodilatation of the afferent arteries, and indirect vasoconstriction of the efferent
arteries, which should (but has not been shown to) cause an increase in the glomerular
filtration rate. There is also an inhibition of aldosterone activity.
These effects make dopamine the inotrope of choice in many situations but there
are drawbacks. The renal effects have not been shown to cause a decrease in
perioperative acute renal failure, length of hospital stay or mortality, though there is a
possibility of converting a low output renal failure into a high output renal failure. The
effect of increased inotropy and chronotropy increases myocardial oxygen demand
and ischaemia may occur. The tachycardic effects may be more marked than with
dobutamine or adrenaline (epinephrine) at equivalent inotropic doses. Other side-
effects include an acute inhibition of prolactin secretion, with a possible detrimental
effect on cell-mediated immune function. Dopamine may exaggerate the catabolic state
found in critically ill patients by inhibiting growth hormone secretion and increasing
basal metabolic rate at moderate doses. There may be down-regulation of the -
receptors and a consequent reduction in the effectiveness of the drug with prolonged
administration or in patients with chronic heart failure.
Dobutamine is a synthetic catecholamine related to isoprenaline. It has predominantly

1 effects with weak 2 and activity. It produces a dose-dependent increase in cardiac
output with a reduction in filling pressures. In patients being treated with do-butamine
for chronic heart failure, the heart rate has been shown to remain relatively unchanged,
but in other settings it may cause a significant increase in heart rate, which is marked in
some patients. It causes a reduction in the systemic vascular resistance and this effect,
combined with the inotropic effect, causes a marked rise in the cardiac index, though
the systemic blood pressure may not rise. It is particularly useful as an agent that
increases oxygen transport, but may have to be given in combination with other agents
to maintain an adequate haemodynamic response, particularly in patients with systemic
sepsis. It has no specific effects on the renal vasculature, but may increase renal blood
flow because of an increase in cardiac output.
Dopexamine is a relatively new synthetic catecholamine with very strong 2 activity

and less pronounced 1, and dopaminergic receptor activity. Its effects are positive
inotropism (less than dobutamine) and peripheral and pulmonary vasodilatation,
causing a marked increase in cardiac output. It causes a tachycardia, particularly at
the higher end of the dose range, which may limit its use in patients with ischaemic
heart disease. It also causes an increase in renal blood flow (dopaminergic effect),
although, as with dopamine, its ability to prevent acute renal failure is not proven. There
may be some gut-protective effect, either by increased splanchnic blood flow or by
redistribution of gut blood flow to the mucosa (the main site of oxygen use in the gut).
Its use in the treatment of patients with systemic sepsis is being investigated.
Isoprenaline is a potent synthetic catecholamine, with strong 1 and 2, but little or no

, activity. It dilates skeletal muscle, renal and mesenteric vascular beds and therefore
decreases systolic and diastolic blood pressure. It is highly chronotropic, and this, in
combination with the induced reduction in coronary perfusion pressure, limits its use in
patients with ischaemic heart disease. Arrhythmias are common. It is a bronchodilator
and may inhibit histamine liberation from mast cells. It is used mainly in the acute
treatment of bradydysrhythmias associated with heart block by increasing automaticity
and reducing refractoriness, in the treatment of pulmonary hypertension (and right
ventricular dysfunction), and heart failure after some forms of congenital heart surgery.
Ephedrine is seldom used primarily for its positive inotropic effects. It has relatively
weak - and -adrenergic activity and is valuable as a pressor agent, particularly in the
treatment of hypotension caused by sympathetic blockade after regional anaesthesia.
The weak inotropic effect may be an advantage in this situation. It is usually given as a
bolus dose of 510 mg i.v. or i.m. repeated as necessary.
Phosphodiesterase inhibitors
The three available phosphodiesterase inhibitors are enoximone, amrinone and
milrinone. Amrinone is not available in all countries and the use of enoximone has
decreased with the introduction of milrinone. They do not depend on -adrenergic
receptor stimulation for their actions and therefore their effectiveness is not altered
by previous -blockade or by the down-regulation of -receptors seen in patients with
chronic heart failure or after prolonged use of catecholamines.
Phosphodiesterase inhibition in myocardium and vascular smooth muscle causes a

secondary increase in cAMP, resulting in an alteration in intracellular calcium balance.
There is positive inotropy and peripheral and pulmonary vasodilatation (the so-called
inodilator action). When used in combination with -agonists phosphodiesterase
inhibitors have an additive effect, and they are usually administered as part of a
combination therapy.
They were primarily used for the treatment of chronic heart failure and as a bridge for
patients awaiting heart transplantation. Recently, they have been used in a variety of
clinical situations, such as acute left or right ventricular failure, and as part of a regimen
for weaning patients from cardiopulmonary bypass.
Milrinone is a second-generation phosphodiesterase inhibitor. This bipyridine

derivative was initially designed for prolonged use in patients with chronic congestive
heart failure. However, in this clinical setting, its use was found to be associated with
increased mortality. It is now used in the short term, in the management of heart failure
and weaning from cardiopulmonary bypass. Unlike amrinone, there appears to be no
thrombocytopenic effect, and it has a shorter half-life than enoximone.
Milrinone causes a rise in cardiac output without increasing myocardial oxygen

consumption and this, in addition to the finding that it aids diastolic relaxation of the
ventricles (lusitropy) and increases coronary artery blood flow, make it an appealing
choice of inotrope in certain circumstances. It decreases systemic and pulmonary
vascular resistances, thereby decreasing afterload and causing a decrease in mean
systemic blood pressure and pulmonary artery pressure. Milrinone has an inotropy:
vasodilatation ratio of 1:20 (compared with 1:4 for amrinone and 1:2 for enoximone).
As a result, it is seldom administered alone but in combination with an appropriate
inotrope or vasopressor. Despite the fact that the -agonists and the phosphodiesterase
inhibitors act through the same final pathway (increased cAMP) there is an additive
effect. Milrinone is arrhythmogenic, which may limit its use in some patients.
Digoxin
Digoxin causes a rise in intracellular calcium and therefore inotropy by inhibiting the
Na-K pump but it may also reduce the neuronal reuptake of catecholamines. It also
reduces activation of the sympathetic nervous system, the reninangiotensin system
and the parasympathetic nervous system. Its use as an inotrope in patients with
congestive heart failure is controversial and in the perioperative period other inotropes
have taken precedence. Its main use is in the treatment of atrial fibrillation and flutter,
and cardiac failure. Low dose digoxin increased the ejection fraction and the exercise
tolerance of patients with congestive heart failure who were receiving concomitant
therapy with either diuretics or ACE inhibitors.
Digoxin has a low therapeutic index, particularly in critically ill patients. The loading
dose is 1 mg in divided doses over 1224 hours given orally or intravenously, aiming
for a plasma concentration of about 1.0 ng/ml. Digoxin toxicity is likely to occur with
concentrations greater than 2 ng/ml, which, in the setting of the perioperative period,
manifest in the form of arrhythmias and other ECG changes.
Class II drugs
Phenylephrine: the main action of the -agonists is peripheral vasoconstriction
mediated by adrenoceptors in peripheral vascular smooth muscle. They also have
inotropic effects mediated by prolongation of the myocardial action potential (increasing
intracellular calcium) and by increasing the sensitivity of the contractile proteins to
calcium, two mechanisms that are unaffected by a down-regulation of the -receptors.
Phenylephrine may be used as an inotrope in patients in whom increasing doses of
noradrenaline (norepinephrine) are required to achieve a desired effect. Under these
circumstances it is best given as an infusion.
Vesnarinone is under investigation. It has effects on the action potential duration of

cardiac muscle and on the sensitivity of actomyosin to calcium. Its inotropic action
may be of value in the treatment of chronic congestive heart failure (the first drug to
demonstrate this) but it has a narrow therapeutic ratio when used in this setting.
Triiodothyronine has been used for some time in high-risk cardiac surgical patients in
whom it reduces stunning after cardiopulmonary bypass. Its role in routine practice is
not clear.
Other vasoactive agents

There are many other agents that are not inotropes, but which, by their actions,
have a consequent effect on myocardial contractility and on haemodynamics. Such
drugs include: nitric oxide, which, delivered through an adapted breathing system,
causes pulmonary vasodilatation; prostacyclin, also a potent pulmonary vasodilator;
and vasopressin, a potent systemic vasoconstrictor. Vasopressin has recently been
used in the treatment of refractory ventricular fibrillation, in catecholamine-resistant
hypotension caused by septicaemia, in haemodialysis-induced hypotension and after
cardiopulmonary bypass. However, its use in these situations is still being investigated,
and it may cause significant toxicity relating to splanchnic vasoconstriction and
thrombocytopenia. u
FURTHER READING
Cuthbertson B H, Hunter J, Webster N R. Inotropic Agents in the Critically Ill. Br J Hosp
Med 1996; 56: 38691.
Feldman A M. Classification of Positive Inotropic Agents. J Am Coll Cardiol 1993;

22(4): 12237.
Fortes M L, Hines R L. Pharmacological Management of Perioperative Left and

Right Ventricular Dysfunction. In: Kaplan J A, Reich D L, Konstadt S N, eds. Cardiac
Anesthesia. Philadelphia: W B Saunders, 1999.
Kellum J A, Pinsky M R. Use of Vasopressor Agents in Critically Ill Patients. Curr Opin
Crit Care 2002; 8: 23641.
Merin R G. Positive Inotropic Drugs and Ventricular Function. In: Warltier D C, ed.
Ventricular Function. London: Williams and Wilkins, 1995.
Skarvan K, ed. Vasoactive Drugs. Bailliere Clinical Anaesthesiology. London: W B

Saunders, 1994.

Postoperative Cardiac
Intensive Care
Jonathan M Handy
Jeremy Cordingley
Jonathan M Handy is Specialist Registrar in the Imperial College, London School

of Anaesthesia. He qualified from University College London School of Medicine and
trained in anaesthetics with a specialist interest in intensive care medicine.
Jeremy Cordingley is Consultant in Intensive Care Medicine at the Royal Brompton

Hospital, London, UK. He qualified from Charing Cross and Westminster Medical
School, University of London, and trained in anaesthesia and intensive care medicine in
London.
This article outlines some of the major considerations in the intensive care of patients
after cardiac surgery.
Management of the cardiovascular system
Cardiac rhythm
Bradycardia and conduction block are common when the patient comes off
cardiopulmonary bypass, particularly after aortic valve surgery, and may persist into the
postoperative period. The usual treatment is pacing via epicardial wires, but atropine
and isoprenaline infusion can be used as temporary measures. The diagnosis of
supraventricular arrhythmias may be aided by the use of an atrial electrocardiogram
(ECG). This is performed by substituting atrial epicardial leads for the upper limb
leads in a standard 12-lead ECG. The resulting ECG produces an exaggerated atrial
depolarization trace making differentiation of atrial arrhythmias easier (Figure 1).
Management should follow conventional lines, though causes such as electrolyte
disturbances, hypoxia, hypercarbia, acidaemia, tamponade and ischaemia should be
identified and corrected rapidly.
1a Surface standard 12-lead ECG demonstrating narrow complex tachycardia.

b Atrial ECG at same time showing atrial flutter with 2:1 block. The patient was subsequently
cardioverted successfully.
Patients with poor left ventricular compliance benefit most from maintenance
of atrioventricular synchrony and active measures should be taken to establish
and maintain this. Atrial fibrillation is common in the first few postoperative days.
Management includes potassium chloride (aiming for a serum potassium level
of 4.55.0 mmol/litre) and magnesium sulphate replacement. Patients who are
haemodynamically compromised should undergo DC cardioversion. Intravenous
amiodarone is commonly administered to stable patients, but DC cardioversion should
be carried out within 24 hours if pharmacological treatment is ineffective. Prolonged
atrial fibrillation requires anticoagulation (increasing the risks of pericardial collection)
and subsequent DC cardioversion preceded by transoesophageal echocardiography
(TOE) to exclude intracardiac clot. Ventricular arrhythmias are uncommon after cardiac
surgery and usually imply recent or continuing myocardial ischaemia.
Temporary pacing systems must be checked daily to ensure adequate pacing

thresholds and to assess underlying rhythm. If the underlying rhythm remains
inadequate after several days, insertion of a permanent pacemaker system is indicated.
The use of two independent artificial pacing systems (usually a long-standing
transvenous system and a temporary epicardial system) simultaneously is not to be
recommended because of the risk of one system being inhibited by the output of the
other, which may be failing to obtain mechanical capture.
Temporary pacing wires should be removed early in a normal working day in order to
reduce the incidence of cardiac tamponade occurring out of hours.
Management of low cardiac output

Ideally, all patients would receive cardiac output monitoring in the perioperative and
postoperative periods, but usually this is reserved for high-risk patients such as
those with poor ventricular function or pulmonary hypertension. Oxygen transport
related goal-directed therapy in cardiac surgical patients has been shown to decrease
morbidity and length of hospital stay but has not been adopted widely. In some
conditions (e.g. types of congenital heart disease, tricuspid regurgitation) the use
of pulmonary artery flotation catheters is either contraindicated or would produce
inaccurate cardiac output measurements. TOE is useful for guiding postoperative
management in difficult cases.
Low cardiac output states (cardiac index less than 2.02.5 litre/min/m2) may present
insidiously postoperatively, and should be considered in patients with metabolic
acidosis, core peripheral temperature gradient persistently more than 2C, oliguria,
tachycardia, obtundation or hypotension. Important causes to identify and treat
rapidly are arrhythmias, decreased preload (hypovolaemia, tamponade, tension
pneumothorax), pump failure (myocardial ischaemia, valve failure, myocardial stunning)
and increased afterload (hypovolaemia, hypothermia and pain).
Although most hearts exhibit varying degrees of stunning after cardiac surgery,
inotropic support is usually weaned rapidly and any delay in weaning warrants
investigation. Tamponade and left ventricular dysfunction may both be associated with
hypotension and raised jugular or central venous pressure. Diagnosis may be aided by
pulmonary artery catheterization and echocardiography, though transthoracic views
are often inadequate in identifying posterior pericardial collections and TOE may be
required. Tamponade cannot always be excluded by TOE and, if there is any doubt
about the diagnosis in a patient with progressive deterioration, resternotomy should be
performed urgently.
Optimization of preload is undertaken with serial fluid challenges. Patients with poor
ventricular compliance may require high left atrial or pulmonary artery occlusion
pressures to maintain an adequate stroke volume. There is continued uncertainty
about the optimal haematocrit after cardiac surgery. For patients without cyanotic heart
disease, the authors usually maintain the haemoglobin concentration above 8 g/dl.
Choice of inotropic support for impaired left ventricular function is a variable area
of practice with little evidence base. For patients with mild-to-moderate ventricular
impairment, dopamine, up to 5 g/kg/min, is often used following cardiac surgery. In
most patients, dopamine is weaned off within 2448 hours. The immunomodulatory
and pituitary effects of dopamine make it unsuitable for long-term use. Dopamine
has no specific reno-protective effects and any improvement of glomerular filtration
rate is related to increased cardiac output. However, because of its ease of use,
dopamine remains a widely used inotropic agent. For patients with moderate-to-severe
impairment of ventricular function a phosphodiesterase inhibitor (e.g. milrinone) is
commonly used. The vasodilatory effects of milrinone usually necessitate concomitant
administration of noradrenaline (norepinephrine) to maintain an adequate systemic
arterial blood pressure. The half-life of milrinone is prolonged in patients with acute
renal failure. Adrenaline (epinephrine) is also used for management of moderate-
to-severe impairment of ventricular function. Undesirable effects include peripheral
vasoconstriction and increased glucose and lactate concentrations.
Additional options for the management of impaired left ventricular function include the
use of an intra-aortic balloon pump (IABP), insertion of a left ventricular assist device
(LVAD) and cardiac transplantation.
Increased systemic vascular resistance is common in the postoperative period.

Pain, hypothermia, hypercarbia, hypoxia and the rebound effects of discontinuing
preoperative antihypertensive therapy should be considered and treated. The risks of
untreated hypertension include myocardial ischaemia, and breakdown of suture lines
and anastamoses. In the case of the latter (particularly aortic root replacement), strict
upper limits for systolic blood pressures should be set and antihypertensive therapy
commenced (e.g. sodium nitroprusside) if these limits are exceeded.
Specific problems
Right ventricular dysfunction is common in patients who have undergone cardiac
surgery. Usually, it is minor and does not delay weaning from mechanical ventilation.
However, some patients with elevated pulmonary vascular resistance (PVR) are at risk
of acute right ventricular failure. Measures used to reduce PVR include hyperventilation,
vasodilators and inhaled nitric oxide or nebulized prostacyclin. These patients should
be weaned from mechanical ventilation slowly and may require tracheostomy.
Endotracheal extubation should occur during daytime hours to ensure extra vigilance.
Evidence of right ventricular failure (tachycardia, rising central venous pressure,
oliguria, low cardiac output, respiratory distress) should prompt early re-sedation and
endotracheal intubation. Severe right ventricular failure can be treated with a temporary
right ventricular assist device.
Ventricular septal hypertrophy causing left ventricular outflow tract (LVOT) obstruction
can be difficult to manage in the postoperative period. In addition to obstruction of
ejection, because of the hypertrophied septum, the high velocity jet in the narrowed
LVOT can cause systolic anterior motion of the anterior mitral valve leaflet, leading to
further outflow tract obstruction. Diagnosis is made with echocardiography. Management
includes maintenance of atrioventricular synchrony, controlling heart rate, ensuring
optimal preload, -blockade, and maintenance of systemic vascular resistance.
Vasodilators and IABP increase ejection velocity in the LVOT and may exacerbate
ventricular obstruction.
Patients with right-to-left intracardiac shunts are at risk of paradoxical veno-arterial

embolization. Meticulous attention should be given to avoiding air and debris entering
venous cannulae and the use of filters should be considered. Right-to-left shunt is
increased if the ratio of pulmonary to systemic vascular resistances increases, resulting
in increased hypoxaemia. Inhaled pulmonary vasodilators can be used to decrease
PVR and vasopressors to maintain or increase systemic vascular resistance.
The systemic inflammatory response syndrome (SIRS) is common after cardiac

surgery. Treatment is supportive and often includes fluid loading and maintenance of
systemic vascular resistance with noradrenaline (norepinephrine). There is increasing
evidence that relative adrenal suppression may be important in critically ill patients.
If rising doses of vasoconstrictors are required to maintain arterial blood pressure,
adrenal dysfunction should be considered.
IABP are often used in the perioperative and postoperative periods. Their use is
associated with a risk of limb and visceral ischaemia due to embolism, malposition
and the inherent risks of anticoagulation. The management of IABP, ventricular assist
devices, surgery for grown-up congenital heart disease (GUCH) and transplantation is
beyond the scope of this article.
Postoperative haemorrhage
Bleeding from chest drains of more than 200 ml for 3 hours or more should prompt
surgical re-exploration. However, bleeding is not always revealed and in patients
with coagulopathy or in whom haemostasis was difficult, a high index of suspicion
should be used with a low threshold for surgical intervention. Haemoglobin, platelet
and coagulation levels should be monitored closely postoperatively. Medical
management includes correction of coagulopathy with adequate heparin reversal,
correction of hypocalcaemia, transfusion of platelets (platelet function may be
abnormal postoperatively) and clotting products; the use of cell-saving devices to
transfuse drained blood; positive end-expiratory pressure (PEEP); head-up tilt; and the
administration of aprotinin and tranexamic acid. Surgical re-exploration in the ICU may
be indicated.
Management of the respiratory system
Following cardiac surgery there is a decrease in vital capacity, functional residual
capacity, total lung capacity, and lung and chest wall compliance. The work of breathing
and the alveolar arterial gradient increase with a reduction in the ratio of partial
pressure of oxygen in arterial blood to the fraction of oxygen in inspired air (PaO2/
FiO2). Following valve surgery there may be an increase in lung compliance, due to
reduction in lung water. The major determinant of prolonged postoperative ventilation
is poor cardiac function emphasizing the importance of cardiac output in contributing
to pulmonary dysfunction. Recent, less invasive, techniques of coronary artery bypass
grafting (off-pump coronary artery bypass, OPCAB) have been used to promote early
postoperative extubation and pulmonary rehabilitation, and several studies have shown
no increase in mortality with significant cost savings. However, both on- and off-pump
bypass surgery result in unfavourable changes to lung and chest wall mechanics and
patients should be selected carefully before considering extubation in theatre.
Postoperative respiratory complications

Atelectasis and left lower lobe collapse are common, and occur more often following
internal mammary artery grafting than with vein grafts alone. Treatment includes
PEEP or continuous positive airway pressure, humidification of inspired gases and
chest physiotherapy. Internal mammary artery grafting is also associated with a
higher incidence of pleural collections, which may require drainage. The incidence of
pneumonia following coronary artery bypass grafting (CABG) and valve surgery is
316% and 57%, respectively. Unless contraindicated, all intubated patients should
be nursed with 30 head-up tilt to reduce the incidence of ventilator-associated
pneumonia.
Phrenic nerve injury with clinically significant diaphragmatic dysfunction is more

common if ice slush is used to cool the heart without a protective insulating pad.
The incidence of acute respiratory distress syndrome (ARDS) or pump-lung following

cardiopulmonary bypass has decreased with changes to techniques (e.g. the
introduction of membrane oxygenators).
Ventilatory support
The incidence of prolonged postoperative mechanical ventilation is increased in
patients with preoperatively decreased lung function, acute pulmonary or neurological
dysfunction and those who require continued cardiovascular support. Mechanical
ventilation decreases the work of breathing and reduces afterload owing to a decrease
in transmural pressure gradient. However, prolonged mechanical ventilation is
associated with an increased incidence of nosocomial pneumonia. In addition, positive
intrathoracic pressure (especially PEEP) may increase pulmonary vascular resistance
and exacerbate right ventricular failure.
Low-risk patients have similar ventilatory requirements to other postoperative patients

and most are extubated within hours of arrival in ICU. Large tidal volumes (over 10
ml/kg) should be avoided in patients with internal mammary artery grafts. Standard
ventilatory modes vary between units and need to be tailored according to individual
patient needs. For example, patients with atelectasis may benefit from higher PEEP
and mean airway pressures, but these manoeuvres can increase pulmonary vascular
resistance. Weaning should follow the usual criteria. Extubation is indicated in an alert,
cooperative patient who is able to protect their airway, with stable cardiovascular and
respiratory function and without excessive bleeding.
Ventilatory management of patients with acute lung injury or ARDS following cardiac
surgery should follow conventional lines with adjustments relevant to the individual
patients cardiovascular physiology.
Temperature
Hypothermia is common after cardiac surgery for several reasons. Deliberately induced
hypothermia is followed by core rewarming via the cardiopulmonary bypass circuit,
however, on discontinuing bypass, heat redistributes to the colder fat layers. Significant
heat is also lost through the surgical field. The resulting hypothermia results in shivering
(with increased oxygen consumption), vasoconstriction (with increased systemic
vascular resistance and hypertension), myocardial irritability and clotting abnormalities.
Rewarming should be active, using forced warm air blankets and warmed intravenous
fluids, and passive by preventing further heat loss. Rapid rewarming should be avoided
because it may result in sudden hypotension due to vasodilation. Hyperthermia should
also be avoided because of the detrimental effects on neurological injury and the
increase in oxygen consumption that may result. Shivering can be controlled with
pethidine, sedation and occasionally neuromuscular blocking drugs.
Renal function and fluid balance

Acute renal dysfunction following cardiac surgery occurs in up to 10% of patients
following CABG. Acute renal failure requiring mechanical renal support is less common
(less than 2% of patients following CABG) but is associated with a greatly increased
mortality. Risk factors for acute renal failure include increasing age, the presence of
carotid artery bruit, congestive heart failure, diabetes mellitus, impaired renal function,
higher body weight and duration of cardiopulmonary bypass.
Patients exposed to chronic or acute ischaemic states (e.g. renal artery stenosis,
diabetes, hypovolaemia, radiocontrast agents), elderly patients and those exposed
to nephrotoxic drugs are more likely to suffer acute renal failure after subsequent
exposure to a surgical insult. Many patients undergoing cardiac surgery have these risk
factors.
The most important factors that decrease the incidence of acute renal failure are
reducing exposure to nephrotoxic agents and maintaining adequate renal perfusion
by careful monitoring and management of cardiac output and systemic arterial
blood pressure. No drug has been demonstrated in large randomized studies to be
specifically reno-protective in the peri- or postoperative cardiac surgical patient.
There are theoretical benefits from using OPCAB instead of cardiopulmonary

bypass techniques with respect to reducing renal dysfunction. However, given that
postoperative renal failure is uncommon in patients without preoperative risk factors,
many studies have been underpowered to show any difference and others have shown
conflicting results.
Continuous veno-venous haemofiltration or haemodiafiltration is the renal replacement

technique of choice in a haemodynamically unstable patient.
Sedation and neurological problems

Various mixtures of drugs provide postoperative sedation, but generally propofol/
opiate combinations are used for short-term sedation and benzodiazepine/opiate
combinations for long-term sedation. There is evidence that long-term sedation should
be stopped daily to allow a degree of neurological recovery and to prevent the side-
effects of over-sedation.
Pain management is extremely important to allow early mobilization, physiotherapy

and respiratory rehabilitation. Patient-controlled analgesia is the most commonly used,
with regular oral or nasogastric analgesia being used when enteral feeding begins.
The use of thoracic epidural analgesia in patients undergoing procedures with full
anticoagulation is controversial because of the risk of epidural haematoma formation.
The ICU is often the first place that postoperative neurological problems are diagnosed.
The rate of neurological complications after cardiac surgery depends on a number
of factors. Surgical risk factors include operations involving calcified valves or an
atherosclerotic ascending aorta, the use of cardiopulmonary bypass, prolonged
surgery, low cardiac output states and gas or debris entering the systemic circulation.
Patient risk factors include previous cerebrovascular accidents or disease, diabetes
and advanced age. The periods of highest risk are during aortic cannulation, onset and
weaning of cardiopulmonary bypass, and removal of calcified valves.
Many complications, including postoperative confusion, associated with

cardiopulmonary bypass are transient, however, some may be prolonged or permanent.
CT is the most common investigation used for diagnosis, though MRI may be required.
Peripheral nerve injuries can occur, as with any prolonged general anaesthetic.
Management of gastrointestinal problems

The incidence of gastrointestinal problems is about 1% after cardiac surgery.
Gastrointestinal bleeding accounts for almost half of these complications, followed
by hepatic dysfunction, intestinal ischaemia, acute cholecystitis and ischaemic
pancreatitis. The clinical manifestations of these conditions may be atypical and may
be masked by postoperative analgesia or sedation. Routine investigations should
include liver function tests, serum lactate, arterial blood gas analysis and serum
amylase with unexpected metabolic acidosis prompting further investigations to
exclude an abdominal cause. Preservation of adequate cardiac output, routine stress
ulcer prophylaxis in patients without full enteral nutrition, and early postoperative
enteral feeding can reduce the risk of these complications. Treatment follows
conventional lines.
Other considerations
The metabolic changes that occur after cardiac surgery are complex and
multifactorial. Surgical trauma, cardiopulmonary bypass, hypothermia, drug
treatments and the transfusion of blood products all contribute. The most
significant changes relevant postoperatively to ICU patients are activation of the
inflammatory and coagulation pathways, and increased gluconeogenesis resulting in
hyperglycaemia. Systemic inflammatory and coagulation activation are multifactorial
and their aetiologies and treatments are beyond the scope of this article. Altered
coagulation may be deliberate (through pharmacotherapy) or pathological, but
is significant because of the risk of bleeding. A fine balance exists between the
commencement of anticoagulant therapy and the immediate postoperative risk
of bleeding. Anticoagulation is often required after prosthetic mechanical valve
insertion, treatment of intravascular or intracardiac thrombus and thromboembolic
prophylaxis (particularly if there are areas of low or turbulent flow). In each case,
the therapeutic range and timing of anticoagulation varies, weighing up the benefits
against the risk of bleeding. For example, aortic valve prostheses pose a low risk
of clot formation in the absence of anticoagulation when compared with mitral
valve prostheses, owing to the high pressures associated with the former. Of
note, pericardial effusions may increase in size on commencement of therapeutic
anticoagulation. Should coagulopathy develop, its aetiology should be sought and
treatment commenced as appropriate. Prophylaxis against thromboembolic disease
should be considered in all patients. Heparin-induced thrombocytopenia should be
considered if the platelet count is falling.
There is compelling evidence supporting tight glycaemic control following cardiac surgery,
though the exact limits with in which blood glucose should be maintained in order to have
a benefit on morbidity and mortality have yet to be established. u

Preoperative Assessment for
Cardiac Surgery
P D Alexander
Andrea Kelleher
P D Alexander is locum Consultant Cardiothoracic Anaesthetist at the Royal Brompton

Hospital, London.
Andrea Kelleher is Consultant Cardiac Anaesthetist at the Royal Brompton Hospital,

London. Her special interests include paediatric cardiac anaesthesia and strategies to
limit bleeding and blood transfusion during cardiac surgery.
The assessment of the patient presenting for cardiac surgery allows the anaesthetist to:
take a history and examine the patient with particular reference to the cardiovascular
disease
plan the anaesthetic approach
educate the patient about the anaesthesia (e.g. tracheal intubation,
invasive monitoring, postoperative intensive care, and the use of intraoperative
transoesophageal echocardiography or regional analgesia)
discuss specific anaesthetic risks including damage to teeth and the potential need
for transfusion of blood and blood products.
History and examination

Most patients presenting for adult cardiac surgery undergo cardiac revascularization.
History taking should be directed towards assessing evidence of previous myocardial
infarction, continuing cardiac ischaemia on exercise or at rest, and pulmonary oedema.
The Canadian Cardiovascular Society Classification of Effort Angina is a widely
accepted method of scoring the severity of anginal symptoms (Figure 1).
The Canadian Cardiovascular Society Classification of Effort Angina
Class 1
Ordinary physical activity does not cause angina. Angina occurs with strenuous
or rapid or prolonged exertion either at work or recreation
Class 2
Slight limitation of ordinary activity. Angina occurs with walking or climbing stairs
rapidly, walking up hill, walking or stair climbing after meals, or in the cold, or
wind, or under emotional stress, or only during the few hours after awakening.
Angina occurs when walking more than two blocks on the level or climbing more
than one flight of stairs at a normal pace and in normal conditions
Class 3
Marked limitation of ordinary physical activity. Angina occurs with walking one to
two blocks on the level and climbing one flight of stairs in normal conditions at a
normal pace
Class 4
Inability to carry on any physical activity without discomfort. Angina may be
present at rest
1
Patients presenting for valvular heart surgery range from those who are seriously ill
(e.g. with infective endocarditis) to those who are relatively asymptomatic, because the
decision to undergo surgery is now often based on changing ventricular dimensions
rather than increasing severity of symptoms. Severe valvular heart disease may
typically present with dyspnoea, syncope or angina. The New York Heart Association
Functional Classification is a widely accepted system for grading dyspnoea secondary
to cardiac disease (Figure 2).
New York Heart Association Functional Classification
Class 1
Patients with cardiac disease but without resulting limitations of physical activity.
Ordinary physical activity does not cause undue fatigue, palpitations, dyspnoea or
angina
Class 2
Patients with cardiac disease resulting in slight limitation of physical activity.
Comfortable at rest. Ordinary physical activity results in fatigue, palpitations,
dyspnoea or angina
Class 3
Patients with cardiac disease resulting in marked limitation of physical activity.
Comfortable at rest. Less than ordinary physical activity results in fatigue,
palpitations, dyspnoea or angina
Class 4
Patients with cardiac disease resulting in an inability to carry out any physical
activity without discomfort. Fatigue, palpitations, dyspnoea or angina may be
present at rest. If any physical activity is undertaken the symptoms of cardiac
insufficiency are increased
Many patients undergoing cardiac surgery have concomitant disease, including

diabetes mellitus, pulmonary disease, hypertension and peripheral vascular disease
(e.g. ascending aortic and carotid atheroma). The presence and severity of associated
disease should be fully evaluated preoperatively because it may have a substantial
impact on the perioperative anaesthetic management, and ultimately the on outcome.
Medication
As a general principle, drugs taken to control hypertension or cardiac disease (e.g.
-blockers, calcium channel antagonists or anti-anginals) must not be stopped
immediately before surgery. A possible exception to this rule is the angiotensin-
converting enzyme inhibitors (e.g. lisinopril) because they may be associated with
profound hypotension during cardiopulmonary bypass. They are often discontinued
2448 hours before surgery.
Aspirin and clopidogrel both irreversibly inhibit ADP-induced platelet aggregation and
should be stopped 710 days before surgery to allow a new population of normally
functioning platelets to enter the circulation and decrease the risk of excessive
postoperative bleeding. Many patients presenting for valvular surgery may be taking
warfarin preoperatively which should be stopped 23 days before surgery to allow the
international normalized ratio (INR) to fall below 2.0. If anticoagulation is essential (e.g.
in the presence of a prosthetic valve) warfarin may be replaced by heparin until the time
of surgery.
Risk stratification
The UK Cardiac Surgical Register data show that in 2000 the national average mortality
for isolated coronary artery bypass grafting was 2.2% and for isolated valve surgery
was 5.5%. The risk is not the same for all patients, so scoring systems have been
developed to attempt to stratify patients according to their individual risk. These range
from simple additive scores such as the Parsonnet Score, to highly complex statistical
algorithms.
The Parsonnet score has been widely used for many years by cardiac surgeons
attempting to predict morbidity and mortality. However, it is heavily weighted towards
factors such as advan-cing age and re-do surgery, the impact of which on mortality has
declined over the last decade, thus diminishing its relevance.
More recently, the Euro Score has become popular. This is a simple additive score
with different weighting and risk factors, which takes into account recent advances in
surgical practice. The score achieved is approximately numerically equivalent to the
percentage risk of death (Figure 3).
Euro Score for Cardiac Operative Risk

Factor Definition Score
Age Per 5 years of age or part thereof from 60 years 1
Gender Female 1
Chronic lung disease Long-term use of bronchodilators or corticosteroids for 1
lung disease
Extracardiac arteriopathy One or more of the following: claudication, carotid occlusion 2
or > 50% stenosis, previous or planned surgery on the
abdominal aorta, limb arteries or carotids
Neurological dysfunction Disease severely affecting ambulation or day-to-day functioning 2
Previous cardiac surgery Involving opening of the pericardium 3
Serum creatinine > 200 mmol/litre preoperatively 2
Active endocarditis Still on antibiotic treatment for endocarditis at the time of surgery 3
Critical preoperative state Preoperative intermittent positive-pressure ventilation, 3
inotropic support, intra-aortic balloon pump or preoperative acute
renal failure
Unstable angina Requiring intravenous nitrates until arrival in the anaesthetic room 2
Left ventricular dysfunction Moderate ejection fraction (3050%) 1
Poor ejection fraction (< 30%) 3
Recent myocardial < 90 days 2
infarction
Pulmonary hypertension Systolic pulmonary artery pressure > 60 mm Hg 2
Emergency surgery Carried out before next available list 2
Cardiac surgery other Cardiac surgery other than or in addition to coronary artery 2
than isolated coronary bypass grafting
artery bypass grafting
Thoracic aortic surgery Ascending, arch or descending 4
Postinfarction septal 4
rupture
The most commonly used anaesthetic scoring systems include the American Society
of Anesthesiologists (ASA) grading system and more recently the Cardiac Anaesthesia
Risk Evaluation (CARE) score, which attempts to evaluate the anaesthetic risk
specifically for patients undergoing cardiac surgery. It is a simple risk classification
based on co-morbid disease (controlled or uncontrolled) and the complexity
and urgency of the surgery (Figure 4). The anaesthetic risks must be discussed
sympathetically with the patient, in the context of the need for surgery. Although it
is uncommon to cancel cardiac surgery on medical grounds or on the basis of a high
risk score, it may be appropriate to delay surgery to allow optimization of the patients
medical condition.
Cardiac Anaesthesia Risk Evaluation (CARE) Score
Score Description Predicted

mortality (%)
1 Patient with stable cardiac disease 0.5
and no other medical problem.
Non-complex cardiac surgery planned
2 Patient with stable cardiac disease 1.1

and one or more controlled medical
problems (e.g. hypertension). Non-
complex cardiac surgery planned
3 Patient with any non-controlled medical 2.2

problem (e.g. unstable angina) or patient
in whom complex cardiac surgery under-
taken
3E As 3 but with emergency surgery 4.5
4 Patient with any uncontrolled medical 8.8

problem and in whom complex cardiac
surgery undertaken
5 Patient with chronic or advanced cardiac 29.3

disease for whom cardiac surgery is
undertaken as a last resort or to save life
4
Investigations
In addition to routine haematological and biochemical investigations before cardiac
surgery, all patients undergo an ECG and chest radiograph. Many UK centres also
screen for hepatitis and multi-resistant Staphylococcus aureus. Patients presenting
for cardiac surgery will have undergone certain specialized investigations, and it is
important that the anaesthetist has an understanding of the principles behind them.
Exercise tolerance test is a non-invasive diagnostic test often used in patients with
suspected ischaemic heart disease. Many different exercise-testing protocols exist,
but the Bruce and modified Bruce protocols are commonly used. The modified Bruce
protocol starts at a lower workload and is used in patients who have had a myocardial
infarct, those whose history suggests symptoms at a low workload, or those who are
elderly or sedentary. The test is conducted in 3-minute stages through which the
patients workload is progressively increased by increasing the speed and incline of
the treadmill. The protocol is continued until one of several end points is reached: a
true positive or negative test, hypo- or hypertension, fatigue, dyspnoea, ventricular
arrhythmias or difficulty in ambulation. The test is described as positive if typical chest
pain or diagnostic ST depression (at least 1 mm at 0.08 s after the end of the QRS
complex) occurs. The test is negative if the patient reaches a specified heart
rate (dependent on age) without chest pain or ST segment changes.
An exercise test is considered strongly positive for triple vessel or left main stem
disease if the systolic blood pressure drops by 10 mm Hg or more, more than five leads
show ST segment changes, and the ischaemic changes occur within 3 minutes of
starting the test and take more than 9 minutes to resolve.
Perfusion imaging patients who are unable to exercise may undergo a thallium
stress test. A common protocol is to infuse dobutamine, 1040 g/kg/min, in
conjunction with intravenous thallium-201. The dobutamine simulates exercise causing
maximal dilatation of the coronary arteries. The patient is scanned with a gamma
camera at peak stress and if there is a fixed coronary stenosis, the artery is unable
to dilate and the blood and thallium are distributed away from the area. Hypoperfused
areas appear on the scan as image defects. The patient is re-scanned 24 hours
later, by which time the thallium will have reached the hypoperfused areas but will
demonstrate very slow clearance, resulting in thallium detection in the areas of the
scan where there was previously a perfusion defect. A persistent hypoperfused area
indicates non-viable myocardium.
The gamma camera is also used in multiple gated acquisition (MUGA) scanning in which
radiolabelled technetium-99 is injected intravenously. The image produced as it passes
through the cardiac chambers can be used to quantify right and left ventricular stroke
volume and therefore function. It is also useful in the assessment of intracardiac shunts
and valvular regurgitation.
CT may be used to provide detailed information about the great vessels (e.g. in aortic
dissection). It is particularly useful in defining cardiac anatomy in patients presenting for
re-do surgery (e.g. the position of the heart in relation to the sternum).
MRI is increasingly valuable as a technique for imaging the heart and great vessels
because the flowing blood produces a unique signal obviating the need for contrast
media or radiographs. It is the procedure of choice in the evaluation of pericardial
disease, intracardiac masses and the assessment of many forms of congenital heart
disease, and is becoming increasingly recognized as a valuable tool in the preoperative
and postoperative evaluation of ischaemic heart disease.
Cardiac catheterization remains the gold standard in the diagnosis of cardiac

pathology, in particular coronary artery disease. A catheter is placed in turn in each
of the two coronary ostia, and dye injected. A 50% reduction in vessel diameter is
equivalent to a 75% reduction in cross-sectional area and represents a significant
stenosis.
Left ventricular ejection fraction, cardiac output, pulmonary vascular resistance and
end-diastolic pressures may be measured during cardiac catheterization. In valvular
lesions, the pressure gradient or alternatively the regurgitant fraction across the valve
can also be estimated.
Echocardiography and stress echocardiography echo-cardiography

(transthoracic, transoesophageal and three-dimensional) has become invaluable in the
diagnosis and pre-operative assessment of many cardiac abnormalities, in particular
valvular disease, allowing the measurement of gradients and the calculation of valvular
areas. Echocardiography is also used to assess systolic and diastolic ventricular
function and to define regional wall motion abnormalities.
Stress echocardiography, using an infusion of dobutamine incrementally increasing

to 20 g/kg/min, is also useful to identify viable myocardium in the presence of
coronary artery disease and to differentiate ischaemic from non-ischaemic myocardial
dysfunction. In the presence of coronary artery disease, low-dose dobutamine may
be expected to increase myocardial blood flow and improve regional wall motion
abnormalities. Conversely, high-dose dobutamine leads to an oxygen metabolic
mismatch in areas at ischaemic risk and results in worsening regional wall motion.
Thus, there is classically a biphasic response to dobutamine stress in ischaemic
heart disease. Segments of the ventricle that remain akinetic or dyskinetic despite
dobutamine infusion are non-viable and represent scar tissue.
Premedication
A common approach to premedication is to prescribe a short-acting benzodiazepine
(e.g. temazepam) 2 hours before surgery. In most cases, this achieves anxiolysis
without significant cardiac or respiratory depression, and may be supplemented if
necessary in the anaesthetic room with intravenous midazolam. In addition, if the
patient is to undergo beating-heart surgery, it may be appropriate to prescribe a
-blocker such as atenolol, 50 mg orally, at the time of premedication, in order to
contribute to the stability of the surgical field. u
FURTHER READING
Depuis J Y, Wang F, Nathan H et al. The Cardiac Anaesthesia Risk Evaluation Score.
Anesthesiology 2001; 94: 194204.
Gothard J W W, Kelleher A A. Essentials of Cardiac and Thoracic Anaesthesia. Oxford:

Butterworth-Heinemann, 1999.
Kaplan J A. Cardiac Anaesthesia. Philadelphia: W B Saunders,1993.
Millner R, Treasure T. Explaining Cardiac Surgery: Patient Assessment and Care.

London: BMJ Publishing Group, 1995.

Principles of Cardiac
Anaesthesia
John W W Gothard
Moira Wattie
John W W Gothard is Consultant Cardiothoracic Anaesthetist at the Royal Brompton

Hospital, London. He qualified from St Marys Hospital Medical School, London. He
has written several textbooks on cardiac and thoracic anaesthesia and has a clinical
practice encompassing all aspects of adult and paediatric cardiac anaesthesia.
Moira Wattie is Specialist Registrar at the Imperial College School of Anaesthesia,

London. She qualified from University College Hospital, London.
There are a number of accepted anaesthetic techniques for cardiac surgery. New
drugs continue to be introduced into clinical practice and there are differences of
opinion about the optimal anaesthetic for a particular cardiac procedure. However,
there is evidence that it is not the initial choice of a particular anaesthetic technique
or group of drugs that is crucial to outcome but rather the manner in which they are
applied in different clinical circumstances. A discussion of all anaesthetic agents and
their cardiovascular effects is beyond the scope of this article but a knowledge of
these agents is essential. The principles of cardiac anaesthesia are outlined below,
but the anaesthetist is also involved in many other aspects of patient care during
cardiac surgery, including the management of anticoagulation and clotting defects,
cardiopulmonary bypass, fluid and electrolyte balance, gas exchange and acidbase
status, inotropic support, pacing techniques and mechanical support of the heart.
Monitoring
The monitoring modalities used for cardiac anaesthesia are listed in Figure 1. Routine
invasive monitoring for all cardiac patients includes arterial cannulation and central
venous access. Pulmonary artery catheters are used routinely in many North American
centres, but in the UK they are used mainly for high-risk cases. Transoesophageal
echocardiography is a rapidly expanding field, which is likely to dominate perioperative
monitoring in the next decade.
Monitoring for cardiac anaesthesia
Essential Optional
ECG (5 lead) Pulmonary artery catheter
Invasive arterial pressure Transoesophageal echo
Central venous pressure Cardiac output
Core temperature As above
Urine output Oesophageal Doppler
Anaesthetic agent analysis Pulse contour analysis
Ventilation Lithium dilution
Tidal volume/respiratory Cerebral function monitors
rate
Airway pressure
End-tidal carbon dioxide
Oxygenation
Inspired/expired oxygen
Pulse oximetry
Arterial cannulation
Cardiac surgery is often associated with sudden changes in blood pressure, and a
safe, reliable, method of measuring these acute changes is required. For this purpose,
a cannula (20 or 22 G) is usually inserted percutaneously into the radial artery of the
non-dominant hand. If the radial artery is to be harvested for use as a conduit during
coronary artery bypass grafting, it is taken from the non-dominant arm, providing there
is adequate collateral flow via the ulnar artery, and the radial artery cannula is placed in
the dominant arm.
In high-risk cases, such as aortic stenosis, left main stem coronary disease and
patients with poor ventricular function, it is advisable to place the arterial line under
local anaesthetic before induction of anaesthesia.
The right radial artery may be preferred if aortic surgery (e.g. repair of coarctation) is
to be undertaken or if an intra-aortic balloon pump (IABP) is likely to be used. This is
because the right subclavian artery is unlikely to be involved in aortic surgery and in
the case of an IABP it will not be occluded by the balloon and is thought to give the
optimal arterial trace for timing balloon inflation. Other arteries (e.g. brachial, femoral,
axillary, dorsalis pedis) can be used to measure systemic arterial pressure. Damage to
the brachial artery can, rarely, result in limb ischaemia because of the poor collateral
circulation at this point, and the femoral artery may be required for insertion of an intra-
aortic balloon or for institution of cardiopulmonary bypass in re-do surgery.
Central venous access

Peripheral venous access will have been established before induction and a large-bore
cannula can be sited in the arm for volume replacement during surgery. Central venous
access is primarily required to measure the filling pressure of the right heart and for
the administration of vasoactive drugs. Additional access may be required to allow the
flotation of a pulmonary artery catheter. The right internal jugular vein is commonly
used because:
it can usually be ballotted in the anaesthetized patient and is easy to cannulate
it can usually be easily located, with ultrasound if necessary
there is a low incidence of complications
pressure recordings are not affected if the innominate vein is stretched on opening
the chest, a manoeuvre that can lead to erroneously high readings with left-sided
lines
multiple catheters can be placed in the same vessel.
A higher anatomical approach to the internal jugular vein is preferable because

pneumothorax and damage to vascular structures within the chest are less likely. The
Seldinger technique is safe and widely practised, though complications relating to
over-zealous use of the dilator have been described. Puncture of the carotid artery
with a small needle is not usually serious, but if this is undetected and a large sheath
is passed into the vessel, surgical repair may be necessary. The subclavian vein is an
alternative site, but is more hazardous.
The National Institute of Clinical Excellence (NICE) has recommended that ultrasound
devices are made available and more widely used to aid central venous cannulation.
Pulmonary artery catheterization and cardiac output measurement

Thermodilution remains the gold standard for clinical determination of cardiac
output but the routine use of pulmonary artery catheters remains a subject of debate.
In certain patients, such as those with poor ventricular function or valve disease,
pulmonary artery catheters facilitate haemodynamic management, including choice
of inotropic drugs. They may also be useful in the management of patients with
significant pulmonary hypertension. The authors practice is to insert a pulmonary
artery catheter introducer sheath following induction of anaesthesia in most patients. A
pulmonary artery catheter can then be introduced easily, if required, at the termination
of cardiopulmonary bypass or once the patient reaches the ICU.
Pulmonary artery catheterization allows measurement of pulmonary artery pressure,

pulmonary capillary wedge pressure, thermodilution cardiac output and mixed venous
oxygen saturation. More sophisticated catheters can measure continuous cardiac
output and/or mixed venous oxygen saturations and some have a pacing facility.
A variety of haemodynamic indices can be calculated from this data (most usefully
systemic and pulmonary vascular resistance) when combined with measurements of
systolic/diastolic arterial pressure and central venous pressure. In difficult cases, this
information may help if separation from cardiopulmonary bypass is not straightforward.
Left-sided filling pressures can be measured directly with a left atrial line inserted under
direct vision at surgery.
Insertion of pulmonary artery catheters is associated with the production of

arrhythmias, pulmonary artery rupture, infection, catheter knotting and
thromboembolism as well as complications related to central venous cannulation.
Less invasive methods of monitoring haemodynamic function and cardiac output during
cardiac surgery include oesophageal Doppler, pulse contour analysis (lithium dilution)
and transoesophageal echocardiography.
Transoesophageal echocardiography (TOE)

The use of intraoperative echocardiography is well established. TOE is now regarded
as an essential monitor (Figure 2) during valve repair surgery and during correction
of some congenital defects. It is also useful to demonstrate adequate de-airing of the
heart and to monitor ventricular function when weaning a patient from cardiopulmonary
bypass. Complications include dental injury, damage to the airway or oesophagus,
bacteraemia and (most importantly) distraction of the operator from patient care.
Indications for transoesophageal echocardiography
Haemodynamic instability
Evaluation of left and right ventricular disease
Global and regional
Systolic and diastolic
Valvular function
Assessment of haemodynamic function
Detection of hypovolaemia
Cardiac tamponade
Acute pulmonary embolism
Dynamic left ventricular outflow tract obstruction
Cardiac surgery
Cardiac valve reconstruction and replacement
Myocardial revascularization (especially poor function)
Surgical correction of congenital heart disease
Aortic dissection
Minimally invasive cardiac surgery
Minimal access heart surgery
Pulmonary embolectomy
Resection intracardiac tumours/thrombi
Aneurysmectomy
Myotomy for hypertrophic cardiomyopathy
Heart transplantation
Induction of anaesthesia
After appropriate monitoring has been established and pre-oxygenation completed,
induction of anaesthesia is commenced, most commonly via the intravenous route in
adults. The drugs used for induction (Figure 3) vary with the intended technique, but
a common approach is to administer a moderate dose of opioid (e.g. fentanyl, 2.55
g/kg) before a sleep dose of etomidate, thiopental (thiopentone) or propofol given by
slow injection. This approach provides a smooth induction with haemodynamic stability
in most cases. Pre-treatment with opioids reduces the dose of induction agent required
and limits, to some extent, the myocardial depression and fall in systemic vascular
resistance associated with them. It may be preferable to give propofol as an infusion
in a target-controlled device, particularly in high-risk cases. Etomidate is widely used
for induction because it appears to have minimal cardiovascular effects, although
reductions in blood pressure occur in patients with cardiac disease or some degree of
hypovolaemia. Substantial falls in arterial pressures can occur in the elderly, in whom
it should be used with care. Etomidate causes pain on injection, myoclonic movements
and adrenal suppression even after a single dose.
Alternative approaches include the use of benzodiazepines, which are commonly used
in North America. Cardiovascular stability is well maintained with intravenous diazepam
and it may be used to facilitate insertion of invasive monitoring lines under local
anaesthetic. Midazolam can be used for induction, but may cause hypotension resulting
from falls in systemic vascular resistance and stroke volume, particularly in combination
with opioids. Ketamine produces a substantial rise in arterial pressure as a result of
sympathetic stimulation. In most cardiac patients, this is not ideal but occasionally
these effects may be advantageous, for example in the patient with a large pericardial
effusion and/or tamponade.
Muscular relaxation
Pancuronium is widely used by cardiac anaesthetists to facilitate intubation and
ventilation. Its sympathomimetic and vagolytic actions were considered advantageous
when the drug was first introduced and coronary artery surgery was in its infancy but
these effects produce an increase in myocardial oxygen demand, which can result in
ischaemia. The improved medical treatment of angina, particularly the use of
-adrenergic receptor blockers in the treatment of ischaemic heart disease, means that
tachycardia and hypertension are unlikely to be a problem if this medication is taken up
to the day of surgery.
Induction agents for cardiac anaesthesia
Drug Cardiovascular Pharmacokinetics Infusion Special

effects considerations
Sodium Reduction in cardiac Slow hepatic Rapid
thiopental output due to direct metabolism accumulation
(thiopentone) cardiac depression
with preservation of
heart rate and SVR
Propofol Significant reduction Rapid metabolism Little accumulation

in SVR and thus MAP largely unaffected in short-term Best avoided in
if given in bolus dose, by renal or infusion outflow tract
largely avoided with a hepatic disease Used to minimize obstruction (e.g.
slow infusion awareness during aortic stenosis
cardiopulmonary or cardiomyopathy)
bypass and for No evidence of
sedation post- neuro-protection in
operatively cardiac setting
Etomidate Minimal cardiovascular Rapid metabolism Associated with Significant adrenal

effects in normal by plasma and increased mortality suppression with
patients hepatic esterases in the critically ill even a single dose
Some reduction in MAP
in those with cardiac
disease and
particularly in the
elderly
Midazolam Modest decrease in Rapid hepatic Accumulates in Can be used as a

MAP and SVR metabolism and long-term infusion, premedication and
renal clearance particularly in the to facilitate line
critically ill insertion under
local anaesthesia
MAP, mean arterial pressure; SVR, systemic vascular resistance
Vecuronium is used increasingly because several studies have shown that residual
neuromuscular blockade is common after administration of pancuronium and may cause
delayed extubation if routine reversal is not used. Vecuronium, with a shorter half-life, has
a stable cardiovascular profile, but may be associated with bradycardia if given shortly
after fentanyl or remifentanil. Rocuronium has a similar haemodynamic profile and has
been recommended for use in cardiac anaesthetic practice. Its rapid onset facilitates
early intubation and its intermediate duration of action means that residual paralysis is
unlikely to be a problem.
Atracurium is not widely used in cardiac anaesthesia except as a continuous infusion.

It may be useful for short non-bypass procedures, but histamine release can cause
hypotension.
Tracheal intubation
Oral intubation is preferred in adults and is well tolerated post-operatively. Nasal
intubation may cause mucosal trauma, resulting in severe haemorrhage following
administration of heparin.
Certain procedures require use of double-lumen endobronchial tubes. These include

descending aortic surgery and thoracoscopic internal mammary artery harvest. The
use of a double-lumen tube allows collapse of the lung on the operative side to facilitate
surgery. A left-sided tube is usually selected to circumvent problems associated with
right upper lobe ventilation.
Maintenance of anaesthesia
Surgery for ischaemic heart disease represents 75% of the total UK cardiac surgical
workload, with 24,000 cases in the year 20002001. The following description of
cardiac anaesthesia is largely applicable to these patients, but the principles are
relevant to all cardiac surgical patients. Specific considerations for patients with valvular
heart disease (about 20% of cases) are summarized in Figure 4.
Valve surgery and anaesthesia
Aortic stenosis
Heart rate/rhythm
Sinus rhythm essential (ventricular filling critically dependent on atrial systole)
Avoid tachycardia (shortens diastole)
Sequential atrioventricular pacing required if heart block presents following
cardiopulmonary bypass
Preload/contractility
Maintain preload and contractility
Systemic and pulmonary vascular resistance

May need to maintain systemic vascular resistance temporarily with
vasoconstrictors to preserve coronary blood flow (e.g. before cardiopulmonary
bypass)
Aortic regurgitation
Heart rate/rhythm
Heart rate optimal at about 90 beats/min (sinus rhythm)
Low heart rates associated with increased diastolic time and increased
regurgitation
May benefit from inodilator therapy

Forward stroke volume can be augmented with vasodilators
Mitral stenosis
Heart rate/rhythm
Ideal heart rate 7090 beats/min
Many patients in atrial fibrillation at time of surgery important to control
ventricular rate in this situation
Inotropic therapy often required following surgery (avoid tachycardia)

Long-standing mitral stenosis can lead to pulmonary hypertension
May require pulmonary vasodilator therapy postoperatively and prolonged
weaning from ventilation
Inhaled nitric oxide therapy has been used in the latter context
Mitral regurgitation
Heart rate/rhythm
Low heart rates deleterious: 80100 beats/min (sinus rhythm) ideal range
Patients often present with atrial fibrillation

Decrease in left ventricular afterload (decrease in systemic vascular
resistance) can reduce the degree of regurgitation through the valve
Pulmonary hypertension may occur with chronic mitral regurgitation (often
combined with mitral stenosis) and require pharmacological treatment
4
The aim of general anaesthesia for cardiac surgery is to produce a state of

unconsciousness in the patient while maintaining myocardial oxygen balance and
minimizing ischaemia. Myocardial ischaemic episodes are minimized if hypertension
(leading to increased myocardial wall tension) and tachycardia are avoided. Anaesthetic
agents alone seldom provide complete haemodynamic control, and additional drug
therapy with a variety of vasoactive agents including nitrates, vasoconstrictors and
inotropes may be required. The introduction of synthetic opioids 30 years ago,
enhanced the anaesthetist's ability to maintain haemodynamic control during cardiac
surgery. High-dose opioid anaesthesia provides this, but recovery is often prolonged
and intraoperative recall may be a problem. Volatile agents provide good intraoperative
conditions, but rapid washout at the end of surgery is associated with sudden
emergence and unstable haemodynamics. A compromise anaesthetic technique is a
combination of an opioid and a volatile agent. Total intravenous anaesthesia is also
widely used, usually a combination of propofol and opioid.
The use of nitrous oxide is controversial in cardiac anaesthesia. It has myocardial

depressant effects, which may be exaggerated if used in combination with opioids. To
avoid this, an air/oxygen mix can be used as the carrier gas for volatile agents. This
also eliminates the possibility that micro air emboli will be enlarged in the circulation
by inward diffusion of nitrous oxide into the air bubbles during the period following
cardiopulmonary bypass.
Inhalational agents: modern inhalational agents (e.g. isoflurane, sevoflurane,

desflurane) have fewer side-effects than older agents such as halothane. On its
introduction to clinical practice, isoflurane was heralded as the ideal inhalational agent
for cardiac anaesthesia because it preserved cardiac output with reduced peripheral
resistance and did not significantly depress myocardial contractility. A number of
studies later suggested that isoflurane could cause a deleterious redistribution of
coronary blood flow, increasing the flow to healthy areas of myocardium by diverting it
from potentially ischaemic areas supplied by diseased coronary arteries the coronary
steal effect. These concerns have largely subsided and it is considered safe when
used at moderate concentrations as part of a balanced anaesthetic technique. There
is no recent evidence demonstrating any major advantage of any of the inhalational
agents for cardiac anaesthesia. In practice, most units in the UK use isoflurane for
adults and reserve sevoflurane for the induction of children.
During coronary artery surgery, myocardial ischaemia with subsequent reperfusion can
lead to ischaemia-reperfusion injury of the myocardium with variable manifestations
ranging from myocardial infarction and myocardial stunning to reperfusion arrhythmias.
Data show that inhalational agents (including isoflurane) given before an ischaemic insult
confer significant protection against this injury. The mechanisms for this effect (Figure
5) include conservation of ATP levels, reduction of calcium overload and free radical
scavenging, thus preserving myocardial myocyte function. This effect is not seen with
intravenous agents such as propofol.

Anaesthesia
Propofol is a well-established, non-cumulative intravenous anaesthetic agent, widely

used in cardiac anaesthesia. It can cause significant systemic hypotension, particularly
following a bolus injection. This effect is principally due to a decrease in systemic
vascular resistance but there may also be an element of myocardial depression.
Propofol should be used only in patients with good ventricular function and avoided
in those with significant outflow tract obstruction (e.g. aortic stenosis, hypertrophic
cardiomyopathy). Propofol is better tolerated if given slowly and is preferably
administered as an infusion, possibly as part of a total intravenous anaesthetic (TIVA)
technique. Propofol is commonly used to provide anaesthesia during the specific
period of cardiopulmonary bypass and has an important role to play in the immediate
postoperative period when ventilated patients can be sedated for a few hours with the
non-cumulative drug.
Propofol has a neuroprotective effect in patients with severe head injuries. This effect
has not been demonstrated in patients undergoing cardiopulmonary bypass.
Opioids: a range of synthetic opioids are available for use in cardiac anaesthesia.
Fentanyl was first used for cardiac anaesthesia in 1978. Since then, its use has been
extensively investigated along with two of its newer congeners, alfentanil and sufentanil.
This group of drugs is reliable and effective for cardiac anaesthesia and is associated
with minimal cardiovascular depression. In the UK, fentanyl is widely used for cardiac
anaesthesia, but there has been a tendency to reduce the dose to facilitate weaning
from ventilation. In this latter respect, much interest has centred around the use of the
opioid remifentanil.
Remifentanil is a potent analgesic opioid agent with an ultra- short half-life (5 minutes)
resulting from metabolism by plasma esterases. It is administered by infusion at a
rate of 0.52 g/kg/min. It has been successfully used with propofol and isoflurane to
produce profound analgesia, haemodynamic stability and suppression of the stress
response during cardiac surgery. Its unique properties allow patients to be weaned from
ventilation within 30 minutes of stopping an infusion.
Initial enthusiasm for remifentanil has been tempered by a number of clinical

observations. It has proved difficult to overlap the termination of remifentanil infusion
with the commencement of an alternative analgesic (e.g. morphine or low-dose
fentanyl). Proponents of TIVA consider this is only a question of attention to detail.
However, if adequate analgesia is not established rapidly, the resultant pain is more
resistant to treatment than if a longer-acting drug had been given throughout.
A bolus dose of remifentanil given at induction of anaesthesia can cause hypotension

and bradycardia in patients with coronary artery disease. It is preferable to introduce
the drug by infusion in these patients.
Neuraxial blockade
Interest in neuraxial blockade for cardiac surgery is increasing, but it is not widely used.
The techniques used to provide intraoperative analgesia during cardiac surgery are
intrathecal opioids and continuous epidural infusion of a low-dose local anaesthetic
and opioid combination. Intrathecal opioids provide good intraoperative and early
postoperative analgesia but can result in respiratory depression, which delays
extubation.
In addition to excellent analgesia, thoracic epidural analgesia may beneficially

affect the outcome of patients undergoing coronary artery bypass grafting through
cardiac sympatholysis and attenuation of the cardiopulmonary bypass-related stress.
Postoperative analgesia and respiratory function is also improved.
Thoracic epidural analgesia improves myocardial oxygen balance in several ways

including selective vasodilatation of atherosclerotic coronary arteries and redistribution
of blood to the subendocardium. In general, cardiac output and systemic vascular
resistance are maintained. Hypertension is less likely to occur on cardiopulmonary
bypass, and hypotension and bradycardia may, occasionally, be associated with thoracic
epidural analgesia.
Spinal and epidural techniques have the potential to cause haematomata around
the spinal cord and subsequent paralysis following the heparinization required for
cardiopulmonary bypass. The incidence of major neurological complications of this
nature is very small, but they are potentially devastating and may be under-reported.
The optimum time for epidural catheter insertion and removal has been debated, but
there is no consensus of opinion. Many practitioners recommend that several hours
should elapse between insertion and heparin administration and site the epidural
catheter the night before surgery in a patient first on the morning operating list. Others
site the epidural just before induction of anaesthesia. Removal of epidural catheters
should be carried out when coagulation is at its most normal, for example, 23 hours
after the last dose of subcutaneous heparin. The timing of catheter removal is difficult
because cardiac surgical patients are often treated with other anticoagulants and may
also have a clotting defect following cardiopulmonary bypass. The place of thoracic
epidural analgesia in cardiac anaesthesia remains uncertain with benefits demonstrated
by some investigators as possibly justifying the potential complications and not by
others. u
FURTHER READING
Arrowsmith J E, Simpson J. Problems in Anesthesia: Cardiothoracic Surgery. London:
Martin Dunitz, 2002.
Gothard J W W, Kelleher A, Haxby E. Cardiovascular and Thoracic Anaesthesia.

Anaesthesia in a Nutshell Series. Oxford: Elsevier Science, 2003.
Kaplan J, Reich D L, Konstadt S N. Cardiac Anesthesia. 4th ed. Philadelphia: W B

Saunders, 1998.

Respiratory Management
following Cardiac Surgery
Brian F Keogh
Brian F Keogh is Consultant in Cardiothoracic Anaesthesia at the Royal Brompton

Hospital, London. His special interests include modes of respiratory support,
particularly in acute severe pulmonary failure.
Patients undergoing high risk, complex or re-do surgery, those with severely
compromised cardiac function or those in whom unexpected perioperative difficulties
have been encountered are generally referred to the intensive care team for
postoperative management. Most cardiac surgical patients do not require this level of
support and can be managed in postoperative cardiac care units, theatre recovery units
or high dependency units as part of fast track protocols. Trainee anaesthetists are
often asked to direct ventilatory support and to assess suitability for extubation in this
lower risk group.
Pulmonary effects of cardiac surgery

Respiratory function is subject to a variety of insults (Figure 1) even during routine
cardiac surgery, though many patients suffer no adverse effects.
Effects of cardiac surgery on pulmonary function
Reduced functional residual capacity

Patchy atelectasis, particularly in dependent zones
Increased V/Q mismatch and intrapulmonary shunt
Ischaemiareperfusion injury
Increased pulmonary capillary permeability
Increased extravascular lung water
The disturbance of lung water homeostasis associated with cardiopulmonary bypass

(CPB) varies from a mild increase in extravascular lung water (EVLW) to severe acute
lung injury or acute respiratory distress syndrome. It is exacerbated by any elevation in
left atrial pressure. All patients undergoing CPB suffer increased EVLW and though this
is less likely with non-bypass re-vascularization procedures, the risk is not eliminated.
Extrapulmonary collections (blood, effusions) or pneumothoraces may combine to
aggravate a reduction in functional alveolar volume.
These effects combine to decrease pulmonary compliance and increase the work of
breathing. In weaning or spontaneously breathing patients, the metabolic cost of this
increase may prove critical in a patient with borderline cardiac reserve. In such patients,
a sudden rise in central venous pressure during weaning or following extubation is
a warning sign of impending cardiopulmonary deterioration. Most cardiac surgical
patients do not suffer such difficulties and proceed through respiratory weaning and
extubation without notable compromise.
Approaches to respiratory support following cardiac surgery

The exact characteristics of ventilatory support in the postoperative period vary in
different units. Flow-generated and pressure-generated mandatory breaths are equally
applicable, though the latter may be uncomfortable for awake patients owing to the
high initial inspiratory flow rate. Patient-initiated breaths should also be supported, most
commonly with pressure support ventilation.
The pathophysiology outlined above results in a reduction of functional alveolar volume

and ventilationperfusion (V/Q) mismatch. Ventilatory conduct should encourage
recruitment and maintenance of lung volume, while avoiding regional over-
distension and the risk of barotrauma. Positive end-expiratory pressure (PEEP) is
almost routinely applied to counteract atelectasis and to increase functional residual
capacity, and it may have favourable effects on the redistribution of increased EVLW.
Typical initial ventilatory settings (Figure 2) allow an initial period of stabilization after
surgery. It may be possible to wean some parameters (e.g. fraction of oxygen in
inspired air (FiO2), oxygen saturation (SpO2)) rapidly. Values of 95% or above should be
achieved, not because they are necessary for adequate oxygen delivery, but because
lower values may reflect pulmonary pathophysiology and the need for intervention.
Typical initial ventilatory parameters following cardiac surgery
Fraction of oxygen in inspired air (FiO2) 0.60.8 (decreased if oxygen

saturation in arterial blood (SaO2) allows)
Tidal volume 1012 ml/kg
Respiratory rate 1012 breaths/min
Inspiratory: expiratory ratio 1:2
Positive end-expiratory pressure (PEEP) 5 cm H2O
Peak pressure limit 30 cm H2O
Pressure support ventilation setting 15 cm H2O
Patients who are mildly desaturated may require an increase in PEEP or mean
airway pressure (longer inspiratory:expiratory (I:E) ratio), lung volume recruitment
manoeuvres (manual hyperinflation or brief increase in ventilator-delivered tidal
volume) or reassessment of their haemodynamic status. Some patients require high
levels of PEEP (> 10 cm H2O) or mean airway pressure and the resultant increase in
intrathoracic pressure may impair cardiac performance, particularly in the presence of
hypovolaemia.
A chest radiograph is mandatory following cardiac surgery to check for fluid or air
collections, to confirm the position of various tubes and catheters and to assess
the state of the lung fields. It is often helpful in directing management. In addition to
ventilatory manipulation (e.g. increase PEEP in bi-basal collapse) the chest radiograph
may suggest the need for diuretic therapy or the introduction of an inodilator to reduce
left atrial pressure.
Preoperative pulmonary function and blood gas measurements, if available, should

be considered in determining target gas exchange values for an individual patient.
In patients with known V/Q mismatch (e.g. those with chronic obstructive pulmonary
disease (COPD)), other lung parenchymal diseases or restrictive disorders (e.g.
obesity), lower levels of oxygen saturation in arterial blood (SaO2) can be readily
accepted. Bronchodilator therapy should be instituted as soon as possible after surgery
in patients with COPD or airway irritability.
Weaning from mechanical ventilation

Weaning from ventilation following routine cardiac surgery does not necessarily
involve a conscious decision but is usually integrated into normal clinical care.
Effective analgesia must be continued throughout the weaning process. For weaning
to proceed successfully, various general criteria (Figure 3) should be satisfied, of
which a satisfactory haemodynamic status is paramount. An after-drop in body
temperature is commonly observed and temperature should approach normal levels
before advanced weaning is attempted. In addition to general criteria, guidelines for
acceptable respiratory parameters can be set (Figure 3) which act as alerts to initiate
reassessment if they are not achieved. These are useful guidelines, which may be
varied in individual patients or in unusual circumstances. For example, in a patient with
known poor ventricular function, respiratory weaning and extubation may be undertaken
successfully with moderate levels of inotropic support or even an intra-aortic
balloon pump in situ.
Criteria for weaning from mechanical ventilation
General
Stable cardiac rhythm
Haemodynamic stability
Low-dose or no inotrope requirement
Acidbase status acceptable
Haemostasis controlled (drainage < 100 ml/hour in adult)
No residual neuromuscular blockade
Approaching normothermia
Adequate analgesia/controllable discomfort
Respiratory
Partial pressure of oxygen in arterial blood (PaO2) > 10 kPa with
fraction of oxygen in inspired air (FiO2) 0.5
PaCO2 < 6.5 kPa
pH > 7.32
Positive end-expiratory pressure (PEEP) 6 cm H2O
Typical criteria for extubation are listed in Figure 4. As the level of respiratory support
decreases, the acceptable level of partial pressure of carbon dioxide in arterial blood
(PaCO2) should be allowed to rise. PaCO2 levels of 7.58 kPa are not unusual in
weaning or extubated patients with acceptable cardiopulmonary parameters who
are receiving adequate analgesia. The decision to extubate is clinically based and a
comfortable, cooperative patient who is neither distressed nor tachypnoeic and has an
acceptable respiratory pattern is likely to succeed, even if arterial blood gas values are
not ideal.
Guidelines for extubation criteria
General criteria apply (Figure 3)

Partial pressure of oxygen in arterial blood (PaO2) > 10 kPa
with fraction of oxygen in inspired air (FiO2) 0.5
PaCO2 < 8 kPa
Respiratory rate < 20/min
Minute volume requirement < 150 ml/kg/min
Satisfactory respiratory pattern
Comfortable, cooperative and neurologically intact patient
Post-extubation management
Patients must be encouraged to cough following extubation and it is vital that adequate
analgesia is administered to allow effective propulsive coughing. Inevitably, some
patients suffer areas of localized collapse, the left lower lobe being the most common,
and this should be treated with intensive physiotherapy and humidified oxygen. High
flow, continuous positive airway pressure (CPAP) systems are commonly used in
patients with pulmonary collapse, pulmonary congestion and obesity, via face CPAP
masks. This is usually well tolerated in cooperative patients, but may prove difficult or
counterproductive in confused patients. Non-invasive positive pressure ventilation may
also be used, via nasal or face mask, but requires patient education and compliance to
be effective.
Respiratory issues in coronary re-vascularization

Internal mammary arteries are commonly harvested for conduit and ipsilateral lower
lobe compression or collapse is common. Extreme care should be taken in lung
hyperinflation if a left internal mammary pedicle graft has been performed because of
the risk of traction disruption of the graft.
Patients may suffer myocardial stunning during surgery and may be at risk of
functional mitral valve regurgitation, due to dilatation of the mitral valve ring. This may
be exacerbated by respiratory weaning. A patient who becomes distressed during
weaning, with a rise in right atrial pressure and relative hypotension, should be re-
assessed with echocardiography. This condition requires venodilatation, usually with
glyceryl trinitrate, in combination with low-dose vasoconstriction, in order to maintain
coronary perfusion. It requires an index of suspicion and correct diagnosis, because
fluid and inotropic therapy, both of which are commonly administered, can increase
regurgitation.
Respiratory weaning failure to progress

Unexpected failure to meet respiratory weaning targets should prompt patient
reassessment. Simple factors include inadequate analgesia, sputum retention and
regional pulmonary collapse. Neurological injury may also present at this time. Occult
fluid or air collections should be excluded. Pericardial effusion or incipient tamponade
may be associated with sudden deterioration in respiratory parameters. Similarly,
deterioration in cardiovascular performance, associated with graft kinking or occlusion,
or impairment of mitral valve function may initially manifest as tachypnoea and
respiratory distress. Echocardiographic re-assessment of cardiac function is indicated,
and may be urgently required in such patients. u

Clinical anaesthesia
Anaesthesia
on CD-ROM
Airway Control
Oliver J Dyar
Oliver J Dyar is Consultant Anaesthetist and Intensivist at the John Radcliffe Hospital,
Oxford, UK. He qualified from University College, Dublin and St Vincent's Hospital,
Dublin, Ireland. He trained in anaesthetics and intensive care in the Nuffield Department
of Anaesthetics, Oxford. His research interests include intravenous anaesthesia and the
use of nitric oxide in the ARDS.
Securing control of the airway is one of the most important skills required of the
anaesthetist. Whether for elective or emergency surgery, and whether the need for
airway control has been predicted or not, the safety of the patient depends on the
anaesthetists ability to intervene to ensure adequate oxygenation and ventilation should
the need arise. The anaesthetist must:
develop the skills of airway assessment and management
be familiar with the equipment and techniques available for control of the airway
be able to choose the appropriate measures for the individual patient.
This contribution focuses on these basic principles.
Assessment of the airway
The anaesthetist must assess the airway before undertaking any anaesthesia. When
general anaesthesia is contemplated, assessment facilitates a planned approach to
anticipated difficulties with laryngoscopy and intubation. When a regional or local
technique is contemplated, the need for airway intervention may also arise, for example,
following respiratory embarrassment as a result of a high spinal or epidural blockade
level, over-zealous sedation, or more rarely, following an allergic reaction to a drug.
The patients previous anaesthetic notes should be consulted if available. It is
important to realize, however, that the patients circumstances may have changed, and
a previously easy intubation may have become difficult (e.g. as a result of pregnancy).
A number of anatomical factors are associated with difficulty in laryngoscopy and
intubation:
obesity, pregnancy
large protruding incisor teeth
short neck, especially in a heavy patient
reduced mobility of the neck (e.g. rheumatoid arthritis)
instability of the neck
reduced mouth opening
intraoral masses
large goitre.
Anatomical assessment
Whether laryngoscopy and intubation would be possible with reasonable ease should
be assessed using a reliable and reproducible bedside method of airway assessment
that has minimal false-positive and false-negative rates. No single test provides this
information, but the modified Mallampati test in conjunction with an assessment of
thyromental distance combines ease with reasonable accuracy.
The modified Mallampati test assesses the size of the base of the tongue in relation
to the size of the oropharynx. The patient sits upright with the head in the neutral
position. The assessor sits in front of the patient at the patients eye level. The patient
opens their mouth as wide as possible. Without phonating, the tongue is protruded as
far as possible. The assessor inspects the pharyngeal structures visible and a score is
allocated according to which structures are visible (Figure 1).
Modified Mallampati test
Class Pharyngeal structures visible

1 Fauces, faucial pillars (the palatoglossal and palatopharyngeal
arches), uvula, soft palate
2 Faucial pillars are obscured leaving the fauces, uvula and soft palate
visible (i.e. posterior pharyngeal wall visible below soft palate)
3 Only the soft palate and the base of the uvula seen (i.e posterior
pharyngeal wall not visible below soft palate)
4 Even the soft palate obscured
The measurement of thyromental distance as recommended by Frerk is obtained by

maximally extending the head on the neck and measuring from the prominence of the
thyroid cartilage to the bony point of the chin.
A modified Mallampati grade of 3 or 4 combined with a thyromental distance of 7 cm
or less gives a bedside assessment system with a sensitivity of 81% and a specificity
of 98% for difficulty with intubation.
The view of the laryngeal structures obtained at direct laryngoscopy is often
classified according to the system described by Cormack and Lehane (Figure 2). In
this system, grades 3 and 4 constitute difficult laryngoscopies. Fairly severe difficulty
with intubation may occur with grade 3, and the use of a bougie/introducer, posterior
to, but held up against the epiglottis may permit blind intubation. With a grade 4 view,
intubation by standard methods is virtually impossible despite optimal positioning.
Cormack and Lehane classification system
Grade Laryngeal structures visible

1 Most of the glottis visible
2 Only the posterior part of the glottis (posterior commissure, arytenoid
cartilages) visible
3 Only the epiglottis visible, no part of the glottis seen
4 Not even the epiglottis seen
2
Airway patency
Partial obstruction of the airway in the awake patient may be caused by masses in
the upper airway (e.g. tonsils, adenoids, tumour), foreign bodies, or epiglottitis. In the
sedated or unconscious patient, laxity of the muscles that normally keep the tongue
anterior to the posterior pharyngeal wall allows the tongue to fall back and obstruct the
airway. Partial obstruction is recognized by noisy inspiration (stridor), tracheal tug, and
dyssynchronous movements of the thorax and abdomen on inspiration.
In normal, unobstructed breathing, the abdomen expands as the diaphragm
descends in inspiration and the thorax expands as indrawn gas fills the lungs. With
obstruction, the abdomen still expands, but if inspired gas cannot be inhaled at
a sufficiently fast rate, the sternum is drawn inwards by the increasing, unrelieved
negative intrathoracic pressure. Partial obstruction and its cause (and therefore ease
of reversal) must be recognized before embarking on anaesthesia. The technique of
airway management is highly modified in the presence of partial obstruction.
Aspiration risk
For elective anaesthesia, the patient is fasted. Solid food, non-clear liquids (especially
those containing milk) and chewing gum should not be consumed in the 6 hours before
anaesthesia. Clear liquids are permissible up to 2 hours before induction.
For emergency anaesthesia, the interval between last food or drink and the injury or
onset of illness is assessed. Gastrointestinal obstruction or other abnormal motility state
(e.g. ileus, diabetes mellitus, renal failure, acute pain) all increase the risk of aspiration
on induction of anaesthesia.
Equipment and techniques for routine airway management
Before embarking on general anaesthesia, the equipment required should be to hand

and its correct function checked. A preoperative checklist such as that proposed by
the Association of Anaesthetists of Great Britain and Ireland is particularly useful (see
Anaesthesia and Intensive Care Medicine 1:2: 65). The minimum equipment required
includes:
source of pressurized oxygen (plus bag-valve-mask or anaesthesia circuit)
selection of face masks
selection of oropharyngeal and nasopharyngeal airways
high-flow suction
Yankauer suction catheter, and selection of narrow-bore suction catheters
two laryngoscopes
selection of tracheal tubes
selection of laryngeal mask airways
Magills forceps
sterile lubricating gel
ties and padding to secure tracheal tube
gum-elastic or other suitable bougie.
For non-emergency anaesthesia, several interventions to control the airway are
available. These range from oxygen administration through a face mask, delivery
of inhalational anaesthesia via an anaesthetic face mask or laryngeal mask airway,
through to tracheal intubation.
Non-relaxant anaesthesia
If relaxant anaesthesia is not required (e.g. for body-surface surgery in the patient not
at risk for aspiration) then inhalational anaesthesia via a face mask is appropriate. In
the absence of flammable anaesthetic agents, the mask is usually clear plastic with an
inflatable rim that provides a good seal in contact with the face. The size of the mask
is determined by the patients size and physical features, but a range of sizes (Figure
3) should be available. For paediatric anaesthesia, the mask should have as little dead
space as possible (e.g. the Rendell-BakerSouchet mask). Nasal masks are indicated
for anaesthesia in the dental chair.
Induction in the absence of airway obstruction may be inhalational or by intravenous
injection of a suitable induction agent. If there is any suggestion of airway obstruction
then inhalational induction or another approach (e.g. awake fibre-optic intubation) is
required.
3 Selection of face masks, including Rendell-

BakerSouchet paediatric masks (lower row).
Supporting the airway

Whatever the means of induction, once the patient is unconscious it is necessary to
support the airway. There is a tendency for the airway to become partially obstructed
at this stage because the tongue falls back against the posterior wall of the pharynx.
Induction will normally have occurred with the patient supine, head resting on a pillow.
This allows the anaesthetist to extend the head on the neck at the same time as
applying a jaw thrust and opening the mouth. To achieve this triple manoeuvre, the
mask is secured on to the face using one or both hands, with the thumbs on the upper
part of the mask, index fingers on the lower part and the rest of the fingers effectively
pulling the patients mandible forward into the mask. It is crucial that unopposed
downward pressure on the mask is not used to obtain a seal between mask and face
because this will close the airway. Likewise, the third, fourth and fifth fingers must
stay on the mandible and must not press on the floor of the mouth, which also tends
to cause obstruction. If it is impossible to open the airway using these techniques,
an artificial airway is required. Two methods are available: the oropharyngeal and the
nasopharyngeal airway (Figure 4).
4a Nasopharyngeal airway.
b Selection of smaller oropharyngeal airways.
The oropharyngeal (Guedel) airway is a curved tube that has a flanged and
reinforced oral end. The flange enables correct positioning at the incisor teeth, and
the reinforcement prevents the patient from obstructing or severing the device by
biting down. This airway is available in a range of sizes (size 34 is usually required
for an adult, Figure 4b), and it is vital that the appropriate size is used for the patient.
An easy way to determine size is to choose the airway in which the length is equal
to the distance between the corner of the patients mouth and the angle of the jaw. If
the airway is too short it tends to push the tongue backwards and cause increased
obstruction. If too long, the device tends to stimulate the larynx, provoking spasm, and
it fails to sit securely with the flange at the front incisors. The Guedel airway is usually
inserted upside-down (the pharyngeal opening facing the roof of the mouth, then
rotated 180 as it passes the back of the tongue). A lightly anaesthetized patient may
gag or cough with this intervention. It may also provoke laryngeal spasm.
The nasopharyngeal airway is a less stimulating intervention. It is a soft curved

tube with a flanged nasal end and a bevelled pharyngeal end (Figure 4a). It is also
available in a range of sizes. Sizes 68 mm (measured as internal diameter) are
suitable for adults, the usual measure is the diameter of the patients little finger. Before
inserting the airway, a safety pin is inserted eccentrically at the flanged end, to prevent
inhalation of the device. The airway should be coated with lubricating gel, and inserted
into either nostril. It is advanced along the floor of the nose in a posterior direction,
and should come to lie with the bevelled end in the oropharynx, behind the tongue and
above the glottis. The eccentric positioning of the pin permits access of a catheter for
suctioning secretions from the pharynx and airway.
Face mask: for brief procedures, anaesthesia can be maintained using a face mask,
with or without airway adjuncts. For longer procedures, when it is desirable for the
anaesthetist to have both hands free, the standard mask can be supported by a
harness. It is now more common to insert a laryngeal mask airway for such procedures.
This has the advantage of maintaining the airway without additional instrumentation, in
addition to providing a more secure airway and providing hands-free operation.
The laryngeal mask airway (LMA) was designed to provide a connection between
the artificial and anatomical airways in a less invasive way than with a tracheal tube,
and yet with greater convenience and reliability than a conventional face mask. The
standard LMA is made from silicone and is designed for multiple patient (up to 40)
uses. It consists of a silicone bowl surrounded by a thin-walled elliptical ring that can be
deflated to form a thin wedge shape, and which when inflated in the space posterior to
the pharynx creates a seal around the laryngeal aperture. This seal permits ventilation
of the airway under positive pressure. It also prevents insufflation of gas into the
oesophagus and stomach, unless high inflation pressures (2030 cm H2O) are used.
The device has a central aperture, with vertical bars, designed to prevent prolapse of
the epiglottis into the tube that connects the mask to the anaesthetic circuit.
The LMA is available in a variety of sizes (Figure 5).
Correct placement is important to ensure a high-performance seal without overinflation
of the cuff, and the appropriate size is chosen for the size of the patient (Figure 6).
The LMA is also available with a flexible, reinforced, non-kinking tube instead of
the standard tube. This type is particularly useful for situations in which the head
may be moved during surgery and for oral and ENT surgery. The intubating LMA is
a development of the standard airway designed to act as a conduit permitting blind
intubation of the trachea using a specially designed silicone tube.
A full description of the recommended technique for inserting the LMA is beyond the
scope of this contribution. Briefly, the device is completely deflated (preferably using a
cuff deflation tool, which will ensure deflation to the correct shape). The patients head
is supported on a pillow, in the classic intubating position. Extension of the head and
flexion of the neck on the thorax is achieved by the non-dominant hand. The posterior
surface of the LMA is lubricated with water-soluble gel. The LMA is held between
index finger and thumb, with the index finger of the operators gloved dominant hand at
the junction of the mask and the tube. The aperture of the device faces caudally. An
assistant holds the patients mouth open, and the device is inserted under direct vision,
with its posterior, lubricated surface firmly against the hard palate. The LMA is pushed,
keeping it firmly against the palate at all times following the palate posteriorly and down
into the hypopharynx. Resistance to insertion is met when the tip of the device is in
the hypopharynx, with the tip resting at the upper oesophageal sphincter. It may be
necessary to push the device using the non-dominant hand, if the inserting finger is
not long enough. The device is released. The cuff is inflated with the recommended
volume of air, at which point the tube may rise from the mouth as the device seats
itself around the larynx. The tube of the LMA is connected to the anaesthetic circuit, if
necessary using a swivel connector.
The LMA may be used to ventilate the anaesthetized muscle-relaxed patient,
provided that the inflation pressures do not exceed about 20 cm H2O. Above this
pressure, the risk of gradual insufflation of the stomach with anaesthetic gas increases.
This increases the risk of regurgitation and aspiration of gastric contents.
5a Standard laryngeal mask airways, sizes

212, 3, 4. b Reinforced laryngeal mask airway,
size 4.
Relaxant anaesthesia
Anaesthesia requiring a muscle-relaxant technique most commonly requires tracheal

intubation. Indications for relaxant techniques and/or intubation are:
provision of clear airway
airway protection from blood, oral or gastric secretions
facilitation of suctioning of airway
prone or sitting patient, airway inaccessible
abdominal, thoracic anaesthesia
likelihood of postoperative respiratory support
administration of positive end-expiratory pressure.
Tracheal intubation
Equipment: in addition to the equipment for inhalational anaesthesia using a face
mask, a suitable laryngoscope, with a spare available, and a range of suitable tracheal
tubes are necessary.
The laryngoscope consists of a handle (which houses the batteries) and a
detachable blade, which has a screw-in bulb. Alternatively, the bulb may be in the
handle, and a fibre-optic bundle transmits the light to the blade. Two basic types of
laryngoscope are available (Figure 7):
curved-blade (usually Macintosh)
straight-blade (e.g. Wisconsin, Seward, Magill).
The curved-blade instruments are most commonly used for adults and larger children:
the tip is placed in the vallecula, anterior to the epiglottis. Forward traction elevates the
epiglottis without touching the posterior surface of the epiglottis. By contrast, straight-
blade laryngoscopes are inserted posterior to the epiglottis and lift it from behind.
These instruments are most often used for smaller children, because the epiglottis is
longer and more floppy in this age group. The blades are available in a number of sizes,
with the Macintosh 3 being suitable for most adults.
Tracheal tubes an extensive range of tracheal tubes is available (Figure 8).
They are most commonly made from polyvinylchloride or polyurethane and are bevel-
ended. They may be plain or have a high-volume low-pressure cuff, which provides a
seal enabling positive-pressure ventilation and preventing aspiration of secretions into
the airway. Uncuffed (plain) tubes are used in children. This avoids the potential for
ischaemic damage on the tracheal lining from high cuff pressure and maximizes tube
size available. The presence of an air leak around the plain tube ensures that the fit
is not too tight.
Tracheal tubes are usually inserted via the mouth, or if necessary via the nose (e.g.
for intraoral surgery). Tube size is measured by the internal diameter, ranging from 2.5
mm to about 10 mm in 0.5 mm increments. The tube is usually cut to the appropriate
length for the patient. Adult males usually require size 89 mm and adult females 78
mm, cut to 2123 cm for oral intubation. For children, the tube size can be estimated
from the formula (age/4 + 4 mm), and length (age/2 + 12 cm), with age being in years.
This is an approximate size, and tubes 0.5 mm greater than and less than the estimated
size should be available.
The tube is connected to the anaesthetic circuit at the proximal end with a tapered
connector of suitable size (see Anaesthesia and Intensive Care Medicine 1:2: 68). The
distal end may have, in addition to the end hole, a side opening (Murphy eye) to allow
passage of gas should the bevelled end be occluded by abutting on the tracheal wall.
Sizes of laryngeal mask airway
Size Patient Cuff volume (ml)

1 Neonates up to 6.5 kg 4
2 Patients 6.520 kg 10
212 Patients 2030 kg 14
3 Children and small adults 20
4 Normal adults 30
5 Large adults 40
b
e
c
f
d g
7 Selection of straight- and curved-blade

laryngoscopes. a Wisconsin, b Seward, c
Oxford, d Soper, e Macintosh size 2, f Macin-
tosh size 3 g McCoy laryngoscope.
a
b
c
d
e
8 Tracheal tubes. Nasal: a cuffed, b plain.

Oral: c North-facing plain polar. Magill pattern
oral tubes: d plain, e cuffed.
Anaesthetic management
Positioning the patient correctly before intubation is crucial. Tracheal intubation
requires approximate collinearity between the axes of the mouth, oropharynx and
larynx. True collinearity of these structures is impossible, but appropriate positioning
can make the difference between a relatively easy laryngoscopy and intubation, and
failure to visualize the larynx at laryngoscopy. The classic intubating position is the
sniffing position: the head is extended on the neck (atlantoaxial extension) and the neck
is flexed on the thorax. For most adults this is easily achieved by having the patient lie
supine on the trolley or bed and placing a pillow under the occiput. If the pillow is too
caudad (elevating the shoulders) then extension of the neck on the thorax occurs. This
almost always makes laryngoscopy more difficult. In small children, the relatively large
head provides the correct position without the use of a pillow.
Induction if the patient is not at risk of aspiration of gastric content, difficulty
with laryngoscopy is not anticipated, and the airway is unobstructed, induction of
anaesthesia is as for the mask techniques outlined above. Following induction, it is
possible, providing the patient is deeply anaesthetized, to perform laryngoscopy and
intubation. This practice is relatively uncommon. More usually, the anaesthetist confirms
that it is possible to ventilate the patient using the mask (with an artificial airway if
needed). Then an intubating dose of a muscle relaxant is given (e.g. suxamethonium,
11.5mg/kg). While the advantages of the speed of onset and quality of relaxation
obtained with suxamethonium are significant, its side-effects include myalgia (which
can be quite severe), occasional profound bradycardia (especially in children, and
particularly likely with second doses of the drug given shortly after a first dose),
hyperkalaemia, and precipitation of malignant hyperthermia in susceptible individuals.
To overcome these disadvantages, an intermediate-duration non-depolarizing drug
such as vecuronium, 0.1 mg/kg, atracurium, 0.5 mg/kg, or rocuronium, 0.6 mg/kg, can
be used. However, they commit the anaesthetist to providing ventilation by mask for a
prolonged period if intubation proves more difficult than anticipated, or is impossible.
With the exception of rocuronium they also take a longer time to achieve good
intubating conditions, which makes them much less suitable for the patient at risk of
aspiration of gastric content. The lungs are usually manually ventilated while awaiting
the onset of muscle relaxation. A mixture of oxygen and the volatile agent chosen to
maintain anaesthesia is used, together with nitrous oxide, if desired. The use of nitrous
oxide reduces the interval allowable for laryngoscopy and intubation. The patient will
become hypoxaemic more rapidly following cessation of ventilation if this gas is used,
because available oxygen stores will be reduced. A peripheral nerve stimulator may be
used to confirm the presence of adequate paralysis, as demonstrated by the absence
of twitch response to a supramaximal stimulus.
Laryngoscopy is then performed. The right hand opens the patients mouth and
the assistant separates the patients lips to expose the teeth. Using a curved-blade
laryngoscope, held in the left hand, the blade is inserted into the right-hand side of the
mouth, and advanced as far as the tonsillar bed. Sweeping the blade into the midline
at this point should displace the tongue to the left, and give a view of the tip of the
epiglottis. The blade is advanced, with force applied along the shaft of the laryngoscope
directed upwards and outwards (at about 3045 to the horizontal). The patients upper
incisors or gum must not be used as a fulcrum. The tip of the blade should enter the
vallecula in front of the epiglottis, and the applied force elevates the epiglottis, exposing
the larynx. The tracheal tube is picked up in the right hand and advanced from the
right-hand side of the mouth, using the natural curvature of the tube to place the tip
in the larynx under direct vision. Once the cuff of the tube is safely past the cords,
the laryngoscope is carefully removed. The anaesthetic circuit is connected to the tube
using a swivel connector and a catheter mount (if desired). The lungs are ventilated and
the cuff of the tube inflated with just sufficient air (or gas mixture) to abolish the audible
leak of gas on inflation of the lungs. Bilateral breath sounds and absence of sounds
of gastric insufflation help confirm placement, however monitoring for appropriate and
continuous concentration of carbon dioxide in the exhaled gas is mandatory.
Extubation anaesthesia is maintained with inhalational agents, and the patient
is ventilated using intermittent positive-pressure ventilation throughout the operation.
At the end of the operation, residual neuromuscular blockade is reversed using a
combination of a cholinesterase inhibitor and a muscarinic blocking drug (to prevent
bradycardia). The drugs most commonly used are neostigmine, 0.05 mg/kg, with
either atropine, 0.02 mg/kg, or glycopyrrolate, 0.01 mg/kg. Secretions and occasionally
gastric content will have accumulated in the pharynx during the procedure. To prevent
aspiration of these secretions and severe laryngeal spasm on removal of the tracheal
tube, these are removed using a Yankauer sucker or equivalent, under direct vision
(with a laryngoscope). The patient is ventilated with 100% oxygen. As the patient starts
to breathe, the circuit is changed to permit spontaneous ventilation, with the reservoir
bag providing visible confirmation of ventilatory effort and volume.
The tracheal tube is removed when the patient is breathing adequately and has
regained protective airway reflexes (the patient is actively resisting the presence of the
tube). The patient may be extubated in the supine position if the anaesthetist is satisfied
that a clear airway can be maintained and the patient is not at risk for aspiration. If
the patient is at risk, then extubation should take place in the lateral position, with the
patient as fully awake as possible. Extubation should be performed during inspiration.
Having deflated the cuff of the tracheal tube, the bag on the anaesthetic circuit is
squeezed to expel secretions above the cuff into the oropharynx, away from the
vocal cords. The tube is removed in a smooth movement, the breathing circuit rapidly
reconnected to an anaesthetic mask, and the mask closely applied to the face.
Partial obstruction of the airway may occur at this stage if the tongue falls back
into the pharynx, or more often because of mild laryngeal spasm. It may respond
to the application of positive end-expiratory pressure. This may be achieved by
partially closing the exhaust valve on the anaesthetic circuit, but the airway pressure
must be monitored. If the airway is obstructed by the tongue, then an oral or
nasopharyngeal airway may be required to relieve the obstruction. When the patient is
breathing adequately, he is transferred to the recovery room, ensuring that he breathes
supplementary oxygen during the transfer.
Recovery
Supplementary oxygen should be administered to all patients in the immediate recovery

period. This is to prevent hypoxaemia that may otherwise occur from the ventilation
perfusion mismatch induced by surgery and anaesthesia, and the hypoventilation that
may ensue from respiratory depressant drugs. Hypoxaemia may also be caused by
dilutional hypoxia following cessation of nitrous oxide.
The duration of oxygen therapy may be limited to 15 minutes for young healthy
patients undergoing minor day- case procedures, but extended for many hours or days
for those with more serious pathology or complicated surgery. Therapy is guided by
pulse oximetry or blood gas estimation, and oxygen therapy is usually titrated to achieve
oxygen saturation greater than 95%.
Oxygen therapy devices may deliver either a variable or fixed concentration of
supplementary oxygen to the inspired gas.
Variable performance devices include nasal prongs and simple Hudson-type face
masks with or without an oxygen reservoir (Figure 9). The oxygen flow delivered to the
device is typically 24 litres/minute, which will be diluted by the air entrained during
inspiration. The concentration of inspired oxygen depends on the oxygen flow rate,
the patients respiratory rate and peak inspiratory flow. Typically, 3040% inspired
oxygen is achieved when 4 litres/minute is delivered to a patient via a Hudson mask,
and this concentration reduces as respiratory rate and inspiratory flows increase, due
to increased air entrainment. The oxygen concentration delivered cannot be predicted
accurately. This is usually of no consequence to a patient on the recovery ward, who
simply needs supplemental oxygen, though the precise concentration is not critical.
The inspired oxygen percentage can be increased further if an oxygen reservoir is
used with the mask, and 80% inspired oxygen may then be achieved using a 1215
litres/minute oxygen flow rate.
a b c
9 Variable performance devices. a Face mask

with oxygen reservoir bag (folded); b simple
Hudson-type oxygen face mask; c nasal
prongs.
Fixed performance devices include face masks with Venturi-type injectors (Figure
10). They achieve a fixed inspired oxygen concentration by ensuring that a high flow
rate of oxygen and entrained air is delivered, in excess of the patients maximum peak
inspiratory flow rate.
The use of a Venturi injector face mask delivers about 60 litres/minute of gas
and so the inspired oxygen concentration is independent of the characteristics of
inspiratory flow. Venturi devices are available to deliver fixed oxygen concentrations
between 24% and 60%. The correct oxygen flow rate must be selected for the
correct Venturi injector, and used with the correct mask. Details are printed on
each Venturi, but typically 2 litres/minute delivers 24% oxygen, and 8 litres/minute
delivers 35% oxygen. Venturi injector devices are not interchangeable with masks
from different manufacturers, because the mask volume allows for adequate mixing of
driving and entrained gases.
Fixed performance devices are often used in the high-dependency setting to enable
accurate assessment of oxygenation, in patients with chronic lung disease who depend
on a hypoxic respiratory drive, and on the general wards.
a b c
10 Fixed performance devices. A selection

of Venturi oxygen masks delivering a 28%, b
35%, c 60% oxgen. d Venturi T-piece deliver-
ing 40% oxygen for use with laryngeal mask
airway, tracheal tube or tracheostomy tube.

Anaesthesia for Laparoscopic
Surgery
Michael W Platt
Michael W Platt is Consultant in the Department of Anaesthesia, St Mary's Hospital,

London. He qualified in Western Australia. His research interests include anaesthesia
and pain relief in the elderly, ethical issues at the end of life and aspects of neuropathic
pain.
Laparoscopic surgery is a revolution in modern surgical techniques and has reduced

postoperative pain, respiratory complications and hospital stay considerably. However,
it produces extra stresses on the heart and lungs, therefore patients should be
screened carefully and the risks explained fully as part of obtaining consent for the
procedure. Anaesthetists should consult their surgical colleagues about the relative
risks in those with cardiac and respiratory disease and should be prepared to cope with
complications as they arise.
History
The earliest recorded references to endoscopy are from Hippocrates in Greece
(460375 BC), who made reference to a rectal speculum. It was only in the 1970s
that the problems of transmitting light, insufflation technology and optical technology
were surmounted sufficiently for gynaecologists to embrace laparoscopic surgery.
Laparoscopic techniques were not supported whole-heartedly by general surgeons
until after 1987, when Mouret performed the first laparoscopic cholecystectomy in
France. Following this, the rapid development of solid state video camera technology
has further broadened the field of laparoscopic surgery.
The advantages of minimally invasive surgery are less ileus, the greatly reduced stress
response to surgery and trauma, reduced acute phase reaction, reduced pain, reduced
post-operative pulmonary dysfunction and reduced hospital stay. These also have
economic advantages.
More procedures are being developed for laparoscopic surgery, including

extraperitoneal inguinal hernia repair and retro-peritoneal nephrectomy and
adrenalectomy. Routine general surgical laparoscopic procedures now include:
oesophagectomy, Nissens fundoplication, gastric banding, oversewing of peptic ulcer,
intestinal resections, including hemicolectomy and col-ectomy, rectopexy and hernia
repair.
Pathophysiology and complications of laparoscopy

The complications of laparoscopy include: haemorrhage, hypotension, decreased
cardiac output, acidosis, pneumothorax, pneumomediastinum, subcutaneous
emphysema, retroperitoneal carbon dioxide (CO2), venous stasis, bradycardia,
increased vagal tone, cardiac arrest, fatal venous CO2 embolism, regurgitation
and aspiration. Many of these complications are the result of peritoneal insufflation
(pneumoperitoneum).
Pneumoperitoneum, the insufflation of the peritoneal cavity, is required to enable a

gas milieu for visualization through the laparoscope (the operating telescope). CO2
is used for laparoscopy because it is highly soluble in blood. Blood can carry large
quantities of CO2 as bicarbonate, carboxyhaemoglobin, and in plasma proteins. Carbon
dioxide is eliminated rapidly and the lethal dose as an embolus is five times that of air.
Usually a CO2 gas embolism resolves rapidly, but if it is large, it can be fatal.
Pneumoperitoneum is achieved by insufflating the peritoneal cavity with CO2 to a

pressure of 1018 mm Hg. The intra-peritoneal insufflation of CO2 to these pressures
causes respir-atory and haemodynamic changes.
Respiratory changes that occur as a result of pneumoperitoneum consist of a

reduction of chest compliance by 3050%. Airway pressures to maintain tidal volume
rise to counter the reduction of chest compliance and the elevation of the diaphragm.
Functional residual capacity of the lungs decreases and there is an increase in
physiological dead space and shunt because of basal compression by the diaphragm
and increased ventilation/perfusion mis-matching, which may result in a reduced
arterial partial pressure of oxygen. Basal atelectasis may persist into the postoperative
period. If minute volume is kept constant, end-tidal CO2 increases due to absorption of
CO2 from the peritoneal cavity. The latter changes are usually countered by increasing
the tidal volume and applying positive end-expiratory pressure (PEEP).
Haemodynamic changes also occur as a result of the pneumo-peritoneum.

Compression of the inferior vena cava leads to a reduction in venous return, potentially
followed by a fall in cardiac output. However, a reflex tachycardia and a massive
increase in peripheral vascular resistance tends to maintain cardiac output at near-
normal levels, by pulling blood centrally from the periphery, but with a concomitant
increase in mean arterial blood pressure. This increase in myocardial work can result
in myocardial ischaemia in those at risk and can lead to infarction, which may not occur
until the postoperative period. Active vasodilatation and blockade are often required
to counter these effects.
Compression of the inferior vena cava causes reduced venous flow from the legs,
resulting in venous stasis and an increased risk of venous thrombosis. Prophylactic
anticoagulation and elastic stockings or pneumatic calf compressors should be used,
especially in the elderly.
Respiratory and haemodynamic changes are affected by the patient's position. For
example, head-up tilt, used for upper abdominal operations (e.g. cholecystectomy,
Nissens fundoplication) further inhibits venous return. Head-down tilt, used for colonic
and pelvic surgery, promotes venous return, but aggravates respiratory changes,
further reducing chest compliance and functional residual capacity and increasing
basal compression.
Other complications of pneumoperitoneum include surgical emphysema, which

can affect most tissues, including the conjunctivae and the scrotal sack. Cardiac
arrhythmias can be secondary to vagal stimulation (bradycardia) or to hypercarbia
(tachyarrythmias). Pneumothorax (including tension pneumo-thorax) may occur,
particularly with upper abdominal procedures such as Nissens fundoplication. Gastric
reflux can occur because of increased intraperitoneal pressure, although retained
gas in the stomach may obstruct the surgeons view for upper abdominal operations.
Pressure on the renal veins and arteries may cause a temporary reduction in renal
function, due to reduced renal blood flow. Major CO2 gas embolus seldom occurs and
is usually the result of accidental direct injection of gas into a major vessel (e.g. the
inferior vena cava). This may cause an obstruction to cardiac output when it reaches
the heart. The treatment is to turn the patient onto the right side immediately and
position them head down, causing the gas embolus to occupy the apex of the right
ventricle, relieving the obstruction to ventricular outflow.
Patients should be assessed carefully preoperatively, focussing on their cardiac
function and reserve, because of the amount of extra cardiac work required during
pneumoperitoneum. Patients with significant cardiac disease and limited cardiac
reserve should be assessed by a cardiologist. It may be that an open procedure or
even cancelling the procedure would be best for the patient. Patients with added risks
of venous thrombosis should be treated prophylactically with fractionated heparin,
elastic stockings and calf compressors during surgery. Surgery for patients with
previously untreated hypertension should be postponed until treatment has stabilized.
Respiratory function should also be assessed. Pulmonary function tests should be
performed in those with significant pulmonary disease. Liver and renal function need
to be ascertained because these organs may also be affected by pneumoperitoneum.
Intercurrent medications (especially antihypertensives) should be given as normal on
the morning of operation. A light sedative, such as a short-acting benzodiazepine, may
be given before surgery.
Perioperative management
A routine intravenous induction is appropriate. It is preferable to intubate and ventilate
patients undergoing laparoscopic surgery. This ensures a secure airway while
ventilating with higher airway pressures and reducing the inherently small risk of
aspiration from gastric regurgitation. A large-bore intravenous cannula should be
placed to allow ready access for the management of major complications. In upper
abdominal procedures a 1216 FG oro- or nasogastric tube is passed to allow egress
of gas from the stomach to facilitate the surgeons view.
Maintenance may be by total intravenous or inhalational anaesthesia. Intermittent

positive-pressure ventilation is preferable, to ensure adequate ventilation in the
presence of the reduced compliance and elevated diaphragm caused by the pneumo-
peritoneum.
Opioid supplementation aids analgesia and improves post-operative analgesia. This

may be as intermittent morphine and diamorphine or as an infusion of a short-acting
agent such as alfentanil or remifentanil.
Monitoring should be the minimum standard of non-invasive blood pressure,

electrocardiograph, end-tidal CO2, anaesthetic gases and pulse oximetry. For patients
who require laparoscopic surgery, but who have very borderline cardiac function,
invasive blood pressure and central venous pressure may be necessary, to allow closer
control of cardiac function, in particular myocardial work. A pulmonary artery flotation
catheter may be considered if there is concern regarding left heart function.
When peritoneal insufflation begins, there is often a reflex tachycardia and significant
increase in blood pressure, even at deep levels of anaesthesia. To avoid hypertensive
crises, with diastolic blood pressures above 120 mm Hg, it is advisable to have
a vasodilator and blocker available. Carefully titrated doses of labetalol can
be effective, with its combined and effects. Occasionally, vagally-mediated
bradycardia, even to the point of sinus arrest, may be seen. In this case, insufflation
should cease immediately, while an appropriate vagolytic (e.g. atropine) is given.
Ventilation should be adjusted to increase tidal volume and PEEP applied to counter the
reduced compliance, elevated diaphragm and increased CO2 load.
At the end of the procedure, it is preferable for the surgeon to infiltrate the small port
wounds with long-acting local anaesthetic to reduce postoperative pain. The raw areas
of tissue that occur after cholecystectomy can contribute to pain, due to carbonic acid
formation by CO2. Spraying the peritoneal cavity with bupivacaine may be effective in
these cases.
Recovery
Pain in the immediate postoperative period can be severe, presumably due mainly to
stretching of the tissues. Shoulder-tip pain is common, secondary to diaphragmatic
irritation. Sitting the patient up and giving systemic analgesia should help this to
settle. Occasionally, large doses of intravenous opioid are required for adequate relief.
However, once the pain is controlled, recovery is rapid and the patient usually goes
home in 23 days.
Postoperative complications
Surgical emphysema is occasionally alarming because it involves much of the trunk. It
is advisable to deflate the scrotal sack before recovery. More generalized emphysema
settles rapidly with time, but a pneumothorax should be excluded. The main problem
with surgical emphysema is pain, which should be controlled systemically. Basal
atelectasis with secondary pulmonary infection may also occur. It is more common in
those with pre-existing pulmonary disease, and should be treated with antibiotics and
physiotherapy. Aspiration may manifest as pleural effusions or rarely as Mendelsons
syndrome. These may require the input of a respiratory physician, but are not usually a
major problem in fasted patients.
The most serious complications are usually haemodynamic. Postoperative myocardial

infarction can occur as a result of the increase in myocardial work during the procedure.
Deep venous thrombosis may occur due to venous stasis in the legs during surgery.
This occasionally presents postoperatively with pulmonary embolus. u
FURTHER READING
Chui P T, Gin T, Oh T E. Anaesth Intens Care 1993; 21(2): 16371.

Anaesthesia for Reconstructive
Free Flap Surgery
Jane Quinlan
Jane Quinlan is Consultant Anaesthetist at the Radcliffe Infirmary and the John
Radcliffe Hospital, Oxford. She qualified from St Thomas Hospital, London, and trained
in anaesthesia in London and Oxford. Her interests include anaesthesia for plastic
surgery and acute pain management.
Reconstructive free flap surgery is a complex method of wound closure for large
wounds not amenable to linear (primary) closure. It involves the transfer of free tissue
(skin, muscle, bone, bowel or a combination) to a site of tissue loss where its circulation
is restored via microvascular anastomoses. A muscle flap produces a more even
contour and better aesthetic appearance than that achieved by a simple skin graft and
provides a better defence against infection. The defect may be caused by trauma,
infection or extensive surgery (e.g. mastectomy, head and neck cancer). The site and
size of the defect determines which flap is used. The most commonly used flaps are
the gracilis muscle for lower leg trauma; latissimus dorsi and rectus abdominis for
breast reconstruction; and pectoralis major and radial forearm flap for head and neck
reconstruction.
In patients with lower third tibulofibular defects, free tissue transfer is typically required.
The bony injury should be repaired and adequate debridement achieved before skin
and muscle coverage begins. This should occur within the first 6 days after injury before
colonization of the wound and the risk of complications increases. In patients with
multiple trauma, any life-threatening injuries must be addressed first and the patients
haemodynamic status stabilized before reconstructive surgery is contemplated.
Flap transfer
The free flap is transferred with its accompanying artery and vein, which are then
reattached to vessels at the donor site using microvascular techniques. The stages of
flap transfer are:
flap elevation and clamping of vessels
primary ischaemia as blood flow ceases and intracellular metabolism becomes
anaerobic (this is dependent on surgical time and lasts 6090 minutes)
reperfusion as the arterial and venous anastomoses are completed and the clamps
released
secondary ischaemia is subsequent to hypoperfusion of the flap (minimized by
appropriate anaesthetic management).
Primary ischaemia
With cessation of blood flow, the flap becomes anoxic. In the presence of anaerobic
metabolism, lactate accumulates, intra-cellular pH drops, ATP decreases, calcium
levels rise and pro-inflammatory mediators accumulate. The severity of the damage
caused by primary ischaemia is proportional to the duration of ischaemia. Tissues with
a high metabolic rate are more susceptible to ischaemia, therefore skeletal muscle
in a flap is more sensitive to ischaemic injury than skin. At the conclusion of primary
ischaemia, the changes in the flap tissue include:
narrowed capillaries due to endothelial swelling, vasoconstriction and oedema
sequestration of leucocytes ready to release proteolytic enzymes and reactive
oxygen intermediates
diminished ability of endothelial cells to release vasodilators and degrade ambient
vasoconstrictors
end-organ cell membrane dysfunction and accumulation of intracellular and
extracellular toxins
up-regulation of enzyme systems to produce inflammatory mediators.
Reperfusion begins with the release of the vascular clamps. Normally, the re-
establishment of blood flow reverses the transient physiological derangement produced
by primary ischaemia. The flap recovers with minimal injury and normal cellular
metabolism is restored. However, an ischaemia/reperfusion injury may result if factors
in the flap are unfavourable. Prolonged ischaemia time or poor perfusion pressure
make this more likely. Reperfusion injury occurs when the restored blood flow allows
the influx of inflammatory substrates that may ultimately destroy the flap.
Secondary ischaemia occurs after a free flap has been transplanted and reperfused.
This period of ischaemia is more damaging to the flap than primary ischaemia. Flaps
affected by secondary ischaemia have massive intravascular thrombosis and significant
interstitial oedema. Fibrinogen and platelet concentrations are increased in the venous
effluent. Although skin flaps can tolerate 1012 hours of ischaemia, irreversible
histopathological changes in muscle can be seen after 4 hours.
Causes of flap failure: the general causes of poor flap perfusion may be classified as
arterial, venous or resulting from oedema. The arterial anastomosis may be inadequate,
in spasm or thrombosed. The venous anastomosis may similarly be defective, in spasm
or compressed (e.g. by tight dressings or poor positioning). Oedema reduces flow to
the flap and may be a result of excessive crystalloids, extreme haemodilution, trauma
from handling or a prolonged ischaemia time. Flap tissue has no lymphatic drainage
and is therefore susceptible to oedema.
Microcirculation: the blood flow through the microcirculation is crucial to the viability
of a free flap. The microcirculation is a series of successive branchings of arterioles
and venules from the central vessels. Regulation of blood flow and oxygen delivery
is accomplished by three functionally distinct portions of the microcirculation: the
resistance vessels, the exchange vessels and the capacitance vessels.
The resistance vessels are the muscular arterioles that control regional blood flow.
Arterioles range in diameter from 20 m to 50 m and contain a relatively large amount
of vascular smooth muscle in their walls. Alterations in vascular smooth muscle tone are
responsible for active constriction and dilation in arterioles and thus control resistance
to blood flow.
The capillaries constitute the network of vessels primarily responsible for the exchange
function in the circulation. Small bands of vascular smooth muscle, the precapillary
sphincters, are located at the arterial end of many capillaries and are responsible for
the control of blood flow within the capillaries.
The venules act as the capacitance vessels, which collect blood from the capillary
network and function as a reservoir for blood in the circulation.
The vascular bed of skeletal muscle has rich adrenergic in-nervation and therefore
has a marked vasoconstrictor response to neural stimulation, primarily through the
resistance vessels. Precapillary sphincters also constrict in response to sympathetic
stimulation, but are sensitive to local factors such as hypoxia, hypercapnia, and
increases in potassium, osmolality and mag-nesium, which may cause relaxation.
Other vasoactive hormones (e.g. renin, vasopressin, prostaglandins, kinins) also have a
role in microvascular control.
Transplanted vessels in a free flap have no sympathetic innervation but are still able to
respond to local and humoral factors, including circulating catecholamines.
The flow behaviour (rheology) of blood in the microcirculation is determined by the red
cell concentration, plasma viscosity, red cell aggregation and red cell deformability.
Following all surgery under general anaesthesia, the changes in blood rheology
include:
increased platelet aggregation and adhesion
an impairment of red cell deformability
an increase in whole blood viscosity
increased clotting factors
increased plasma fibrinogen and red cell aggregation
disturbance of fibrinolysis.
Normal levels of 2,3-diphosphoglycerate (2,3-DPG) are required for optimal red

cell deformability. After blood transfusion, this deformability is impaired owing to the
negligible amount of 2,3-DPG in stored blood.
Physiology
The physiological status of the patient has a major influence on the viability of the
transferred tissues, so the conduct of anaesthesia and postoperative management
have a direct effect on outcome. Surgery is long (often 68 hours) with multiple sites
for tissue trauma, resulting in extensive blood and fluid losses as well as heat loss. The
resulting hypovolaemic vasoconstriction and hypothermia, if not corrected, compromise
blood flow to the flap and result in flap failure.
Even with good fluid management, blood flow to a flap may decrease by 50% for 612
hours postoperatively. The guiding principle of anaesthesia for free flap surgery is the
maintenance of optimum blood flow. The determinants of flow are summarized by the
HagenPoiseuille equation:
Laminar flow = Px r4 x
8xxl
where: P is the pressure difference across the tube, r is the radius of the vessel, is
viscosity and l is the length of the tube.
From this we may deduce that the goals of anaesthesia for free flap surgery are
vasodilatation, good perfusion pressure and low viscosity.
Vasodilatation
Vessel radius is the most important determinant of flow, for the vessels supplying the
flap as well as those in the flap.
Temperature the patient should be kept warm in theatre, the recovery room and the
ward for the first 2448 hours. This is best achieved by raising the ambient temperature
in theatre and by using a warm air blanket. Active warming should begin before the start
of anaesthesia because patient cooling occurs rapidly after induction of anaesthesia.
In an awake patient, the central core temperature is higher than that of the peripheral
tissue and skin temperature. After the induction of anaesthesia, vasodilatation modifies
the thermal balance between compartments. The volume of the central compartment
enlarges leading to a decrease in its mean temperature, while the temperature of the
peripheral and skin compartments increases. At thermoregulation, the size of the
central compartment becomes smaller owing to vasoconstriction, which leads to an
increase in the mean temperature, although the peripheral and skin temperatures fall.
In addition to vasoconstriction, hypothermia also produces a rise in haematocrit

and plasma viscosity, the aggregation of red blood cells into rouleaux, and platelet
aggregation. These effects may reduce the microcirculatory blood flow in the flap.
Fluid peripheral vasoconstriction due to an underestimation of fluid losses is

common. There are two operating sites in free flap transfer: the donor site and the
recipient site. Both have insensible fluid losses and both may have blood losses. A
warm theatre environment also increases fluid loss. Modest hypervolaemia reduces
sympathetic vascular tone and dilates the supply vessels to the flap. An increase in
central venous pressure of 2 cm H2O above the control measurement can double the
cardiac output and produce skin and muscle vasodilatation. Figure 1 gives a guide to
fluid management.
Guide to fluid management
Crystalloids
1020 ml/kg to replace preoperative deficit
48 ml/kg/hour to replace insensible losses
Colloids
1015 ml/kg for haemodilution
To replace blood loss
Blood
To maintain haematocrit at 30%
Dextran
Often given postoperatively
1
Anaesthesia isoflurane has the advantage over other volatile anaesthetics and
propofol that it causes vasodilatation with minimal myocardial depression. Propofol
inhibits platelet aggregation which could reduce the risk of thrombosis. This may be due
to an effect of intralipid on the plateleterythrocyte interaction, and by the increased
synthesis of nitric oxide by leucocytes.
Vasospasm of the transplanted vessels may occur after surgical handling or after
damage to the intima of the vessels, and can occur during surgery or postoperatively.
The surgeons may use topical vasodilators such as papaverine, lidocaine (lignocaine)
or verapamil during the operation to relieve the vasospasm.
Sympathetic blockade epidural, brachial plexus or interpleural local anaesthetic

infusions, used intraoperatively and postoperatively, provide sympathetic blockade to
further dilate vessels. Concerns have been raised that the sympathetically-denervated
transplanted vessels would be unable to dilate after lumbar epidural blockade, resulting
in a steal effect reducing flap blood flow. In fact, provided any hypotension due to the
sympathetic block is treated appropriately, blood flow to the flap improves as a result of
the increased flow through the feeding recipient artery. Other advantages of epidural
analgesia include a reduction in intraoperative and postoperative blood loss and vessel
spasm; a lower incidence of deep venous thrombosis; improved diaphragmatic function
and more rapid post-operative recovery. Good analgesia reduces the level of circulating
catecholamines and avoids the vasoconstrictor response to pain.
Perfusion pressure
The preservation of a good perfusion pressure with wide pulse pressure is essential
to flap survival. Appropriate anaesthetic depth and aggressive fluid management
are usually all that is needed. Most inotropes are contraindicated owing to their
vasoconstrictive effects, but if required, dobutamine and low-dose dopamine could be
used.
Viscosity
Isovolaemic haemodilution to a haematocrit of 30% improves flow by reducing viscosity,
reducing reperfusion injury in muscle and increasing the number of patent capillaries,
which decrease tissue necrosis. Further reductions in haematocrit do not provide
much more advantage because the curve of viscosity versus haematocrit flattens
off markedly (Figure 2). If the haematocrit falls further, the marginally improved flow
characteristics from a lower viscosity may then be offset by a reduction in oxygen
delivery:
DO2 = CO x [(Hb x sat x 1.34) + (PaO2 x 0.003)]
A low haematocrit also increases myocardial work, therefore care should be taken in
patients with poor cardiac reserve.
Br J Anaesth 57:

2
Practical conduct of anaesthesia
Monitoring
In addition to basic monitoring, these patients require invasive blood pressure
monitoring to enable safe manipulation of the perfusion pressure. Direct measurement
of arterial pressure gives a continuous record of the pressure and is more accurate than
non-invasive indirect techniques. An arterial cannula also provides access to blood gas
analysis and haematocrit estimations.
Central venous pressure reflects cardiac filling pressures and can be manipulated to
increase cardiac output.
Core temperature measurement is essential when active warming is instituted. A

nasopharyngeal or rectal probe is used intraoperatively for a continuous reading, while
intermittent tympanic or axillary measurements are used in the recovery and ward
areas.
Peripheral temperature is also measured because a fall in skin temperature can

reflect hypovolaemia and vasoconstriction. A difference of less than 2oC between core
and peripheral temp-eratures indicates a warm, well-filled patient. The temperature of
the skin flap is sometimes monitored postoperatively because a drop in temperature
may herald flap failure. However, this is not a sensitive test, because by the time the
temperature has fallen the flap will have suffered sufficient vascular damage to render it
virtually unsalvageable.
Urine output is another indicator of volume status. A urine output of 12 ml/kg/hour

should be maintained intraoperatively and postoperatively with appropriate fluid
management. Diuretics are contraindicated in these operations because volume
depletion compromises flap survival.
Induction
Active warming starts before the patient is asleep. The ambient temperature in theatre
is raised to about 2224oC, a level high enough to reduce patient heat loss, but not too
hot to be uncomfortable for the theatre staff. The patient is covered in a hot air blanket
before induction of anaesthesia and this remains in place while the patient is prepared
for theatre. Once in theatre, the blanket is moved to enable surgical access, but with as
much surface area coverage as possible.
If appropriate, a regional block is inserted, preferably to cover the free flap recipient
site (rather than the donor site) for the full benefit of the sympathetic block. The patient
is intubated and ventilated; and a large gauge peripheral line, central line, arterial line,
urinary catheter and core temperature and skin temperature probes are positioned.
Nitrous oxide diffusion into air in the stomach combined with gastric stasis results in
gastric distension, with associated post-
operative nausea and vomiting. A nasogastric tube is therefore sited at intubation, left
on free drainage, then aspirated and removed at the end of the operation.
Fluid, administered through a fluid warmer, is started in the anaesthetic room to

compensate for preoperative dehydration.
Maintenance
Careful positioning of the patient is imperative for such a long operation. Limbs are
positioned and supported to avoid neuro-logical damage or vascular compression.
Eyes are taped and lightly padded to reduce the incidence of corneal abrasion and
prevent drying of the cornea.
Prophylaxis against deep venous thrombosis is necessary for all patients.

Subcutaneous heparin or low-molecular-weight heparin is given preoperatively, while
anti-embolism (TED) stockings and compression boots are used intraoperatively.
The patient is ventilated to normocapnia. Hypocapnia increases peripheral vascular

resistance and reduces cardiac output, while hypercapnia causes sympathetic
stimulation. If the surgeon uses the microscope for vessel preparation or anastomosis
on the chest or abdomen, the tidal volume is reduced to minimize movement in and out
of the surgeons field of vision. The respiratory rate is then increased to maintain minute
ventilation.
Controlled hypotension is useful during the initial dissection and is most easily achieved
using epidural local anaesthetic and/or isoflurane. An infusion of glyceryl trinitrate may
be added if needed.
Crystalloids are used to replace the preoperative fluid deficit from starvation and to
cover intraoperative insensible losses. The latter are high because the warm theatre
increases evaporative losses from the two operating sites. Excessive use of crystalloid
may precipitate oedema in the flap.
Hypervolaemic haemodilution is achieved using colloids.
Blood gas analysis and haematocrit measurement should be carried out at the start of
the operation and repeated every 2 hours.
By the time the flap is reperfused, the patient should be warm, well-filled and
sympathetically blocked with a high cardiac output.
Emergence and recovery

The patient should wake up pain-free. Analgesia is maintained postoperatively with
local anaesthetic infusions for regional blocks, intravenous patient-controlled analgesia,
or both. Coughing and vomiting increase venous pressure and reduce flap flow, so
smooth emergence and extubation are needed. The principles of perioperative and
postoperative care are listed in Figure 3. u
Principles of perioperative and postoperative care
Maintain high cardiac output

Normal arterial blood pressure (systolic >100 mm Hg)
Low systemic vascular resistance
Normothermia
High urine output (> 1 ml/kg/hour)
Effective analgesia
Haematocrit 3035%
Monitoring of blood flow in flap (Doppler postoperatively)
3
FURTHER READING
MacDonald D J F. Anaesthesia for Microvascular Surgery. Br J Anaesth 1985; 57:
90421.
Sigurdsson G H, Thomson D. Anaesthesia and Microvascular Surgery: Clinical Practice
and Research. Eur J Anaesthesiol 1995; 12: 10122.

The Anaesthetic Machine
Michael OConnor
Ian Taylor
Duncan Parkhouse is Consultant Anaesthetist in the Swindon and Marlborough NHS

Trust, UK. He qualified from Bristol University and trained in Bristol, Swindon, Adelaide,
Australia, and Oxford. He is an examiner in the Primary FRCA and is involved in
education as a Postgraduate Clinical Tutor.
Ian Taylor is Specialist Registrar in Anaesthesia in the Swindon and Marlborough NHS
Trust, UK. He qualified from Bristol University and is training at the Wessex School
of Anaesthesia, based in Southampton, UK. His interests are vascular and obstetric
anaesthesia.
Many anaesthetic machines incorporate patient monitoring; conventionally this is

considered separately and will not be discussed here.
Types of anaesthetic machine

Demand and intermittent flow machines
The patients inspiration controls the flow of fresh gases. Such machines have been
used for dental anaesthesia (e.g. the McKesson anaesthetic machine) and for military
field anaesthesia (the Triservice apparatus).
Continuous flow machines (Boyles machine)

Continuous flow machines are encountered in day-to-day hospital practice in the
UK. The driving force for gas flow is compressed gases. This contribution discusses
continuous flow machines.
Pressures in the anaesthetic machine
Units of pressure
To understand the anaesthetic machine, it is important to be able to relate the
various different units that are used to describe pressure; 1 atmosphere pressure is
approximately:
101 kPa
760 mm Hg
1035 cm H2O
1 bar
15 psi.
Absolute and gauge pressure

Absolute pressure is pressure above that in a vacuum.
Gauge pressure is pressure above atmospheric. Pressures in the anaesthetic
machine are always quoted as gauge pressures.
All pipeline pressures are 400 kPa except for pressure in the air pipeline used to
drive equipment such as orthopaedic drills, which is 700 kPa. Cylinder pressures are
reduced to a machine working pressure of 400 kPa by pressure regulators (see below,
page 66).
Pressure downstream of the flowmeters can range between zero (i.e. 1 atmosphere
pressure), when the common gas outlet is open to the atmosphere, and about 33 kPa
if the common gas outlet is completely obstructed and the safety valve in the back bar
vents to the atmosphere.
Measurement of pressure
Cylinder and pipeline pressures are measured by a Bourdon pressure gauge (Figure
1). This is an aneroid (i.e. without liquid) gauge consisting of a coiled tube attached
at one end to the gas supply and at the other to a pointer. The pressure of the gas
causes straightening of the coil and thus movement of the pointer over the colour-
coded, labelled and calibrated dial (Figure 2). The gauge is faced with heavy glass and
designed such that leaks vent from the back of the valve casing and do not blow out the
glass.
Bourdon pressure gauge
Dial
Coil
Coil straightening
Pointer
Pressure
2 Bourdon pressure gauge.
Pressure regulators
Although sometimes referred to as pressure-reducing valves, the term pressure
regulators is preferred because their function is not simply to reduce pressure, but in
doing so to allow more accurate control of flow and to make up for the fall in cylinder
pressures as they empty.
Figure 3 demonstrates the function of a pressure regulator. The principle is similar
to that of the pressure-relief valve (see Anaesthesia and Intensive Care Medicine 1:3:
107) except that there are two chambers, one of high pressure and the other of low, and
two discs of different areas.
Pressure regulator
Diaphragm (A) Spring
Regulated
low-pressure
Low-pressure outlet (p)
chamber
Valve (a)
High-pressure
chamber
High pressure (P)

With a constant force applied by the spring acting on the large diaphragm
(A) to open the valve, and the opposing high pressure (P) of the inflow gas
acting on a small area (a) to close the valve, there is equilibrium between
the high- and low-pressure chambers. To balance the equilibrium and
keep the valve open, the pressure in the second chamber is thus
reduced. Thus: P x a = p x A, where P = pressure in the high-pressure
chamber; p = pressure in the low-pressure chamber; A = area of large
diaphragm; a = area of small diaphragm.
Adjustment of the tension in the spring and thus the force it applies to
the discs, regulates the pressure at the outlet to produce a constant
operating pressure. As the inlet pressure falls during use of the cylinder,
the force from the spring opens the valve wider, allowing more gas to flow
into the second chamber and maintaining pressure at the outlet. The
opposite happens if the inlet pressure rises, resulting in valve closure and
thus less flow into the second chamber.
Flowmeters
Rotameters
Flow in most anaesthetic machines is measured by a variable orifice flowmeter known
as a rotameter. A rotameter consists of a bobbin that floats in a glass tube with a
diameter that increases with height up the tube. The pressure drop across the bobbin
remains constant, and as flow increases it rises up the tube.
The two important properties of the gas flowing through a rotameter that influence
its calibration are:
viscosity
density.
Gas flows in the annulus between the bobbin and the tube. At the lower end of the
tube the annulus is long with respect to its cross-sectional area, and flow is laminar
and dependent on the viscosity of the gas. Higher up the tube, the cross-sectional area
of the annulus is greater, the gas is effectively flowing through an orifice, and flow is
turbulent and dependent on the density of the gas (Figure 4).
Flowmeter
Turbulent flow
Laminar flow
Bobbin
Laminar flow around the bobbin at the bottom of the tube, turbulent flow
at the top. NB Pitch of the rotameter tube has been greatly exaggerated
4
Features of rotameters
For any given gas, the flow through a rotameter depends on both its viscosity and its
density. Rotameters therefore have to be calibrated individually for the gas they will be
measuring.
The bore may be varied to measure low flows accurately.
The back plate may be luminous.
Calibration is from the lowest accurate point, not zero.
Accuracy is 2%.
In many machines there is a constant low flow of oxygen.
Potential sources of inaccuracy in rotameters

If the tube is not truly vertical, the annulus between the tube and the bobbin is
altered.
Static electricity can cause inaccuracies. To minimize this, glass is conductive and
sprayed with antistatic material.
Dust can collect on the bobbin or within the tube.
Tubes may be damaged. In the UK, the oxygen rotameter tube is on the left (said
to be because Boyle was left-handed). This can mean that any damage to the tubes
would preferentially leak oxygen and result in the delivery of a hypoxic mixture. Many
manufacturers now arrange the order in which the gases finally mix so that oxygen is
the last gas added to the mixture.
The top-sealing washer may be defective.
The carbon dioxide bobbin may become stuck at the top of the tube.
Back pressure from a minute volume divider such as a Manley ventilator increases
the density of the gas and may cause the rotameter to under-read by about 7%.
Atmospheric pressure affects density. Low pressure gives over-reading.
Temperature affects density and viscosity. Increased temperature causes decreased
density and increased viscosity.
Vaporizers
Vaporizers are discussed elsewhere.
Safety
The anaesthetic machine has several in-built safety features that vary from machine
to machine. The commonly found features that are of importance to anaesthetists are
listed in Figure 5.
Perhaps the most important safety feature is that the machine should always be
checked in a systematic fashion before use. The Association of Anaesthetists of Great
Britain and Ireland has published a useful checklist, part of which is reproduced in
Figure 6. These checks must be performed at the beginning of each theatre session.
Anaesthetic machine safety features
Non-interchangeable pipeline outlets (often referred to as Schrader connec-

tors, though this is really a trade name)
Pipelines are coloured and marked with the name of the gas
Non-interchangeable screw thread connectors connect the pipeline to the
anaesthetic machine
The pin index system prevents accidental connection of the wrong cylinder
to the wrong yoke
Cylinders are coloured and marked with the name of the contents
Grease can be flammable or explosive in contact with gases at high pres-
sure. A Bodok seal (see below) makes a gas-tight connection between
cylinder and yoke
There are pressure gauges for pipelines and cylinders
Rotameter knobs are identified by the oxygen knob being a distinctive colour
and shape and more prominent
The oxygen rotameter outlet may be diverted to enter the gas flow last
Oxygen and nitrous oxide rotameters may be linked to prevent delivery of a
hypoxic mixture
The oxygen bypass can provide oxygen at high flow (> 30 litres/minute)
directly to the common gas outlet
There is an oxygen failure warning device triggered by a dropin the oxygen
pressure, which also vents the flow of anaesthetic gases to the atmosphere
to prevent delivery of a hypoxic mixture
Vaporizer fillers are keyed to prevent a vaporizer being accidentally filled
with the wrong agent
Vaporizers may be arranged so that only one can be turned on at a time
There is a machine pressure-relief valve in the back bar that prevents the
pressure rising above about 33 kPa
The machine is serviced regularly by a qualified engineer
Bodok seal.
Anaesthesic machine safety checks
Anaesthetic machine Operate the emergency oxygen bypass control and ensure that
Check that the anaesthetic machine and relevant ancillary flow occurs without significant decrease in the pipeline supply pres-
equipment are connected to the mains electrical supply sure. Confirm that the oxygen analyser display approaches 100%
(where appropriate) and switched on during this test. Ensure that the emergency oxygen bypass control
Careful note should be taken of any information or labelling ceases to operate when released
on the anaesthetic machine that might refer to its current
status Vaporizers
Check that the vaporizer(s) for the required volatile agent(s)
Oxygen analyser are fitted correctly to the anaesthetic machine, that any back bar
locking mechanism is fully engaged and that the control knobs
The oxygen analyser should be placed where it can monitor
rotate fully through the full range(s). Ensure that the vaporizer is
the composition of the gases leaving the common gas outlet
not tilted.
The analyser should be switched on, checked and calibrated
Turn off the vaporizers
according to the manufacturers instructions
Check that the vaporizer(s) are adequately filled and that the
filling port is tightly closed
Medical gas supplies Set a flow of oxygen of 5 litres/minute and, with the vaporizer
Identify and take note of the gases that are being supplied turned off, temporarily occlude the common gas outlet. There
by the pipeline, confirming with a tug test that each pipeline should be no leak from any of the vaporizer fitments and the
is correctly inserted into the appropriate gas supply terminal flowmeter bobbin should dip.
Check that the anaesthetic apparatus is connected to a Turn each vaporizer on in turn and repeat this test. There should
supply of oxygen and that an adequate reserve supply of be no leak of liquid from the filling port.
oxygen is available from a spare cylinder After this test, ensure that the vaporizers and flowmeters are
Check that adequate supplies of any other gases intended turned off
for use are available and connected as appropriate. All Should it be necessary to change a vaporizer at any stage, it is
cylinders should be securely seated and turned off after essential to repeat the leak test.
checking their contents. Carbon dioxide cylinders should not Failure to do so is one of the most common causes of critical
incidents
normally be present on the anaesthetic machine. A blanking
Removal of a vaporizer from a machine in order to refill it is not
plug should be fitted to any empty cylinder yoke
considered necessary
All pressure gauges for pipelines connected to the anaes-
thetic machine should indicate 400 kPa
Check the operation of flowmeters, ensuring that each
control valve operates smoothly and that the bobbin moves
freely through its range without sticking. With only the
oxygen flow control valve open and a flow of about 5 litres/
minute, check that the oxygen analyser display approaches
100%.
Turn off all flow control valves Source: Association of Anaesthetists of Great Britain and Ireland. Checklist
for Anaesthetic Apparatus, 1997.
FURTHER READING
Association of Anaesthetists of Great Britain and Ireland. Checklist for Anaesthetic
Apparatus, 1997.
Moyle J T B, Davey A. Wards Anaesthetic Equipment. 4th ed. Philadelphia: Saunders,
1998.

Artificial Ventilation in the
Operating Theatre
Elaine M Wilson-Smith
J Duncan Young
Elaine M Wilson-Smith is Anaesthetic Specialist Registrar and Neuroanaesthesia

Fellow at the Radcliffe Infirmary, Oxford, UK. She qualified from Guys Hospital,
London, and has trained in anaesthetics in Leicester, Alder Hey Hospital, Liverpool, and
Oxford.
J Duncan Young is Clinical Reader in Anaesthetics at the Oxford Radcliffe Hospitals

Trust. He qualified from Southampton University and trained in anaesthesia and
intensive care in Southampton, Oxford and North America. His interests include
artificial ventilation and techniques to improve arterial oxygenation in ICU patients.
Ventilators are used in two main settings: the operating theatre and the ICU.
In the operating theatre, ventilators are used to maintain ventilation in anaesthetized,
intubated, pharmacologically paralysed patients who have predominantly normal lungs.
These ventilators are designed to interface with anaesthetic gas circuits to allow varying
concentrations of oxygen, anaesthetic gases and volatile agents to be delivered to the
patient. Most theatre ventilators are relatively simple, mechanical or electromechanical
devices that do not have patient-sensing capabilities.
Ventilators are often used in the ICU to ventilate patients with abnormal lungs, who
require only air and oxygen as respiratory gases; these patients are seldom paralysed
and often require only partial respiratory support. The ventilators used are almost all
complex, computer-controlled devices with sensitive mechanisms to detect the patients
respiratory efforts.
This contribution discusses ventilators for theatre use, though many of the basic
principles apply to ICU devices.
Classification of anaesthetic ventilators
Ventilators can be classified according to their function and operation.

Functional classification is the most common and clinically useful system. It is
based on the pattern of gas that the ventilator generates during inspiration, and the
mechanism that cycles between inspiration and expiration (Figure 1).
Operational classification is based on parameters such as power source or driving
mechanism. Operational classification is not covered in this contribution.
Ventilator classifications were devised when most ventilators had only one mode
of ventilation. Examples of such ventilators are the Manley ventilator (a time-cycled
pressure generator), the Nuffield 200 ventilator (a time-cycled flow generator)
and paediatric theatre ventilators (time-cycled pressure generators). Modern theatre
ventilators and all ICU ventilators can operate in two or more ventilatory modes and so
do not fit neatly into one single category of the traditional functional classification.
Functional classification of the respiratory cycle

during intermittent positive-pressure ventilation
Inspiration Pressure generator
Flow generator
Active process
Pressure
Cycling Time
Cycling Cycling
trigger Volume
EI IE Flow
Passive
process
Expiration
Based on Mapleson classification. I, inspiration; E, expiration
Functional classification of ventilators

The important difference between pressure and flow generators is the pattern of gas
flow produced during inspiration. This influences the effects of changes in airway
resistance, or lung and chest wall compliance, or if there is leak of delivered gases
from the system. A summary of the important differences between pressure and flow
generators is shown in Figure 2. Knowledge of the basic respiratory mechanics is vital
to understanding ventilatorpatient interactions.
Pressure generators and flow generators

Pressure generator Flow generator
Decelerating flow Constant flow
Flow
Time Time
Volume
Time Time
Inspiration Expiration Inspiration Expiration
Flow pattern varying with Flow pattern predictable

respiratory resistance and Tidal volume predictable
compliance Peak pressure varying
Tidal volume varying with with respiratory
respiratory resistance and resistance and
compliance compliance
Peak pressure predictable
Resistance, compliance and time constants: the pressure required to cause gas to
flow into the lungs has two components:
that required to maintain gas flow along the airways, overcoming airways resistance
that required to overcome the elastic recoil of the respiratory system, determined by
compliance.
The interaction of these components determines the time constant (TC).
TC defines the rate of a simple (first-order) exponential process. It is equivalent
to the time taken for the exponential process to complete if it were to continue at the
same rate as that at which it began. TC describes how fast the lungs fill with a constant
applied airway pressure or how fast they empty during expiration. (TC = compliance x
resistance.) It increases with increasing resistance (e.g. in asthmatics) and decreases
with decreasing compliance (e.g. in pulmonary fibrosis).
Resistance is a measure of the resistance to gas flow. The major site of respiratory
resistance is in the medium-sized bronchi, but total respiratory resistance during
positive-pressure ventilation also includes the contribution of the endotracheal tube
and to a lesser extent the circuit. In a patient with normal lungs, this increases the total
respiratory resistance from 2 to 4 6 cm H2O/litre/second.
Compliance describes the elasticity of the respiratory system, or the ease with
which it inflates, and is measured as the volume change per unit pressure. Total
respiratory compliance consists of combined lung and chest wall compliance and is
normally 5070 ml/cm H2O.
Within the normal working range of the lung compliance is constant though it
decreases at extremes of volume. The contribution to compliance from the ventilator
circuit is usually small. The exception is during anaesthesia in neonates and infants
when the tidal volume is small compared with the circuit volume, and compression of
gas within the circuit can make it difficult to ensure that accurate and adequate tidal
volumes are delivered (Figure 3).
Effect on artificial ventilation increased airways resistance and reduced lung
and chest wall compliance are the most clinically significant changes in respiratory
mechanics affecting artificial ventilation. Some causes are shown in Figure 4.
Resistance, compliance and time constant

Compliance High compliance Low compliance
Compliance is a measure of the elasticity and ease of
Small Large expandability of the respiratory system
Alveoli force
force Normal chest wall and lung compliance is 50 ml/cm H2O
Small volume change, Potential delivered tidal volume = pressure x compliance
Large volume change, easy to inflate stiff to inflate
Resistance
High resistance Low resistance
Slow Fast Resistance is a measure of resistance to airflow
gas gas Normal airways resistance is 24 cm H2O/litre/second
inflow inflow
Time constant Time constant = resistance x compliance
Resistance Time constant describes the speed of filling of a
The time taken for a lung unit to fill lung unit
Pressure
depends on: Normal time constant = 0.2 seconds
the speed of gas inflow resistance Filling and emptying of a lung unit is 95% complete in
the total volume change compliance Compliance 3 x time constant
Causes of increased airways resistance and reduced respiratory

compliance
Increased airways resistance Reduced respiratory compliance
Bronchospasm asthma, Within lung pulmonary

chronic obstructive airway oedema, adult respiratory
disease (COAD) distress syndrome, fibrosis,
Mucosal swelling asthma, atelectasis
COAD Around lung pleural
Luminal obstruction effusion, upward
excessive secretions compression from abdominal
Foreign body tumour contents when supine,
Emphysema dynamic especially if obese
airway compression during Chest wall surgeon
Low lung volume compressing chest, expiration
retractors, scoliosis, contractures
Pressure and flow generators: an understanding of the different types of ventilator

and how they function helps predict the behaviour and limitations of each type of
machine when resistance and compliance of the lungs change (Figure 5).
Pressure generators a pressure generator applies a preset positive-pressure
waveform to the airway for the duration of inspiration. In its simplest form this pressure
is constant (Figure 6).
If the inspiratory time is sufficiently long, the respiratory compliance determines
the tidal volume delivered when a given airway pressure is applied. The respiratory
compliance decreases linearly with lung size, therefore a pressure generator set at
1520 cm H2O delivers an appropriate tidal volume to a small child or an adult with
normal lungs.
Pressure generators can maintain the required airway pressure, even in the
presence of a leak, within reasonable limits. As a result, the main use for pressure
generators in anaesthetic practice is to ventilate children. The cricoid ring is the
narrowest point of the airway in children. The insertion of endotracheal tubes can
lead to compression of the tracheal mucosa against the cricoid cartilage, resulting in
pressure necrosis. This can be avoided by using uncuffed endotracheal tubes; the
presence of an air leak during inspiration confirms that the endotracheal tube is not
lodged tightly in the cricoid ring.
The pressure generator ensures that adequate tidal volumes are delivered because
a consistent pressure is maintained despite the leak. Paediatric patients, particularly
neonates, are prone to ventilator-induced lung damage, and constant pressure
generators ensure that even when lung dynamics change, the applied pressure remains
constant.
Pressure generators are designed for use with normal lungs that remain
normal during surgery (delivered tidal volume = pressure x compliance.) The main
disadvantage of a pressure generator is that tidal volume is determined by compliance
and reductions in compliance may cause significant reductions in delivered tidal volume
and minute ventilation. Therefore, pressure generators may not be appropriate when
precise control of arterial carbon dioxide tension (PaCO2) is important, for example,
during neurosurgery.
Flow generators (Figure 7) are devices that produce a constant gas flow
independent of respiratory compliance or resistance. The volume delivered per unit time
remains constant even in the presence of high airway pressures. All flow generators
need a high-pressure gas source. This can be delivered by compressing bellows or by
using proportional control valves, which control gas flow from the pipeline supply.
The delivered tidal volume is determined by control of the inspiratory flow rate and
inspiratory time. The peak and mean airway pressure generated depends on the tidal
volume, inspiratory flow rate, respiratory compliance and resistance.
The main advantage of a constant flow generator is that a constant tidal volume and
minute ventilation are maintained even when the mechanics of the lung are changing.
The tidal volume can be set precisely and minute ventilation is predictable and
consistent, giving precise control of PaCO2.
The main disadvantage is the potential for high airway pressures and barotrauma if
changes in lung mechanics occur. There is also no ability to compensate for leaks. Flow
generators are used mainly for adults, particularly where lung mechanics are abnormal,
and when precise control of PaCO2 is required.
Cycling parameters - cycling is the process of stopping one phase of ventilation and
changing to the next. This occurs twice within each delivered breath. For the purposes
of classification, cycling marks the end of inspiration and the beginning of expiration.
Ventilators may be:
time-cycled cycling occurs after preset time
volume-cycled cycling occurs after preset volume delivered
pressure-cycled cycling occurs after preset pressure attained
flow-cycled cycling occurs when flow falls below a preset value.
Time cycling is the most common technique. Flow cycling is used in inspiratory
pressure support in the ICU but seldom in theatre. Volume and pressure cycling are
used infrequently. In most ventilators, cycling from expiration to inspiration is by time.
Advantages and disadvantages of pressure and flow generators
Pressure generators Flow generators
Advantages Protection from high airway pressures Ability to maintain a constant tidal volume
and barotrauma and minute ventilation even with significant
Compensate for leaks changes in lung mechanics
Precise control of PaCO2
Disadvantages Hypoventilation as a result of changes Potential for high airway pressures and
in lung mechanics barotrauma
Inability to compensate for leaks
Constant pressure generator

Inspiration Expiration
Weight
A weight resting on inflating bellows results in a constant
Flow
pressure, P1, being applied during inspiration. At the start

of inspiration P1 > P2, so gas flows into the lung. Once
P2 = P1 gas inflow will cease. Delivered tidal volume will
vary with compliance, rate of gas inflow with resistance Time
P1
Inspiratory valve
Volume
P2
Time
Expiratory valve
Pressure
Time
High-pressure, high-resistance flow generator

Heavy weight Inspiration Expiration Flow is
maintained at
the expense of
Flow
High pressure potentially high

High-resistance airway pressures
P1 Time
flow resistor
A constant flow
High-pressure Volume = flow x time for a preset time
Volume
P2 will deliver a
safety valve
constant tidal
volume
Time
A constant flow is obtained by having a large pressure
difference between P1 and P2, most of the pressure Compliance
drop occurring across the flow resistor. Changes in P2
Pressure
from altered lung dynamics will have little effect on the Resistance
overall P1/P2 relationship and so gas flow will remain
constant. Gas flow would stop only if P1 = P2. To avoid
the patient being exposed to such a potentially high
pressure, a safety valve is always included in the Time
inspiratory limb of the system. This is usually set at
45 cm H2O.
Single- and double-circuit ventilators

In a single-circuit ventilation system the anaesthetic gas is also the driving gas. A well-
known example is the Manley ventilator, where the fresh gas flow set on the rotameters
is divided into tidal volume (hence the term minute volume divider). The fresh gas flow
powers the ventilator and is also delivered to the patient.
In a double-circuit ventilation system the anaesthetic gas and the driving gas are in
separate circuits. The clearest example of this is a bag in bottle or bellows ventilator.
The anaesthetic gas is contained within the circuit and a set of bellows, which act as
a reservoir. After delivering the tidal volume, the bellows refill during expiration. The
bellows are contained within an air-tight cylinder and a separate high-pressure driving
gas is used to pressurize the cylinder periodically, compressing the bellows and thereby
generating inspiratory gas flow. Most modern circle/ventilator systems are double
circuits.
Bellows can be of the standing or hanging variety. Standing bellows rise as they
refill; hanging bellows are mounted inverted and fall as they refill. The advantage
of standing bellows is that a leak of anaesthetic gases will be noticed by a failure of
the bellows to rise to the full height. This is especially useful during low-flow circle
anaesthesia. Hanging bellows are usually weighted at the base and entrain room air if
there is a circuit leak.
The Nuffield 200 series of ventilators are functionally double circuit. Although there
is no physical separation of the driving and fresh gas flow, the configuration of these
ventilators ensures that fresh (anaesthetic) gases and driving gas do not mix. This is
achieved by using a connector hose with an internal volume that is greater than the tidal
volume.
Pulmonary physiology and the effects of intermittent positive-pressure

ventilation (IPPV)
When a patient breathes spontaneously the expansion of the chest wall creates a
negative pressure relative to atmospheric pressure between the visceral and parietal
pleura. The transpulmonary pressure gradient created causes the lung to expand and
fill. Thus, during inspiration the intrathoracic pressure is negative.
During IPPV the patient makes no respiratory effort and the transpulmonary
pressure gradient required to expand the lung is generated by raising the airway
pressure. With inspiration, intrathoracic pressure is positive. During artificial ventilation
the mean intrathoracic pressure is increased compared with spontaneous ventilation
and this has effects on the respiratory, cardiovascular, renal and endocrine systems.
The effects of IPPV are wide ranging and must be viewed in the context of the position
of the patient on the operating table and the effects of general anaesthesia.
Normal respiratory physiology and the effects of general anaesthesia

The primary function of ventilation is to move air in and out of the lungs so that carbon
dioxide can be eliminated and arterial oxygenation maintained. In healthy individuals it
is the requirement to eliminate carbon dioxide that is the prime determinant of minute
ventilation. A normal tidal volume is about 500 ml in an adult (8 ml/kg); of this, about
150 ml (2 ml/kg) remains in the conducting airways (anatomical dead space), and the
remaining 350 ml enters the alveoli and is available for gas exchange. The respiratory
rate depends on the requirement for carbon dioxide elimination, but is usually 1015
breaths per minute in adults. Effective ventilation maintains a normal arterial PaCO2 of
4.55.5 kPa and an arterial oxygen tension (PaO2) of 13.5 kPa in healthy young adults
breathing room air.
Functional residual capacity (FRC): the various subdivisions of lung volume that
can be determined by spirometry, whole-body plethysmography or helium dilution
are shown in Figure 8. Of these, the most important for anaesthesia and the care
of patients in the ICU is FRC. FRC is the end-expiratory volume of the lungs and is
determined by the balance between:
the elastic recoil of the lungs
the outward recoil of the chest wall
the respiratory muscle tone
the position of the diaphragm.
FRC gradually reduces with age and is reduced on lying supine (by 500800 ml) as
a result of upward displacement of the diaphragm by the abdominal contents. This
effect is enhanced in patients with abdominal distension or obesity. During general
anaesthesia, reduction in diaphragmatic and chest wall tone and function lead to a
reduction in FRC of about 20%. The effects of general anaesthesia and the supine
position are additive, and can cause a significant reduction in FRC.
Lung volumes (70 kg adult) Maximum inspiration

6
5
Volume (litres)
1 FRC Maximum expiration
0 Time
Normal values
Functional residual capacity 2.5 litres Vital capacity 3.55.5 litres
Inspiratory reserve volume 2.53.0 litres Total lung capacity 6 litres
Tidal volume 0.50.6 litres Minute ventilation 7.5 litres/minute
Expiratory reserve volume 1.5 litres Alveolar ventilation 5 litres/minute
Residual volume 1.52 litres Vd/Vt 0.3
Closing capacity (CC) is the lung volume at which small airway closure begins.
Closing volume is an alternative term that is equivalent to CC minus residual volume
(RV). Normally CC is less than FRC, but they converge with increasing age. When
FRC decreases to below CC, airway closure occurs during normal expiration and the
resulting decrease in ventilation to areas of the lung distal to the closure worsens the
ventilation-perfusion (V/Q) relationship. FRC usually remains greater than CC when
supine until about 45 years of age but the additional reduction in FRC that occurs
during general anaesthesia makes it more likely that FRC will fall below CC during
anaesthesia. The resulting increase in V/Q mismatch leads to a decrease in arterial
oxygenation, which is normally countered by increasing the inspired oxygen fraction.
Distribution of ventilation and perfusion: during spontaneous ventilation in an

upright position, distribution of ventilation and perfusion are not uniform throughout the
lungs. Blood flow increases linearly from the top to the bottom of the lungs as a result
of the effects of gravity on the low-pressure pulmonary circulation. The lower zones
ventilate better than the upper zones because the dependent parts are on a more
compliant (i.e. steeper) part of the pressure-volume curve. During normal inspiration,
diaphragmatic contraction is enhanced in the parts of the diaphragm most displaced,
aiding increased ventilation of the dependent parts of the lung (Figure 9).
Ideally, ventilation and perfusion at the alveolar level should be matched. Alveolar
ventilation should equal perfusion and the V/Q ratio equal 1. In this situation no
ventilation or perfusion is wasted. However, the normal V/Q ratio is 0.8. The further
the V/Q ratio deviates from 1, the more inefficient the ventilatory process becomes
(Figure 10).
In the supine position, the gravitational effects on the lung are more limited, and
perfusion is more homogeneous. However, the reduction of FRC, which is compounded
by anaesthesia and the patient's position, leads to uneven ventilation because of airway
closure and the tendency of the dependent portions of the lung to reduce in volume
more than the superior parts (compression atelectasis).
Therefore, in the supine position (especially under anaesthesia) V/Q relationships
worsen. This tends to cause hypoxaemia, which, because it is caused by a V/Q
mismatch rather than a true shunt, can be reversed with added inspired oxygen.
Distribution of ventilation and perfusion in the lungs

10 mBar
Ventilation Normal V/Q ratio = 0.8
increases
down
Relative blood flow

the lung 2.5 100%
mBar
Volume
50%
Transpulmonary pressure Top Bottom

Vertical distance along lung
Ventilation increases from the apex to
Perfusion increases on moving down
the base. Dependent parts of the lung
the lung. The low-pressure pulmonary
are on a more compliant part of the
circulation is affected by gravity
pressurevolume curve
Ventilation and perfusion

V V
Intrapulmonary right to left Dead space from
shunt from perfusion without ventilation without
ventilation perfusion
No ventilation
Q V/Q = 0 Q
Shunt
PAO2 PAO2
No PaO2
PaO2
flow
No perfusion
V/Q =
Alveolar PO2 determines end capillary PO2 Dead space
V
O2 supply determined
V by alveolar ventilation
Underventilated Normal alveolus
alveolus
Q
End
PAO2 PAO2
capillary PAO2
Q
O2
PaO2
O2 in = ventilation V
PaO2 PAO2
O2 out = flow Q
In an ideal alveolus capillary PO2 (PaO2) comes close to alveolar PO2 (PAO2). PAO2 is determined by the balance between the rate of O2 uptake by
the pulmonary capillaries (Q) and continued supply of O2 by alveolar ventilation (V). The rate of O2 removal is determined by the rate of O2
consumption (metabolic rate). In an under-ventilated alveolus, the supply of O2 is reduced. If O2 uptake continues, the result is for PAO2 to fall and
so PaO2 will fall
10
Hypoxic pulmonary vasoconstriction (HPV): when the alveolar PO2 or, to a lesser
extent, the mixed venous PO2 decreases, smooth muscle contraction occurs in small
pulmonary arterioles. This diverts blood from unventilated areas to better-ventilated
areas and helps minimize the effects of V/Q imbalance. Volatile anaesthetic agents as
well as many vasodilators (e.g. sodium nitroprusside) inhibit HPV, worsening the effects
of V/Q mismatching.
Respiratory effects of IPPV

Changes in distribution of ventilation: the preferential ventilation of the non-
dependent parts of the lung in the anaesthetized, supine position is increased by IPPV.
The non-dependent areas are more compliant than the dependent zones after induction
of anaesthesia and muscle relaxation, and so preferentially expand in response to
positive pressure. This effect is further exaggerated if the lungs have an increased
density, as in the adult respiratory distress syndrome or in patients with cardiogenic
pulmonary oedema. It is also compounded by compression of basal areas of the lung
as a result of the upward displacement of the paralysed diaphragm.
Changes in distribution of perfusion: normal distribution of perfusion is usually

maintained during IPPV. However, in the presence of high intra-alveolar pressures,
compression of the alveolar capillaries occurs and flow stops. Capillary pressures
are lower in the upper zones because of the effect of gravity on the low-pressure
pulmonary circulation, and these zones are particularly vulnerable to increases in
airway pressure. These preferentially ventilated upper zones now have much reduced
flow and V/Q mismatch is further increased. This is more likely to occur when mean
airway pressures are high and with the use of positive end-expiratory pressure (PEEP).
PEEP is the application of a residual positive pressure to the airway at the end of
expiration instead of atmospheric pressure. This improves oxygenation by increasing
FRC and thus reduces the effects of airway closure and lung volume reduction on V/Q
relationships. PEEP may also reopen previously collapsed lung units and maintain their
patency (alveolar recruitment).
Barotrauma is the result of excessive pressure gradients between alveoli and the
interstitium, with rupture occurring. Air can spread along perivascular spaces into the
mediastinum, pericardium, up into the neck, down into the abdomen or into the pleural
cavity (pneumothorax). Risk factors include:
large tidal volumes
excessive inflation pressures, especially > 40 cm H2O
use of PEEP
non-uniform lung disease
increased airway resistance.
Recently, the term volutrauma has been used in the ICU setting. This refers to
overdistension of normal areas of the lung by the high pressures required to inflate the
diseased areas.
Other respiratory effects of IPPV: during general anaesthesia with intubation and
ventilation, there is loss of the ability to cough and so secretions are retained. Inhaled
anaesthetics and cold, dry gases inhibit ciliary activity in the bronchial tree, again
leading to a tendency to retain secretions. In addition, if the anaesthetic gases are not
warmed and humidified, the respiratory tract can be a major source of heat loss.
Cardiovascular effects of IPPV

The major effect of IPPV is to reduce cardiac output via a reduction in venous return. In
most patients, this can be counteracted by fluid loading (e.g. 5001000 ml crystalloid).
There are additive effects on the pulmonary circulation and heart, but their relative
contribution is thought to be minor, and significant changes occur only with high mean
airway pressures.
Cardiac output: a decrease in cardiac output occurs when beginning IPPV, which
can cause significant hypotension. The increase in mean intrathoracic pressure during
inspiration with positive-pressure ventilation causes the low-pressure veins in the chest
to be compressed. Cardiac output falls because of the reduction in venous return to
the heart. The decrease in cardiac output and mean arterial blood pressure can be
particularly marked in patients who are hypovolaemic or have limited cardiovascular
reserve and is further worsened by PEEP. The expected fall in cardiac output can be
reduced by prompt infusion of fluids to increase central venous pressure and maintain
venous return.
Effects of IPPV on pulmonary vascular resistance and the heart: increased

pulmonary vascular resistance occurs when airway pressures are high, from direct
compression of alveolar capillaries. As pulmonary vascular resistance increases, there
is an increase in right ventricular afterload and right ventricular end-diastolic volume.
If end-diastolic volume becomes significantly raised, bulging of the intraventricular
septum into the left ventricular cavity can occur, reducing left ventricular compliance
and reducing left ventricular stroke volume. In addition, the increased wall tension in
the right ventricle, coupled with a reduced arterial pressure, can compromise right
ventricular perfusion in compromised patients. The final effect is right heart strain
further augmenting a reduction in cardiac output. Paradoxically, in patients with
existing heart failure, the increase in transpulmonary pressure transmitted to the thorax
can occasionally help to off-load the left heart by reducing venous return from the
pulmonary veins, thus reducing left atrial pressures. Left ventricular performance may
then improve.
Other effects of IPPV

Renal: mechanical ventilation causes a reduction in urine volume, and thus sodium and
water retention. A fall in renal perfusion pressure associated with the reduced cardiac
output and a rise in renal venous pressure as a result of impedance of venous return,
along with increased levels of antidiuretic hormone associated with IPPV, are thought
to be important. An increase in sympathetic stimulation triggered by baroreceptors
sensing the changes in pressure and flow may also contribute. The renal effects are
persistent and are not fully reversed with fluid infusion or improvement in cardiac
output.
Liver: the reduction in cardiac output and increased venous pressure leads to a
fall in hepatic blood flow proportional to the drop in cardiac output. Hepatic blood
flow may be reduced by up to 50% and hepatic metabolism is reduced. This can be
reversed by infusion of fluid. The increased venous pressure caused by the positive
intrathoracic pressure can cause hepatic venous congestion, and hypocapnia will lead
to vasoconstriction.
Endocrine: antidiuretic hormone levels are increased during IPPV, with corresponding
increases in renin and angiotensin levels. This contributes to salt and water retention.
Practical aspects of positive pressure ventilation
Adequate ventilation requires an adequate tidal volume and minute ventilation to be

delivered, time for gas distribution and gas exchange to occur, and sufficient time for
expiration to be completed. Adequate ventilation results in a normal PaCO2 tension
(4.55.0 kPa), and in anaesthetic practice this is usually estimated by the end-tidal
carbon dioxide tension (PE'CO2). In patients with normal lungs the arterial PaCO2 is
about 0.5 kPa greater than the PE'CO2. PE'CO2 is measured from alveolar gases from
all ventilating lung units with a spread of V/Q ratios. Units with high V/Q ratios have a
reduced alveolar PCO2 and so dilute the gas from units with a V/Q ratio close to unity.
This relationship is lost in patients with lung disease; arterial blood gas monitoring may
be required in these patients. The minute volume and tidal volumes used should aim for
peak airway pressures of 1520 cm H2O in most patients.
Arterial oxygenation is determined primarily by the inspired oxygen, which should
never be below 30% (FiO2 0.3) initially. The required inspired oxygen is determined
by the saturation recorded by the pulse oximeter; 95% or greater is appropriate. After
monitoring the effect of the initial settings in each patient, appropriate alterations can be
made to suit the individual.
Initial IPPV settings for routine general surgical cases

Adults:
flow generator mode of ventilation
tidal volume 810 ml/kg
respiratory rate 1012 breaths/minute
inspiratory/expiratory (I:E) ratio 1:2
Fi O2 0.4 (40% oxygen)
maximum airway pressure 30 cm H2O.
If a circle absorber system is in use, an initial fresh gas flow of 6 litres/minute should be
used.
A tidal volume of 810 ml/kg is appropriate for adults. An I:E ratio of 1:2 allows
sufficient time for equilibration in inspiration and time for full expiration, in relation to the
TC of normal lung. A starting inspired oxygen concentration of 40% helps to prevent a
fall in PaO2 and overcomes the expected increase in V/Q mismatch that occurs during
IPPV. Barotrauma is avoided if peak pressures are kept below 30 cm H2O.
Flow generators are the preferred method of ventilation in adults. A reliable and
predictable tidal volume and minute ventilation can be achieved even when there
are alterations in lung mechanics from pre-existing lung disease or when temporary
peroperative changes occur related to the effects of patient positioning and surgery.
Children:
pressure generator mode of ventilation
inspiratory pressure 20 cm H2O irrespective of weight
respiratory rate 3040 breaths/minute for neonates; 2025 breaths/minute for
infants; 1520 breaths/minute for older children
I:E ratio 1:2
Fi O2 0.5 (50% oxygen).
Owing to their increased basal metabolic rate relative to their weight, neonates and
infants have an oxygen requirement (6 ml/kg/minute) twice that of adults. As a result,
they have a high carbon dioxide production, hence the need for a high respiratory
rate. Young children also have a reduced FRC, high CC and relatively high airways
resistance with low respiratory compliance. Their increased metabolic rate and
relatively low FRC means they have limited oxygen stores and so their arterial oxygen
saturation falls rapidly if ventilation is inadequate. Loss of respiratory gases as an air
leak from around their uncuffed endotracheal tube is expected and indeed desirable. It
provides evidence that the endotracheal tube is not so tightly fitting as to cause tracheal
mucosal compression at the level of the cricoid ring. Pressure generators, which
compensate for gas losses and limit peak pressures, are commonly used in paediatric
anaesthesia. At puberty, differential growth of the cricoid ring and laryngeal aperture
means that the larynx becomes the narrowest part of the airway as in adults, so cuffed
tubes may then be used.
Safety issues
Detection of ventilator disconnection

Anaesthetized, paralysed patients are wholly dependent on the ventilator and the
anaesthetist to keep them alive. In this respect, a paralysed patient is much more
vulnerable than one who is breathing spontaneously. The anaesthetist should be
alerted to a disconnection promptly by a disconnect alarm, which may also indicate
when inadequate ventilation is occurring.
Disconnections can be sensed by:
loss of the rhythmic increase in airway pressure
reduction in expired gas volume
loss of expired carbon dioxide.
Monitoring of airway pressures and exhaled CO2 are part of minimum monitoring
requirements during mechanical ventilation.
Airway pressure sensors are either aneroid gauges or, more commonly, electronic
pressure transducers. The gauge the anaesthetist uses for monitoring and the alarm
system are often separate devices. Airway pressure alarms detect an increase above a
threshold pressure. If an increasing pressure that exceeds the threshold is not detected
in the preset time, an alarm is sounded. This system does not normally detect a blocked
endotracheal tube, but an alarm for the excessive inspiratory pressures generated in
this scenario is usually incorporated in the same system.
Expired tidal volume or expiratory flow over time can also be measured. A minimum
preset volume must be exhaled at a frequency above the preset minimum rate or the
alarm will be triggered. Expired tidal volume is usually measured by integrating the
expired flow signal.
Capnographs are fitted with limit alarms and often with apnoea detectors, which
detect apnoea from the carbon dioxide waveform. In addition, respiratory movements
are sometimes sensed via ECG leads and as a very late indicator, pulse oximeters will
alarm if significant arterial desaturation occurs.
Ventilator checks
The anaesthetist is responsible for the state of the equipment he or she uses. It is
expected that equipment is systematically checked before use. Although on occasion
this may be delegated to trained assistants, the final responsibility lies with the
anaesthetist. To this end, guidelines for machine checks have been issued by the
Associaton of Anaesthetists of Great Britain and Ireland (Figure 11). With the increasing
use of sophisticated, electronically controlled anaesthesic machines and ventilators, a
generic checklist must be used only with reference to the manufacturers suggested
protocol for each machine.
Ventilator checks
Ensure that ventilator tubing is correctly configured and securely attached

Set the controls for use and ensure that an adequate pressure is generated during the
inspiratory phase
Check that the pressure relief valve functions
Check that the disconnect alarm functions correctly
Ensure that an alternative means to ventilate the patients lungs is available
Source: Association of Anaesthetists of Great Britain and Ireland. Checklist for Anaesthetist
Apparatus, 1997.
11
FURTHER READING
Hedenstierna G. Respiratory Measurement. (Principles and Practice Series). London:
BMJ Publishing Group, 1998.
Oczenski W, Werba A, Andel H. Breathing and Mechanical Support. Oxford: Blackwell
Science, 1996.
Sykes K, Young J D. Respiratory Support in Intensive Care. (Principles and Practice
Series). 2nd ed. London: BMJ Publishing Group, 1999.
West J B. Respiratory Physiology The Essentials. Baltimore: Williams & Wilkins,
1990.
West J B. Respiratory Pathophysiology The Essentials: Baltimore: Williams & Wilkins,
1998.

Breathing Systems
Gordon W G French
Gordon W G French is Consultant Anaesthetist at Northampton General Hospital,

UK. He qualified from Glasgow University and trained in Nottingham and Oxford. His
research interests include the detection of silent myocardial ischaemia perioperatively,
the use of starches for volume preloading in obstetric anaesthesia and modes of
paediatric resuscitation teaching.
A breathing system is the name given to apparatus that delivers and removes gas and
vapour to or from a patient. The three main functions of the breathing system are:
to supply adequate oxygen
to remove carbon dioxide
to supply adequate inhalational anaesthetic agent.
The perfect system has yet to be developed but the ideal breathing system should:
be simple and safe
deliver the intended mixture
allow manual and intermittent positive-pressure ventilation (IPPV) in all age groups
be efficient (able to use low gas flows)
protect the patient from barotrauma
be sturdy, lightweight yet compact
be easy to scavenge
be cheap.
Essential components of a breathing system
Tubing (hose): originally this was carbon-impregnated rubber (an antistatic design),
corrugated to prevent kinking, but it was heavy and prone to perishing. Modern tubing
is usually plastic, disposable or designed for single use, and often has a smooth
inner bore that reduces resistance to airflow. Early systems had various means of
inter-linking tubes, including tapered metal connectors that pushed into each other
and screw mountings. These were manufactured in various sizes, with many systems
being non-interchangeable, clearly a dangerous situation. The International Standards
Organization (ISO.5356, 1987) and British Standard (BS 3849) recommend the
following sizes for all breathing systems:
30 mm tapered connections for scavenging hose to breathing systems
22 mm taper for connections within breathing systems
15 mm connections between the breathing system and the endotracheal tube.
An upstream male connector traditionally fits into a downstream female part. The
ISO 15 mm standard connector is cumbersome for small paediatric endotracheal tubes
(26 mm internal diameter). Smaller, lighter 8.5 mm connectors may be used, which
have adapters to connect to the 15 mm standard system. Tapered connections between
plastic, metal and rubber can be locked by giving them a slight twist after connecting.
Systems designed for repeated use can usually be autoclaved, which does not affect
their connectors. Single-use systems often distort if heated, making the connectors
unsafe.
There is controversy among practising anaesthetists as to exactly what for single
use only means. Clearly it would be expensive to use a new breathing system for
each patient, and almost certainly unnecessary. Many departments employ a cost-
effective compromise by using a new disposable antibacterial filter for each patient,
but only changing the actual breathing system weekly. It may be changed more often
depending on clinical need (e.g. after use in a patient with known lung infection such
as tuberculosis).
Reservoir bag: this stores fresh gas when the patient is exhaling and accommodates
the high peak inspiratory flow rates during inspiration. Made of rubber or plastic, the
common adult size is 2 litres and 0.5 litres for children, but some ventilators use other
sizes up to 6 litres. The bags motion allows observation of ventilatory patterns but
does not reflect the tidal volume accurately. As the bag stretches, the pressure in its
walls reaches a limit of about 40 cm H2O (Laplaces law); further distension does not
result in greatly increasing pressures. This partly protects the lungs from barotrauma
should the breathing system outlet become obstructed, such as when the adjustable
pressure-limiting (APL) valve is left fully screwed down. An open-ended reservoir bag is
commonly used in paediatric circuits, allowing manual ventilation and assessment of the
compliance of a childs lungs (e.g. Mapleson type F).
APL valve: this is a one-way, spring-loaded valve consisting of a thin, lightweight

disc (made of hydrophobic material) held by an adjustable spring against knife-edged
seating. This arrangement (Figure 1) reduces the area of contact between the disc and
the seating, lessening any surface tension that condensed water vapour might create,
causing the disc to stick. The disc prevents movement of air into the system when
the patient inhales, but opens at low pressure (about 1 cm H2O) to allow exhaled and
surplus gas to be vented during expiration. When fully screwed down, modern valves
open at about 60 cm H2O positive pressure, acting as a safety feature.
Expired gases can be conveniently scavenged by surrounding the valve with a hood.
If the valve is sucked open continuously by a faulty scavenging system, a huge increase
in the dead space of the apparatus will result. The APL valve should be fully open
during spontaneous respiration, partially closed during manual IPPV and fully closed
during ventilator IPPV.
Cross-section of an adjustable pressure-limiting valve

Valve screw top
Scavenging hood
Spring
Disc
Pathway of gas
when valve is open
Classification of breathing systems
The historical development of breathing systems was largely based on the intuition and
practical experience of individual anaesthetists. As a result, there are many different
systems. One classification based on function is described below.
Non-rebreathing systems
Non-rebreathing systems use one-way valves to separate inspired and expired gases.
When the patient inspires, the expiratory valve closes and the inspiratory valve opens,
allowing inhalation of fresh gas. There is usually a reservoir bag on the inspiratory limb,
which provides enough gas for the maximum peak inspiratory flow rate (often > 30
litres/minute), and collects fresh gas when the inspiratory valve is closed in expiration. It
may also allow for manual-assisted ventilation. Resuscitation devices commonly include
a bag constructed of foam-lined rubber or silicone, which remains inflated in the
resting state, in addition to a thin-walled reservoir bag. Manual ventilation is provided
by squeezing this bag, which automatically refills from the oxygen inlet and reservoir
bag when hand pressure is released. The fresh gas flow (FGF) should at least equal
the patients required minute volume. Examples are resuscitation devices such as the
Ambu bag, Laerdal silicone resuscitator, drawover units and the Triservice apparatus.
Rebreathing systems
In rebreathing systems, the inspiratory and expiratory gases can mix in the tubing and
re-inhalation of expired gas can occur. Rebreathing refers to inhaling part or all of the
previously exhaled tidal volume. In particular, it is the inhaling of previously exhaled
carbon dioxide (i.e. alveolar gas) which is of most concern to the anaesthetist. A system
is efficient if it can preferentially vent alveolar gas, retaining dead space (non-carbon-
dioxide-containing) gas and thus use an FGF that approximates to the patients alveolar
minute ventilation. The extent of carbon dioxide rebreathing thus depends on the FGF
flushing the expired gas away before the next inspiration. The normal respiratory
cycle consists of an inspiration followed immediately by expiration, but there is then
an expiratory pause. It is during this period that the FGF flushes the system. In
1954, Mapleson classified five commonly used systems according to their efficiency
at eliminating expired carbon dioxide in spontaneously breathing patients (Mapleson
systems AE). An F system was added in 1975 (Figure 2).
The Mapleson classification of anaesthetic breathing systems and adaptations

Mapleson type Recommended General points
fresh gas flow
System A Spontaneous a, b, c Efficient for spontaneous, not for IPPV
a Magill FGF AMV Heavy, especially at patient end
(70 ml/kg/minute) Unsuitable for children < 25 kg because large dead space
IPPV b Lack: coaxial, APL and reservoir bag at machine end
FGF
b Lack 23 x AMV Inspiratory gases through outer (30 mm) tube
Expiratory via inner (14 mm)
c Parallel c Parallel Lack: separate inspiratory and expiratory tubes
Lack FGF
System B Spontaneous FGF near patient end. Performs similarly in both modes.
23 x AMV Seldom used
FGF IPPV
23 x AMV
System C Spontaneous Similar arrangement to system B. The large-bore

23 x AMV tubing to bag is shorter
IPPV a Waters to and fro circuit: inefficient but small size
FGF 23 x AMV and simplicity means useful for resuscitation and patient
transfers
b Waters canister: heavy because incorporates a 1 lb
soda lime container between bag and mask or ET tube
Channelling occurs if incompletely packed. Nylon pot
scourer compresses at bag end. Filter at patient end
prevents soda lime dust movement. NB Filter to
patient = dead space. Easily sterilized. Now little used.
Superseded by circle absorber systems
System D Spontaneous Inefficient for spontaneous but good for IPPV

FGF 23 x AMV Manley ventilator on spontaneous ventilation
IPPV mode is a Mapleson D
AMV Safety problems include kinking of inner tube
(70 ml/kg/minute) Disconnection of inner tube increases dead space. Both
lead to hypoxia and hypercarbia
a Bain a Bain: coaxial D. Length of tube does not affect properties
(180540 cm). FGF through inner tube (opposite to Lack)
Ventilate with Penlon 200 replacing bag.
Connecting tube long > 500 ml (usually 1 m)
to prevent driving gas entering circuit. Lightweight, easy
to scavenge. Ga in expiratory limb warm inspiratory gases
FGF
System E Spontaneous Used for children up to 30 kg. Low resistance, small

FGF
23 x AMV dead space, lightweight, no valves. Inefficient but used for
IPPV spontaneous and IPPV. Expiratory limb is reservoir
23 x AMV and should be > VT to prevent air entraining
Ayres T-piece: developed for neuro/cleft palate surgery
System F Spontaneous Jackson Rees modification. Reservoir bag allows rate and
23 x AMV chest compliance to be monitored, ventilation by hand
FGF
IPPV and continuous positive airway pressure application.
23 x AMV Barotrauma and humidification a problem
AMV, alveolar minute volume; FGF, fresh gas flow; IPPV, intermittent positive-pressure ventilation; VT, tidal volume
Mapleson A: classically describes the Magill system. The APL valve and any
scavenging device make this system cumbersome at the patients end. Lack solved this
problem by creating a co-axial arrangement where the expiratory gases were carried
up an inner hose to the APL and scavenging system, both of which were thus distant to
the patient. However, this system is bulky, even though it is less weighty at the patients
end. In addition, if the inner tube breaks and this goes unrecognized, the system may
become dangerous because carbon dioxide elimination is drastically reduced. It is also
difficult to use with a ventilator. A parallel hose breathing arrangement (parallel Lack)
eliminates this problem.
The Mapleson A system is an efficient system for spontaneous ventilation because
it selectively vents alveolar gas through the APL valve. The first part of the exhaled tidal
volume (non-carbon-dioxide-containing dead space gas) is retained in the system and
is available for inhalation during the next breath. This efficiency is lost when the system
is used for IPPV.
Mapleson B and C: in both systems the FGF, reservoir bag and APL are near the
patient, creating a compact and portable system. However, they are both inefficient and
only the Waters to and fro system is commonly used, mainly for patient transport and
in postoperative recovery units.
Mapleson D: exhaled gas passes into a reservoir bag along with the fresh gas, so
rebreathing occurs unless the FGF is high. The system is efficient for IPPV.
The Bain system is a coaxial version, which is particularly useful for limited-access
surgery because of its light weight and the fact that the tubing can be lengthened
without affecting the flow characteristics. The system can be connected to a ventilator
by replacing the reservoir bag with tubing connected to a ventilator such as the Penlon
Nuffield 200. The tubing should be of sufficient length to prevent the ventilator driving
gas entering the breathing system (in practice > 500 ml or 1 metre of standard hose). In
this system, the FGF is along a narrow internal tube (the opposite of the Lack system),
and the expired gas moves along the outer tube, usefully heating up the dry FGF. It
is vital that the inner tube is intact because disconnection leads to a huge increase in
dead space and possible hypercarbia or hypoxia.
Mapleson E: the Ayres T-piece is a valveless, lightweight system, with low internal
resistance and dead space. In inspiration, gas is inhaled from both the inspiratory and
expiratory limb. The volume of the expiratory limb needs to be at least equal to the tidal
volume or air may be entrained. If it is too large, then rebreathing can occur because
expired gas may not have vented to air before the next inhalation. Occluding the outlet
intermittently allows IPPV.
Mapleson F: adding an open-ended reservoir bag to the expiratory limb of the Ayres
T-piece allows manual control of ventilation, observation of breathing and assessment
of lung compliance. Some continuous positive airway pressure (CPAP) is also achieved
with the system during spontaneous respiration, which, in an infant, may help to
increase the functional residual capacity. Scavenging is a problem for both the
Mapleson E and F systems. The routine use of capnography allows the FGF to be
tailored precisely to achieve normocapnia in individual patients for all these systems.
Humphrey ADE system (Figure 3) is one of a number of hybrid systems that has
become popular. It is a low-flow multipurpose system that appears to combine the best
of the Magill, Lack and T-piece systems but not their disadvantages. It is cost effective
in all modes, being more efficient than the Magill for spontaneous ventilation. The
15 mm, smooth-bore tubing has one-quarter of the resistance to flow of 15 mm
corrugated tubing, which allows use in adults and children; 8.5 mm tubing is available
for neonates. The reservoir bag, APL, scavenging shroud and a pressure-limiting valve
are all located on the Humphrey block. The system tubing connects to the patient
via a symmetrical Y-piece, which probably accounts for much of its efficiency as it
produces less turbulence than the conventional Magillpatient interface. One lever
allows conversion from A mode to E mode, with only a slight increase in FGF being
required to eliminate rebreathing. In E mode, the reservoir bag and APL are isolated
from the system, and the expiratory tubing acts as the reservoir limb of a T-piece. This
is open to the atmosphere via a port on the block to which a bag squeezer ventilator
such as the Manley Servovent or Penlon Nuffield 200 or 400 can be attached. The D
mode could be engaged by simply attaching a reservoir bag and APL to this port for
spontaneous ventilation, but this is much less efficient than the A mode.
The APL valve provides positive end-expiratory pressure of 1 cm H2O without
increasing the airway resistance of the apparatus. The APL valve does not have to be
screwed down for IPPV, except if used in the A mode. However, there is a long orange
valve seat stem that can be temporarily held down instead. This also moves slightly
during spontaneous respiration and gives a visual indication of respiratory movement.
A separate 60 cm H2O pressure-limiting valve lies behind the APL valve on the block.
This is always in-line, whatever mode is being used. The system can be fixed on to
the anaesthetic machine via a locking nut. A 500 g soda lime canister (lifespan 12
hours), which has a low resistance to flow and is autoclavable, can be fitted in front
of the block. This circle system arrangement requires no other alterations in FGF for
adults or children.
The entire system is MRI compatible, being made of plastic and brass. In addition,
tubing lengths of over 3 m can be used without compromising its function. The main
disadvantages are that it protrudes out of the anaesthetic machine, is heavy and can be
knocked, which theoretically could fracture old anaesthetic machine outflow pipes.
b
e
g
c
f
3 Humphrey ADE system. a adjustable pressure limiting valve with scaveng-

ing; b lever in A position; c soda lime carbon dioxide absorber; d pressure relief
(60 cm H2O) valve; e port for ventilator; f reservoir bag; g fresh gas flow. Fresh
gas flow: A mode (lever up) = 50 ml/kg/minute; E mode (lever down) = 70 ml/kg/
minute. Children start at 3 litres/minute.
Systems using carbon dioxide absorbers

The circle system (Figure 4) was first described in the 1920s. It uses soda lime to
absorb exhaled carbon dioxide. Partial rebreathing of other exhaled gases can thus be
undertaken, depending on the arrangement of the components and the FGF.
Circle systems can be classified as follows:
semi-open no rebreathing, very high FGF, APL valve wide open
semi-closed rebreathing occurs, low flow, APL valve partly closed
closed FGF inflow exactly matches uptake by patient; complete rebreathing of
exhaled gases after carbon dioxide uptake and APL valve fully closed.
A circle system consists of:
FGF source
inspiratory and expiratory unidirectional valves
inspiratory and expiratory corrugated tubes
a Y-piece connector
an APL valve or pop-off valve
a reservoir bag
a canister containing a carbon dioxide absorbent.
Fresh gas enters the circle by a connection from the common gas outlet of the
anaesthetic machine. Various arrangements of components are possible, but there are
three golden rules to prevent carbon dioxide rebreathing.
A unidirectional valve must be located between the patient and the reservoir bag on
both the inspiratory and expiratory limbs of the circuit. These valves commonly have a
clear plastic cover so that their correct movement can be observed during use.
The FGF cannot enter the circuit between the patient and the expiratory valve.
The APL valve cannot be located between the patient and the inspiratory valve.
The most efficient circle system has the unidirectional valves near the patient
and the APL valve just downstream from the expiratory valve. This arrangement
conserves dead space gas and preferentially eliminates alveolar gas. The advantages
and disadvantages of a circle system are listed in Figure 5.
Nitrogen washout at the start of anaesthesia, non-nitrogen-containing gas
(unless medical air is being used) is inspired and body nitrogen passes into the lungs.
This effectively reduces the oxygen concentration in the alveoli and circle system,
producing a potentially hypoxic mixture. The use of high flows of gas at the start of
anaesthesia can washout this nitrogen. Pre-oxygenation with 100% oxygen for 710
minutes is also effective and can theoretically then allow low circle FGF to be used
from the start. Basal metabolic oxygen requirements are about 250 ml/minute, but to
allow for leaks in the circle and patient variability, 500 ml/minute oxygen is the minimum
recommended flow rate. Low flow anaesthesia is usually regarded as less than 1
litre/minute FGF.
The uptake of volatile agents is highest initially. Fast FGF inflows and large minute
volumes produce fast induction of anaesthesia as well as facilitating denitrogenation. As
equilibrium is reached, the expired concentration of volatile agent begins to reflect the
inspired value, and flows can be reduced. The exhaled gases are added to the fresh
gas and have a dilutional effect on the concentration of oxygen and vapour, which will
be proportionally greater at low flows. A potentially hypoxic alveolar concentration of
oxygen can develop as the FGF reduces. Using an inspired oxygen concentration of
50% to prevent these low oxygen levels in the circle was customary before the advent
of in-line gas/vapour analysers. However, this was associated with an increased chance
of awareness if the inspired volatile concentration was not increased to compensate for
the lower inspired nitrous oxide and volatile concentrations.
Vaporizers can be placed outside (VOC) or inside (VIC) the circle (Figure 6). Most
modern vaporizers tend to be outside the circle (e.g. Back bar units such as a TEC
vaporizer) and are accurate at low flows. With this set-up, the concentration of volatile
gas in the circle is reduced with increased patient uptake and low FGF (due to the
dilutional effect of exhaled gas), until uptake reduces and equilibration begins to occur.
With a vaporizer in the circle (e.g. Goldman vaporizer), both the fresh and exhaled gas
(which already contains vapour) pass through the vaporizer. When the FGF is low and
alveolar ventilation high, the concentration of volatile will rise. Thus the concentration
of the alveolar and circle vapour is a function of ventilation. In spontaneous ventilation,
with deepening anaesthesia and depression of ventilation, the concentration of volatile
gas will fall and result in the patient becoming lighter, a useful safety feature. However,
low flow controlled ventilation may result in high levels of volatile gas.
Future developments in circle technology may incorporate the VIC arrangement but
use a system of vapour injectors instead of the vaporizer. This would be linked to a
feedback mechanism incorporating circuit vapour analysis.
Carbon dioxide absorption closed or semi-closed circle systems require carbon
dioxide absorption to make rebreathing possible. Desirable features of a carbon dioxide
absorption mechanism are lack of toxicity (intrinsic or with common anaesthetics), low
resistance to air flow, low cost, ease of handling and efficiency. Soda lime and baralyme
are the two formulations commonly used for carbon dioxide absorption (Figure 7). Both
need water but because baralyme contains water as a barium hydroxide octohydrate
salt it performs better in dry climates. Soda lime (but not baralyme) is capable of some
regeneration after exhaustion. Maximum absorbency of both systems is 26 litres of
carbon dioxide per 100 g absorbent.
Dyes (acids or bases) are also added, which change colour as the hydrogen ion
concentration changes:
ethyl violet (colourless to violet; fluorescent light deactivates it)
phenolphthalein (white to pink)
Clayton yellow (red to yellow)
ethyl orange (orange to yellow)
mimosa z (red to white).
The chemical reaction in soda lime is:
CO2 + H2O H2CO3
H2CO3 + 2NaOH [KOH] Na2CO3 [K 2CO3] + 2H2O + heat
Na2CO3 [K 2CO3] + Ca(OH) 2 CaCO3 + 2NaOH [KOH]
Some carbon dioxide reacts directly with calcium hydroxide but this is much slower.
In baralyme the carbon dioxide acts directly with barium hydroxide and much more
water is released. In the UK, the size of granules is 48 mesh (a compromise between
surface area for absorption and air flow resistance). Mesh refers to the number of
openings per linear inch in a sieve through which the granules pass. A 4-mesh screen
indicates four quarter-inch openings per linear inch.
Soda lime and baralyme are not inherently toxic, but at low flows intrinsically
produced acetone can accumulate and has been linked to nausea and vomiting.
Carbon monoxide can also accumulate at low flows of dry gas (e.g. oxygen running
overnight) leading to the formation of carboxyhaemoglobin.
The volatile agent trilene degrades into dichloroacetylene (a neurotoxin causing
cranial nerve damage and encephalitis) and phosgene (a potent pulmonary irritant
causing adult respiratory distress syndrome).
Sevoflurane and halothane are slightly unstable in soda lime, the rate of degradation
increasing with temperature. Sevoflurane degrades into several compounds. Compound
A (a vinylether) has been associated with lung haemorrhage and renal tubular necrosis
in rats, but neither compound has been shown to cause problems in humans. Many of
these problems are resolved by flushing the system regularly.
Ideal circle set-up

Adjustable Fresh gas flow (FGF)
pressure-limiting
(APL) valve
Reservoir CO2 absorber

bag
One-way valves
Unsuitable position Unsuitable position

for FGF for APL valve
4
Properties of a circle system
Advantages Disadvantages
Heat/moisture Multiple connections
conservation Valves can stick
Easy scavenging Open leads to rebreathing
Reduced cost Closed leads to asphyxia
Small dead space Bulky
Good for long cases Inefficient for short cases
Soda lime changeover a hazard
Gas analyser necessary for accuracy
Potential for infection
Properties of vaporizers
Inside the circle Outside the circle
Low internal resistance High internal resistance
Low efficiency desirable (plenum)
Higher concentrations at High efficiency desirable
low fresh gas flow Lower concentrations at low
fresh gas flow (diluted)
Properties of soda lime and baralyme

Soda lime Baralyme
Calcium hydroxide (94%) Calcium hydroxide (80%)
Sodium hydroxide (the Barium hydroxide (the
catalyst) (5%) catalyst) (20%)
Potassium hydroxide (1%) More stable so does not
Silica (calcium and sodium contain silica
silicate harden it and reduce Denser and 15% less
dust formation) efficient than soda lime
System checks
All systems should be checked visually for broken parts and disconnections and a
push-and-twist connector test performed. In addition, there are checks specific to
individual systems.
Occluding Mapleson types B and C causes their reservoir bags to fill, testing the
air-tightness of the system. Releasing the valve causes the bag to deflate if the valve
is functioning normally.
The Bain system inner tube can be tested in two ways. Occluding the end of the
inner tube causes the rotameter bobbin to dip and the pressure alarm/valve to blow
if there are no leaks/disconnections up to that point. Occluding the patient end of the
system will fill the reservoir bag, testing overall air- tightness. Releasing the occlusion
causes the bag to deflate, then continue to empty as a result of the negative pressure
caused by the Venturi-effect of the fast FGF leaving the inner tube. The connection
of the inner tube can also be visually inspected because the outer corrugated tubing
is often made from transparent plastic. This outer tubing may also be temporarily
disconnected and a secure inner tube connection confirmed.
To carry out the low-pressure circle leak test, the end of the system should be
occluded and the APL valve closed off. The system is filled using the oxygen flush until
the airway pressure gauge registers 30 cm H2O. The pressure should remain at
30 cm H2O if no leaks are present.
FURTHER READING
Humphrey D, Brock-Utne J G, Downing J W. Single Lever Humphrey ADE Low Flow
Universal Anaesthetic Breathing System. Can Anaesth Soc J 1986; 33(6): 698718.

Cleaning, Disinfection and
Sterilization of Equipment
Duncan Parkhouse
Jonathan Warwick
Duncan Parkhouse is a Military Anaesthetic Trainee. He joined the Royal Army

Medical Corps as a medical cadet while a medical student at University College
Hospital, London. During his anaesthetic training he has spent time at both military and
NHS Hospitals including St Marys Hospital, the Brompton Hospital and the National
Hospital for Neurology and Neurosurgery, London.
Jonathan Warwick is Consultant Anaesthetist at the Radcliffe Infirmary, Oxford, UK.

His special interests are anaesthesia for plastic surgery and head and neck surgery.
Hospital-acquired infections have significant implications for the morbidity and mortality
of patients as well as for the economics of health care. The protection of patients
and medical staff from medical equipment that has come into contact with patients
or their body fluids, requires the adoption of various processes enforceable by law.
Changes in these laws and guidelines, published by the Department of Health and the
Medical Devices Agency, are expected in the near future. One of the reasons for the
introduction of new guidelines is the development of new variant CreutzfeldtJakob
disease, which is resistant to the standard methods of decontamination used in hospital
sterile services departments.
Contamination is the soiling or pollution of an inanimate object with harmful,

potentially infectious, material. In the clinical setting, this is most likely to be organic
material or microorganisms. Contamination may place the patient at risk and may
adversely affect equipment.
Decontamination is a method used to remove contamination and prevent

microorganisms reaching a susceptible site in large enough numbers to initiate
infection or other adverse effects. The three methods of decontamination routinely used
are cleaning, disinfection and sterilization. The method of decontamination chosen
takes into account the infection risk from the reprocessed piece of equipment. The risk
is dependent on:
the amount of contact the patient has with the piece of equipment (i.e. how invasive)
the susceptibility of the patient (i.e. immunocompromised, potential hypersensitivity)
the nature, extent and amount of microbial contamination on the piece of equipment
(the bio burden).
The type of equipment and its intended use determine the method of
decontamination used (Figure 1). The manufacturer should provide instructions for
cleaning, disinfection and sterilization techniques that are effective without affecting the
performance of the equipment.
It is essential that records are kept to demonstrate the number of times an
item has been decontaminated and the effectiveness of each process. The
documentation should allow patients to be traced in the event of any malfunction in the
decontamination process.
Risk of contamination for equipment and suggested decontamination process

Risk Application of equipment Recommendation
High In close contact with a break in the skin or Sterilization
mucous membrane
For introduction into sterile body areas
Intermediate In contact with mucous membranes Sterilization or disinfection

Contaminated with particularly virulent or easily
transmissible organisms
Before use on immunocompromised patients (Cleaning may be acceptable in
some agreed situations)
Low In contact with healthy skin Cleaning

Not in contact with patient
Single use equipment

Manufacturers should state in the product literature any restrictions on the number
of re-uses. Any device deemed by the manufacturer as unsuitable for reprocessing
is labelled single use. Devices labelled single patient use may be used for an
extended period of time or intermittently on the same patient. Users who disregard
the manufacturers guidelines, for example by reprocessing single use items or
reprocessing more than the recommended number of times may be transferring legal
liability for the safe performance of that product from the manufacturer to themselves or
the organization for which they work.
Many anaesthetic departments routinely use disposable anaesthetic breathing
systems marked as single use for extended periods with multiple patients. The
wisdom of this practice is the subject of much controversy. The advantages of these
breathing systems include safety (often pre-assembled with fewer opportunities for
connection errors by the user), lightweight and low cost if used on several patients. The
disadvantage is that this practice may contravene the manufacturers recommendation
for single use only and risk transmission of infection. The responsibility for use of
equipment marked single use then lies with the hospital. Departments of anaesthesia
should have an operational policy on the management of breathing systems marked for
single use. This may include:
the use of a new bacterial (heat and moisture exchanger type) filter for each patient
change of all breathing systems weekly
change of breathing system following use on a patient with known or suspected lung
infection
change of breathing system whenever there is visible contamination from blood or
body fluids.
Cleaning
Cleaning physically removes contaminants without necessarily destroying
microorganisms. It removes organic material and is required before disinfection or
sterilization.
Manual cleaning
Manual cleaning does not disinfect. It should be used only when other mechanical
methods are inappropriate or unavailable.
Immersion wearing appropriate protective clothing, the cleaner should submerge
the device in compatible water/detergent solution at the correct dilution and not
exceeding 35C. It is important to ensure that the cleaning solution reaches all surfaces
of the device, including lumen surfaces. Endoscopic equipment that may be totally
immersed for cleaning is marked with a blue line, usually around the eyepiece adjacent
to the focussing ring. The device should be brushed or agitated to remove any visible
contaminants. The device should be thoroughly drained and rinsed in clean water. This
method is generally satisfactory for the routine cleaning of laryngoscopes between
patients. Disinfection with an alcohol spray is then commonly used.
Non-immersion wearing appropriate protective clothing, the cleaner should immerse
a cleaning cloth into the detergent solution and wring it out. The equipment should
be cleansed by wiping its surfaces. The surfaces should be hand dried using a cloth,
hot air dryer or drying cabinet. This method of cleaning is often used for electrical or
electronic equipment which cannot be immersed in water.
Mechanical cleaning
Mechanical cleaning uses automated washers to clean equipment and often combines
cleaning with disinfection.
Thermal washer cleaning occurs by continually spraying the equipment with water
and detergent during a timed cycle. During the first process, cleaning occurs at 35C.
The second wash heats the surface of the equipment to a minimum temperature of
71C for a minimum of 3 minutes, 80C for 1 minute, or 90C for 1 second to disinfect
it.
Chemical washer the first part of the cleaning process is the same as the thermal
washer. Disinfection occurs by exposing the equipment to an approved disinfectant for
a particular period of time at less than 60C. The residue disinfectant is then removed
by a rinse cycle.
Ultrasonic cleaners are often incorporated into washer disinfectors. These work
by rapidly forming bubbles in the liquid, which immediately collapse (cavitation). This
cavitation agitates the liquid, producing a highly effective cleaning system. The process
does not disinfect.
Disinfection
Disinfection is used to reduce the number of viable micro-organisms, but it may not kill
all microbial agents such as some viruses and bacterial spores.
Low temperature steam disinfection

Low temperature steam disinfection is also known as pasteur-ization. It kills most
vegetative microorganisms and viruses by exposure to moist heat. The equipment
is exposed to dry saturated steam at a temperature of 73C for at least 10 minutes
at below atmospheric pressure. The low temperature steam kills vegetative
microorganisms and some heat-sensitive viruses. It cannot be used for sealed, oily
or greasy pieces of equipment or those with sealed cavities due to the variation in
pressure.
The advantages of this system are its broad spectrum of disinfection, it is non-
toxic, non-corrosive and the equipment is relatively safe and simple to use. The
disadvantages are that it requires a trained operator and that much equipment is
unsuitable for disinfection in this way. The capital cost of the disinfector is high and the
equipment is fixed and not portable.
Boiling water disinfection

Boiling water is an effective disinfectant against many microorganisms. Immersing a
piece of equipment in soft water and boiling at 100C for at least 5 minutes produces
disinfection. Boiling inactivates most non-sporing microorganisms, fungi, viruses and
some heat-sensitive spores. This method is not used if a better method is available. It
is unsuitable for heat-labile pieces of equipment, hollow or porous items into which the
water will not penetrate, or tubing over 1 metre in length.
The advantages are that boiling water has a broad disinfecting effect. The process
is non-toxic and inexpensive. The disadvantages are that boiling water is a potential
cause of injury. Following disinfection, items are wet and unfit for immediate use and
must be allowed to dry and cool, which may allow recontamination. There is also no
method of checking the efficacy of the process.
Washer disinfectors
Washer disinfectors are described above. They inactivate all microorganisms except
bacterial spores and some heat-resistant viruses. They are unsuitable for equipment
that may be heat labile or corroded by chemical disinfectant, and for hollow or porous
equipment that does not allow all surfaces to come into contact with the chemical
disinfectant or heat.
These methods are safe for the operator. There is minimal handling of the equipment
by staff and therefore a low risk of recontamination. Another advantage is that they
combine cleaning and disinfection. The disadvantages are the high cost of the
equipment and the requirement for trained staff.
Liquid chemical immersion

Liquid chemical immersion relies on good contact between the chemical disinfectant
and the equipment. The equipment therefore requires thorough cleaning beforehand.
It is then immersed in the chemical disinfectant, ensuring that the disinfectant reaches
all surfaces. The equipment is immersed for a predetermined time depending on
the chemical disinfectant used. The spectrum of activity also depends on the type of
chemical disinfectant used (Figure 2).
The method is unsuitable if the corrosive nature of the chemical disinfection may
damage the equipment or if the equipment has areas inaccessible to liquid. It requires
trained staff wearing protective clothing. It is potentially toxic, corrosive or volatile.
Also, the equipment may have to be hand dried after disinfection allowing possible
recontamination.
Equipment disinfectants commonly used and their spectrum of activity and physical properties
Disinfectant Microbiological activity Stability Inactivation Corrosive/ Irritant

by organic damaging
matter matter
Spores Mycobacteria Bacteria Viruses1
Enveloped Non-
enveloped
Glutaraldehyde +++ +++ +++ +++ +++ Moderate No No Yes
2% (slow) (fixative)
Peracetic acid +++ +++ +++ +++ ++ Poor No Slight Slight

0.20.35% (< 1 day)
Alcohol (ethyl None ++ +++ +++ ++ High Yes Slight No

alcohol) (fixative) Flammable
6080%
Peroxygen None + +++ +++ ++ Moderate Yes Slight No

compounds ( 7 days)
Chlorine-releasing +++ +++ +++ +++ ++ Poor Yes Yes Yes

agents >1000 (< 1 day)
ppm average Cl2
Clear soluble None +++ +++ + None Good No Slight Yes

phenolics
0.62%
Quarternary None Variable Moderate + +++ Good Yes No No

ammonium
compounds
1
Activity varies with concentration of product.
Sterilization
Sterilization is used to produce an object free from viable microbial organisms including
viruses and bacterial spores. There are several types of sterilizer (Figure 3).
Steam
When steam is pressurized it reaches a temperature greater than that of boiling water
at atmospheric pressure and destroys or renders non-viable, bacteria, viruses and their
spores. For this process to be effective, direct contact between the pure dry saturated
steam and the object being sterilized is required at the specific temperature and in the
absence of air. The temperature reached by the object determines the time required
for sterilization. The lowest temperature recommended is 121C for 15 minutes; the
highest temperature of 134C requires only 3 minutes.
This process is effective against all microorganisms with a significant safety factor.
Problems occur with wrapped items because all air must be removed. To overcome
this, porous load sterilizers are used, which incorporate a vacuum pump. Air is removed
before steam is added. This is the most commonly used method for sterilization in
hospitals today (Figure 4). However, it cannot be used for any material that cannot
withstand the temperatures or pressures required for sterilization (e.g. thermo-labile
plastics, fibre-optic endoscopes).
The advantages of this process are that steam is non-toxic, non-corrosive and a
highly effective sterilizing agent. This system can be incorporated into a fully automated
process on a large scale, coping with a high turnover of equipment. Disadvantages are
that the operator must wear protective clothing to avoid direct contact with the steam.
Different types of hospital sterilizers
Types of sterilizer Use Minimum time / temperature

Steam sterilizer
Porous load Wrapped instruments, dressings, utensils 134138C for 3 minutes
Fluid cycle Fluids in sealed containers 121124C for 15 minutes,
or 115C for 30 minutes
Unwrapped instruments Unwrapped instruments and utensils 134138C for 3 minutes
Hot air sterilizer Oils, powders, heat-resistant instruments 160C for 2 hours
that must be kept dry
Low temperature steam Heat-sensitive equipment 73C for 3 hours
formaldehyde sterilizer
Ethylene oxide Heat-sensitive equipment Various temperatures and
times
Dry hot air

In this process, sterilization takes place by raising the ambient temperature. Typical
processes consist of 160C for 2 hours, 170C for 1 hour, 180C for 30 minutes. If all
the items are completely clean and dry before this sterilization process starts, then all
microorganisms will be killed. However, it cannot be used for materials that would be
damaged by these temperatures (e.g. rubber, plastic).
Dry heat can be used to sterilize stable powders, waxes and non-aqueous liquids.
It is also effective for non-stainless metals, hollow needles and glass syringes.
However, the sterilization time is long compared with other methods, and items have
to cool slowly afterwards. Many pieces of equipment cannot withstand these high
temperatures for the allocated time.
Ethylene oxide
Ethylene oxide at ambient pressure and temperature vaporizes easily and thus has
good penetrative properties. It is also non-corrosive and has a wide spectrum of activity
against bacteria, spores, fungi, viruses and other living cells. Sterilization is usually
carried out at 2060C for 224 hours.
Ethylene oxide is most often used under three different conditions:
normal atmospheric pressure using undiluted ethylene oxide the gas is very
flammable, and so is often diluted to reduce explosion risk
ethylene oxide with a diluent gas such as nitrogen at a pressure of 2 bar
ethylene oxide diluted with carbon dioxide at a pressure of 6 bar.
This process should not be used if heat sterilization is possible. Organic material
has a marked protective effect and therefore prior cleaning is essential. Ventilatory or
respiratory equipment is contraindicated. Ethylene oxide does not penetrate plastic;
therefore items must be wrapped in sterilization paper.
Ethylene oxide is a highly effective sterilizing agent. In particular it is used to sterilize
single use medical items that would be damaged by the excessive heat used in other
sterilization methods. Disadvantages of ethylene oxide are that it is toxic and long
periods of aeration are required after sterilization therefore turn-around time is long.
The process is expensive and there are significant health and safety issues concerning
ethylene oxide and the equipment required to use it. Because of this, ethylene oxide is
not often used in hospitals but is commonly used by industry.
Low temperature steam and formaldehyde

This process uses a combination of dry saturated steam and formaldehyde, which
together kill vegetative bacteria, spores, fungi and most viruses. Objects are placed in
the sterilizer to allow maximum contact with the steam. Air is actively removed from the
container and replaced by dry saturated steam at 73C at subatmospheric pressure.
Formaldehyde is entrained as the steam enters the sterilizer.
The subatmospheric pressure may damage hollow objects. Formaldehyde may
be corrosive with certain materials and some fabrics may absorb formaldehyde. This
method cannot be used for items contaminated with body fluids, because the proteins
in the fluids congeal and produce hard fixed deposits.
Advantages of the process are that it can provide dry, packaged items in a sterile
form and the process is fully automated. Disadvantages are that the process is
complex and formaldehyde is toxic, irritant and possibly mutagenic. The equipment
required is also expensive, with the added problem of toxic waste products.
Irradiation
Irradiation uses rays or accelerated electrons. A dose greater than 25,000 Gray
produces sterility. Irradiation is often used to sterilize single use items on an industrial
scale. It has a broad spectrum of activity. Irradiation can cause significant degradation
of materials and is unsuitable for the resterilization of hospital equipment.
The advantages are that it is reliable on an industrial scale for heat-labile pieces of
equipment. However, irradiation can damage equipment particularly on re-exposure.
Monitoring the process and the required safety equipment is expensive.
Special circumstances
Recent work has identified that the prion strain causing bovine spongiform
encephalopathy (BSE) in cattle has infected humans, manifesting itself as a novel
human prion disease, new variant CreutzfeldtJakob disease (vCJD). The abnormal
prion protein is a new class of transmissible agent that demonstrates resistance to the
standard methods of sterilization used in hospital sterile services departments.
Affected individuals accumulate prion protein in lympho-reticular tissues (e.g.
appendix, tonsils), as well as in the CNS. The number of people incubating the disease
is unknown, and there are concerns that prions might be transmitted iatrogenically
via contamination of surgical instruments. Such risks remain unquantified, and there
have been no identified cases involving vCJD transmission via surgical instruments. All
neurosurgical instruments used on patients suspected of carrying vCJD are destroyed.
However, there are significant implications for the safety of surgical instruments in ENT
and other surgical practice.
The Spongiform Encephalopathy Advisory Committee (SEAC) has recommended
that, where feasible, the move to single use instruments is appropriate. From January
2001, the Department of Health requires tonsillectomy and adenoidectomy to be
performed using single use instruments in England and Wales. The recommendations
are that instruments used to dissect or cut lymphoid tissue are to be disposed of.
Anaesthetic equipment may also provide theoretical risk for prion disease transfer. This
risk is as yet unquantified and accepted practice is continuing to evolve. It is likely that,
in the near future, anaesthetic practice will change to incorporate disposable, single
patient use equipment wherever possible (e.g. disposable laryngoscope blades and
laryngeal mask airways).

Critical Incidents:
The Cardiovascular System
Joy E R Beamer
Jonathan Warwick
Joy E R Beamer is a locum Consultant Anaesthetist at the Horton Hospital, Banbury,

UK. She was recently awarded a CCST in Anaesthetics. She qualified from St
George's Hospital Medical School, London, and undertook a specialist registrar training
programme in the Oxford Region.

He qualified from Birmingham University Medical School and trained in anaesthesia
in the Royal Air Force. Further training as a Senior Registrar in the NHS was spent
in Oxford. He now specializes in anaesthesia for plastic surgery and head and neck
surgery.
Hypertension
Hypertension is a common critical incident during anaesthesia. Whether it is harmful

depends on its severity, cause and duration, and on the condition of the patient. These
factors also determine how actively it needs to be treated. Hypertension is difficult to
define because of observer and subject variation, and the arbitrary nature of cut-off
values, but definitions include:
elevation of blood pressure at least 15% above patients baseline
systolic blood pressure greater than 160 mm Hg and/or a diastolic blood pressure
greater than 95 mm Hg. Figure 1 lists the causes of hypertension during or persisting
after anaesthesia.
Causes of hypertension during or persisting after anaesthesia
Inadequate anaesthesia/analgesia
Tracheal intubation/extubation
Inadequate muscle relaxation
Pre-existing hypertensive disease
Hypoxaemia
Hypercapnia
Aortic clamping
Raised intracranial pressure, cerebral ischaemia or cerebrovascular accident
Drugs (e.g. ketamine, adrenaline (epinephrine))
Metabolic disorders (e.g. malignant hyperpyrexia, thyroid crisis,
phaeochromocytoma, carcinoid syndrome)
Postoperative urinary retention, pain, anxiety
Complications
Cardiovascular hypertension may precipitate myocardial ischaemia (especially
subendocardial), infarction or failure.
Neurological cerebral haemorrhage may result, especially in patients with
vascular malformations. Cerebral oedema or encephalopathy are less common
complications of uncontrolled hypertension.
Haemorrhage at the operation site or from pre-existing vascular malformations.
Renal severe hypertension may precipitate acute renal failure.
Management
Management of hypertension should be directed towards the underlying cause. The
usual cause is inadequate anaesthesia for the level of surgical stimulation being
employed and treatment requires an increase in the inhalational or intravenous
anaesthetic drug, or an increase in analgesia. Confirmation of the diagnosis may
require a trial of therapy. If the cause of the hypertension cannot be diagnosed
or removed, an appropriate antihypertensive drug may be used. The following are
examples of drugs commonly used.
Labetalol combined - and -blockade; dose 520 mg i.v. over 2 minutes with
increments up to 200 mg. Onset 530 minutes, duration 50 minutes.
Metoprolol 1 (cardioselective) blockade; 2 mg increments slow i.v., maximum dose
15 mg.
Esmolol rapid onset; short half-life of 9 minutes; 500 g/kg loading dose; 50200
g/kg/minute infusion.
Nifedipine calcium-channel blocker, sublingual or intranasal; onset 15 minutes
following a 10 mg dose.
Phentolamine -blockade; 0.52 mg i.v., repeated as necessary, rapid onset, short
half-life 1015 minutes.
Hydralazine direct-acting arteriolar dilator, peak action after about 20 minutes
following 1020 mg slow i.v. injection over 20 minutes. Onset occurs after 1520
minutes; duration is 26 hours.
Glyceryl trinitrate arterial and venous dilator; use 1 mg/ml solution i.v. (preferably
a central vein) via syringe driver, dose 10200 g/minute, maximum effect after 12
minutes.
Sodium nitroprusside arteriolar dilator; very rapid response, administered by
continuous intravenous infusion via a dedicated vein, 0.51.5 g/kg/minute. Direct
arterial blood pressure recording is mandatory. Doses greater than 4 g/kg/minute may
cause cyanide poisoning.
Hypotension
Mild-to-moderate falls in blood pressure are common during anaesthesia, but seldom
result in any harm to the patient. It is difficult to determine what is a dangerous level of
hypotension; it depends on the duration of hypotension and the patients preoperative
medical condition. Two signs of inadequate myocardial perfusion are the development
of ST segment depression and ectopic beats. Increased ventilationperfusion mismatch
secondary to pulmonary hypotension causes a fall in oxygen saturation (SpO2). In
awake patients receiving regional anaesthesia, nausea and dizziness are common
symptoms of excessive hypotension. The lower limit of cerebral, renal and hepatic
autoregulation occurs at a mean arterial pressure of about 60 mm Hg in otherwise
healthy individuals.
Causes
Anaesthesia
Volatile agents produce a dose-related fall in blood pressure (vasodilatation,
myocardial depression, impaired baroreceptor response).
Induction agents cause a dose-related fall in blood pressure owing to a
complex combination of effects involving myocardial depression, vasodilatation, altered
baroreceptor reflex and bradycardia (especially propofol).
Opioids may precipitate histamine release and vasodilatation. Larger doses are
associated with bradycardia.
Non-depolarizing muscle relaxants may produce hypotension secondary to
histamine release.
Positive-pressure ventilation increases intrathoracic pressure and produces a
decrease in venous return and cardiac output.
Spinal and epidural anaesthesia produce sympathetic blockade. This results in
vasodilatation, reducing venous return, cardiac output and systemic vascular resistance.
Although reflex vasoconstriction occurs above the level of the block, blood pressure
usually falls. Higher blocks (T4 or above) obtund the cardiac sympathetics, preventing
a compensatory tachycardia.
In obstetrics, aortocaval compression impairs venous return and in combination with
spinal and epidural anaesthesia may produce profound hypotension.
Hypovolaemia, regardless of aetiology, becomes less concealed following induction

of anaesthesia owing to impairment of compensatory mechanisms. Hypotension then
ensues. Hypovolaemia may occur in patients with:
trauma or burns
gastrointestinal disease (e.g. haematemesis, melaena, small bowel obstruction,
acute inflammatory bowel disease)
dehydration from poor fluid intake, vomiting or diarrhoea
metabolic disorders (e.g. diabetic ketoacidosis, diabetes insipidus, hypercalcaemia).
Surgical causes of hypotension include:

haemorrhage
head-up position
excessive intra-abdominal pressure during laparoscopic surgery may impair venous
return causing hypotension
release of aortic cross-clamping or lower limb tourniquets causes an acute fall in
systemic vascular resistance and blood pressure secondary to vasodilatation in the
ischaemic tissues.
Cardiovascular disease may lead to hypotension:

ischaemic heart disease with impaired cardiac contractility (including unstable
angina and recent myocardial infarction)
heart failure
valvular heart disease (mitral or aortic stenosis and regurg-itation)
dysrhythmias (fast atrial fibrillation, complete heart block)
hypertension, especially if poorly controlled
others (e.g. myocarditis, cardiomyopathy, constrictive pericarditis, myocardial
contusion, tamponade, aortic coarctation, congenital cardiac anomalies).
Cardiovascular medication such as -blockers, angiotensin-converting enzyme

(ACE) inhibitors, calcium antagonists, nitrates, 1-antagonists (prazosin) and centrally
acting 2-agonists (e.g. clonidine, methyldopa) may cause hypotension.
Autonomic neuropathy produces impaired baroreceptor response and may be

present in a variety of disease states:
diabetes mellitus (incidence and severity increase with the duration of the disease)
GuillainBarr syndrome
spinal cord injury and following cerebrovascular accident
Parkinsons disease
AIDS.
Other causes
Anaphylaxis may result in massive histamine-mediated vasodilatation, producing
Pulmonary embolus from deep vein thrombosis, or emboli from air, carbon dioxide
or fat may reduce cardiac output. Hypotension is accompanied by desaturation and a
fall in end-tidal carbon dioxide.
Management
Identify and remove the precipitating cause.
Increase fraction of oxygen in inspired air (FiO2) to maintain SpO2.
Position patient supine, possibly with the legs raised to improve venous return.
The head-down position is no longer recommended because it also raises cerebral
venous pressure and therefore cerebral perfusion pressure may not be improved.
Give a rapid intravenous infusion. The type and amount of fluid depends on
aetiology and patient factors. A useful guide is to infuse 10 ml/kg of colloid or 20 ml/kg
crystalloid initially and assess the response.
Vasopressors may be considered, particularly if the cause of hypovolaemia is non-
haemorrhagic (e.g. ephedrine, 36 mg i.v., metaraminol, 0.51.0 mg i.v., or phenylephrine,
0.51.0 mg i.v.).
Consider an infusion of a positive inotrope (e.g. adrenaline (epinephrine),
dobutamine) or vasoconstrictor (e.g. noradrenaline (norepinephrine)).
Massive haemorrhage
Bleeding is a significant cause of mortality and morbidity because of the loss of blood
volume and its constituents and also the effects of infusions of products aimed at
compensating for the loss. Massive blood transfusion can be defined as the transfusion
of blood, blood products and fluids equivalent to the circulating blood volume in any
24-hour period. The most profound physiological, haematological and biochemical
effects occur in those who have the most rapid loss and replacement therapy.
Causes of massive haemorrhage include:

trauma
major elective surgery such as orthopaedic or vascular surgery, especially rupture
or dissection of the aorta
during pregnancy and the puerperium (e.g. massive antepartum or post-partum
haemorrhage)
urgent operations and/or procedures in patients with abnormalities of haemostasis
or coagulation.
Management
Measuring blood loss: the quantity of blood lost can be estimated by a number of
methods.
Weighing swabs and measurement of blood aspirated into suction apparatus. With
major haemorrhage, these methods become less useful because a considerable
amount of blood is spilled on to the drapes and floor. In traumatized patients, major
blood loss may have occurred before arrival in hospital or may be concealed in the
chest or abdomen, or in the limbs and pelvis at the site of fractures.
Measuring packed cell volume. Blood lactate concentration gives an indication of the
adequacy of organ perfusion.
Clinical observation. The monitoring of cardiovascular variables such as heart
rate, arterial pressure, capillary return, central venous pressure, and in some cases
pulmonary capillary wedge pressure and cardiac output, allows a clinical impression of
the adequacy of volume resuscitation to be made.
Compensatory mechanisms initially maintain the blood supply to vital organs. Unless
adequate and appropriate corrective measures are taken, these mechanisms will
decompensate. With increasing volumes of blood loss, there is an increase in heart
rate, decrease in stroke volume, reduced pulse pressure, increased respiratory rate
and a reduction in cerebral blood flow leading to a reduction in conscious level. These
compensatory mechanisms are less efficacious in the elderly and very young and may
be impaired by disease or medication. Figure 2 shows the relationship between the
changes in vital signs and the volume loss from the circulation.
Relationship between the changes in vital signs and the volume loss from the circulation
Blood loss (ml)

750 7501500 15002000 2000
Loss as % of blood volume 15 1530 3040 40
Heart rate < 100 > 100 > 120 140
Blood pressure Normal Normal Decreased Decreased
Pulse pressure Normal Decreased Decreased Decreased
Capillary return Normal Slowed Slowed Slowed
Respiratory rate (breaths/minute) 1420 2030 > 30 35
Urine output (ml/hour) > 30 2030 515 Negligible
Mental status Normal Anxious Confused Drowsy
Suggested volume replacement Crystalloid Crystalloid/colloid Blood Blood
Active management: the rapid and effective restoration of an adequate circulating

blood volume is the primary responsibility of the anaesthetist during periods of heavy
blood loss.
Establish adequate venous access by siting at least two large-bore cannulae to
allow rapid fluid infusion. The most important pre-determinants of the flow rate of fluid are
the diameter of the cannula and the ability to apply a continuous pressure of 2300 mm
Hg via a pressurized infusion system. Crystalloids and synthetic colloids may be used
initially and should be followed by the administration of blood if bleeding continues.
Commence intravenous fluids internationally accepted practice is to use Hartmann's
solution as the initial resuscitation fluid for trauma and burns. The success of initial
resuscitation in an acutely hypovolaemic patient probably depends more on adequacy of
repletion than on which fluids are used. For a given blood volume expansion about twice the
volume of crystalloid compared with colloid is required. In practice, combined therapy using
both crystalloids and colloids is often used.
Fluids should be warmed a transfusion system should have the ability to
transfuse blood at fast flow rates (up to 500 ml/minute) and at temperatures greater
than 35C. Some systems use a constant-pressure infusion device combined with an
efficient blood warmer and a purpose-designed blood-warming coil (e.g. Level One).
Priming or flushing blood through the system after fluid containing calcium has been
used (such as Haemaccel) should be avoided, because this may cause blood clot
formation in the tubing by reversal of the anticoagulant effect of citrate.
Blood should be taken for grouping and cross-matching, for coagulation studies
and for biochemical analysis. Accurate identification of transfusion specimens and
of designated units of blood, platelets and fresh frozen plasma (FFP) is particularly
important in patients undergoing massive transfusion. It should be noted that most
incompatible blood transfusions occur in emergency situations. For operations where
significant blood loss is anticipated, replacement therapy should be available in
advance of surgery.
Red cell transfusions are given to increase the haemoglobin concentration and
thus improve or normalize the delivery of oxygen to the tissues. The haemoglobin
concentration at which blood transfusion is commenced depends to a certain extent
on the individual patient (e.g. elderly patients are at greater risk of complications from
anaemia). A haemoglobin value below 8.5 g/dl would be an indication to transfuse in
all apart from the younger fitter patient. A postoperative haemoglobin level of about 10
g/dl is widely accepted as a general guideline in adult surgical patients. However, it is
more appropriate to base transfusion decision on a clinical assessment of the patient.
If a major surgical procedure is planned, it may be possible to decrease the amount of
donor blood transfusions by using an automated cell saver system.
About 80% of patients who have massive haemorrhage develop diffuse ooze from
raw or cut surfaces. The causes are multifactorial but include relative hypothermia,
abnormal platelet function, dilution of clotting factors, consumption of factors and
enhanced fibrinolysis. It is critically important to monitor platelet numbers and the
coagulation process during major bleeding and its resuscitation. The platelet count
falls steadily with the transfusion of each successive unit of blood. Platelet infusion is
indicated if there is:
a platelet count less than 50 x 109 /litre and there is impending surgery or an invasive
procedure
diffuse microvascular bleeding and transfusion greater than one blood volume and a
platelet count of 50 x 109 /litre or less, or the result is unavailable
diffuse microvascular bleeding following cardiopulmonary bypass and the platelet
count is 100 x 109 /litre or less, or the result is unavailable
bleeding in a patient with a qualitative platelet defect, regardless of platelet count.
Moderate deficiency of coagulation factors is common in massively transfused
patients, but does not contribute to microvascular haemorrhage until levels fall below
20% of normal. These levels are reliably reflected by prolongation of the prothrombin
(PT) and activated partial thromboplastin times (aPTT) to values of more than 1.5 times
the control value. If the PT and aPTT are more than 1.5 times normal, 4 units of FFP
should be given. If PT and aPTT are prolonged and fibrinogen is less than 0.8 g/litre,
cryoprecipitate is indicated.
Arterial and central venous lines may be sited to allow rapid blood sampling, for
acidbase and potassium status, and the direct measurement of arterial and central
venous pressures. The central venous catheter also provides access for intermittent
bolus administration of drugs or drug infusions.
A urethral catheter should be passed unless contraindicated by pelvic or urethral
injury, and urine output monitored.
Core temperature should be measured continuously and every effort made to
prevent heat loss. Hypothermia causes platelet dysfunction, reduced metabolism of
citrate and lactate and an increased tendency to cardiac arrhythmias. This may result in
bleeding diathesis, hypocalcaemia, metabolic acidosis and cardiac arrest.
Arrhythmias
Arrhythmias are one of the most commonly reported critical incidents. About 12% of
patients undergoing anaesthesia develop arrhythmias; this increases to 30% in patients
with cardiovascular disease. Treatment may not be required; this depends on the nature
of the arrhythmia and its effect on cardiac output. Single supraventricular or ventricular
ectopic beats, and slow supraventricular rhythms, do not require treatment unless
cardiac output is compromised.
Management
Fluid, electrolyte and acidbase disturbances should be corrected preoperatively.
Particular attention should be paid to the level of potassium ions in the plasma
because they have a vital role in the generation of the resting membrane potential
and thus muscle and nerve function. Patients with hypokalaemia may be prone to
the development of supraventricular or ventricular extrasystoles and tachycardias.
ECG changes of hypokalaemia include a long PR interval, ST depression, T wave
flattening and a prominent U wave. Rapid treatment is indicated if arrhythmias are
present. Intravenous administration of potassium supplements should not exceed 0.5
mmol/kg/hour.
Continuous intraoperative ECG monitoring is essential. The ECG gives no indication
of cardiac output or tissue perfusion, therefore the detection of an abnormal cardiac
rhythm should be followed by clinical assessment of the circulation. An absent pulse,
severe hypotension or ventricular tachycardia or fibrillation should be treated as a
cardiac arrest.
Correcting the precipitating factor is often the only treatment required. Hypoxaemia
and inadequate anaesthesia or analgesia must be excluded. Factors associated with
the development of arrhythmias are listed in Figure 3.
Intervention with a specific antiarrhythmic agent or cardioversion is indicated if there
is:
a risk of developing ventricular tachycardia or fibrillation (e.g. frequent, multifocal
ectopic beats, or R on T complexes)
a significant decrease in cardiac output (causing dizziness or hypotension)
evidence of myocardial ischaemia (causing chest pain or ST segment changes).
Factors associated with the development of arrhythmias
Preoperative conditions
Ischaemic heart disease
Pre-existing arrhythmias
Hypertension
Valvular heart disease
Electrolyte disorders
Medications (theophylline, 2-agonists, tricyclic antidepressants)
Others (thyrotoxicosis, myocarditis, cardiomyopathies, trauma, drug and
solvent abuse)
Anaesthetic factors
Hypoxaemia
Hypo/hypercapnia
Hypo/hypertension
Laryngoscopy
Drugs (e.g. volatile anaesthetic agents, suxamethonium, central venous
pressure lines)
Surgical factors
Catecholamines
Exogenous (e.g. infiltrated adrenaline (epinephrine))
Endogenous (inadequate analgesia, inadequate anaesthesia)
Autonomic stimulation
Oculocardiac reflex
Laryngoscopy, bronchoscopy, oesophagoscopy
Carotid artery and thyroid surgery
Peritoneal and visceral traction
Peritoneal insufflation
Direct stimulation of the heart
Cardiac and thoracic surgery
Embolism
Thrombus, fat, air, carbon dioxide, amniotic fluid
Others
Limb reperfusion
Aortic cross-clamping
Bradycardia can be treated with an anticholinergic agent such as atropine, 0.6 mg i.v.,
or glycopyrrolate, 0.20.4 mg i.v. If the bradycardia is refractory to treatment, cardiac
pacing or an intravenous infusion of isoprenaline, 0.510 g/minute, may be indicated.
An anticholinergic drug may be given prophylactically if there is risk of bradycardia (e.g.
strabismus surgery or following a second dose of suxamethonium).
Sinus tachycardia associated with myocardial ischaemia may be controlled by

administration of a -blocker such as metoprolol, 2 mg increments slow i.v., maximum
dose 15 mg, or esmolol, 500 g/kg, loading dose followed by 50200 g/kg/minute
infusion.
Junctional rhythms are usually associated with the use of halothane. A reduction in
concentration and/or changing the volatile agent is indicated. An anticholinergic drug
may restore sinus rhythm.
Accelerated nodal rhythms may be precipitated by an increase in sympathetic tone

in the presence of sensitizing volatile agents. Treatment includes adjusting the depth of
anaesthesia and/or changing the anaesthetic agent.
Supraventricular tachycardia (SVT) can occur in susceptible patients, such as Wolff

ParkinsonWhite or other pre-excitation syndromes. Treatment of SVT consists of:
carotid sinus massage
adenosine, 312 g i.v.
DC cardioversion if haemodynamic decompensation is present
if there is no decompensation give verapamil, 510 mg slow i.v. over 30 seconds; the
injection should stop when the SVT is controlled
in sepsis-related or refractory SVT, volume loading plus amiodarone, 300 mg i.v. by
infusion over 20 minutes, then 900 mg over 24 hours
if the patient is thyrotoxic a -blocker is useful.
Atrial fibrillation or flutter is often seen as a paroxysmal increase in the ventricular

rate in patients with pre-existing atrial fibrillation or flutter. Having corrected any
precipitating factors, the therapeutic options include:
digoxin, 10 g/kg by slow i.v. injection over 20 minutes, repeat after 4 hours
according to response, maintenance dose 125500 g/day. Peak effect after 2 hours.
Slows the ventricular rate and is a positive inotrope
amiodarone produces a more rapid ventricular response and may re-establish sinus
rhythm, give 300 mg i.v. by infusion over 20 minutes, then 900 mg over 24 hours
-blockers, especially in thyrotoxicosis, in combination with digoxin (e.g. propranolol
1 mg slow i.v. repeated every 2 minutes, maximum 5 mg)
cardioversion is an option if the ventricular rate is fast with a clinically reduced
cardiac output.
Premature ventricular contractions are common in healthy patients. Perioperatively
they seldom progress to more serious arrhythmias unless there is underlying
hypoxaemia or myocardial ischaemia. An underlying cause should be sought
before antiarrhythmic agents are considered. If associated with a slow atrial rate,
increasing the sinus rate with an anticholinergic drug will abolish them. Halothane
lowers the threshold for catecholamine-induced ventricular arrhythmias; this is
exacerbated by hypercapnia. Halothane should be used with care in patients receiving
sympathomimetic drugs (including local anaesthetics containing adrenaline), and in
patients taking tricyclic antidepressants and aminophylline.
Ventricular tachycardia and fibrillation should be treated as a cardiac arrest.
Malignant hyperthermia
Malignant hyperthermia is a rare inherited complication of general anaesthesia

triggered by inhalational agents or suxamethonium in susceptible patients. The
inheritance is complex and it is a genetically heterogeneous condition. These patients
have a defect in intracellular calcium binding within the sarcoplasmic reticulum of
skeletal muscle cells. Calcium ions are released on exposure to trigger agents,
which initiates widespread skeletal muscle contraction and generalized membrane
permeability. There is severe metabolic disturbance and catabolism runs unchecked,
because raised levels of myoplasmic calcium ions result in increased production
of pyruvate and heat. A successful outcome relies on making an early diagnosis,
discontinuation of trigger agents, prompt treatment with intravenous dantrolene and
supportive care. The mortality today has decreased to about 25% owing to increased
awareness, monitoring and prompt treatment. The mode of presentation is variable and
a high index of suspicion is required for early diagnosis.
Signs of malignant hyperthermia include:

unusual muscle rigidity following suxamethonium (especially masseter spasm)
unexplained tachycardia and arrhythmias
rise in end-tidal carbon dioxide
metabolic acidosis
fall in oxygen saturation
hyperkalaemia
rise in core temperature (about 12C/hour)
evidence of a coagulation disorder, oozing from wound sites.
Management
Immediate actions
Discontinue inhalational agents and inform the surgeons. Stop surgery if feasible,
make the operating site safe and close wounds.
Continue sedation or anaesthesia with a total intravenous technique. Hyperventilate
with 100% oxygen using a clean breathing system. Change the circle system using
fresh soda-lime, or use a non-rebreathing system.
Immediately instruct staff to prepare dantrolene and commence as soon as available
in an intravenous infusion of 1 mg/kg repeated at 10 minute intervals up to 10 mg/kg.
Remove drapes, fully expose the patient and promote surface cooling with
avoidance of vasoconstriction.
Insert an arterial line to aid monitoring, and allow regular estimation of arterial blood
gases, potassium and creatine kinase.
Monitor the patients core temperature.
Intermediate actions
Control life-threatening dysrhythmias (e.g. -blockers).
Control hyperkalaemia with intravenous glucose or insulin.
Control metabolic acidosis by hyperventilation, consider sodium bicarbonate (24
mmol/kg) if acidosis is severe (e.g. pH < 7.0).
Later actions
Send blood for clotting screen (PT, aPTT, fibrinogen).
Catheterize the patient. Test their urine for myoglobin. Collect samples for
vanillylmandelic acid estimation to exclude phaeochromocytoma. Promote diuresis with
intravenous fluids and mannitol, 0.5 g/kg over 20 minutes.
Request a chest radiograph. Send blood for full blood count, biochemistry and
thyroid function tests.
Notify the intensive care unit.
Repeat the creatine kinase estimation in 24 hours.
Consider other diagnoses such as recreational drug ingestion (e.g. Ecstasy),
neuroleptic malignant syndrome or myopathy.
Future care
The patient and their family should be counselled as to the likely diagnosis and
the implications for future anaesthetics. Wearing a Medic-Alert bracelet should
be encouraged. The patient and immediate family should be referred for further
investigation and muscle biopsy to:
UK MH Investigation Unit, Academic Unit of Anaesthesia
Clinical Sciences Building
St Jamess University Hospital Trust
Leeds LS9 7TS
Tel: 0113 206 5274
Emergency hotline: 07947 609601
Future anaesthetic care can be provided safely with the avoidance of trigger agents
the volatile anaesthetics and depolarizing muscle relaxants. Prophylactic dantrolene
is not recommended. Phenothiazines, antidepressants and haloperidol have been
suggested as possible trigger agents, because of the similarity between malignant
hyperthermia and the neuroleptic malignant syndrome, but this is unlikely. All other
anaesthetic drugs appear to be safe.

Critical Incidents:
The Respiratory System
Orlando J Warner
Jonathan Warwick
Orlando J Warner is Specialist Registrar in Anaesthetics at the Oxford Radcliffe

NHS Trust Hospital, Oxford, UK. He qualified from the Royal London Hospital Medical
School. For the past 2 years he has been the Advanced Trainee in Neuroanaesthesia
at the Department of Neuro-surgical Critical Care and Anaesthetics, Radcliffe Infirmary,
Oxford.

surgery.
A critical incident during anaesthesia is any event that may result in actual or potential
harm to the patient if uncorrected. It may cause severe morbidity or even mortality. It
is often preventable by a change in practice. Incident reporting is the key to preventing
future disaster. There is observer bias concerning which incidents are recorded, and the
problem for anaesthetists is to distinguish between a critical incident and the normal
course of clinical practice.
This contribution deals with life-threatening problems in the management of the
respiratory system including the clinical and physiological presentation of some
commonly encountered critical incidents and their treatment. All may be a cause
of alarming cyanosis under anaesthesia. Not all the problems discussed can be
prevented and so some may not meet the precise definition of critical incidents. The
recommendations aim to provide the anaesthetist with fast and effective solutions that
may be used in clinical, examination or simulation situations. In all cases, the trainee
anaesthetist must request senior help at the earliest opportunity.
Aetiology
The 2000 report of the National Confidential Enquiry into Perioperative Deaths
(NCEPOD) cites hypotension, hypoxaemia, arrhythmia and cardiac arrest as the most
common critical events that occur during or immediately following surgery. It also
concludes that modern anaesthetic equipment, when properly checked, is very reliable.
Human factors often play a major role in the aetiology of adverse events (Figure 1).
Factors involved in avoidable deaths
Error of judgement
Error of clinical expertise
Lack of experience
Lack of assistance
Lack of equipment
Equipment failure
Preparation is an important factor in predicting and treating these events and should
involve:
thorough preoperative patient assessment
check of all anaesthetic equipment
appropriate selection of drugs
appropriate level of clinical expertise.
The Association of Anaesthetists of Great Britain and Ireland (AAGBI) has recently
published new recommendations for standards of monitoring during anaesthesia
and recovery. The Royal College of Anaesthetists (RCA) has a web page (http:
//www.rcoa.ac.uk/critincident/ciweb.html) that deals with the processing of critical
incidents. The RCA is committed to setting up a national database so that even rare
incidents can be reported and acted on. Critical incidents should be discussed locally at
regular departmental audit meetings to complement the process of clinical governance.
Respiratory obstruction and increased peak airway pressure
Obstruction to the airway is an immediate threat to life and is the most common
critical incident registered. The airway can be considered as the conducting pathway
responsible for the delivery of oxygen from anaesthetic machine to the alveolar/
blood interface. Thus, obstruction may occur from outside or within the patient. The
anaesthetic machine, breathing system and connections must be checked to ensure
their patency and correct function before anaesthesia.
Obstruction of the airway within the patient may arise from the upper, supraglottic
region, to the lower bronchiolar region. It may be caused by the devices used during
anaesthesia or result from airway anatomy, pathology or trauma. Figure 2 shows some
of the likely causes of airway obstruction in the perioperative period.
Possible causes of airway obstruction
Supraglottic
Tongue
Periglottic abscess, tumour, haematoma
Regurgitation of solid material
Blood or secretions
Laryngeal mask airway (LMA) or tracheal tube luminal occlusion or misplacement
Laryngeal
Laryngospasm
Tumour or oedema
Post-thyroidectomy (laryngeal nerve injury)
LMA or tracheal tube luminal occlusion or misplacement
Tracheal or bronchial
Aspiration
Asthma
Anaphylaxis
Pneumothorax
Pulmonary oedema
Tracheal obstruction by retrosternal goitre
Respiratory obstruction during induction of anaesthesia
Preoperative evaluation of the airway is vital and should include mouth opening,
dentition, Mallampati score, jaw movement, thyromental distance and neck movement.
The aim is to predict which patients may present difficulty with direct laryngoscopy and
intubation and those in whom difficulty may arise with airway maintenance following
loss of consciousness, such as those with:
obesity or a bull neck
limited mouth opening (e.g. trismus, following infection, trauma)
restricted head and neck movement (e.g. severe ankylosing spondylitis, rheumatoid
arthritis)
stridor resulting from tumour, trauma, infection or haem-atoma
upper airway soft tissue swelling (e.g. burns, pre-eclampsia). About 10% of reported
critical incidents occur in the anaesthetic room. Patient monitoring during induction of
anaesthesia should follow the guidelines established by the AAGBI. The patient must
be monitored adequately during this stage of anaesthesia. If the required equipment is
unavailable, induction should take place in the operating theatre.
Induction of anaesthesia in patients with upper airway obstruction requires
specialized expertise. Management must involve a clear plan of how to proceed in the
event of total airway obstruction during induction. These patients are best managed
in the operating theatre with surgeons gowned and ready to perform immediate
tracheostomy under local anaesthesia if necessary.
In routine practice, airway obstruction that occurs following induction is apparent
from:
paradoxical (see-saw) chest movement (when breathing spontaneously)
noisy airway
absent or diminished movement of the reservoir bag
absent or diminished capnograph trace
increased airway pressure (when mechanically ventilated)
progressive oxygen desaturation.
Simple airway manoeuvres such as chin lift and jaw thrust, often combined with
the insertion of a correctly sized oropharyngeal or nasal airway are necessary to
maintain airway patency following induction. In apnoeic patients or those requiring
assisted ventilation, bag and mask ventilation by two operators is more effective than
that provided by one operator (Figure 3), allowing more effective face mask application
and upper airway management. Manual ventilation with bag and mask is then easier to
perform. If management is difficult, it is important to switch to 100% oxygen and call for
senior help early on.
If airway obstruction persists, a laryngeal mask airway (LMA) often corrects the
situation. While tracheal intubation provides a definitive airway, it may be difficult to
insert in a patient who has not received muscle relaxants. Neuromuscular blockade
should never be administered unless airway patency can be assured. However, if
airway maintenance is lost following the administration of muscle relaxants then swift
direct laryngoscopy and tracheal intubation should be attempted. Some patients
(e.g. those with adenotonsillar hypertrophy, the obese or heavy snorers) are often
easy to intubate despite having a difficult airway to maintain with bag and mask. The
LMA is also the technique of choice following a failed intubation if subsequent airway
management is difficult. Numerous reports testify to the ability of the LMA to provide a
clear airway following a failed intubation. The Combitube may also be useful, though it
is less commonly used in the UK. Both are supraglottic airway devices, therefore it is
unlikely that the Combitube will provide a clear airway if the LMA does not.
Cant intubate, cant ventilate (CICV)
The inability to intubate or ventilate a patient is rare, with an estimated incidence of

1/10,000 anaesthetics. It occurs when alveolar ventilation cannot be maintained despite
best attempts at intubation and bag-mask ventilation (Figure 4).
Analysis of closed-claims in the USA revealed that the most common predisposing
factor in the development of CICV was repeated and continued attempts at intubation.
With each successive period of re-oxygenation between intubation attempts, bag-mask
ventilation became increasingly difficult as laryngeal oedema evolved. The anaesthetist
should limit intubation attempts to a maximum of three. The decision must be made
early to abandon further attempts at intubation and the anaesthetist must use an
alternative airway device, or wake the patient. The main causes of CICV are:
repeated failed attempts at intubation
airway or neck trauma
burns to the head and neck
pregnancy (especially pre-eclampsia)
tumour (e.g. larynx)
infection.
Requirements for optimum best attempts

Optimum best bag-mask ventilation
Correctly sized oral or nasal airway
Two-operator technique
Optimum best laryngoscopy
Trained anaesthetist (3 years' training)
Optimal intubating position
Optimal external laryngeal manipulation
Optimal laryngoscope
4
The optimal intubating position is shown in Figure 5. Flexion of the cervical spine, and
extension of the head at the atlanto-occipital joint, aligns the glottis with the visual axis.
In the obese or pregnant woman at term, this may require at least one pillow under
the shoulders and two pillows beneath the head and neck. Anaesthetic induction and
tracheal intubation should be avoided when patient positioning is not ideal.
Optimum

intubating
position
The larynx should be manipulated from the front of the neck by the operators free hand
to help provide the best view. This position is maintained by the anaesthetic assistant
while intubation is performed. Optimum external laryngeal manipulation does not mean
cricoid pressure, which may further distort the view and make direct laryngoscopy
more difficult. Optimum manipulation involves direct manipulation of the thyroid
cartilage of the larynx. The application of backwards, upwards and rightwards pressure
aligns the laryngeal inlet more closely with the visual axis. Correct optimum external
laryngeal manipulation is shown in Figure 6.
Aligning the laryngeal inlet with the visual axis

The choice of laryngoscope blade is important. A useful guideline is to change the

length of blade once, and the type of blade once, to achieve the best view. A variety
of blades is available in clinical practice. The standard Macintosh blade (size 3) may
need to be changed to a longer blade (size 4) or to a levering blade such as the McCoy.
The McCoy blade can be successful in improving the laryngoscopic view by one
grade (Cormack and Lehane grade 3 to 2). The Belscope blade has a 45 angle and a
detachable prism, and may similarly improve a grade 3 view. The Polio blade is inclined
at an angle greater than 90 to the handle, which may aid insertion into the mouth
(Figure 7).
7 Laryngoscope blades:
a Macintosh size 4;
b Macintosh size 3;
c McCoy size 4;
d McCoy size 3;
e Belscope;
f Polio;
g straight blade (Seward);
h left-hand Macintosh,
i Huffman prism.
If a CICV situation occurs, an LMA should be inserted immediately. There are many
reports describing the successful use of the LMA in this situation but no controlled
clinical studies. The type of LMA used is probably unimportant. A 2 cm mouth opening
is required to insert an intubating LMA.
Failure of the LMA to enable ventilation and oxygenation means that emergency
tracheal access is necessary. There must be no delay because the situation is critical
in a patient with marked hypoxia. Tracheal access is best achieved via the cricothyroid
membrane by needle puncture, percutaneous cricothyrotomy or surgical cricothyrotomy.
The precise technique depends on: the equipment available; the experience of the
anaesthetist; and the nature of the emergency.
It is impossible to give firm recommendations but whatever the means used,
the immediate aim is to achieve oxygen delivery to the trachea (and alveoli) via the
cricothyroid membrane. This membrane lies subcutaneously between the cricoid and
thyroid cartilages of the larynx and in the adult measures 1 x 3 cm. It will accept a
tracheal tube of maximum size 7.0 internal diameter (ID). Paired cricothyroid arteries
arise from the superior border and pass laterally. The patients head and neck should
be extended to bring the cricothyroid membrane closer to the skin surface to facilitate
access. Placing a sandbag or 1 litre fluid bottle between the patients scapulae may
help to achieve this.
Needle cricothyrotomy is minimally invasive but requires a jet ventilator to achieve

satisfactory alveolar ventilation. A cannula is inserted via the cricothyroid membrane
(Figure 8), free aspiration of air confirms correct placement. Resistance through the
cannula is too high to enable conventional bag ventilation. Simple emergency systems
can be constructed using green oxygen tubing connected to a flowmeter (e.g. 10-15
litres/minute). A side hole or three-way tap allows for intermittent insufflation by finger
occlusion of the hole. The green oxygen tubing is inserted into the barrel of a 2 ml
syringe which then allows connection to the cannula. The free end is connected to
an oxygen flowmeter or to the anaesthetic machine via a 15 mm connector. Oxygen
insufflation techniques provide tracheal oxygen delivery but not satisfactory carbon
dioxide elimination. It is recommended that all sites where anaesthesia is administered
have access to a jet ventilator. The inspiratory time of about 1 second should be
followed by a 3 second expiratory time. It is unlikely that airway obstruction is absolute
and passive exhalation will occur via the glottis. If this is deemed inadequate a second
cannula should be placed to allow exhalation and prevent overinflation and barotrauma.
A needle cricothyrotomy is a temporary measure and preparations should be made for
a formal tracheostomy.
Specific cricothyroid cannulae are available for emergency tracheal access (Figure
9). The Ravussin 13 G jet ventilation catheter (VBM Medical) is flanged to simplify
fixation, and has both Luer-lock and 15 mm connections. The Cook 6 F emergency
transtracheal catheter is spiral reinforced and kink-resistant; a standard 14 G
intravenous catheter is easily kinked and difficult to fix. The main complication of the
technique is incorrect needle position and subcutaneous/mediastinal emphysema.
9 Cricothyrotomy needles.
a 13 G Ravussin jet ventilation
catheter (VBM Medical);
b 6 F Cook emergency transtracheal
catheter;
c 14 G Venflon cannula.
Percutaneous cricothyrotomy allows emergency placement of a tracheal tube to

allow more conventional ventilation via bag and mask. Several commercial kits are
available, which differ in insertion technique (Seldinger or non-Seldinger), size of tube
(3.5-6.0 ID), and time taken for tube placement. There are insufficient data to make
recommendations concerning the optimum technique and the anaesthetist should be
familiar with the equipment available in their hospital. A non-Seldinger kit (e.g. VBM
Quicktrack, 4.0 mm ID) generally allows the most rapid access by direct cricothyroid
puncture using a large diameter sharpened stylet. A Seldinger technique (e.g. Cook
Melker kit 3.5-6.0 mm ID) may be safer to perform but requires several stages including
the use of a dilator. All techniques require familiarization. Complications include
bleeding, malposition and subcutaneous emphysema.
Surgical cricothyrotomy rapidly provides a definitive airway, though it requires more

surgical experience and bleeding is likely to be considerable. It is ideally suited to the
emergency trauma setting in the presence of severe maxillofacial, neck or laryngeal
injury. Thorough training is necessary for this seldom performed but life-saving
procedure. Practising on the sheeps larynx provides a realistic training model.
With finger and thumb either side, the cricothyroid membrane should be stabilized.
A 22 scalpel blade is used to make a 2 cm vertical skin incision to part the skin.
The scalpel should then be horizontally inserted into the cricothyroid membrane,
perpendicular to the skin. This incision should be enlarged laterally. The scalpel handle
should be inserted through the cricothyroid incision and rotated through 90, then
removed. A well-lubricated size 7.0 ID cuffed tracheostomy tube should be inserted.
The main complications are bleeding and malposition.
Respiratory obstruction during the intraoperative period
If respiratory obstruction occurs during surgery, the following procedure will help to
diagnose the cause of obstruction (Figure 2) and guide appropriate action to correct the
situation. Surgery can then recommence.
100% oxygen should be commenced.
The surgeons should be alerted to the problem and advised to stop surgery. The
surgical stimulation may have caused the obstruction. Procedures such as dilation of
the cervix or anus may precipitate severe stridor especially if anaesthesia is light.
The anaesthetic delivery circuit should be checked rapidly.
If it is patent, the obstruction must be within the patient.
Access to the airway may be difficult, especially in head and neck surgery. Extreme
circumstances of continued patient deterioration require the complete uncovering of
surgical drapes and exposure of the airway.
The upper airway should be checked for secretions, signs of regurgitation or obvious
tube or LMA obstruction. The mouth and trachea should be suctioned if indicated.
The capnograph confirms alveolar ventilation by displaying a carbon dioxide trace.
Absence of a trace is a sign of complete airways obstruction. The normal capnograph
trace may change in airways obstruction with a characteristic marked upslope to the
alveolar plateau.
The urgency of the situation is indicated by the oxygen saturation. If there is any
doubt about the tracheal tube position, immediate replacement is needed. An LMA will
need repositioning or changing to a tracheal tube. Careful observation of the chest wall
during manual ventilation may show unilateral or little chest movement. Auscultation of
the chest may detect unilateral air entry, wheeze or absent breath sounds. Withdrawing
the tracheal tube slightly may alleviate this if the distal end has migrated to the
endobronchial position, or is in contact with the carina.
Fibre-optic bronchoscopy will confirm the position of the tracheal tube and that
there is no intraluminal obstruction such as a sputum plug, blood clot or in rare
circumstances, an endoluminal tumour.
Bronchospasm during anaesthesia
Bronchospasm is reversible airways obstruction most commonly associated with

patients who have asthma or chronic chest disease. The incidence of asthma is 5-
10% with a higher prevalence in children. Smokers and patients with upper respiratory
tract infection are also at increased risk of bronchospasm. Bronchospasm occurs as
a result of smooth muscle constriction within the respiratory subepithelial layers in
the bronchioles. It may be accompanied by other pathological effects (e.g. mucosal
oedema, cellular infiltrates, mucus secretion, desquamation of surface epithelial cells,
goblet cell hyperplasia) which exacerbate smooth muscle contraction. Contraction
is stimulated by neural or paracrine effects. Chemical mediators such as histamine
and products of arachidonic acid, the leukotrienes, may act locally to initiate
bronchoconstriction.
Bronchospasm is not the only cause of intraoperative wheeze (Figure 10). Luminal
occlusion from eccentrically inflated tube cuffs (cuff herniation) used to occur with red
rubber tracheal tubes, but modern disposable materials have made this complication
less common, however the tracheal tube cuff should not be over-distended. The
old adage if in doubt take it out remains true. A monophonic wheeze developing
immediately after intubation may indicate tube occlusion, or a distal position next to the
carina or within a bronchus.
Bronchospasm is suggested by:
increased respiratory effort, tachypnoea and intercostal recession (if spontaneously
breathing)
expiratory wheeze (wheeze throughout the respiratory cycle may indicate
obstruction within the breathing equipment)
rise in inspiratory airway pressure (if mechanically ventilated). Management of
wheeze while under anaesthesia is as follows.
The surgeons should be alerted and asked to stop surgery.
100% oxygen should be delivered and anaesthesia deepened. Bronchospasm may
result from a depth of anaesthesia that is too light for the degree of surgical stimulation.
This includes stimulation of the airway by the anaesthetist. All modern inhalational
agents are bronchodilators.
The breath sounds over both lung fields and over the stomach should be listened to.
Capnography confirms tracheal intubation. Tracheal tube position should be adjusted if
necessary. Signs of pulmonary oedema or tension pneumothorax should be sought.
The position of the tracheal tube should be adjusted if necessary.
The airway should be checked and the trachea should be suctioned looking for signs
of aspiration.
Full monitoring should be in place. Extreme tachycardia and cardiovascular collapse
suggest anaphylaxis.
The treatment of bronchospasm includes the following.
The inspired concentration of volatile anaesthetic agent should be increased.
The patient should be treated with continuous inhaled salbutamol nebulizers, 5
mg, and ipratropium, 500 g, until the wheeze settles. This is best delivered using a
separate oxygen cylinder with nebulizer attachment, connected to the tracheal tube on
the patient side of any heat/moisture exchange filter.
If wheeze persists, aminophylline, 250500 mg (5 mg/kg) i.v.in 500 ml normal saline
over 20 minutes can be given (if notalready treated with theophylline or aminophylline
preparations); continue with an infusion of 0.5 mg/kg/hour if needed.
If bronchospasm is severe, salbutamol, 250 g bolus i.v. over 510 minutes may be
given, and continued as an infusion of 5 g/minute, adjusted according to the heart rate
and bronchospasm response.
It may be necessary to adjust ventilator settings. A longer expiratory time may be
needed to allow more complete exhalation, though a short inspiratory time will produce
higher peak inspiratory pressures. An I:E ratio of 1:2 or 1:1.5 is usual.
Hydrocortisone, 200 mg i.v., is not immediately effective but provides bronchospasm
relief within 612 hours.
Management of anaphylaxis will be covered in CLINICAL ANAESTHESIA.
Causes of intraoperative wheeze
Endobronchial intubation
Mechanical obstruction of the tracheal tube
Bronchospasm
Anaphylaxis
Pulmonary oedema
Tension pneumothorax
Aspiration of gastric contents
10
Failure to breathe
A delay in the return of spontaneous respiration following anaesthesia is most

commonly the result of an imbalance between the:
patient requirements of anaesthesia and analgesia (differences caused by normal
variation and the effects of coadministered drugs or disease)
doses of drugs used
timing of their administration.
In all patients, maintain ventilation to ensure satisfactory oxygenation and carbon
dioxide removal. The patient is likely to be unconscious and usually all that is required
is more time. If there is continued apnoea, inconsistent with the clinical picture, then a
careful evaluation of the cause is needed. The patient should be reassured if they are
conscious.
Assess neuromuscular block a train-of-four ratio of 75% is usually adequate
for satisfactory ventilation following anaesthesia. The presence of four good twitches
with absent fade implies adequate reversal. Modern nerve stimulators (e.g. the train-
of-four watch) can provide more accurate assessment of neuromuscular function by
measurement of thumb acceleration (and thus force, because the mass of the thumb is
constant). The standard 1 ml ampoule of glycopyrrolate, 0.5 mg/neostigmine 2.5 mg, is
the correct reversal dose for a 50 kg patient. The ability to sustain a 5-second head lift
from the pillow is a useful clinical indicator of neuromuscular recovery. Figure 11 shows
factors that prolong the action of a non-depolarizing neuromuscular block.
Factors that may increase duration of non-depolarizing neuromuscular

block
Hypokalaemia
Hypothermia
Hypocarbia
Neuromuscular disease (e.g. myasthenia gravis, Eaton-Lambert syndrome)
Inhalational anaesthetic agents
Aminoglycosides
Calcium antagonists
Magnesium
Local anaesthetics
Lithium
Frusemide
11
Partial reversal of neuromuscular block presents as respiratory inadequacy together

with jerky, uncoordinated gross muscular movement. Laryngeal muscle weakness can
produce airway obstruction and stridor. The best treatment is to:
reassure the patient (they may be distressed and feel unable to breathe, with
tachycardia and hypertension) and administer 100% oxygen
help allay anxiety by giving midazolam, 2 mg i.v. or reintroduce general anaesthesia
for a short period of time
correct any underlying cause
administer further neostigmine (with glycopyrrolate) to a total of 70 g/kg i.v.
(maximum dose 5 mg) if necessary.
Plasma cholinesterase activity if suxamethonium (or mivacurium) has been
used and return of adequate neuro-muscular function is delayed, it is likely that
plasma cholin-esterase activity is decreased. This may be an inherited abnormality
of cholinesterase activity or an acquired reduction in enzyme activity (Figure 12).
The genetic variants have autosomal dominant inheritance, and the prevalence of
homozygotes for the atypical gene is 1:2500 of the Caucasian population. Only
homozygotes display significantly prolonged apnoea. This may produce many hours of
continued paralysis. The patient will come to no harm providing ventilation is supported
and adequate sedation is continued (e.g. propofol, 46 mg/kg/hour). Neuromuscular
block should be monitored with a nerve stimulator and eventually wears off. Infusion
of fresh frozen plasma containing cholinesterase enzyme speeds recovery of neuro-
muscular function. The benefits must be balanced against the cost and infection risk.
Acquired conditions (Figure 12) that reduce plasma cholinesterase activity may slightly
increase suxamethonium duration.
Factors that may cause decreased plasma cholinesterase activity
Congenital
Autosomal dominant inheritance of abnormal enzyme Four alleles have been
identified: E1n normal, E1a atypical, E1f fluoride-resistant, E1s silent
Acquired
Infections
Malignancy
Chronic disease
Liver disease
Renal failure
Pregnancy, oral contraceptives
Hypothyroidism
Drugs (monoamine oxidase inhibitors, ecothiopate eye drops,
organophosphorus compounds, chemotherapy)
12
Doxapram is a central respiratory stimulant that may reverse the respiratory

depression caused by general anaesthetic agents and potent analgesics. It does not
reverse the other effects of opioids. It acts by direct stimulation on the carotid body
chemoreceptors. A maximum dose of 1.5 mg/kg slow i.v. can be given.
Benzodiazepines flumazenil can be used to reverse the central sedative effects
of benzodiazepines. It has a shorter half-life than midazolam and diazepam, and
therefore re-sedation is possible. Flumazenil, 200 g i.v., should be given followed
by 100 g i.v. every minute as necessary. The maximum total dose is 1 mg. While
benzodiazepines may contribute to postoperative sedation, they seldom cause apnoea
unless large doses are used or the patient is elderly and frail.
Opioid drugs if excessive narcotic is suspected, then give naloxone by titrating
dose to effect. Dilute 400 g in 10 ml normal saline and give 12 ml every few minutes
to achieve the desired effect. It is important not to use excessive naloxone to prevent
reversal of the analgesic effect. Pain, hypertension and tachycardia may result. The
patient must be observed closely for the next 46 hours because the duration of the
naloxone effect may be shorter than that of the opioid.
Check end tidal carbon dioxide tension (PE'CO2 ) hyperventilation during
anaesthesia results in reduced respiratory drive. Spontaneous ventilation is unlikely to
occur until the partial pressure of carbon dioxide in arterial blood (PaCO2) and PE'CO2
have normalized. The addition of 5% carbon dioxide to the inspiratory gas mixture was
common in older anaesthetic practice to stimulate respiratory drive. Hazards associated
with carbon dioxide use, in particular the inadvertent use of carbon dioxide from
incorrect flowmeter settings, have removed the use of this gas from modern practice.
The PE'CO2 should be allowed to rise by itself by either reducing minute volume, or
adding dead space into the breathing system (e.g. disconnection of the absorber from a
circle system).
Body temperature hypothermia delays recovery from anaesthesia, prolongs
the duration of neuromuscular blockade and is an important cause of postoperative
hypoventilation. The fall in core temperature that occurs with anaesthesia should
be anticipated and minimized using passive or active rewarming (see Anaesthesia
and Intensive Care Medicine 1:3: 122). Continued ventilation in the recovery area
or ICU may be required until rewarming is completed and spontaneous ventilation is
satisfactory.
Neurological vital signs an intracranial bleed during surgery is a rare cause of
continued unconsciousness and apnoea. It may occur as a result of an undetected
head injury in patients undergoing surgery for trauma, or coincidentally in patients with
cerebrovascular disease. A CT scan is required for diagnosis.
Investigations in the patient who fails to breathe following anaesthesia should
include:
blood gases, electrolytes and glucose
body temperature
neuromuscular function (nerve stimulator)
ECG and chest radiograph
CT head scan
blood for serum cholinesterase activity if indicated.
Air embolism
If bubbles of gas enter the circulation, they may accumulate in the right ventricle.
Unlike liquid, gases are compressible, and therefore adequate ejection of blood is not
achieved, reducing stroke volume and cardiac output. This can present clinically as
a minor fall in blood pressure, hypoxaemia or complete cardiovascular collapse with
electromechanical dissociation. If a patent foramen ovale is present, or any other shunt-
causing communication between the right and left sides of the heart, the air could enter
the systemic circulation and cause neurological injury or coronary artery embolism and
infarction (paradoxical air embolism). The effects of air embolism depend on the:
volume of air entrained
rate at which it enters the circulation
general condition of the patient.
Experiments in dogs suggest that volumes greater than 20 mlare potentially fatal.
Some operations carry an increased risk of air embolus (Figure 13). Air may be
entrained into an open vein when the venous pressure is subatmospheric. Air embolism
occurs in 2550% of all craniotomy operations in the sitting position and the incidence
has reduced now this position is seldom used. The prone position with head tongs
appears to be safer for posterior fossa surgery.
Procedures with increased risk of air embolus
Posterior cranial fossa neurosurgery (especially in the sitting position)

Lumbar laminectomy and head and neck surgery when the vertebral column
is positioned above the level of the heart
Hepatic surgery that carries a risk of opening the inferior vena cava
Any patient with a central venous pressure catheter in situ that may result in
accidental entrainment of air
Varicose vein ligation
Surgery combined with low venous pressures (e.g. in children)
13
Signs that alert the anaesthetist to the development of air embolism are usually
detected by monitoring. Early diagnosis allows prompt institution of preventive
measures before the situation becomes critical. The signs of air embolus include:
sudden fall in PECO2 despite unchanged ventilatory settings (if breathing
spontaneously the patient may develop respiratory distress)
turbulent blood flow (monitored by precordial Doppler probe; conventional
auscultation may reveal continuous millwheel murmur as a late sign)
pulmonary artery pressure increases during air embolism (it is not often monitored)
arterial hypotension
tachycardia, dysrhythmias or cardiac arrest.
Management (Figure 14) comprises prevention of further air entrainment, attempts
to remove the air and supportive measures.
Management of air embolus
Ventilate the patient with 100% oxygen. Stop nitrous oxide administration
Flood the surgical site with normal saline, wet packs, and apply bone wax to
any area of exposed bone cortex. Manually compress the proximal veins to
stop further air entrainment
Attempt to increase venous pressure

Position patient head down (or surgical site down)
Give rapid fluid bolus (250500 ml) and observe effects
Use vasopressors if the arterial blood pressure is severely affected
Compression of the abdomen
Activation of antigravity venous compression device (G suit) if fitted
If a central venous catheter (CVC) is in situ, try to aspirate air from all
lumens. Insert a CVC (right internal jugular or subclavian) if one is not
present
The left lateral position may transfer air from the pulmonary artery to the right
ventricle, thereby improving pulmonary flow (there is little evidence that this
is of benefit)
Give cardiopulmonary resuscitation if required
14
Pneumothorax
The pleural cavity usually exists only as a potential space between the parietal pleura
(attached to the innermost intercostal muscle, the transversus thoracus), and the
visceral pleura (continuous with the lung parenchyma). A pneumothorax occurs when
this potential cavity is opened, either by breaching the chest wall structures (an open
pneumothorax), or by injury to the lung parenchyma (a closed pneumothorax).
The clinical management is concerned with releasing the accumulation of air from
the cavity and correcting the chest wall injury. Understanding the anatomy of the chest
cavity allows cause and effect to be identified rapidly.
The dome of the lung protrudes superiorly above the thoracic inlet to the level of the
6th cervical vertebra. The tip of a needle inserted towards the internal jugular vein could
pass more posteriorly where it may cross the pleural space and enter the apices of the
lung parenchyma. This is possible even with a relatively high approach.
The inferior part of the chest cavity extends to the costo-diaphragmatic recess. This
reaches to the crura of the diaphragm at the level of the 12th thoracic vertebrae. The
cavity can be entered inadvertently in this low position by surgery to the renal bed or
lower thoracic and upper lumbar vertebrae.
The mediastinal pleura lies against the vertebral bodies, oesophagus, aorta, large
veins, heart and trachea. Damage to many of these mid-chest structures could allow air
or blood to enter the pleural cavity. Trauma from accidents or surgical instrumentation
of the oesophagus or trachea may cause this.
The signs and causes of a developing pneumothorax while under general
anaesthesia are shown in Figure 15; some or all may be present depending on the
nature of the pneumothorax (simple or under tension), its speed of onset, the general
health of the patient and whether they are breathing spontaneously or are mechanically
ventilated.
Signs and causes of pneumothorax
Signs Causes
Hypoxaemia Central venous catheter insertion
Wheeze Penetrating or blunt chest trauma
Increasing airway pressure Diaphragmatic, tracheal,
oesophageal or cardiac surgery
Unilateral chest wall motion Chest drain clamping
Reduced air entry Spontaneous bullae rupture
Hyperresonance
Distended neck veins
Shock
Shifted trachea away from
affected side
15
In trauma patients, pneumothorax should be identified and treated by chest drain

insertion before anaesthesia to avoid the dangers of tension pneumothorax following
the start of positive pressure ventilation (Figures 16 and 17). If there is obvious
chest injury, but no clinical sign or chest radiograph appearance of pneumothorax,
prophylactic bilateral chest drains may be indicated. The risks of chest drain insertion
must be balanced against the consequences of a tension pneumothorax developing
during interhospital or intrahospital transfer or during the perioperative period.
Immediate management of a tension pneumothorax is chest decompression using
a 14 G cannula inserted in the midclavicular line and second intercostal space. This
should be followed immediately by formal chest drain insertion.
16 Right-sided tension pneumothorax 17 Left-sided simple pneumothorax

requiring immediate needle requiring chest drain before anaesthesia.
decompresion followed by chest
drainage. Gross mediastinal deviation
is shown to the left.

Electrical Hazards: Their
Causes and Prevention
John Moyle
John Moyle is Consultant in Palliative Medicine in Milton Keynes and a Chartered

Engineer. He trained with Philips Electrical Industries. He read medicine at St
Bartholomews Hospital, London and trained in anaesthesia and intensive care at Kings
College Hospital, London.
Before 1940 there was little electrical equipment in the operating theatre apart from
crude radiofrequency diathermy. Since then there has been an invasion of electronic
monitoring equipment and many surgical tools are electrically powered. The operating
theatre and ICU are unique in electronic engineering because deliberate electrical
contact is made with the human body.
The body should be protected from electric current. The body may be considered as
an electrolyte solution, which is a good conductor of electricity, contained in a leather
bag. Dry leather is a good electrical insulator but conducts electricity easily when damp
especially with electrolyte-containing liquids such as sweat.
Electrical injury is caused primarily by the intensity of the current passing through.
Current is dependent on the potential difference or voltage across the body and the
resistance of the tissues through which it passes (Ohm's law).
I= E
R
where: E, potential difference (volts); R, resistance (ohms); I, current (amperes)

Severity of injury also depends on the current pathway through the body,
environmental factors and the pre-existing health of the patient.
Pathophysiological effects
The pathophysiological effects of electricity range from a mild tingling feeling to
ignition in extreme cases. Any electrical current passing through a resistance loses
some energy by conversion to heat. The amount of heat generated depends on the
current and the value of the resistance; this may be beneficial and forms the basis
of coagulation by radiofrequency diathermy. Electricity may stimulate excitable tissues,
both nerves and muscles. In a controlled way, this effect may be used medically
(e.g. peripheral nerve stimulator, defibrillation). Direct currents, even of low intensity,
may cause electrochemical effects. Very high currents, generated by high voltages,
cause arcing or sparking and char the tissues. This effect may be harnessed when
radiofrequency diathermy is used to cut tissues.
Complications of the inadvertent application of electric currents to the body are:
cardiopulmonary arrest
cardiac arrhythmia
skin and tissue damage
associated injuries caused by gross muscle contraction.
In the hours after an electric shock there may be further heart rhythm disturbances,
hypoxia and electrolyte disturbances, and acute renal failure due to myoglobinuria. It
is difficult to predict the effect of electricity on the body because of variables such as
body size, proportion and general health. Pre-existing heart problems make the heart
more susceptible to arrhythmias.
The current pathway through the body dictates the type of injury. Current passing
through the head or across the thorax may cause loss of consciousness and respiratory
arrest with or without ventricular fibrillation. Current passing from hand to hand (Figure
1) may cause ventricular fibrillation. Current passing vertically through the body is more
likely to cause cardiac muscle damage and injury to other vital organs especially the
spinal cord. These injuries depend on the intensity and duration of the current.
The resistance of the human body is not uniform, therefore electricity does not pass
evenly through it. Skin resistance is low and allows electricity to pass easily, especially
when wet with sweat. Blood has a relatively low resistance, therefore highly vascular
areas or inflamed areas of skin have lower resistance. The highest skin resistance is
found over heavily calloused areas such as the palm or sole.
The pathway of the current inside the body depends on the resistance of each
tissue type. Tissues with the lowest resistance (the best conductance) are nervous
tissue, blood, mucous membranes and muscle; the poorest conductors are tendon,
bone and fat.
Direct and alternating currents have different effects on the body. Direct current
of sufficient intensity causes short duration muscle spasm which may throw the
victim from the source. There may be a disturbance of heart rhythm and blunt
mechanical trauma. Alternating current, especially at 50 Hz (60 Hz in North America)
is approximately three times more dangerous than direct current. Alternating current
(40110 Hz) causes continuous muscle spasm or tetany. As the flexor muscles are
more powerful than the extensors, tetany may cause the victim to grip the offending
conductor more tightly, thus prolonging the duration of current. Local diaphoresis also
reduces skin resistance at the point of contact thus increasing the current.
50 Hz (or 60 Hz) is a bad choice of frequency for the public utility electricity
supply because it is the frequency to which the body is most sensitive. At higher
frequency the body is progressively less sensitive to the excitable effects of electricity.
Radiofrequency surgical diathermy uses frequencies greater than 100 kHz at which
comparatively large current may be passed, taking advantage of the heating effects of
electricity without affecting excitable tissues.
Effects of hand-to-hand 50 Hz alternating current
1 mA Tingling sensation
5 mA Pain
15 mA Severe pain with local muscle spasm
50 mA Respiratory muscle spasm
80100 mA Dysrhythmias, pump failure, ventricular fibrillation
Electrical safety
The basic principle of electrical safety is to prevent the body becoming part of an
electrical circuit. This requires good design of equipment, cables and connectors. Even
with the highest quality of design, the user has the responsibility of using and handling
equipment sensibly.
The conventional single-phase mains supply has two conductors: live and neutral.
The live conductor is at a voltage dependent on the supply, normally 220240 volts (110
volts in the USA) with respect to the neutral conductor which is tied to earth at the
substation. A safety or earth conductor may also be present which is connected to earth
locally and therefore may be at a slightly different potential from the neutral conductor. It
is unusual to get an electric shock from the neutral conductor alone but a circuit may be
completed between a live conductor or component and either the neutral conductor or,
more commonly, an earth pathway (Figure 2). This condition may be eased by the use
of an isolation transformer (Figure 3) which will protect against electrocution via earth
but not between earth and neutral. Isolation transformers are the most common form of
basic protection with medical equipment and are often contained inside the equipment.
(Further isolation is required when connection is made directly to the patient, this is
described below.)
Conductor with earth pathway

Conductor with isolation transformer

Electrocution depends on the duration of exposure and current. The shorter the
duration, the higher the current required before damage is done. The earth leakage
or residual circuit breaker stops the current passing through the body before any
serious damage occurs. This phenomenon is used as the final level of protection
from electrocution in the domestic situation and is commonly used commercially
for power tools. The principle of the earth leakage circuit breaker (ELCB) is shown
in Figure 4. The ferrite ring forms the core of an electrical transformer. The live and
neutral conductors pass together through the ring, forming a single-turn primary of
the transformer. The secondary of the transformer consists of many turns of much
finer wire and is connected to a solenoid. When the solenoid is energized it breaks
the supply. In the normal state, current passes down the live conductor, through the
appliance and back through the neutral conductor. The current in the neutral is equal
and opposite to that in the live and so their magnetic fields are cancelled out and
no current is generated in the secondary winding. If some current leaks out of the
appliance due to a fault or someone touching a live part, there is an imbalance between
the live and neutral and a much amplified current is generated in the secondary,
energizing the solenoid and disconnecting the supply.
Earth leakage circuit breaker

4
Microshock: electrocution of the intact human body is commonly referred to as
macroshock to distinguish it from microshock in which smaller currents can lead to
cardiac dysrhythmia or arrest because one of the points of contact is on or in the heart.
50 Hz mains electricity at a current as low as 50 A by this route may have serious
consequences. Contact may be made with the heart during thoracotomy but a more
common and less obvious route is via electrolyte solutions in catheters in or near the
heart. Therefore, any equipment that might make connection with the heart must be
specially designed to protect against the unintentional passage of these very small
currents. Such equipment includes ECG recorders, intravascular pressure monitoring
systems, pacemakers and defibrillators.
Leakage current may be defined as electric current that has passed through
insulators. It is difficult to design equipment with perfect insulation. The reduction of
leakage in medical equipment requires special design features. The designer has to
ensure that no electrically live parts are accessible. Any outer metal casing has to
be connected to earth; an extra layer of insulation may also be used the double
insulation often used on power tools. These techniques may make a piece of medical
equipment safe to be in the patient environment. However, if there is any possibility
of connection with the heart, special isolation techniques have to be employed by the
equipment designer to ensure that any leakage current is less than 10 A. This is a
stringent limit to achieve.
Safety standards
All medical equipment manufacturers have to comply with published international
standards. Each nation also has its own standards organization; in the UK it is the
British Standards Institute (BSI). To make standards applicable on a worldwide basis,
all national organizations cooperate to write international standards. The International
Standards Organization (ISO) deals with everything excluding electricity; the
International Electrotechnical Committee (IEC) deals with the standards of anything
electrical. Both the ISO and the IEC are based in Geneva.
IEC-60601 is the basic standard for medical equipment. It classifies equipment in
two ways; the method of electrical protection and the degree of protection.
Class I equipment uses a protective earth connection to the outer conductive
casing.
Class II protection is by double insulation. The degree of protection required is
classified as B, BF or CF (C, intra cardiac or near cardiac; F, floating) as shown in
Figure 5. Figure 6 shows the same symbols, with the indication that the equipment may
withstand a defibrillator pulse without damage.
Symbols indicating equipment is able to withstand

a defibrillator pulse
Two values of leakage current are given for each category; the lower refers to the
equipment in its normal state; the higher value is the maximum allowable leakage
current with a single fault condition (SFC). The Standard lists the allowable SFCs for
each type of equipment. All medical equipment has to be marked with symbols to show
the degree of protection. Figure 7 includes other relevant safety markings that are
published in IEC 60601.
Alternating current
3 Phase alternating current
3 Phase alternating current with neutral
Direct current
Protective earth (ground)
Earth (ground)

Neutral conductor (only on permanently
installed equipment)
Equipotentiality

Fires and Explosions
John Moyle

College Hospital, London. He teaches physics and clinical measurement to trainee
anaesthetists.
Less emphasis is placed on the risk of fire and explosion in the operating theatre
today than previously mainly because the use of flammable agents has decreased;
for example, ether and cyclopropane are no longer used in anaesthesia. This has
lead to a false sense of security and little attention to fire safety. It must not be
forgotten that alcohol as an antiseptic and dry drapes are flammable and that the
microenvironment around a patient may have an increased concentration of oxygen.
Nitrous oxide supports combustion better than oxygen. There are also new sources of
ignition, such as the intense energy at the end of fibre-optic light pipes and surgical
lasers as well as the dangers associated with the use of surgical diathermy.
Fire and explosion

Fire or explosion occurs when a substance combines with an oxidizing agent with the
release of energy. The reaction requires activation energy to trigger it (Figure 1). If the
reaction occurs slowly, heat may be the only obvious evidence, though it usually leads
to fire. If the reaction proceeds rapidly, large amounts of heat, light and a rapid increase
in pressure occur, making sound; this is an explosion. Fire burns slowly at atmospheric
pressure at a temperature of 200500C. An explosion is a fast, sudden increase in
pressure to a high level at a much higher temperature than fire.
If the rate of liberation of heat is equal to the amount of heat required to maintain
the process, the flame will stay still as long as the reactants are made available by
convection. If the rate of generation of heat is larger than that required to continue
activation, the flame will travel through the mixture. The greater the difference, the
greater the likelihood of the reaction travelling so fast that a shock wave occurs; this
is an explosion.
On a molecular basis, combustion is a chemical process. In oxidation, the
intermolecular bond energy of the end products is less than the bond energy of the
reactants and the excess energy is dissipated as heat. To induce the initial deformation
of the molecules which allows the rearrangement of these bonds, activation energy has
to be added to the system; in the case of fires and explosions this is usually in the form
of heat. When the oxidation process begins, positive feedback has to occur to maintain
the reaction; if not, the process would cease immediately, before the reaction was
complete.
The speed of reaction is greatest for a stochiometric mixture: defined as a mixture in
such proportions that none of the reactants is left at the end of the reaction.
Fuel
A gas or vapour may be flammable over a range of concentrations with lower and upper
limits of flammability. The stochiometric concentration occurs between these limits.
Limits of flammability vary depending on the atmosphere in which the flammable gas
or vapour is found (Figure 2).
Anaesthetic gases and vapours are not the only flammable substance that may put
the patient at risk.
Methane and hydrogen are found in bowel gas.
Alcohol forms the basis of many skin preparation solutions and is in the exhaled
gases of the inebriated. Isopropyl alcohol is commonly used to clean the skin before
cannulation. Methyl alcohol is used in spirit burners and by down-and-out alcoholics.
Drapes are often applied to the patient before the alcohol in skin preparation solution
has evaporated completely. There may be a high concentration of the vapour, and even
some of the liquid alcohol, beneath the drapes.
Some surgeons use hydrogen peroxide to clean wounds. It rapidly decomposes by
enzyme catalysis when poured on to open wounds, producing a froth of hydrogen and
oxygen; the gas given off is highly flammable.
Dry cotton or paper drapes are flammable.
The plastic compounds used in the manufacture of conventional tracheal tubes may
become flammable in high concen-tration of oxygen and high ignition energy levels.
2
Oxygen
Oxygen in the air is the usual source of oxygen involved in a fire. Figure 3 shows
that the risk of ignition of any flammable gas or vapour is increased with increased
concentration of oxygen above ambient level. Any fire burns more vigorously if the
concentration of oxygen is increased.
Nitrous oxide is not combustible but it vigorously supports combustion.
Risks of fire and explosion arise from the strong oxidizing action of nitrous
oxide and from its thermodynamic instability. At about 400C, nitrous oxide
breaks down to oxygen and nitrogen and if this comes into contact with
combustible material, fire or explosion may result. The concentration of oxygen
and nitrous oxide is increased around the mouth and upper airways if a tracheal tube
or laryngeal mask does not seal perfectly. There is often an increased concentration of
oxygen and nitrous oxide trapped between the patient and the surgical drapes.
Limits of flammability of gases and vapours encountered in the operating theatre1
Gas or vapour Air Oxygen Nitrous 30% oxygen 20% oxygen

oxide 70% nitrous oxide 80% nitrous oxide
L2 U L U L U L U L U
Diethyl ether 1.9 48 2.0 82 1.5 24
Cyclopropane 2.4 10 2.5 60 1.6 30
Ethyl chloride 4.0 15 4.0 67 2.0 33
Enflurane 4.0 5.75 4.25
Isoflurane 6.0 7.0 5.25
Halothane 4.75 3.25
Methoxyflurane 7.0 5.0 28 4.6
Trichloroethylene 9.0 65
Fluoroxene 4.0
Hydrogen 4.0 74 4.6 94 5.8 86
Methane 5.3 15 5.4 59 4.0 40
Sevoflurane 12 11
Isopropyl alcohol 2.5 12
Methyl alcohol 6.0 36.5
Ethyl alcohol 3.3 19
This is a compilation of information from a number of sources

1
L, lower limit; U, upper limit.

2
All values are percentages.
Ignition source
Sources of ignition may be sparks generated by static electricity, flames or hot
surfaces. Even shaking a bottle containing an organic compound in combination
with a peroxide, may cause ignition.
The flash point of a liquid is the lowest temperature at which it gives off enough
vapour to form an ignitable mixture with air. At flash point, the vapour will burn, but
only briefly because inadequate vapour is produced to maintain combustion. The flash
point of a liquid is always quoted but is of less significance to theatre staff than the
autoignition temperature.
The autoignition temperature is the minimum temperature above which a
flammable mixture is capable of extracting enough energy from the environment to
self-ignite. Figure 4 shows the flash points and autoignition temperatures of some
compounds in the operating theatre.
If anaesthetic agents that are flammable at clinical concen-trations are used, care
must be taken to keep any possible source of ignition outside the zone of risk. There
are two zones of risk around the anaesthetic machine, breathing circuit and head and
neck of the patient:
5 cm if only air is used as the source of oxygen
25 cm if nitrous oxide and/or oxygen are used.
Equipment must be marked as AP where air is the only source of oxygen and APG
when nitrous oxide or high oxygen concentrations are used.
Possible sources of ignition

Open flames are an obvious source of ignition; they comprise spirit and gas
burners, matches and cigarette lighters.
Hot surfaces may cause ignition if the temperature is above the autoignition
temperature of the liquid, vapour or solid. In some cases the high temperature of a
surface is obvious because it glows or is incandescent.
Hot wire filaments used for cautery may be of high enough temperature to cause
ignition. Miniature filament bulbs used in old-fashioned endoscopes may have a surface
temperature of 250C; sufficient to ignite diethyl ether in air.
Light sources powerful light sources and fibre-optic light-guides have replaced
miniature light bulbs but they should always be extinguished when not in use because
the energy emitted from the light-guide when not connected to an instrument is intense
enough to cause a burn on a surgical drape or the skin. The likelihood of igniting a
drape is higher if the concentration of oxygen or nitrous oxide is high in the atmosphere
trapped beneath it.
Surgical lasers see below.
Sparks due to current electricity, as in radiofrequency surgical diathermy and static
electricity, are the most obvious sources of ignition in surgical practice. Even sparks that
are so small as to be almost invisible may be of sufficient energy to cause ignition.
Sudden increase in gas pressure causes gases to heat. Therefore it is important
that no oil, grease or other flammable substance comes into contact with oxygen or
nitrous oxide under high pressure.
Lasers
The energy emitted from the tip of a laser applicator is extremely high. The risk of
causing ignition is higher than with any other source of emission. Extreme care must be
taken to ensure that a laser beam does not come into contact with anything flammable.
Any drapes or swabs in the vicinity must be kept wet with water. Care must also be
taken to ensure that the beam is not inadvertently reflected on to a flammable surface.
If the laser is being used in the mouth, the trachael tube should be of a non-flammable
type or be suitably protected. In the case of laser in the bronchi or trachea the oxygen
concentration should be 21% or only slightly higher.
Precautions
Avoid the use of flammable liquids, gases and vapours.
Keep unsuitable equipment out of zones of risk when flammable anaesthetic agents
are in use.
Observe antistatic precautions.
Remember bowel gases are flammable.
Relative humidity should not be less than 50% (a dry atmosphere promotes the
generation of static electrical charge).
At least 1520 changes of air per hour in the operating theatre will reduce the risk
of build-up of flammable vapours.
High energy light sources must not remain on dry drapes (these sources are of high
enough energy to damage tissues).
Radiofrequency surgical diathermy is a potent source of ignition energy; evaporation
of flammable skin preparation solutions must be complete and the atmosphere cleared
of the vapour before diathermy is used.
Flash points and autoignition temperatures of flammable liquids

encountered in the operating theatre
Compound Flash point (oC) Autoignition

temperature (oC)
Methyl alcohol 16 385
Ethyl alcohol 12 363
Diethyl ether 45 160
Isopropyl alcohol 11.7 455.6

Induction of Anaesthesia
James Austin
James Austin is Specialist Registrar in Anaesthesia in Oxford, UK. He qualified in

Cape Town, South Africa and trained in Anaesthesia in Reading, UK.
Induction is the process that produces a state of surgical anaesthesia in a patient.

The term is used only in the context of general anaesthesia and not with local
anaesthesia. It is the first step in the process of anaesthesia whereby the patient
is rendered unconscious, preventing both awareness of, and response to, surgical
stimuli. Anaesthesia and physiological sleep are different because sleep has structured,
specific EEG patterns and endocrine changes, whereas anaesthesia is associated with
a diffuse damping-down of EEG function and a stress-type endocrine response.
The process of induction should ensure patient safety, produce a state of
unconsciousness, ensure optimal conditions for the surgeon and prepare the patient
for waking and recovery.
Before anaesthesia is induced, the anaesthetist must:
assess the patient as completely as circumstances allow, and
institute preoperative preparations (e.g. intravenous fluids, sedative drugs,
analgesics)
discuss the surgery with the surgeon, particularly in complex or unusual cases
plan the anaesthetic technique
ensure all necessary equipment and drugs are available, and that the equipment
is working.
On arrival in the anaesthetic suite, the anaesthetist must ensure:
the correct patient has arrived
the correct operation is planned on the correct side
consent has been given
jewellery or prostheses have been removed or declared
blood for transfusion is available if required.
Anaesthetic room
In the UK, most inductions take place in a dedicated anaesthetic room; however, in
many other countries induction takes place on the operating table in theatre. The main
advantage of using a dedicated induction room is the quicker change-around as the
theatre is cleaned and prepared between patients. If staffing permits, induction may
take place while the previous case is being completed. A separate induction room also
avoids the psychological stress (for some patients) of seeing the operating theatre. The
anaesthetic room must be equipped with the necessary anaesthetic and monitoring
equipment for the induction to be completed safely. The duplication of equipment
between anaesthetic room and operating theatre may be a financial constraint in some
locations. In urgent cases, with potentially unstable patients or with the morbidly obese,
theatre is the best place for induction, because it saves the time, physical hazards and
period of reduced or absent monitoring associated with transfer.
Equipment checks: successful induction requires planning and attention to detail.

Before the procedure begins, checks of the anaesthetic machine must have been
completed and the following must be available:
the patient must be on a tilting bed or trolley
two working laryngoscopes (in case of bulb failure), including standard and long
blades (sizes 3 and 4)
a selection of laryngoscope blade types (e.g. the Macintosh and the McCoy levering
blade)
a selection of tracheal tube sizes, with their cuffs checked
suction equipment
equipment to deal with difficult or failed intubation, including oral and nasal airways,
gum-elastic bougie, laryngeal mask
standard monitoring equipment (e.g. pulse oximeter, ECG, capnometer, blood
pressure monitor).
Monitoring
In addition to the clinical observations made by the anaesthetist, the Association

of Anaesthetists of Great Britain and Ireland has published recommendation for
standards of monitoring equipment during anaesthesia and recovery. Monitoring should
be instituted before induction whenever possible and should consist of a pulse oximeter
(ideally with continuous display of pulse rate and plethysmography), an ECG and non-
invasive arterial blood pressure monitoring. Following unconsciousness, other variables
should also be monitored, including:
carbon dioxide (using a capnometer)
the anaesthetic vapour concentration
body temperature
neuromuscular function if muscle relaxants are used (assessed using a nerve
stimulator)
invasive arterial or central venous pressures and urine output monitoring may be
required.
Induction methods
Most anaesthetic inductions are performed using intravenous or inhalational (gas)

induction; each has advantages and disadvantages (Figure 1). Less commonly,
induction may be carried out by the intramuscular route in uncooperative patients,
children or those with difficult venous access. Ketamine,10 mg/kg, provides up to 30
minutes of surgical anaesthesia, but induction times are unpredictable (1545 minutes)
and recovery is slow. Rectal induction with thiopentone, methohexitone, chloral hydrate
or benzodiazepines was popular for children at one time, but is seldom used now. Oral
induction is effectively a heavy sedative or premedicant, rather than induction, and
recovery time is prolonged.
There are several tasks to be accomplished with any form of induction:
last-minute preliminary checks (as specified above)
establish monitoring
establish intravenous access
produce unconsciousness
secure the airway
establish ventilation
commence analgesia (systemic or local)
position the patient
establish maintenance of anaesthesia.
Intravenous and inhalational induction

Intravenous Inhalation
Advantages Advantages
Rapid onset Does not require IV access
Patient comfort Useful for children
Airway protection in rapid- Useful for adults with needle-phobia
sequence induction
Disadvantages Disadvantages
Contraindicated in patients Slow induction
with a difficult airway Excitement phase
Risk of vomiting
Risk of arrhythmias
Volatile agents contraindicated in patients
susceptible to malignant hyperpyrexia
Intravenous induction
Pulse oximetry and ECG monitoring should be established before intravenous access
because occasionally a cardiovascular event (e.g. vasovagal syncope) occurs during
cannulation. Intravascular access commonly consists of a simple venous cannula;
however, complex cases may require an arterial line, a central venous line and/or a
pulmonary artery catheter. These may be sited with local anaesthesia before induction,
to provide additional monitoring if haemodynamic instability is expected.
Following intravenous access, preliminary drugs (e.g. analgesics, antibiotics, anti-
emetics) may be given. These vary according to the clinical circumstances and a
detailed discussion is beyond the scope of this article. A regional analgesic block, if
required, may also be given at this stage. Whether to insert the block before or after the
patient is anaesthetized is the subject of some controversy (Figure 2).
Advantages of regional nerve blockade performed either before or after

induction
Before induction After induction

Patient cooperation with Patient preference
correct positioning Correct positioning may be
Patient may provide easier (e.g. patients with painful
feedback to minimize neural fractures or skeletal deformity)
damage by needle or injection
Less requirement for
anaesthetic monitoring
Pre-oxygenation: some anaesthetists routinely pre-oxygenate their patients before

induction. The correct technique is for the patient to breathe 100% oxygen via an
anaesthetic circuit and close-fitting mask for about 3 minutes of tidal volume breathing.
Alternatively, pre-oxygenation by three vital capacity breaths has been demonstrated
to be effective. The aim is to replace nitrogen-containing air in the resting volume of
the lungs (the functional residual capacity, FRC) with a high oxygen concentration. The
gas within the FRC acts as an important oxygen store, and therefore pre-oxygenation
lengthens the time before hypoxaemia occurs following the onset of apnoea. This may
provide valuable time in which the airway can be secured if an unexpectedly difficult
airway is encountered. Mask phobia and the difficulties in achieving a mask seal in
non-compliant patients and children are the only significant contraindications to pre-
oxygenation. Pre-oxygenation is mandatory in rapid-sequence induction.
Intravenous drugs: slow, smooth injection of an intravenous anaesthetic agent usually

results in loss of consciousness in less than 1 minute. Thiopentone, for example, starts
to work in a period of one armbrain circulation time. This is the period of time taken
for the drug to travel from the site of injection (the arm) to the site of action (the brain)
and is about 15 seconds in a healthy patient. The dose is carefully titrated according to
patient response. Typical induction doses for healthy individuals are shown in Figure 3,
but dose reduction may be required in:
patients who are less fit
the elderly or frail
neonates
patients with hypotension or poor cardiac reserve
patients with chronic renal or liver disease
patients with raised intracranial pressure
patients who have been premedicated.
It can be difficult to judge when enough induction agent has been given. Care and
experience are needed to titrate dose to effect but some indicators include:
loss of response to verbal command
loss of eyelash reflex (in which brushing the eyelash produces a blink response)
relaxation of a motor posture (e.g. a raised arm or a grip on an object)
cooperation with bag/mask ventilation.
The eyelash reflex has conventionally been regarded as a good end-point for
thiopentone induction, but it is less reliable in propofol induction, for which loss of verbal
response or motor relaxation is a more useful end-point.
Induction doses of intravenous drugs

Drug Typical adult induction Notes
dose (mg/kg)
Propofol 1.52.5 Popular and widely used drug associated with rapid and clear-headed'
recovery. Rapid metabolism and lack of cumulative effects has made it popular
for total intravenous anaesthesia
Thiopentone 35 (2.5% solution) The gold-standard against which all other drugs are judged. Smooth induction
in one armbrain circulation time
Methohexitone 11.5 (1% solution) Lowers the convulsive threshold, mainly used in anaesthesia for
electroconvulsive therapy
Etomidate 0.20.3 Marked cardiovascular stability makes this drug popular for use in unstable
patients
Ketamine 0.52 Useful for sedation with profound analgesia. Increases pulse rate and blood
pressure and useful for the induction of patients suffering from acute trauma
Midazolam 0.150.5 A benzodiazepine that may provide stable induction for the elderly and frail, in
combination with an opioid
3
Further procedures: the induction agent may be followed by a muscle relaxant,
particularly if tracheal intubation is planned. It is important to confirm that the patients
lungs can be ventilated via a bag and mask before paralysing. A muscle relaxant should
not be given until it has been confirmed that ventilation is possible. Once anaesthesia
is adequate, a clear airway is established using a simple face mask (with or without
an oral or nasal airway), laryngeal mask airway or tracheal intubation. If the level of
anaesthesia proves to be inadequate to allow an airway or tracheal tube to be tolerated,
it may be deepened either with supplementary doses of intravenous agent, or by
ventilating with volatile anaesthetic. With the airway secure, ventilation can continue by
the patients own effort, by manual hand ventilation, or by mechanical ventilator.
At this stage, further invasive procedures may take place, such as additional
vascular access, regional blocks, bladder catheterization, passing of a nasogastric tube
or insertion of a temperature probe.
Transfer to theatre: if anaesthesia has been induced in the anaesthetic room, the
patient is now transferred to theatre. This is potentially hazardous because for a short
time the patient is separated from monitoring equipment and the mechanical ventilator.
The patient is also potentially unstable because of the effects of induction drugs and
is at risk of injury during the physical transfer. It is the anaesthetists responsibility to
guarantee the patients safety. It should be ensured that ventilation and anaesthetic
maintenance are re-established in good time, that tubes and lines are not dislodged,
and that changes in clinical condition are detected promptly, in particular, cardiovascular
instability, desaturation or signs of waking from anaesthesia.
Once in theatre, the priorities are:
prompt transfer on to the operating table
prompt re-establishment of ventilation
prompt re-establishment of anaesthetic maintenance if using volatile anaesthetic
drugs
check correct drug delivery if using intravenous maintenance technique
prompt re-establishment of monitoring equipment
safe positioning of the patient
commencement of maintenance fluids and temperature control.
Rapid-sequence induction
Rapid-sequence induction is used to decrease the risk of aspiration if the patient
may have a full stomach, for example in an emergency. In patients presenting for
elective surgery, a period of starvation of 2 hours for clear fluids, or 6 hours for
food, is considered appropriate. Bowel obstruction, incompetent lower oesophageal
sphincter, pregnancy and gastroparesis caused by disease, pain or drugs such as
opiate analgesics are also causes of a potentially full stomach.
The incidence and severity of aspiration of gastric contents are made worse by
the nature, volume and pH of the gastric solution. Mendelsons studies on aspiration
pneumonitis showed that aspiration of solid particles produced more damage than
purely fluid aspirates. A potential gastric aspirate greater than 25 ml in volume and/or
with a pH less than 2.5 is considered dangerous, though there is little direct clinical
evidence for this. In these at-risk patients it is sensible to attempt to raise gastric
pH, and to try to promote gastric emptying. Pre-medication with ranitidine, 50 mg
i.v., to decrease gastric acidity, and metoclopramide, 10 mg i.v., to enhance gastric
emptying and increase the tone of the lower oesophageal sphincter is popular with
some anaesthetists; both take at least 1 hour to take effect. A non-particulate antacid,
such as sodium citrate, 30 ml of 0.3 M solution orally, given on leaving the ward or
arriving in the anaesthetic room, further neutralizes residual stomach acid, but at the
expense of raising gastric volume further.
Some anaesthetists advise that a nasogastric tube should be passed to drain the
stomach, but it is uncomfortable and may induce vomiting. The counter argument is
that any vomiting is better done while the patient is fully awake with protective airway
reflexes. If a nasogastric tube is already in place it should be aspirated. If the gastric
contents are still acidic on litmus test, consideration should be given to instilling sodium
citrate. The old practice of inducing vomiting with ipecac or apomorphine is no longer
advised.
The rapid sequence of drug administration aims to produce unconsciousness and
intubation conditions as rapidly as possible. The airway is swiftly protected by a cuffed
tracheal tube without prior inflation of the lungs via bag and mask. This is to prevent
possible gastric distension with an increased risk of gastric reflux. It is performed with
the help of a trained assistant, competent in the technique of cricoid pressure.
Muscle relaxants are administered before the airway is controlled, and in this way
rapid-sequence induction breaks an important rule of anaesthesia. Careful preoperative
assessment of potential airway difficulty is therefore vital, and rapid-sequence induction
must not be performed if this assessment predicts difficulty with intubation. The trainee
anaesthetist must seek further advice, because an awake intubation technique may
then be indicated.
Pre-oxygenation is mandatory, though it may be difficult to achieve in children. Pre-

oxygenation reduces the need to ventilate the lungs before intubation. The correct
technique is described above. Oxygen must be delivered via an anaesthetic breathing
system capable of delivering 100% oxygen; standard Hudson type face masks are
inadequate.
Drug injection: the chosen drug is rapidly adminstered (Figure 3). Thiopentone is the
drug of choice because of its rapid onset of action in one armbrain circulation time,
but propofol or etomidate are alternatives, albeit slightly slower-acting. The use of rapid-
acting opioids such as alfentanil, 10 g/kg, or fentanyl, 1 g/kg, helps to reduce the
pressor response to laryngoscopy.
Cricoid pressure: or Sellicks manoeuvre, is traditionally practised in rapid-sequence

induction and is applied by the anaesthetic assistant as the patient starts to lose
consciousness. Pressure is applied to the cricoid cartilage to compress it against the
oesophagus, preventing passive regurgitation of stomach contents.
If active vomiting occurs, it is recommended that cricoid pressure be removed to
prevent oesophageal rupture suction, head-down tilt and turning the patients head
to one side is then used instead. Otherwise, cricoid pressure is removed only on the
instruction of the anaesthetist, once the airway has been secured with a cuffed tube.
Occasionally, it may be removed to facilitate an intubation that is being made more
difficult by its continued application.
Muscle relaxation: suxamethonium, 1.5 mg/kg, is the drug of choice. Its rapid onset
produces ideal intubating conditions, with a peak effect of muscle relaxation within 50
seconds of injection. It is important to allow the drug time to work, and not to begin the
intubation sequence before muscle fasciculations have subsided.
The duration of apnoea is usually about 5 minutes in healthy individuals, and thus
spontaneous respiration may be re-established early in the event of a failed intubation.
Suxamethonium is contraindicated in patients with:
previous allergy
susceptibility to malignant hyperpyrexia
myotonia
severe burns, muscle damage or paraplegia (of over 1 weeks duration)
known raised serum potassium.
In these patients, rocuronium, 0.60.9 mg/kg, may provide relaxation as rapidly
as suxamethonium, but with longer duration. Rocuronium is also the drug of
choice in patients with reduced or absent plasma cholinesterase activity, in whom
suxamethonium has a long and unpredictable duration of action.
Intubation: the trachea is intubated with a cuffed tube following unconsciousness and
muscle relaxation. Uncuffed tubes are used in children to avoid local pressure on
the tracheal wall and to maximize the internal diameter of tube available. If difficulty
is encountered with direct laryngoscopy, then simple steps may be taken to facilitate
intubation:
manipulate the larynx (the assistant providing the cricoid pressure may be distorting
the view of the larynx)
change to a larger blade laryngoscope
change to a different type of blade (e.g. a McCoy levering blade)
use the gum-elastic bougie (this thin, flexible stylet may be used to pass through the
cords providing a track over which the tracheal tube can be railroaded).
Before the cricoid pressure is released, the correct position of the tube must be
checked carefully by auscultation and capnometry. Once the cuff has been inflated and
the airway has been secured, a nasogastric tube should be passed and aspirated, if
not done previously. The rest of the anaesthetic proceeds as usual; but at the end of
the procedure extubation should take place with the patient awake, with their protective
airway reflexes re-established, positioned on their side in a head-down tilt, and with
suction available.
Failed intubation drill if the trachea is not successfully intubated, a failed
intubation drill must be followed:
cease further attempts at intubation
call for help
maintain cricoid pressure
insert an oral airway
hand-ventilate via bag and mask using 100% oxygen
await return of spontaneous respiration
once spontaneous ventilation has returned, turn the patient into the lateral
position with head tilted down and await return of consciousness.
A decision to abandon further attempts at intubation must be made early and certainly
before arterial desaturation supervenes. The prime concern of the anaesthetist is
patient safety. The safest option following failed intubation is to wake the patient. Once
the effects of the intravenous induction agent and muscle relaxant have worn off,
consideration must be given to how to proceed. This requires consultation with a senior
anaesthetist and may involve an awake intubation technique.
Inhalational induction
Gas induction, controversially, is often used as a means of inducing anaesthesia
(particularly in a child) without having to site an intravenous cannula first. However,
in the event of difficulties (e.g. laryngospasm, arrhythmias) instant intravenous access
should be available, because otherwise the anaesthetist controlling the airway will
be unable to attempt rapid cannulation. For this reason, some anaesthetists seldom
perform gas induction; others permit gas induction if a second anaesthetist is present
to assist with intravenous cannulation. Gas induction of children and adults has taken
place without intravenous access for over 150 years, in most cases safely and without
incident.
Indications: gas induction (with intravenous access) is indicated for patients in whom
airway difficulties are expected. In these cases, the patient continues to breathe
spontaneously throughout and apnoea is avoided, since it may then be impossible to
manually ventilate the lungs with bag and mask.
Upper airway obstruction is an important indication for inhalation induction,
and in these circumstances fibre-optic techniques for intubating the trachea are
contraindicated for fear of producing complete airway obstruction. However, in patients
with an unobstructed difficult airway, the increasing availability of fibre-optic intubation
equipment and the growing skill of anaesthetists in awake intubation techniques may
reduce the need for gas induction. The difficult airway may best be secured even before
anaesthesia is induced.
Technique: there is controversy over whether to induce in 100% oxygen or to use

nitrous oxide as well.
Concurrent use of volatile and nitrous oxide exploits the second-gas effect for a
cumulatively more rapid induction. The rapid absorption of the second gas (nitrous
oxide) has the effect of increasing the alveolar concentration of the first agent. The
partial pressure of anaesthetic gas in the alveolus reflects the partial pressure of
anaesthetic in the brain and hence the anaesthetic effect.
Pre-induction, with 33% oxygen and 66% nitrous oxide only, may render a child
sleepy enough not to resist when the odour of the volatile agent is added. Clearly the
more nitrous oxide is used the more anaesthetic effect is achieved; but likewise the less
reserve there is against desaturation. A minimum of 30% oxygen should be given.
Induction in 100% oxygen is least smooth, but should laryngospasm occur, it is
an advantage to have as much of the lung FRC filled with oxygen as possible. This
maximizes oxygen stores and thus delays the onset of hypoxaemia.
Conventional practice for inhalational induction with halothane is to start with a low
inspired concentration of 0.5%, and to increase it by 0.5% every four breaths up to
4%.
Sevoflurane has greatly enhanced gas induction, because it is faster, better tolerated
by patients, and is less arrhythmogenic than halothane. It has been suggested that
the lower incidence of arrhythmias has contributed to a decrease in dental anaesthetic
deaths in recent years. The high blood-gas solubility of sevoflurane accounts for its
rapid onset and offset. Because sevoflurane is less pungent it is often used in high
concentrations (maximum 8% on most vaporizers) for faster induction.
Enflurane is seldom used for gas inductions because it is slow; isoflurane and
desflurane are almost never used because they are pungent and irritating to the airway.
The last-minute checks before inhalational induction are the same as those for the
intravenous route. Monitoring should be established; some children make this difficult,
but ECG should be the minimum monitoring instituted. Induction should ideally take
place via a tight-fitting face mask (even small leaks may significantly delay induction).
However, the use of a cupped hand may be less threatening to a small child in the
first instance.
Single-breath induction has been described with halothane and sevoflurane. A
Mapleson A breathing system containing a 4-litre reservoir bag is filled with a maximum
concentration of volatile anaesthetic (4% halothane or 8% sevoflurane) in 66% nitrous
oxide and 33% oxygen. The patient is asked to exhale to residual volume, then, via
a tight-fitting mask, to inhale a full vital-capacity breath of gas, and then to hold
their breath for as long as possible. This technique produces a faster induction than
conventional tidal volume inhalational induction in cooperative adults. In the case of
single-breath 8% sevoflurane, the speed of induction is comparable with induction with
intravenous propofol. It may be a useful technique to use in cooperative needle-phobic
adults, but it offers few other advantages.
Four main variables determine the speed of inhalational anaesthetic induction.
The inspired partial pressure of the anaesthetic agent relative to its minimum
alveolar concentration (MAC) alters the speed of induction. MAC is the partial pressure
of the agent, expressed in volumes %, which at equilibrium prevents gross muscle
movement in response to a skin incision in 50% of patients. It is thus the effective dose
in 50% of patients and is a measure of anaesthetic potency.
The faster the patient breathes, or the greater the alveolar ventilation, the faster the
alveolar partial pressure of the agent approaches the inspired partial pressure. In a
child, crying speeds up gas induction by increasing minute ventilation.
The higher the cardiac output the more anaesthetic agent is removed from the
alveoli and hence the slower the partial pressure rises in the alveoli. Thus, an anxious,
hyperdynamic patient is slow to induce, whereas a shocked patient with a low cardiac
output is quicker.
The higher the solubility of an agent (i.e. a high blood-gas solubility coefficient), the
more the agent will dissolve in blood and thus a lower partial pressure will be generated.
Agents with a low solubility (e.g. sevoflurane) result in more rapid induction.
During a gas induction, most patients pass briefly through a phase of excitability
during which they may be agitated and at increased risk of laryngospasm or, more
rarely, arrhythmias. If a child is being induced, it is useful to warn the parents of this
disinhibition in advance. The disinhibition is not remembered by the patient.
Once the patient is unconscious, anaesthesia should be deepened, assisting
the ventilation by hand, using bag and mask if necessary. If not already obtained,
intravenous access should be secured, which requires the help of an assistant. Muscle
relaxants may then be given intravenously to assist in securing the airway. If the patient
is sufficiently deeply anaesthetized, as evidenced by a regular respiratory pattern and a
forward gaze in eyes with small pupils, the airway may be secured (even by intubation)
purely under inhalational anaesthesia. Nevertheless, it is valuable to have intravenous
access before attempting to manipulate the airway, in case any untoward airway
reflexes are produced (e.g. arrhythmias, laryngospasm). With the airway secured, the
remainder of the induction sequence proceeds as above.
Historical note
In 1937, Arthur Guedel published Inhalational Anaesthesia a Fundamental Guide, three

chapters of which were devoted to his observations of premedicated patients responses to
gas inductions with nitrous oxide, the ethers, chloroform and cyclopropane
Guedels stages of anaesthesia
Stage Definition Features

1 Analgesia From beginning to Sedation
loss of consciousness Loss of eyelash reflex1
2 Delirium Loss of consciousness Agitation, vomiting,
to onset of rhythmic arrhythmias
breathing Eyes deviated
3 Surgical
1st plane Onset of rhythmic Loss of eyelid reflex
breathing to loss of Loss of conjunctival
eyeball movement reflex1
2nd plane Loss of eyeball Loss of laryngeal
movement to onset of and gag reflexes
intercostal paralysis Loss of corneal reflex1
3rd plane Onset to completion of
intercostal paralysis
4th plane Complete intercostal Dilated pupils
paralysis to respiratory Loss of carinal reflex1
arrest
4 Respiratory Respiratory arrest to Loss of anal reflex
paralysis death
1
Not described in Guedels original monograph
Induction in children
Children from about 3 months of age until the teenage years are generally more
anxious, or less able to control their anxiety, than adults. The preoperative visit is
important in children because meeting the anaesthetist and having the procedure
explained calms the fears of children and parents. If the child is old enough, address
your conversation to him or her. Explain in detail what will happen, and invite the
parents and child to ask questions. Where possible, bring relevant equipment,
particularly a face mask for gas induction, for the child to become familiar with.
Topical local anaesthetic cream such as EMLA (a eutectic mixture of lignocaine and
prilocaine) or amethocaine gel is desirable if awake intravenous access is planned.
Marking visible veins in advance helps the nurse to cover the right spots. Both
preparations are similarly effective in clinical practice though onset and duration of
action differ (Figure 4).
It has become common for parents to accompany children to the anaesthetic room,
and this is generally helpful. Smaller children may best be anaesthetized on a parents
lap a well-positioned hug serves to comfort the child and to restrain them during
intravenous cannulation or gas induction. Strapping for the cannula, and the induction
drugs, should be on hand for swift application once access has been obtained.
For gas induction, a sideways hug helps to immobilize all the limbs, while the
anaesthetists hands control the head.
For intravenous cannulation, a face-to-face hug (Figure 5), with the childs arm
under the parents arm, helps to immobilize the arm and restrict the childs view of
cannulation.
The older child may prefer or need to be anaesthetized on the trolley. If the trolley
permits, it is useful to raise the back until just before (or even during) induction itself.
This more upright position allows the child a better view of their surroundings, and
hence a feeling of more control and less anxiety.
Children should be treated with respect at all times. They should be spoken to
in non-condescending language they can understand if something is going to be
unpleasant, it should be acknowledged. The alternative is for the child to become
suspicious and uncooperative for even the most innocuous procedure. There is no
formula that will ensure every paediatric induction is smooth and trouble-free; some
children will be understandably fractious despite all efforts to calm them.
Comparison of EMLA cream and amethocaine gel

EMLA cream Amethocaine gel
Constituents Lignocaine 2.5%, Amethocaine 4%
prilocaine 2.5%
as an oil/water
emulsion
Presentation White cream, 5 g Clear gel, 1.5 g

per tube per tube
Application 2 g minimum 1 hour 1 g 3045 minutes

before venepuncture, before venepuncture.
maximum 5 hours Remove after 45 minutes
Duration Efficacy declines soon Efficacy remains 46
after cream is hours after application
removed
Skin effects Usually transient Usually transient
paleness redness
May produce redness May produce itching
and oedema and oedema
Contra-indications Not for children Not for children

< 1 year < 1 month
5 Hugging the child face to face helps to immobilize the arms.
Further Reading
Association of Anaesthetists of Great Britain and Northern Ireland.Recommendations
for Standards of Monitoring During Anaesthesia and Recovery. 1994.
Sear J W. Induction of Anaesthesia. In: Aitkenhead A R, Jones R M, eds. Clinical
Anaesthesia. London: Churchill Livingstone, 1996: 15572.

Induction of Anaesthesia in
Special Circumstances
Christopher F Kearns
Christopher F Kearns is Consultant Anaesthetist in the Nuffield Department of

Anaesthetics, The Radcliffe Infirmary, Oxford, UK. He qualified from Charing Cross
Hospital and trained in anaesthesia and intensive care at St Bartholomews Hospital,
London, in Toronto, Canada, and at Oxford. His clinical interest is neuroanaesthesia. He
organizes the Oxford Primary FRCA courses.
A full stomach
The pulmonary aspiration of acid gastric contents has long been recognized as a major
risk of anaesthesia. Patients are normally asked to fast preoperatively to allow sufficient
time for gastric emptying. However, induction of anaesthesia in the presence of a full
stomach may be unavoidable when normal gastric emptying is impaired, or when the
urgency of surgical intervention overrides the requirement for a patient to have fasted
adequately. Gastric stasis, ileus and reverse peristalsis may accompany obstruction
or perforation of the gastrointestinal tract. Trauma, pain and its treatment with opioids
delays gastric emptying. Gastric motility may also be abnormal in the presence of
diabetes mellitus or obesity and in these circumstances no period of fasting may be
considered to be safe. The hazards of induction of anaesthesia in these circumstances
are listed in Figure 1.
If the patient has a full stomach an attempt to reduce intragastric volume and
acidity before anaesthetic induction is desirable. Gastric fluid may be removed through
a gastric tube, or if there is time and no contraindications by giving a prokinetic
agent (e.g. metoclopramide, 10 mg i.v.). The pH of the gastric contents may be
increased by the ingestion before induction of a non-particulate alkali, usually 30 ml of a
0.3 molar solution of sodium bicarbonate.
Induction of anaesthesia in the presence of a full stomach
Hazards Management
Pulmonary aspiration of Reduce gastric volume
gastric contents Raise intragastric pH with alkali
Use of cricoid pressure
Rapid sequence induction
Unanticipated failure to Preoxygenation

intubate Rapid sequence induction
Failed intubation drill

Rapid sequence induction is the anaesthetic technique indicated in the presence of a
full stomach (Figure 2). It aims to reduce to a minimum the period during which the
airway is unprotected after induction of anaesthesia and before inflation of the cuff of
a correctly placed tracheal tube.
During preparation for rapid sequence induction, a skilled assistant should carefully
identify and hold the cricoid cartilage between the thumb and forefinger, ready to apply
cricoid pressure as anaesthesia is induced. Cricoid pressure (Sellicks manoeuvre)
correctly applied with adequate, but not excessive, force compresses and occludes
the upper oesophagus between the flat posterior surface of the cricoid cartilage and
the body of the sixth cervical vertebra, preventing reflux of gastric contents without
distorting the view at laryngoscopy. If a gastric tube is already in place, it should not be
removed but should be allowed to act as a gastric vent.
The main risk of rapid sequence induction is that there is no prior opportunity
to ensure that intubation or mask ventilation will be possible after induction. Good
preparation for intubation is vital and it is essential that all equipment is checked,
suction equipment and aids to oxygenation are ready and the patient is in an optimum
intubating position.
The patients lungs should be preoxygenated. This is achieved by allowing the
patient to breathe 100% oxygen through a tightly fitting mask and anaesthetic circuit
for about 3 minutes. When apnoea occurs at induction, the lung rests at end tidal
volume where there is equilibrium between the elastic recoil of the lungs and the
chest wall. Arterial oxygen desaturation follows when the oxygen content within the
functional residual capacity (FRC) of the lungs is exhausted. During preoxygenation,
the nitrogen in the FRC will be displaced, increasing the oxygen content of this
reservoir substantially and delaying the onset of cyanosis after induction of apnoea.
Despite these measures, arterial oxygen desaturation is accelerated by the presence
of a reduced FRC (e.g. obesity), a raised metabolic oxygen demand (e.g. sepsis) or a
combination of the two (e.g. late pregnancy).
Rapid sequence induction requires the use of rapidly acting induction and paralysing
agents injected intravenously in quick succession. Most intravenous induction agents
cause loss of consciousness within one armbrain circulation time in the following
doses: thiopental (thiopentone), 24 mg/kg, etomidate 0.20.3 mg/kg, propofol 23
mg/kg. In UK practice, suxamethonium, 1.5 mg/kg, remains the neuromuscular blocking
agent of choice because it provides optimum intubation conditions in the shortest time.
Once the correct position of the tracheal tube is verified clinically and by
capnography and after the cuff has been inflated, cricoid pressure can be released.
In case of failure to intubate, the duration of action of the induction and paralysing
agents is critical. Despite the additional time made available by preoxygenation, it may
be impossible to see the larynx or intubate the patient. It is then essential to revert to a
well-rehearsed failed intubation drill. The effects of the common induction agents wear
off in a few minutes and the choice of suxamethonium is reinforced by its short duration
of action. The temptation to give a second dose of the drugs and prolong attempts
at intubation should be resisted. At this point, resumption of patient oxygenation is
the priority.
Selection of intubation aids and equipment for cricothyroid puncture

Skilled assistant applying cricoid pressure
Patient on surface that can be tipped head down
Suction switched on with catheter under pillow
Optimal patient intubating position
Good quality venous access with running intravenous infusion
Preoxygenation with 100% oxygen through close fitting face mask
Single sleep dose of intravenous induction agent
Single adequate intravenous dose of suxamethonium (e.g. 1.5 mg/kg)
After head injury

Induction of anaesthesia and tracheal intubation after head injury (Figure 3) is indicated
when:
the patients airway or oxygenation is compromised
the patient has a depressed level of consciousness (Glasgow Coma Score of 8
or less)
in the presence of agitation
before emergency surgery
in preparation for safe transfer to either CT scanner or to a neurosurgical centre.
It is vital to prevent secondary brain injury due to hypoxia, hypotension, hypercapnia
or uncontrolled rises in intracranial pressure. The patient is assumed to have a full
stomach so a rapid sequence induction with preoxygenation and cricoid pressure is
indicated. In addition, patients presenting with a severe head injury must be assumed
to have suffered a cervical spine injury. Cricoid pressure is applied using a two-handed
technique, the second hand supporting the back of the cervical spine. Another assistant
is required to provide manual in line stabilization of the spine during induction because
any cervical collar has to be temporarily removed to facilitate intubation. Coexisting
facial injuries need to be assessed carefully because they may affect intubation by
displacing, distorting or obstructing the airway.
Careful monitoring of cardiovascular status is required. It may not be practical to
monitor blood pressure invasively before induction, but non-invasive measurements
should be made frequently. Suppression of the hypertensive response to intubation
requires an intravenous induction agent, though the dose may have to be reduced
in the presence of depressed consciousness. Lidocaine (lignocaine), 1 mg/kg, may
also be given for this purpose. After induction there should be a smooth transition
to maintenance sedation, which may include opiates, to avoid fluctuations in blood
pressure.
Suxamethonium is associated with a transient rise in intracranial pressure, but this
potential for harm is outweighed by its advantage of rapidly producing optimal intubating
con-ditions and thereby reducing the risk of hypoxia. A peripheral nerve stimulator
will help to ensure adequate neuromuscular blockade before intubation, and that a
non-depolarizing agent is given in time to prevent coughing and facilitate controlled
ventilation as the effect of suxamethonium wears off.
Tracheal and gastric tubes should not be placed nasally, for fear of breaching a
skull base fracture. Constriction or distortion of neck veins that could result in cerebral
venous hypertension should be avoided when securing the tracheal tube and applying
a cervical collar. Arterial hypotension must be actively investigated and treated, while
moderate hypertension should be tolerated because this may be a normal response to
intracranial hypertension, preserving cerebral perfusion pressure.
Induction in head injury
Hazards Management
Full stomach See Figure 1

Cervical spine injury assumed In line stabilization of neck
Two-handed Sellick manoeuvre
Rising intracranial pressure Adequate dose of induction agent
Adequate neuromuscular blockade
Smooth transition to maintenance sedation and
paralysis
Reduced cerebral perfusion Avoid hypotension
pressure
Facial injuries Intubation facilitated or made more difficult
Skull base fracture Avoid nasal intubation
Upper airway obstruction
The management of the patient with obstruction of the upper airway, including the
larynx, is a vital skill for anaesthetists (Figure 4). Adequate diagnosis of the airway
pathology and the derangement of normal anatomy should precede discussion of
the management plan between senior anaesthetic and ENT staff. An alternative
strategy must also be agreed so that there is a back-up plan before proceeding. The
management plan should be explained clearly to the patient, whose cooperation will be
required.
Induction in airway obstruction
Hazards Management
Potential for airway obstruction Senior help present
in expert hands
Abnormal anatomy Information from imaging or endoscopy
Loss of muscle tone in upper air- Inhalation induction or awake tracheostomy

way at induction may precipitate
complete obstruction
Obstruction during inhalation Back-up plan in place

induction with scrubbed ENT surgeon for surgical
airway
4
Assessment of the patient may elicit stridor (inspiratory noise) at rest, which
suggests that the airway is more than 50% narrowed. Results of radiographs, CT or
MRI scans or nasendoscopy should be available. In their absence it may be appropriate
to perform endoscopic examination by fibrescope via a topicalized and vasoconstricted
nasal passage. The site of obstruction must not be approached with the fibrescope
because attempted fibre-optic intubation may be impossible and may be hazardous,
but endoscopy may provide important reconnaissance information. If there is doubt
about the feasibility of intubation, then an awake surgical tracheostomy under local
anaesthesia should be considered.
If intubation is likely to be possible, an alternative strategy must be in place before
embarking on induction of anaesthesia. A scrubbed ENT surgeon must be present
ready for immediate intervention and opening of a surgical airway.
The usual technique for induction of anaesthesia in the presence of upper airway
obstruction is an inhalation induction. Most experience has been obtained with
halothane although use of sevoflurane is growing. Gradual induction of anaesthesia
while maintaining spontaneous ventilation and airway muscle tone may allow adequate
depth of anaesthesia for intubation without airway closure. Should there be no
obstruction, no manipulation of the airway or laryngoscopy is allowed before adequate
depth of anaesthesia is achieved as judged by the pupils coming to lie centrally. It is
vital that no neuromuscular blockade or intravenous sedation is used before the airway
is safely secured.
Obstruction of the airway during inhalation induction prevents further uptake of
anaesthetic agent, therefore allowing anaesthetic depth to lighten and the patency
of the upper airway to be restored. An awake surgical tracheostomy should then be
performed under local anaesthesia.
FURTHER READING
Mason R A, Fielder C P. The Obstructed Airway in Head and Neck Surgery.
Anaesthesia 1999; 54: 6258.
Oldroyd G J, Dearden N M. Management of Acute Head Injury. In: Van Aken H ed.
Neuroanaesthetic Practice, Fundamentals of Anaesthesia and Acute Medicine. London:
Vanner R G, Asai T. Safe Use of Cricoid Pressure. Anaesthesia 1999; 54: 13.

Maintenance of Anaesthesia
James Austin

Cape Town, and trained in Anaesthesia in Reading, UK.
This contribution is an overview of what is meant, and required, by maintenance of

anaesthesia. Many of the topics are covered in greater detail in separate contributions;
the aim here is to put these topics in context.
Maintenance of general anaesthesia involves four priorities:
keeping the patient safe
keeping the patient comfortable
presenting the best possible operating conditions for the surgeon
preparing the patient for the postoperative period.
Keeping the patient safe
There are several aspects involved in keeping the patient safe:

airway, breathing and circulation
temperature control
monitoring
positioning.
Airway: this will usually have been established at the time of induction. However, it
should not be assumed that this remains secure. Airway disconnection or obstruction
may occur and the anaesthetist must be able to detect and correct these incidents
promptly, assisted by monitors such as the capnograph, pulse oximeter, disconnect
alarm and airway pressure monitor. Movement of the tracheal tube (either towards the
right main bronchus or withdrawal from the trachea) or dislodgement of the laryngeal
mask airway (LMA) are particularly likely to occur when patients are transferred to the
operating table or when changes are made to patient position. These periods require
increased vigilance by the anaesthetist. The integrity of the airway should be rechecked
both clinically and by monitoring after each patient movement.
Tracheostomy, rigid bronchoscopy or one-lung thoracic surgery may require
intraoperative changes to the airway. The anaesthetist must be prepared for such
changes and, if necessary, should formulate a plan with the surgeon in advance as to
how the airway will be managed.
Breathing will often depend on whether muscle relaxants are being employed as part
of the anaesthetic technique. Although the use of muscle relaxants is not essential for
controlled ventilation, they are usually employed for ventilated patients. Surgical factors
often influence the decision to use muscle relaxants. For example, abdominal surgery
is greatly facilitated by muscle relaxation. In specialized surgery, such as ophthalmic
surgery or neurosurgery, where the slightest move or cough may have disastrous
consequences and carbon dioxide must be controlled, paralysis is ideal. Otherwise,
anaesthetists have widely differing views as to whether breathing should be controlled.
Some anaesthetists use muscle relaxants almost routinely for any operation lasting
longer than about 30 minutes, on the basis that carbon dioxide retention is avoided,
potent short-acting opioids can be used without fear of respiratory depression, and
good lung aeration with avoidance of atelectasis may be easier to achieve. Others
control ventilation less often unless indicated for reasons of airway management or
the requirements of surgery. Some advantages and disadvantages of paralysis and
ventilation are listed in Figure 1.
The technique of paralysing and ventilating may be preferred when a tracheal tube
is present. It is likely that a relaxant will already have been given to enable intubation.
Also, the presence of a tube within the trachea is a potent stimulus, and unless local
anaesthesia has been applied to the respiratory tract, a deeper level of anaesthesia
may otherwise be needed for the patient to breathe spontaneously without coughing.
Lighter planes can be tolerated when a laryngeal mask or oropharyngeal airway are
employed, because these devices are less stimulating to the patient. Paralysing and
ventilating may also be used for longer operations, where carbon dioxide control and
prevention of atelectasis is important.
However, avoiding relaxants wherever possible can reduce two important
complications of general anaesthesia:
unrecognized awareness patient movement usually warns of light anaesthesia
before the patient becomes aware
accidental hypoxia the spontaneously breathing patient may maintain oxygenation
even in the event of circuit disconnection.
Use of muscle relaxants and controlled ventilation
May allow lighter anaesthesia because reflex May allow unrecognized awareness as a result of inadequate
activity is abolished by neuromuscular blockade anaesthesia
Facilitates abdominal surgery by relaxation of abdominal Reliance on ventilation equipment and circuit integrity to
muscles maintain alveolar ventilation
Intracranial and intraocular pressure control by regulation of PaCO2 Possible side-effects of muscle relaxant drugs (e.g. histamine
release, vagal blockade, malignant hyperpyrexia)
Allows effective ventilation during, for example, thoracic surgery,
prone positioning or long procedures Need for reversal of neuromuscular blockade
Allows use of potent opioids to reduce the surgical stress response Possible contraindication in patients with a difficult airway.
in major surgery Absence of spontaneous respiration may render ventilation
impossible
May improve surgical conditions by facilitating a hypotensive
technique and lowered PaCO2 When there is requirement to monitor neuromuscular function
(e.g. facial nerve during surgery on the parotid gland
Decreases intraoperative atelectasis or acoustic neuroma)
Decreases energy requirements and tissue carbon dioxide Contraindicated in some myopathies
production
Ventilator settings most anaesthesia ventilators are time-cycled and volume- or

flow-driven. A rate, usually with a ratio of inspiratory time to expiratory time (I:E), and a
tidal volume or flow need to be set. Most adults have a minute volume of 80100 ml/kg,
therefore a tidal volume of 8 ml/kg (e.g. 500600 ml) and a rate of 10 breaths/minute is
a good starting point; this can be adjusted according to the observed end-tidal partial
pressure of carbon dioxide (PECO2). For routine surgery, a PECO2 of about 4.5 kPa should
be aimed for. If metabolic rate and cardiac output (and hence pulmonary perfusion) are
assumed to be constant, then PE CO2 varies inversely with the alveolar ventilation.
In general, an I:E ratio of 1:2 is often the best compromise between maintaining
low inflation pressures (e.g. 1520 cm H2O), satisfactory oxygenation (Sp O2 > 95%) and
adequate carbon dioxide removal (PECO2 4.5 kPa). However, this can be decreased to
1:1.5 or even 1:1 to prolong inspiratory time. This may be useful in some patients to
help decrease high airway pressures (e.g. > 2530 cm H2O) or improve oxygenation
(e.g. in the obese). Some patients with asthma or chronic airway disease may benefit
from a longer expiratory time to allow the lungs to empty, and an I:E ratio of 1:3 or
1:4 may be preferable.
Children have a proportionately higher minute ventilation than adults up to
200 ml/kg in infancy, approaching adult values weight-for-weight by about age 10
years. Given that their tidal volume is slightly less weight-for-weight than adults
(7 ml/kg), this increased minute volume must be provided for by an increase in rate.
For example, in a 5 kg infant, a minute volume of 1000 ml might be provided by 30
breaths each of about 33 ml/minute.
However, paediatric ventilation is complicated by the obligatory leak around the
uncuffed tube. Volume control is unlikely to inflate the lungs to the set volume
(especially if a Newton valve is used with T-piece ventilation). This is usually overcome
by increasing the tidal volume by titrating against inflation pressure and/or PECO2. Some
modern anaesthesia ventilators have pressure control capabilities (e.g. the Draeger
Julian). Specific compliance varies little with age, therefore pressure control mode can
be used to deliver an inflation pressure of 1520 cm H2O. This provides an adequate
tidal volume for any age, despite small to moderate leaks, as long as lung compliance
is normal.
Regardless of the mode of ventilation, a fresh gas flow must be selected. This
depends on the breathing system in use as well as the size of the patient. A high flow
should be used initially (e.g. 6 litres/minute), regardless of the circuit being used. This
allows time for denitrogenation and equilibration of inhaled anaesthetic agent during this
early period of rapid anaesthetic uptake. After about 10 minutes, flows can be reduced
considerably if the system permits. The circle system with carbon dioxide absorber is
widely used, and modern lightweight valves and low-resistance tubing make it suitable
for paediatric use well below the traditional lower patient weight limit of 20 kg. With
appropriate monitoring of gas concentrations within the circle, this permits total fresh
gas flows of 1 litre/minute or less. Higher flows are required for T-pieces such as the
Bain and Jackson Rees systems. Formulae exist for each of these circuits to predict
the flow of fresh gas required per kilogram patient weight to eliminate rebreathing
for controlled and spontaneous respiration. However, a more practical approach is
to reduce the fresh gas flow gradually, stopping when rebreathing of carbon dioxide
begins to appear on the capnograph.
General anaesthesia, particularly when using volatile anaesthetic agents, causes
the development of atelectasis in the dependent parts of the lung and impairs the
pulmonary vascular response to hypoxia (hypoxic pulmonary vasoconstriction). These
two factors produce a small but noticeable degree of shunt, usually about 10%. This
can be corrected by giving anaesthetized patients higher inspired oxygen than the
21% present in air; 30% is usually given, though this can be titrated against observed
oxygen saturation.
Circulation: appropriate fluid management is an important component of anaesthetic

maintenance. Intravenous fluid requirements may range from none in short and
relatively non-invasive procedures, to many times the circulating volume in long and
traumatic procedures. Fluid requirement consists of:
replacement of existing deficit crystalloid or blood
metabolic maintenance requirements crystalloid
replacing additional ongoing losses crystalloid, colloid or blood.
Existing deficit in the adult elective surgical patient, who has been starved
for at least 4 hours preoperatively (and sometimes much longer), a deficit of 500 ml
of crystalloid can be assumed. This deficit is generally well tolerated and does not
necessarily need replacing, but it decreases the patients margin of reserve against
any further losses, or against ongoing postoperative dehydration as a result of nausea
or vomiting. Many anaesthetists routinely administer 5001000 ml of crystalloid in all
patients except those at risk from fluid overload (e.g. those with renal or cardiac failure).
There is evidence to suggest that this may improve the quality of early recovery and
help to decrease postoperative nausea.
In the emergency patient, fluid deficit may be considerable, as a result of either
trauma-related blood loss, or anorexia, vomiting and/or interstitial (third-space) fluid
loss from surgical pathology. In either case, the deficit should be assessed and
replaced with the appropriate fluid. The larger the deficit, the more important that it be
replaced before induction, whenever circumstances permit. The exception to this rule is
during major ongoing blood loss, such as a ruptured aortic aneurysm or major trauma,
where the priority is stopping the bleeding rather than prolonging attempts to normalize
the circulation preoperatively.
Maintenance for many patients this is the least important component of
intraoperative fluid management the average adult requirement of about 100 ml/hour
is negligible in the context of a short procedure and other fluid losses. However, in small
children, maintenance requirements are proportionately larger and more significant.
Paediatric maintenance fluid is usually calculated according to: 4 ml/kg/hour for the first
10 kg, plus 2 ml/kg/hour for the next 10 kg, plus 1 ml/kg/hour for the remainder. Thus,
a 25 kg child would have a maintenance requirement of 40 + 20 + 5 = 65 ml/hour. The
smaller the child, the less reserve there is for managing without ongoing maintenance
fluids, and the greater the impact of preoperative starvation.
Infants have small glycogen reserves, and therefore need intravenous dextrose (e.g.
as 5% dextrose in 0.18% saline) as maintenance to sustain their blood sugar levels.
For longer procedures, careful attention must be paid to electrolyte balance, because
infants have less ability to correct excessive salt loads or water loads.
Ongoing losses the most significant aspect of intraoperative fluid management
can be the most difficult to estimate.
Losses from extravascular spaces (e.g. gastrointestinal, evaporative, third-space
fluid losses) are usually crystalloid losses. Evaporative losses can be large an adult
may lose in excess of 1 litre/hour from a laparotomy or thoracotomy wound, and even
larger amounts from extensive open skin wounds such as burns or large graft sites.
There is no way of measuring these losses directly, and measures such as blood
pressure, pulse rate or central venous pressure (CVP) provide only an indirect measure
of total body water. Urine output may be the most useful clinical measure. Blood tests
such as plasma urea, sodium and haematocrit may provide information regarding the
hydration state, and plasma electrolytes and haematocrit are now commonly available
from blood gas machines.
Losses also occur from the intravascular space (i.e. blood). Losses in suction
bottles may be complicated by wash, faeces, urine or amniotic fluid. Visual estimates
of blood loss on swabs are often inaccurate weighing of swabs is more precise, but
still neglects losses on drapes, gloves and instruments. A dilutional technique relies
on washing all swabs, instruments and gloves in a fixed volume of water, which can
then be measured colorimetrically to give an accurate measure of blood loss. Such
instruments are not widely available. Intravascular loss may be estimated indirectly from
clinical measures such as blood pressure, pulse rate or CVP, though other anaesthetic
factors such as the balance between surgical stimulation and depth of anaesthesia
complicate these measures. Estimation of haemoglobin is useful only when adequate
intravascular volume has been replaced. Blood losses may initially be replaced by
colloid solution (e.g. a gelatin solution or hydroxyethyl starch), but larger losses (> 20%
blood volume) may require replacement by packed-cell blood. Very large losses (> 1
blood volume) may require supplementation with fresh frozen plasma and/or platelets to
maintain clotting function.
In practice, it is likely that fluid losses are under-replaced in many patients. This
is offset by the hormonal stress response to surgery: aldosterone, cortisol and
antidiuretic hormone levels rise and atrial natriuretic peptide falls; all contribute to
postoperative water retention.
Temperature control: there is now good evidence that the maintenance of a
physiological body temperature reduces postoperative morbidity. Patients suffering from
head injury or undergoing certain neurosurgical procedures are possible exceptions.
Shivering increases oxygen consumption, and predisposes to myocardial ischaemia,
dysrhythmias, hypotension and acidosis. Hypothermia also increases susceptibility to
infection and tends to lengthen hospital stay.
Temperature control is of particular importance in patients at the extremes of age
(who have less intrinsic control over body temperature and a larger surface area-to-
volume ratio through which to lose heat), in operations involving open body cavities,
and in all patients undergoing lengthy procedures. About 20% of trauma patients who
arrive at hospital are hypothermic (core temperature < 35C).
A change in core temperature as a result of general anaesthesia is a three-phase
response.
The first phase is a brisk fall in core temperature as a result of vasodilatation, caused
by redistribution of heat to the peripheries. Core temperature may be as low as 35.5C
in some patients after transfer to the operating theatre from the anaesthetic room.
The second phase is a slower but more sustained fall as a result of accelerated loss
of heat to the environment from the warmer peripheries.
The third phase is a stable equilibrium at a lower core temperature.
It is important to note that the anaesthetic itself brings about these changes, which
are independent of the nature of the surgery, though surgery may modify the pattern.
The use of spinal or epidural anaesthesia instead of general anaesthesia reduces, but
does not abolish, the three-phase response described above.
Passive rewarming is the prevention of heat loss, typically by raising the
temperature of the environment. Passive rewarming can serve to modify only the
second phase of the heat loss response. Covering with blankets or the use of foil
space blankets decreases heat loss by reduced transfer of heat by convection,
conduction, evaporation and radiation.
Dry inspired anaesthetic gases need to be humidified, and a heat and moisture
exchange filter in the breathing system reduces heat loss by evaporation from the
respiratory tract (latent heat). Low flows in a circle system (e.g. 1 litre/minute) further
reduce the quantity of dry gas needing to be humidified and help retain heat and
moisture within the breathing system.
A normal operating room temperature of 21C is a compromise between that which
is warm enough for the patient, but cool enough for the comfort of theatre personnel. An
increase in theatre temperature (e.g. to 25C) helps to reduce the gradient for heat loss
in patients at high risk (e.g. young children, patients with extensive burns).
Active rewarming is the addition of heat into the patient. It may be used to prevent
or reverse the first phase of the temperature drop. The local environmental temperature
can be raised so much that the transfer of heat is reversed. Warm air convection
blankets (e.g. the Bair Hugger) are considered as active rewarming.
Intravenous fluid warmers play an increasingly important role the greater the volume
of intravenous fluid given. A fluid-warming device should be used in all at-risk patients
and especially when stored blood is administered. Ventilatory gases may be warmed
using a heated humidifier. Overhead radiant heaters may be used when a large area
of the body needs to be exposed, and neonates may undergo surgery on an open
incubator such as the Resuscitaire.
Cardiopulmonary bypass represents the ultimate in active rewarming, but is practical
only in cardiothoracic surgery or in uncommon resuscitation situations.
Care is needed not to overheat the patient and temperature monitoring is necessary
when active rewarming methods are used. Monitoring probes are available for a
variety of body cavities, including nasopharynx, oesophagus, rectum, bladder and
tympanic membrane. In routine clinical practice, core temperature is usually measured
by nasopharyngeal or rectal temperature probes. Surface temperature monitors do
not reflect core temperature, but the coreperipheral gradient may provide a useful
measure of peripheral vasodilatation. A gradient of less than 2C implies good
peripheral perfusion.
Monitoring: the Association of Anaesthetists has published recommendations on

standards of monitoring. A summary is given in Figure 2.
Blood sugar should be monitored in infants and diabetic patients. The blood sugar of
diabetic patients should be known before anaesthesia is given, and should be estimated
every 12 hours during routine surgery.
The Association of Anaesthetists summary of standards of monitoring
The Association of Anaesthetists of Great Britain and Ireland strongly

recommends that the standard of monitoring used during general
anaesthesia should be uniform in all circumstances irrespective of the
duration of anaesthesia or the location of administration
An anaesthetist must be present throughout the conduct of general
anaesthesia
Monitoring should be commenced before induction and continued until the
patient has recovered from the effects of anaesthesia
These recommendations also apply to the administration of local
anaesthesia, regional analgesia or sedation where there is a risk of
unconsciousness or cardiovascular or respiratory complications
The anaesthetist should check all equipment before use. Monitoring of
anaesthetic machine function during the administration of anaesthesia
should include an oxygen analyser with alarms. During spontaneous
ventilation, clinical observation and a capnometer should be used to detect
leaks, disconnection, and rebreathing and high pressure in the breathing
system. Measurement of airway pressure, expired volume and carbon
dioxide concentration is strongly recommended when mechanical ventilation
is employed
A pulse oximeter and capnometer must be available for every patient
It is strongly recommended that clinical observation of the patient should be
supplemented by continuous monitoring devices displaying heart rate, pulse
volume or arterial pressure, oxygen saturation, the electrocardiogram and
expired carbon dioxide concentration. Devices for measuring intravascular
pressures, body temperature and other parameters should be used when
appropriate. It is useful to have both waveform and numerical displays
Intermittent non-invasive arterial pressure measurement must be recorded
regularly if invasive monitoring is not indicated. If neuromuscular blocking
drugs are used, a means of assessing neuromuscular function should be
available
Additional monitoring may be required in certain situations. These
recommendations may be extended at any time on the judgement of the
anaesthetist
Positioning: an unconscious patient cannot move to relieve an uncomfortable position,

and it is the anaesthetists responsibility to prevent discomfort from becoming damage.
The anaesthetist is also responsible for protecting the patient during movement on and
off the operating table, and during changes of position. Traditionally, the anaesthetist
has particular responsibility for the head and airway. It must be ensured that all
members of the team are working to a common agenda and with coordinated timing.
It is usually easiest and safest to disconnect as much equipment as possible before
moving the patient.
Prophylaxis against venous thromboembolism the thrombotic process often
starts intraoperatively. It is difficult to identify patients at high risk, though coexisting
medical illness, major surgery, malignancy, trauma (especially hip and pelvis), obesity,
high-dose oestrogen therapy and age greater than 40 years are well-known risk factors.
Thromboprophylaxis should commence before anaesthesia; gradated compression
stockings and low-dose unfractionated heparin, 5000 IU s.c. twice daily, continued until
full mobilization, is popular and effective. When positioning for surgery, raising the heels
on foam pads prevents venous stasis in the calves. Intermittent pneumatic compression
pumps assist venous return, but it is not known whether this reduces the incidence of
postoperative pulmonary embolism.
Keeping the patient comfortable

Traditionally, the main components of anaesthetic maintenance are unconsciousness
(hypnosis), analgesia and absence of movement. Some advantages and disadvantages
of using muscle relaxants have been discussed. Keeping the patient unconscious and
relieving the pain of surgery are now considered.
Maintenance of unconsciousness is usually achieved by anaesthetic drug delivery

via the inhalational or intravenous route, or both. The intramuscular route is seldom
used in hospital practice owing to the relatively slow onset of drug action, unpredictable
duration and delayed recovery. Ketamine, 10 mg/kg, is the only useful intramuscular
agent, with an onset of 510 minutes producing up to 30 minutes of anaesthesia. It has
a role in the provision of emergency anaesthesia in difficult locations.
Inhalational route this is the most widely used technique, using a volatile
anaesthetic agent with or without nitrous oxide. It therefore requires a supply of
compressed gas, a vaporizer and a breathing system for drug delivery. Compressed
gas may not be required if a drawover type vaporizer is used.
The potency of an inhaled anaesthetic agent may be described in terms of its
minimum alveolar concentration (MAC). MAC is defined as the alveolar concentration
of the anaesthetic agent which at equilibrium is required to prevent gross reflex
muscular movement in response to a standardized skin incision in 50% of healthy,
unpremedicated patients. It is therefore a measure of anaesthetic potency, and is the
effective dose in 50% of the population (ED50). It should be borne in mind that not all
operations are a standardized skin incision. The amount of anaesthetic needed to
remove a foreign body from the nose is very different from that needed for an anal
stretch. It is important to know the MAC of individual inhalational agents and the factors
on which they depend (Figures 3 and 4).
Of any given inhalational anaesthetic, 0.71.3 MAC will anaesthetize 95% of the
population. MACs are also additive: 0.5 MAC of nitrous oxide (52%) plus 0.5 MAC of
isoflurane (0.6%) is equivalent to 1 MAC of any other inhalational agent given alone.
The principle of MAC acts as a useful guide. It allows the anaesthetist to select
a vapour concentration that is likely to maintain unconsciousness. The state of
anaesthesia is related to the partial pressure of anaesthetic within the brain, which
is taken to be equivalent to the alveolar partial pressure. This can be measured by
analysis of the end-tidal partial pressure of the anaesthetic agent. What is dialled on
the vaporizer or the nitrous flowmeter is not necessarily what is in the patients alveoli
the fresh gas flow takes time to equilibrate both with the dead space of the circuit and
with the uptake by the patient. Observing how the ratio of end-tidal to inspired partial
pressure varies with time can assess this rate of uptake (or wash-in).
MAC is useful to estimate the amount of anaesthetic required. In clinical practice
this must be adjusted against indicators such as pulse rate, blood pressure, respiratory
rate, patient movement, pupillary size, lacrimation and sweating. Many of these
variables may be abolished by factors other than anaesthetic depth. Tachycardia may
be prevented by co-administered -blockers, hypertension masked by hypovolaemia,
respiratory rate and patient movement abolished by paralysing drugs, and pupillary
size altered by use of opioids or anti-muscarinic drugs. Thus, lacrimation and sweating,
though crude indicators of inadequate anaesthesia, reflect the need for clinical
observation in addition to monitoring.
Minimum alveolar concentration (MAC) of inhalational anaesthetic agents
Anaesthetic MAC in MAC in 70%

agent oxygen (%) nitrous oxide
Halothane 0.75 0.29
Enflurane 1.68 0.57
Isoflurane 1.15 0.50
Sevoflurane 2.0 0.8
Desflurane 69 2.53.5
Factors affecting minimum alveolar concentration
Decrease Increase No change

Increasing age Decreasing age Gender
Alcohol Alcohol Duration of
(acute ingestion) (chronic ingestion)
anaesthesia
Nitrous oxide Hyperthermia Time of day
Analgesics Hyperthyroidism Hypercarbia
Sedatives and hypnotics Hypocarbia
Hypotension
Hypothermia
Hypothyroidism
Hypoxia
4
Intravenous route a popular alternative to inhalational anaesthesia is total
intravenous anaesthesia (TIVA). Many intravenous anaesthetics have been used for
TIVA, including barbiturates, ketamine, etomidate and propofol. The pharmaco-kinetic
profile of propofol makes this drug the most commonly used for TIVA. It has a high
clearance (13001900 ml/minute), short metabolic half-life (60100 minutes) and
inactive metabolites. For short procedures, propofol may be administered following
initial intravenous induction by intermittent bolus with no special infusion equipment
(e.g. 50 mg as required every 35 minutes).
For longer procedures, the advent of reliable electronic syringe pumps, and in
particular the development of target-controlled infusion (TCI) software, have contributed
to the widespread use of TIVA techniques. Some advantages and disadvantages of
inhalational or TIVA maintenance are shown in Figure 5.
Consider a three-compartment model: vascular space, richly perfused organs, and
poorly perfused organs plus clearance. A large initial bolus of propofol is needed to fill
the vascular compartment, namely the induction dose. Thereafter an initially high rate
of infusion is needed to keep up with losses to the richly perfused compartment until
it approaches saturation. Then a slower rate is required to keep up with losses to the
poorly perfused but difficult to saturate compartment, and with metabolic clearance.
The Bristol regimen reflects these kinetics. This regimen aims to maintain a plasma
propofol concentration of about 3 g/ml by giving patients receiving 67% nitrous oxide
an initial bolus of 1 mg/kg, followed immediately by infusion at 10 mg/kg/hour for 10
minutes, then 8 mg/kg/hour for 10 minutes, then 6 mg/kg/hour thereafter. A dose of
10 mg/kg/hour is equal to the patient's weight (in kg) as ml/ hour of 1% propofol
hence a 60 kg patient will initially receive 60 ml/hour of 1% propofol. At the end of
the operation, switching off the propofol allows rapid redistribution from the vascular
compartment (and therefore from the richly perfused compartment also) to the still
unsaturated third compartment. It is this rapid redistribution that allows a prompt wake-
up even after a long period of TIVA.
TCI microprocessor-controlled technology (e.g. as incorporated in the Graseby 3500
Diprifusor syringe pump) requires manual input of patient age, weight and desired
plasma concentration. The pump then administers propofol according to the three-
compartment pharmacokinetic model incorporated into its software. Change to a higher
propofol concentration is achieved by a rapid zero-order infusion, and the plasma
concentration is calculated until the new predicted value is reached. Change to a lower
concentration is achieved by temporary cessation of drug infusion until the predicted
plasma level falls to the required level, followed by continuation of infusion at a lower
rate. The system is used in a similar fashion to adjusting the vaporizer setting during
inhalational anaesthesia; the predicted plasma concentration of drug is analogous
to the end-tidal concentration of the inhalational agent. Maintenance of satisfactory
anaesthesia requires a plasma concentration of propofol of 26 mg/ml, depending on
patient fitness, coexisting drug therapy and degree of surgical stimulation.
Comparison of inhalational anaesthesia and total intravenous anaesthesia (TIVA) maintenance techniques
Inhalational maintenance TIVA
Cost-effective (especially when used with low-flow circle systems) Independent of airway for drug delivery. May be advantage
Predictable population pharmacokinetics and confidence in anaesthetic in, for example, jet ventilation techniques
depth achieved No specialized equipment is essential. More suitable
Ease of measurement of end-tidal partial pressure technique for patient transport and difficult locations
Minimal metabolism of modern agents, no accumulation and Rapid increase in anaesthetic depth possible by
clearance independent of patient hepatic and renal function administration of intravenous bolus
Low incidence of postoperative nausea and vomiting and
better quality of early recovery (especially for propofol)
No contraindication in malignant hyperpyrexia
Requires conventional tidal ventilation for drug delivery Requires patent and dependable intravenous access.
Requires specialized equipment (e.g. vaporizer, anaesthetic Undetected failure may result in awareness
machine, agent analyser) Drug accumulation with prolonged infusion
Concern regarding tissue and organ toxicity (especially hepatotoxicity Inability to measure plasma concentration directly has led
following repeat halothane exposure) to concerns about possibility of awareness
All volatile anaesthetics are known triggers for malignant
hyperpyrexia
Environmental pollution
Analgesia: modern inhalational or intravenous anaesthetic drugs possess little

analgesic activity, with the exception of ketamine. For all but the simplest procedures,
analgesia must be provided by systemic analgesics (usually opioids) or by local
anaesthetics. Analgesia has several effects.
It reduces the required MAC (or plasma concentration) of co-administered
anaesthetic drugs. Analgesia is an important component of the balanced anaesthetic
technique.
It reduces the immediate autonomic activity in response to pain. Sympathetic
stimulation otherwise results in cardiovascular and respiratory responses that may lead
to myocardial ischaemia and dysrhythmias.
It reduces the neuroendocrine stress response caused by surgery.
Opioid analgesics such as fentanyl, 15 g/kg, reduce circulating concentrations
of the stress hormones that increase after moderate and major surgery (e.g.
noradrenaline, adrenaline, cortisol, growth hormone, glucagon, antidiuretic hormone).
The stress response is largely detrimental and leads to increased catabolism, metabolic
rate and oxygen consumption. This response is not significant in minor surgery.
The short-acting synthetic opioid drugs such as fentanyl and alfentanil are widely
used to provide intraoperative analgesia. Fentanyl, a synthetic opioid structurally
related to pethidine, is the most popular (12 g/kg for minor procedures, onset
12 minutes, duration 30 minutes). Its potency and minimal effect on pulse and blood
pressure make it commonly used for the provision of intense analgesia during surgery.
These drugs are unsuitable for routine use in postoperative analgesia because of their
short duration of action and their tendency to produce marked respiratory depression.
They are commonly substituted by longer-acting analgesics (e.g. morphine 0.10.2
mg/kg i.v.) towards the end of the procedure to provide pain relief following surgery.
Pre-emptive analgesia laboratory work suggests that noxious stimuli produce
hypersensitivity in the pain pathways both centrally and peripherally. Larger doses
of analgesics are then required to have an effect. If systemic analgesia or local
anaesthetics are used to prevent the initial pain, this hypersensitivity is reduced. This is
the basis of pre-emptive analgesia, but its clinical significance is disappointing.
Providing the best possible operating conditions
The surgeon hopes for two things from his patient during the operation: not to move,
and not to bleed. If the anaesthetist has succeeded in keeping the patient safe and
comfortable as described, then the patient is unlikely to move. The anaesthetist can
also help to minimize bleeding.
Tourniquets are ideal for extremity surgery. Traditionally, a 90-minute time limit is
imposed on upper limb tourniquets (usually at 250 mm Hg), and a 120-minute limit
on lower limb tourniquets (usually at 300 mm Hg). This is arbitrary; the longer the
tourniquet is on, the greater the potential for damage. The main risk is ischaemic
damage to nerves directly under the tourniquet; distal ischaemia is likely to take 46
hours to become significant. If antibiotics are necessary, they should be given at least a
few minutes before exsanguination.
Sickle-cell disease is an absolute contraindication to tourniquet use, because
sickling of haemoglobin S may be induced by the local hypoxia and acidosis.
Positioning adequate venous drainage from the operative site is ensured by
careful attention to patient positioning. Raising the operative site above heart level
decreases arterial and venous pressures. Arterial pressure falls by 2 mm Hg for each
2.5 cm vertical height. Head-up tilt is commonly used in head and neck surgery to
decrease bleeding, but there is a risk of venous air embolism.
Hypotensive anaesthesia moderate reduction of systolic blood pressure (e.g. to
7080 mm Hg) in otherwise fit patients may greatly improve the operative field. It must
be used with caution in patients with coronary, cerebral, renal or peripheral vascular
diseases who are at risk from ischaemic events. Techniques for deliberate hypotension
are outside the scope of this contribution.
Non-steroidal anti-inflammatory drugs used intraoperatively may increase blood
loss during surgery.
Blood gases carbon dioxide is a local vasodilator, and moderate hypocapnia (e.g.
PCO2 4.04.5 kPa) contributes to a dry surgical field.
Preparing the patient for the postoperative perio
The maintenance period is often a convenient time to complete the necessary

anaesthetic record and drug prescription charts. During anaesthesia, it should be
considered what else may be done while the patient is unconscious to enhance his or
her postoperative course. This includes the following.
Venous access must be sufficient for postoperative requirements. A central venous
line should be sited if access is likely to be difficult or prolonged, or to enable central
venous monitoring. A subcutaneous cannula for analgesic administration may avoid the
need for injections, especially in children.
A nasogastric tube is more comfortably inserted while the patient is asleep, and its
position can be checked during laparotomy.
Analgesia ideally, the plan for postoperative pain control should be formulated
before anaesthesia, and discussed with the patient. Balanced analgesia is the concept
of using several analgesics with differing modes of action, thus reducing dose-related
side-effects and enhancing overall analgesic effect. Typically this may involve local or
regional analgesia in combination with opioids, non-steroidal anti-inflammatory drugs
and simple analgesics (e.g. paracetamol).
Antiemetics should be given in particular to patients receiving opioids, and those at
high risk of postoperative nausea and vomiting (PONV). High risk includes patients with
a history of previous PONV or motion sickness, certain operations (e.g. gynaecological,
middle ear or strabismus surgery) and female gender.
Oxygen all anaesthetics (with the exception of ketamine) induce about 10%
shunt. Atelectasis, impaired hypoxic pulmonary vasoconstriction, diffusion hypoxia from
nitrous oxide use, opioid-mediated hypoventilation and other factors contribute to
making the postoperative patient prone to hypoxia. Added oxygen (e.g. 3040% via
a simple face mask) should be administered in the immediate recovery period to all
patients for about 15 minutes, guided by pulse oximetry. Subsequently, the need for
added oxygen must be determined for each patient depending on factors such as age,
pre-existing disease and the nature of anaesthesia and surgery.
Fluids there must be clear instructions for postoperative fluid intake. Elective
day-surgery patients will drink when ready, but in-patients and those undergoing major
procedures require intravenous fluids to replace continuing fluid losses and provide
maintenance. How far in advance fluids can be prescribed depends on the accuracy
of prediction of future needs.
Thromboprophylaxis stockings for prevention of thrombo-embolic disease
and/or regular heparin should be prescribed where indicated by local policy.
Antibiotics should be prescribed at the surgeon's discretion.
Monitoring the anaesthetist should understand the routine standard of monitoring
on the postoperative ward and ensure that it meets the needs of the patient. Specific
requirements must be clearly communicated, such as hourly urine output, hourly
blood pressure, overnight Sp O2 or any other observ-ations in an at-risk patient. Action
that should be taken if the observation deviates from the desired targets should be
documented.

Medical Gas Storage, Suction
Devices and Humidifiers
Ian R Taylor
Michael OConnor
Ian R Taylor is Specialist Registrar in Anaesthesia at the Princess Margaret Hospital,

Swindon, UK. He qualified from Bristol University and is training in Anaesthesia at
the Wessex School of Anaesthesia, Southampton, UK. His interests are vascular and
obstetric anaesthesia.
Michael OConnor is Consultant Anaesthetist in the Swindon and Marlborough NHS

Cylinders
Medical gas cylinders are made of molybdenum steel to ensure they are
strong and able to withstand high pressures, but are also relatively light
in weight. They are constructed as a seamless tube and consist of a
body, shoulder and neck. They are colour coded according to British and
International Standards (BS1319C and ISO32) to identify their gas contents (see
Figure 7, page 109). Cylinders are manufactured in different sizes from A, the smallest,
to J, the largest. Size E cylinders are usually attached to the anaesthetic machine and
size J cylinders make up manifolds.
The cylinder valve fits into the cylinder neck by a screw thread mechanism, to permit
safe, controlled use of its contents. The junction between the cylinder and valve melts
in the presence of intense heat, thus allowing escape of gas and minimizing the risk of
explosions. Between the neck and cylinder valve is a plastic disc, the colour and shape
of which denotes the year in which the cylinder was last examined (Figure 1).
1 Cylinder neck disc.
Cylinder body
The cylinder body is colour coded and engraved with:
test pressure
date of last test performed
chemical symbol of contents
tare weight (i.e. weight of empty cylinder).
It is also labelled (Figure 2) with the name and symbol of the gas it contains, its volume,
pressure and minimum purity (Figure 3). The label gives additional information relating
to storage, use (in conjunction with the Medical Gases Data Sheet) and safety matters.
The safety points highlighted are:
compressed gas
flammability status
avoidance of oil or grease because spontaneous combustion can occur with high-
pressure gases.
2 Cylinder label.
Cylinder size, volume, pressure and purity of contents
Gas Cylinder Volume Pressure Purity

size (litres) of gas at 15oC (kPa) (%)
Oxygen E 680 13700 99.5

Nitrous oxide E 1800 4400 98.0
Air E 640 13700 21.0 (oxygen)
Carbon dioxide C 450 5000 99.0
Storage
Cylinders must be stored under cover, in a dry, clean and well-ventilated area, away
from extremes of temperature.
Smoking or the use of a naked flame in the storage area is prohibited.
Moisture or exposure to chemicals can lead to the corrosion of the cylinder or its
valve.
Cylinders should be kept in the upright position or horizontal on shelves to avoid
direct damage to the valves.
Cylinders should be used in a sequential manner to ensure that no cylinder remains
in storage for too long.
Full and empty cylinders should be kept apart.
Testing
During manufacture, one in every 100 cylinders is cut into strips and tested for tensile
strength. Cylinders in circulation are tested on a 5-yearly basis by:
exposure to hydraulic pressure of about 22,000 kPa (far in excess of the pressures
encountered in daily use)
filling with water under pressure to assess expansion and elastic recoil
internal endoscopic inspection.
Test date details are recorded on the plastic disc between the cylinder valve and the
neck and engraved on to the cylinder body.
Filling
Medical gases are stored either in the gaseous state (oxygen and air) or as a mixture
of the liquid and vapour (nitrous oxide and carbon dioxide). Cylinders that contain liquid
should be used only in the upright position. Gases and vapours stored in cylinders must
be free of water vapour to avoid the formation of ice (secondary to a fall in temperature
on cylinder opening), which may block the exit valve. For cylinders containing gas
alone, the contents can be assessed directly by measuring the pressure using a
Bourdon gauge (see Anaesthesia and Intensive Care Medicine 1:2: 65). In the case of
cylinders containing both the liquid and vapour phases the situation is more complex.
The contents of these can be determined only by subtraction of the tare weight from the
cylinder weight because the pressure within will not fall until the liquid has completely
vaporized, assuming the temperature stays constant.
During nitrous oxide use, the liquid within the cylinders cools owing to the uptake of
latent heat of vaporization. Condensation or ice may form on the outside of the cylinder.
In such circumstances, the cylinder gauge pressure may fall despite there being liquid
nitrous oxide in the cylinder owing to the fall in saturated vapour pressure of nitrous
oxide following the drop in temperature of the liquid. However, once the gas flow is
turned off the temperature returns to that of the atmosphere and the gauge pressure
returns to that at the beginning of use. Carbon dioxide is used at low flows so the
chances of ice forming are low. Liquid is less compressible than gas, therefore cylinders
containing nitrous oxide or carbon dioxide are only partially filled with liquid. Any change
in pressure within the cylinder is minimized, thus reducing the chance of cylinder
rupture should the temperature rise.
The filling ratio is that between the mass of liquid contained in the cylinder and the
mass of water that it could contain if filled to the top. The filling ratios for nitrous oxide
and carbon dioxide are both 0.75 in temperate climates and 0.67 in the tropics.
Filling ratio = Mass of liquid

Mass of water
Cylinder valve
Cylinder valves are made of brass and screw into the cylinder neck. There are four
types of valve:
pin-index valve block
bull-nose valve
hand-wheel valve
star valve.
A pin-index valve is used on all cylinders that are to be attached to an anaesthetic
machine. It is an international system (ISO2407) designed to prevent the fitting of the
incorrect gas to the yoke and is fully detailed in the British Standard BS1319.
The system is made up of two components.
Two pins projecting from the yoke, which are arranged in a gas-specific
configuration in relation to the valve outlet
Two holes within the valve block on the cylinder with a corresponding pattern for
the designated gas (Figure 4).
This arrangement ensures that it is impossible to fit the incorrect cylinder to the yoke.
The pin-index valve block on the cylinder is engraved with:
tare weight
chemical symbol for contents
cylinder owner
pressure of hydraulic test.
4 Pin-index valve holes on the cylinder.
Cylinder use
New or refilled cylinders are supplied from the manufacturer with a plastic dust cover
over the valve to avoid dirt contamination. Before use, this cover should be removed
and the valve transiently opened to expel any dirt or grease from the outlet. This
reduces the chance of debris entering the anaesthetic machine and is known as
cracking the cylinder.
The cylinder is mounted on to the anaesthetic machine by engaging the pins on the
yoke with the holes in the valve block. It is secured by tightening the wing nut.
Before use, the cylinder should be opened gently to ensure that there are no leaks,
either from the cylinder valve itself or at the point of attachment to the yoke on the
anaesthetic machine. A possible reason for gas leakage at the pin-index junction is the
absence of the Bodok seal. This is an aluminium-rimmed neoprene washer that sits
between the outlet on the valve block and the yoke on the anaesthetic machine. Gentle
opening of cylinders minimizes sudden surges of high-pressure gas that may damage
the pressure gauge or regulator.
Suction systems
Suction systems form part of the piped medical gases and vacuum systems (see page
107) and must comply with specifications detailed in BS4957. Portable and fixed suction
systems are available to accommodate the differing circumstances of use. General
operating principles are the same for both systems. Outlets from the central piped
vacuum system must have the capability of maintaining a vacuum of at least 53 kPa
below atmospheric pressure (101.3 kPa) and supporting a flow of 40 litres/minute.
Suction apparatus and nozzle: suction nozzles are made of either firm plastic (e.g.
Yankauer) or metal. They should have a smooth tip to prevent damage to the soft
tissues of the oropharynx. The tip often has more than one hole to allow continuation
of suction should one hole become blocked. Suction tubing is constructed of semi-rigid
plastic to minimize kinking, with a smooth internal surface to limit resistance to flow. The
tubing must be of sufficient length to be practical to use, but it should be remembered
that the length and width of a tube influences the laminar flow within it, according to the
laminar flow = Pr4

8L
where: P = pressure gradient along tube, r = tube radius,

L = tube length, = viscosity of liquid.
Thus, short, wide tubing maximizes laminar flow.
Reservoir: the reservoir must be of sufficient size to contain the estimated volume of
suctioned material, but not so large that it increases the time taken for the vacuum to
build up. Most reservoir vessels are constructed of clear material to allow the contents
to be visualized and are graduated to permit accurate assessment of aspirate volume.
Disposable liners are commonly used to reduce staff exposure to potentially infective
material. A floating ball valve within the collection vessel prevents material from
entering the control unit and the vacuum source if the container overfills.
Vacuum control regulator unit: this unit is usually situated between the reservoir
and the vacuum source (Figure 5). Its function is to allow adjustment of the degree
of vacuum applied to the distal suction tubing. The vacuum control adjuster acts as a
variable orifice (either directly or by way of a spring acting on a diaphragm) to adjust the
force of vacuum, which is indicated on a gauge. Within the unit is a filter and some form
of float valve to provide protection from particulate matter.
Distribution pipeline network: between the terminal outlet and the control unit there
is a colour-coded (yellow) flexible hose with a specific Schrader probe connection, as
for piped medical gases.
Terminal outlet: the terminal outlet of the vacuum pipeline consists of a labelled, self-
sealing valve, fronted in yellow, that accepts a probe with indexing collar to prevent
misconnection.
d 5 Vacuum control regulation unit.

a vacuum gauge, b vacuum control, c filter, d float valve.
Filter unit: filters are sited within the control unit, but also in the case of piped medical
gases and vacuum systems between the terminal outlet and the central vacuum source.
They remove particulate matter and bacteria from the system to prevent blockage and
contamination.
Central pump: the role of the pump is to generate subatmospheric pressure within the
system. Pumps are commonly driven by electrical, pneumatic or manual means (Figure
6). The piston, diaphragm and rotary devices shown in Figure 6 all require some form of
energy source (usually electricity) to drive mechanical pumps. In contrast to these, the
gas-powered pump works on the Venturi principle and the bellows require manual input
to generate subatmospheric pressure.
The type of pump is determined by the specific requirements of the suction unit. For
example, most portable units use a manual pump, whereas a rotary-driven pump may
be used when a large volume of aspirate is anticipated. The pump expels its exhaust
gases, via a silencer, to the atmosphere at a suitable site, such that staff and patients
are not exposed to the pollution.
Vacuum pumps
Piston Diaphragm High-vacuum

pump pump rotary pump
Low-vacuum Rotary pump using

rotary vane pump an Archimedean wheel
Gas-powered pump using

the Venturi principle Bellows pump
Adapted from: Moyle J T B, Davey A. Wards Anaesthetic Equipment. 4th

ed. London: WB Saunders, 1998. By courtesy of the publisher.
Humidification devices
Humidification strictly refers to the addition of water vapour to air. Humidification of

dry, cold anaesthetic gases as they enter the patients airway is important because dry
gases result in drying of the mucosal surfaces, abnormal ciliary function and increase
in the viscosity of respiratory tract secretions. Loss of these protective mechanisms
can cause mucus plugging, atelectasis, reduction in gas exchange and an increased
susceptibility to infection. Also, heat energy due to latent heat of vaporization is lost by
the patient in warming and humidifying dry, cold anaesthetic gases.
Aims: under normal circumstances, the upper respiratory tract warms and humidifies
the air to an absolute humidity (i.e. mass of water vapour in a given volume of air
at specified temperature and pressure) of 34 g/m3 at 34oC in the trachea and 44 g/
m3 at 37oC in the alveoli. These values equate to fully saturated air whereby the air
contains the maximum possible water vapour at specified temperature and pressure.
Achievement of these values is the gold standard for humidification. The different
efficiencies of various humidifiers are shown in Figure 7.
Approximate efficiency of humidifiers

Normal level in upper trachea
Cold water bubble through
100% saturation
Heat and moisture exchanger at 37C
Heated water bath

Heated Bernoulli
nebulizer and anvil
Ultrasonic nebulizer
(adjustable)
0 25 34 44 50 75 100
Absolute humidity (g/m3)
The exact values depend on the model of humidifier used.
Adapted from: Davis P D, Parbrook G D, Kenny G N C. Basic Physics and
Measurement in Anaesthesia. 4th ed. Oxford: Butterworth-Heinemann, 1995.
By courtesy of the publisher.
Types of humidifiers
Heat and moisture exchanger (HME) is the most commonly employed humidifier in
day-to-day anaesthetic practice (Figure 8). It consists of a sealed unit that is placed
within the breathing circuit. The exchanger contains a structure usually of either
sponge or mesh, of large surface area, on to which water is absorbed. Absorption is
maximized if the mesh is made of a hygroscopic material such as paper coated with
calcium chloride or glass fibre. An additional role of some devices is to act as bacterial
filters because over 99.99% of bacteria will not pass through pores of less than 0.2
microns. HMEs work on the principle that the moisture from expired gas condenses
on to the mesh material within the device as it cools. The mesh is also warmed as the
cooling moisture emits latent heat. As gas is inhaled it is warmed and humidified, thus
exchanging heat and moisture. The advantages of the system are that it is:
lightweight
compact
disposable
efficient (6070% relative humidity at 3034oC, equating to absolute humidity of
about 2535 g/m3)
passive (requires no external power source)
inexpensive.
The disadvantages are:
increased dead space
increased resistance to breathing
single-patient use.
8 Heat and moisture exchanger.

Cold water bath humidifier (Figure 9): this operates by bubbling inspiratory gas
through or over a cold water bath. The advantages are it is simple and safe. The
disadvantage is that it is inefficient.
Hot water bath humidifier (Figure 10): inspiratory gases are bubbled through, or
pass over, a warm water reservoir. The contact surface area is increased in some
devices by the use of wicks or multiple bubble holes. The water temperature must be
rigidly regulated to attain a balance between maximum humidification, bactericidal
activity and heating, with the risk of thermal injury to the patient. This is achieved by the
use of a thermostatic control and temperature monitoring within the circuit close to the
patient. A water trap must be included on the patient side of the system and the whole
apparatus must be below patient level to limit the risk of condensed water in the tubing
entering the breathing circuit directly. The system is efficient but the disadvantages are:
risk of scalding
bacterial growth if temperature falls below 60oC
condensation of water within tubing.
9 Cold water bath humidifier.
10 Hot water bath humidifier.
Nebulizers: the principle of nebulizers is to add tiny droplets of water to the inspired
gas. Strictly speaking nebulizers are not humidifiers because they add water droplets
not vapour to the gas. Nebulizers have the potential to produce water droplets of
varying sizes. The result of this is that very small droplets pass into the alveoli and thus
risk fluid overload, whereas large droplets risk being deposited in the breathing circuit
or upper airway. Ideal droplet size is 15 microns. Nebulizers are highly efficient but
they can be expensive and water overload may occur, especially in ultrasonic devices.
There are three commonly encountered methods by which nebulizers produce water
droplets.
Venturi principle water is entrained into a jet of gas that breaks it into droplets
(Figure 11). Some systems also contain a solid object (anvil) into which the droplets are
propelled, thus further reducing their size. Droplet size averages 24 microns. Back
pressure from a breathing system can affect the efficiency of the device by reducing
water entrainment. Some nebulizers incorporate a heater to increase their efficiency.
Spinning disc a rapidly rotating disc that throws off tiny water droplets.
Ultrasonic high-frequency ultrasound waves fragment water into tiny droplets. The
water may be dropped on to a vibrating surface or the device may be immersed in a
water bath. Droplets 12 microns in size are produced.
Gas-driven nebulizer
Water
droplets
Water
reservoir
High-pressure
gas
11
FURTHER READING
Aitkenhead A R, Smith G. Textbook of Anaesthesia. 3rd ed. London: Churchill
Livingstone, 1998.
Al-Shaikh B, Stacey S. Essentials of Anaesthetic Equipment. Edinburgh: Churchill
Livingstone, 1995.
Davis P D, Parbrook G D, Kenny G N C. Basic Physics and Measurement in
Anaesthesia. 4th ed. Oxford: Butterworth-Heinemann, 1995.
Moyle J T B, Davey A. Wards Anaesthetic Equipment. 4th ed. London: WB Saunders,
1998.

Medical Gases and their
Delivery
Ian R Taylor
Michael OConnor


Medical gas
In the UK, most hospitals have piped medical gases and vacuum systems (PMGV)
for convenience and economic reasons. The vacuum component of this system is
discussed on page 114.
The pipeline network carries medical gases from central bulk storage sites to hose
outlets in the walls of anaesthetic rooms, theatres and wards. The responsibility for
this section of the PMGV is principally that of the hospital pharmacy, supplies and
engineering departments. Anaesthetists have responsibility for the section of pipeline
between the terminal outlet and the anaesthetic machine. The bulk store for medical
gases is usually a series of cylinder manifolds (Figure 1). In the case of oxygen, the
cylinder manifold is often used as a reserve because most hospitals store oxygen in
a vacuum-insulated evaporator (VIE) (Figure 2). The cylinder manifold is divided into
a primary unit, which is in use, and a secondary unit in reserve. As the pressure in
the primary unit falls, the supply is automatically switched to the secondary unit and
an alarm sounds to alert the staff to replace the empty cylinders. When there is actual
or impending supply failure the alarm usually sounds in the switchboard area of the
hospital.
The pipes are constructed of high-grade copper alloy to prevent degradation of
gases and are de-greased to reduce the risk of combustion or explosion. They are
labelled at regular intervals along their length and are separated from other pipelines
within the hospital to avoid confusion. Within the network of pipes there are valves to
control the supply to individual theatres or a complete department, in the event of fire
or pipeline damage. These are lever-operated, non-lubricated valves housed in clearly
accessible units usually behind a breakable glass cover (Figure 3).
The pressure within the pipelines is regulated at about 400 kPa.
1 Cylinder manifolds.
2 Vacuum-insulated evaporator.
3 Pipeline lever safety valve.
Terminal outlet connection

Outlet points (Figure 4) for each of the piped medical gases have specifically labelled,
shaped, colour-coded and non-interchangeable Schrader sockets to prevent connection
of the incorrect gas supply to the flexible hoses supplying the anaesthetic machine.
These must comply with the British Standard codes (BS5682) and be labelled as
such. Each terminal outlet is a self-sealing valve unit of specific size to receive the
corresponding collar-indexed probe of the flexible hose.
To ensure correct connection and function of the outlet valve, the probe is firmly
inserted and a sharp tug applied to ensure full engagement and opening of the valve.
This simple procedure is known as the tug test.
4 Terminal gas outlets.
Flexible pipeline
A flexible pipeline carries medical gases from the terminal outlet to the anaesthetic
machine. The terminal outlet probe (Schrader probe; Figure 5) is fitted with an indexing
collar of a specific diameter for each gas, which will fit only the corresponding gas
socket on the terminal outlet valve. In addition, each collar has a notch that fits over a
pin within the socket to prevent rotation of the hose once installed. The entire assembly
is constructed so that rapid probe insertion or withdrawal can be performed single-
handedly and that once withdrawn the terminal outlet unit is self-sealing.
The flexible hose is made of a high-quality copper alloy with antistatic and
bacteriostatic properties. It is colour coded and labelled in accordance with the gas
it carries.
The hoses are connected to the anaesthetic machine by a non-interchangeable
screw thread unit. This unit consists of a probe unique to each gas and a nut to screw
the assembly on to the machine. A stainless-steel ferrule is crimped over the whole unit
to seal the connection and prevent its removal (Figure 6).
5 Schrader probe.
6 Non-interchangeable screw thread.
Safety
Pipelines and flexible hoses: guidance for manufacturers, installers and maintenance
engineers is in accordance with BS5682 (1987) and Health Technical Memorandum
2022 (1994). Pipelines for each of the medical gases are manufactured in different
locations within the factory to prevent accidentally mixing up their unique features, for
example, connection of the wrong terminal probe, non-interchangeable screw thread
fitting or incorrect colour coding.
Pipelines and flexible hoses are steam cleaned, dried and sealed at both ends after
internal inspection before being transported to their installation site. This is to prevent
contamination and particulate matter from entering the gas supply. In the event of
damage to, or technical failure of any part of the pipeline, it must be returned directly to
the manufacturer for repair or replacement.
The pharmacy, supplies and engineering departments within each hospital are
responsible for the pipeline supply. This includes testing of gases for purity and identity
after installation of new pipelines.
The anaesthetist is responsible for ensuring that the flexible hoses are correctly
engaged and that the corresponding gas passes into the anaesthetic machine. Correct
engagement is checked by using the tug test and the identity of the gas by using
the single-hose test. This is done by attaching the oxygen pipeline to the anaesthetic
machine, turning on all the flowmeters and ensuring that gas flows only through the
oxygen flowmeter and that it is detected by an oxygen analyser fitted at the common
gas outlet.
Cylinder gas supply: cylinders and their use in conjunction with the anaesthetic
machine are covered elsewhere in Anaesthesia and intensive care medicine.
Medical gas pressure

Working pressures within cylinder and piped medical gas supplies are outlined in Figure
7.
Pressure monitoring and display of both pipeline and cylinder gases is performed by
Bourdon gauges. The Bourdon gauge is an aneroid (i.e. without liquid) gauge consisting
of a coiled tube, attached at one end to the gas supply and at the other end to a pointer.
The pressure of the gas causes straightening of the coil and thus causes movement of
the pointer over the colour-coded, labelled and calibrated dial. The gauge is faced with
heavy glass and designed such that leaks vent from the back of the valve casing and
do not blow out the glass.
Cylinder and pipeline colour coding and pressures
Body colour Shoulder colour Pressure (kPa) at 15oC
Cylinder
Oxygen Black White 13700
Nitrous oxide Blue Blue 4400
Carbon dioxide Grey Grey 5000
Air Grey White/black 13700
Pipeline
Oxygen White 400
Nitrous oxide Blue 400
Air (clinical use) Black 400
Air (power tool use) Black 700
Pressure regulators: throughout the medical gas supply network the pressure within
the system is closely regulated. This is vital for the protection of both equipment and
patient. Measures to maintain a near-constant pressure are found in many sites and
usually take the form of a pressure relief valve or a pressure regulator (see Anaesthesia
and Intensive Care Medicine 1:2: 66). Both devices are also present within the
anaesthetic machine.
Pressure relief valves are designed to allow escape of gas above a certain set
pressure. In the case of the VIE this protects the oxygen storage equipment from
damage from pressure above 1690 kPa. Similar valves are positioned downstream of
pressure regulators within the pipeline supply in case of regulator failure. These are
set slightly above 400 kPa.
The principle on which the valve works relates to an equilibrium between two
opposing forces: that exerted by the spring and that generated by the gas itself (Figure
8).
Pressure relief valve
Force exerted by spring (F)
Disc area (A)
Gas pressure (P)
F=PxA
As the disc area is constant, and the force exerted by the spring to close
the valve is pre-set, once the gas pressure within the system exceeds this
closing force, the valve opens and gas escapes
Adapted from: Aitkenhead A R, Smith G, eds. Textbook of Anaesthesia.
3rd ed. London: Churchill Livingstone, 1998. By courtesy of the publisher.
Medical gases
Oxygen
Manufacture: industrial manufacture is by the fractional distillation of liquid air. This
involves the removal of carbon dioxide and then the separation of oxygen and nitrogen
by means of their different boiling points.
Oxygen may also be produced by oxygen concentrators, which extract oxygen
from air. This process involves the passing of air through a sieve of zeolite (aluminium
silicate), which absorbs the nitrogen, leaving oxygen and a trace of argon. The
equipment for this process used to be bulky, but recently smaller units suitable for home
use have been developed. A maximum concentration of 95% pure oxygen can be
produced using these devices.
Storage: oxygen is stored either as a gas in cylinders or as a liquid in a VIE. In the

UK, cylinders used for oxygen storage are black with a white shoulder (Figure 9); in the
USA they are green. The oxygen is stored at a pressure of 13700 kPa at 15oC. Where
piped medical gases are used, oxygen is also stored in cylinder manifolds. In cylinders,
oxygen is a gas and the volume of oxygen remaining in the cylinder is directly related to
the measured pressure, according to Boyles law.
9 Cylinders. From left: oxygen, nitrous oxide, air,

carbon dioxide.
The VIE (Figure 10) is a thermally insulated device similar to a large vacuum
flask. Oxygen is stored within this vessel at about 160oC and at a pressure of 510
atmospheres (5001000 kPa). The low temperature is maintained by the vacuum
surrounding the main chamber and by heat energy being lost from the liquid oxygen
as it evaporates (latent heat of vaporization). Under normal working conditions, oxygen
evaporates and passes through the pressure regulator to reduce its pressure to 400
kPa, and then enters the pipeline supply. If demand for oxygen is low, the internal
pressure gradually rises until a safety valve opens at 1690 kPa to release gas to the
atmosphere. When demand for oxygen is great, the control valve opens allowing liquid
oxygen to pass through the pressure-raising superheater and vaporizer, evaporate and
enter the pipeline supply. The superheater is a coil of uninsulated copper pipe.
The VIE (Figure 2) can be found outside all hospitals that use piped gases and
may be supported by a tripod structure. Two of these legs support the weight of the
evaporator, while the third is a weighing device to allow the mass of liquid contained to
be measured. Modern designs stand on four legs and the contents are calculated by
measuring the pressure difference between the top and bottom of the vessel.
Dial
Coil
Coil straightening
Pointer
10
Pressure
11 Cylinder yoke.
Delivery: oxygen is delivered from a central supply (i.e. a manifold or VIE) or directly
from cylinders. Central oxygen supply is via the pipeline system described above. Direct
cylinder supply of oxygen to the anaesthetic machine involves the connection of the
cylinder valve to the cylinder yoke (Figure 11) on the back of the machine.
Carbon dioxide
Manufacture: carbon dioxide is manufactured by heating calcium or magnesium
carbonate in the presence of their oxides. Other sources are as a by-product of the
manufacture of hydrogen, fermentation of beer or the combustion of fuel.
Storage: in the UK, carbon dioxide is stored in grey cylinders (Figure 9) at a pressure
of 5000 kPa at 15oC, as a liquid in equilibrium with its vapour.
Distribution: unlike the other medical gases, carbon dioxide is not distributed via a
central pipeline. The attachment of carbon dioxide cylinders to anaesthetic machines
has declined in recent years to minimize the risk of accidental administration during
anaesthesia. The present guidelines issued by the Association of Anaesthetists of
Great Britain and Ireland state that carbon dioxide cylinders should not be routinely
fitted to the anaesthetic machine.
Air
Manufacture: air for medical use is compressed, cleaned and filtered before use.
Storage: compressed air for anaesthetic use is stored in grey cylinders with black
and white shoulders (Figure 9) at a pressure of 13,700 kPa at 15oC. In the USA, the
cylinders are yellow.
Distribution: pipeline air is sourced from either a manifold (Figure 1) or, more
economically, from an air compressor. It is important to know that air for clinical use is
regulated to a pressure of 400 kPa, whereas that for the use of surgical power tools is
supplied at 700 kPa. The terminal outlet for compressed air is colour coded black and
white, labelled and has a non-interchangeable connection (Figure 4).
Cylinders are attached directly to the anaesthetic machine by connection of the
cylinder valves to the cylinder yoke. A larger portable cylinder may be attached via a
flexible hose.
FURTHER READING
Livingstone, 1998.
Livingstone,1995.
1998.
Yentis S M, Hirsch N P, Smith G B. Anaesthesia and Intensive Care
A to Z. An Encyclopaedia of Principles and Practice. 2nd ed. Oxford: Butterworth-
Heinemann, 2000.

Perioperative Fluids
E Anne Thornberry
E Anne Thornberry is Consultant Anaesthetist at the Gloucestershire Royal

Hospital, Gloucester, UK. She qualified from Kings College, London, and trained in
anaesthesia in Chester, Bristol and Southampton. She has a special interest in obstetric
anaesthesia.
Any surgery under anaesthesia can upset the patients normal fluid status through
preoperative restriction of oral intake of fluids. The degree of disruption depends on
the patients medical condition, the nature of the surgery and the choice of anaesthetic.
Factors to consider when planning perioperative fluid management are listed in Figure
1.
Maintenance requirements: normal values for daily fluid and electrolyte requirements
are shown in Figure 2. Dextrose 4% with saline 0.18% contains 30 mmol/litre of sodium
and is often used for basal fluid therapy.
Determinants of perioperative fluid requirements
Maintenance requirements
Preoperative deficits
Blood loss
Third-space losses
Transcellular fluid losses
Effects of anaesthetic agents and technique
Maintenance fluid and electrolytes
Adults
40 ml/kg/day
Children
100 ml/kg/day for first 10 kg
50 ml/kg/day for second 10 kg
25 ml/kg/day for each subsequent kg
Na+ = 11.5 mmol/kg/day

K+ = 1 mmol/kg/day
Preoperative assessment of the fluid status of the patient requires an appropriate
history, examination and investigations.

The following questions should be asked.
How long has the patient been starved?
Do they have an intravenous infusion in progress?
Have they any reason to expect excessive losses?
Are they taking diuretics?
Are they pyrexic?
Have they been vomiting or do they have a nasogastric tube in situ?
Have they got diarrhoea or had a bowel preparation?
Could they have third-space losses or occult bleeding?
Have they any symptoms of fluid overload?
The physical examination includes evaluation of the mucous membranes and skin
turgor, and measurement of the vital signs, including orthostatic changes. Ascites,
pulmonary oedema and pleural effusions should be sought. Measurement of urine
output may be useful.
Investigations
A normal haematocrit value may indicate that the patient has a normal fluid status or it
may reflect someone with anaemia who is also dehydrated. A raised serum urea with a
normal creatinine level may indicate dehydration. Raised urinary sodium levels, specific
gravity and osmolality all reflect the normal homeostatic response to water depletion
and can be used to monitor progress with resuscitation. The signs and symptoms of
water depletion are described in Figure 3.
Estimation of total body water deficit
Deficit of For example in Signs and symptoms

body weight a 70 kg man
Up to 5% 3.5 litres Thirst

Dry mouth
510% 3.57 litres Decreased skin turgor

Decreased intraocular pressure
Tachycardia
Orthostatic hypotension
Tachypnoea
Oliguria
Skeletal muscle weakness
Drowsiness
1015% 710.5 litres Severe hypotension

Tachycardia
Anuria
Confusion/coma
3
Signs and symptoms of uncorrected acute blood loss
Volume lost For example in Signs and symptoms

a 70 kg male
10% 490 ml Thirst

Venoconstriction
20% 980 ml Mild increase in heart rate

Systolic blood pressure normal
Slight rise in diastolic pressure
Decreased urine output
30% 1470 ml Tachycardia > 120/minute

Moderate hypotension
Tachypnoea
Cool, clammy, pale
Anxious/aggressive
Oliguria
40% 1960 ml Severe hypotension and

tachycardia
Tachypnoea
Anuria
Mental confusion
50% 2450 ml Coma
Fluid losses
Blood loss: the signs and symptoms of unreplaced blood loss (Figure 4) can help
to estimate acute losses if accurate measurements cannot be made. Estimates of
intraoperative blood losses are derived from measuring or estimating observed losses.
Prediction of postoperative losses requires knowledge of the type of surgery and
expected postoperative bleeding, combined with measurement of losses in the drains,
vital signs, and haemoglobin and haematocrit levels.
Third-space losses are caused by sequestration of extracellular fluid into the tissues.
The composition of this fluid is the same as that of interstitial fluid and losses after
major bowel resection may be as great as 8 ml/kg/hour. The extent of third-space
losses depends on the severity of injury to the tissues.
Transcellular fluid losses: nasogastric aspirate can be measured but pleural

effusions and ascites must be estimated. Losses from evaporation occur from the
surgical site and during a laparotomy these can be as much as 10 ml/kg/hour.
Effects of anaesthetic agents and techniques

Ventilation with dry anaesthetic gases increases the pulmonary losses from
evaporation. General and regional anaesthesia tend to decrease the patients blood
pressure by a reduction in sympathetic tone, vasodilatation or myocardial depression.
Vasopressors and intravenous fluids are used to minimize these effects, complicating
the assessment of perioperative fluid status. Central venous pressure monitoring can
be invaluable in helping to manage more complex cases.
Choosing perioperative fluids

Crystalloids
Dextrose solutions disperse through all the body fluid com-partments and are
required to replace combined intracellular plus extracellular water depletion. Once any
deficit has been replaced, dextrose is used only perioperatively as part of the basal
water requirements or in a diabetic regimen.
Physiological saline disperses throughout the extracellular fluid compartments and is

commonly used perioperatively to replace blood loss, transcellular losses, evaporation
and third-space losses. Only one-third remains in the intravascular compartment
and therefore three times the volume of the blood loss must be given if saline is used
as a replacement. When large volumes of saline are administered there is a risk of
developing hyperchloraemic acidosis.
Ringers lactate (Hartmanns solution) behaves as normal saline in distribution. It is

often used as the first-choice replacement fluid because the electrolyte content more
accurately mimics the extracellular fluid. Its constitution varies between laboratories
but in general it contains 137 mmol/litre sodium, 4 mmol/litre potassium, 3 mmol/litre
calcium and 142 mmol/litre chloride. There are fewer risks of electrolyte disturbances
if large volumes are administered but it is hypotonic and large volumes reduce plasma
osmolality.
Colloids
The contents of the commonly used colloids are listed in Figure 5.
Properties of commonly used colloids
Average molecular Sodium Potassium Chloride Calcium

weight (mmol/litre) (mmol/litre) (mmol/litre) (mmol/litre)
Haemaccel 35,000 145 5.1 145 6.2

Gelofusine 35,000 154 0.4 154 0.4
Hetastarch 450,000 154 0 154 0
Dextran 70 70,000 150 0 150 0
in saline
Albumin 4.5% 70,000 150 2 120 0
Colloids used for intravenous therapy have an increased osmolality with respect to
plasma and can increase plasma volume by more than the volume infused by attracting
water from the interstitial fluid compartment. Consequently they are used predominantly
to replace intravascular losses and are unsuitable for the treatment of dehydration.
The length of time a colloid stays in the intravascular compartment depends on the
shape, size and charge of the molecules suspended and the porosity of the capillary
endothelium.
Gelatins are colloid solutions derived from animal gelatin. They have an average
molecular weight of 35,000 but there is a wide variation in molecule size. The two
commonly used gelatins are Haemaccel, which is urea linked, and Gelofusine, which
is a succinylated gelatin. Their intravascular persistence is low, about 23 hours with
Gelofusine and less for Haemaccel. Gelatins are the colloids most likely to induce an
anaphylactoid reaction. Cross-matching is unaffected by the use of gelatins. In vitro
studies suggest they interfere with clotting and platelet aggregation but in clinical
practice little effect is seen.
Hydroxyethyl starches (HES) are modified natural polymers of amylopectin, which
are metabolized by amylase. They are divided into high, medium and low molecular
weight starches according to the range of molecular weights in the solution. Hetastarch
is a 6% solution with an average molecular weight of 450,000 and a mean molecular
weight of 70,000. The intravascular persistence of Hetastarch is over 24 hours. Some
enters the interstitial space and is taken up by the reticulo-endothelial system where it
can persist for years. Hexastarch and pentastarch are lower metabolic weight starch
solutions. High molecular weight HES solutions can cause a coagulopathy by reducing
factor VIII and von Willibrand factor. The lower the average molecular weight of the
solution the less effect it has on coagulation. The maximum recommended dose is
33 ml/kg/day, though this has often been exceeded without any adverse effects.
Anaphylactic reactions have been reported, but the incidence is low.
Dextrans are branched polysaccharides produced by the action of bacteria on a

sucrose medium. Dextran solutions are divided by their average molecular weight
into 10% Dextran 40 (molecular weight 40,000) and 6% Dextran 70 (molecular weight
70,000). Dextran reduces blood viscosity, reduces platelet adhesiveness and increases
fibrinolysis. Doses higher than 1.5 g/kg can increase bleeding. Only Dextran 70 is
used for short-term plasma expansion. Severe anaphylaxis is uncommon but has been
reported.
Albumin has a molecular weight of 69,000 and is a naturally occurring plasma protein
that contributes significantly to the maintenance of plasma oncotic pressure. It has been
used as a colloid to treat critically ill patients with hypoalbuminaemia but there is no
evidence that this improves outcome. Recent research has suggested it may worsen
outcome but this is not proven. The increasing cost of production of albumin has
significantly reduced its use in clinical practice.
Crystalloidcolloid controversy
It has been argued that colloids are more appropriate than crystalloids for the
replacement of intravascular losses because they stay in the intravascular compartment
longer, necessitating a smaller volume of replacement and a more rapid result. As
stated above, the intravascular persistence varies significantly between the different
colloids, while this argument holds for hydroxyethyl starches it is not so strong for the
gelatins.
Opponents of colloids emphasize the incidence of ana-phylaxis with colloids, which

does not exist with crystalloids. The pragmatists suggest that the normal physiological
response to an acute intravascular deficit is to draw water in from the interstitial fluid
compartment and therefore it makes sense to initiate resuscitation with a crystalloid and
then to continue with a colloid if the loss becomes significant.
Blood and blood products

Red cell transfusions: the indication for a red cell transfusion is to increase the
oxygen-carrying capacity of the blood by raising the haemoglobin concentration
of patients with acute or chronic anaemia. The extent to which it should be raised
depends on the balance between oxygen consumption and supply, with the aim of
avoiding tissue hypoxia. Factors that affect perioperative oxygen consumption are body
temperature, sympathetic activity, metabolic activity, heart rate and drug therapy.
New safety requirements are making blood products more complex and expensive
to produce. Recent research suggests the traditional trigger of a haemoglobin
concentration of 10 g/dl for perioperative transfusion is too high. The rate of blood loss
also needs to be taken into consideration when deciding to transfuse. Suggested British
Society for Haematology guidelines are summarized in Figures 6 and 7.
Need to transfuse based on an estimate of lost circulating

volume
Volume lost Indication for transfusion
15% Only if superimposed on existing anaemia

or
Patient unable to compensate because of severe
cardiac or respiratory disease
1530% As above
or
In the presence of continuing blood loss
3040% Transfusion should be considered
> 40% Transfuse
Need to transfuse based on consideration of haemoglobin

concentration
Haemoglobin Indication for transfusion

concentration
< 7 g/dl Transfuse
710 g/dl Transfuse patients who would tolerate

anaemia poorly (e.g. those with cardiac or
respiratory disease, those over 65 years
of age)
> 10 g/dl No indication

7
Concerns about the safety of transfusion have encouraged the development of

alternative strategies to minimize the need for homologous transfusions. These include
the use of autologous pre-donation of blood, acute normovolaemic haemodilution,
intraoperative cell salvage, preoperative administration of erythropoietin and the
development of blood substitutes.
Fresh frozen plasma is valuable because it contains all the clotting factors. It is used
to correct a coagulopathy due to a concurrent illness, the use of anticoagulants or a
dilutional coagulopathy. A coagulation screen should be requested to establish the need
for fresh frozen plasma, although in the presence of a massive haemorrhage, fresh
frozen plasma may be given before laboratory results are available if there are clinical
signs of impaired coagulation.
Platelets should be given only if there is clinical and laboratory evidence of abnormal
coagulation.
Blood substitutes
There are three different areas of research in progress: free haemoglobin solutions,
encapsulated haemoglobin cells, and perfluorocarbon emulsions.
Haemoglobin-based oxygen carriers: free haemoglobin has been used as a red

blood cell substitute for decades but initially there were many adverse effects including
hypertension, bradycardia, renal dysfunction and a short intravascular retention time.
A problem was the lack of 2,3-diphosphoglycerate (2,3-DPG) and the higher pH of
plasma compared with that inside the red blood cell. There is also an increase in
oncotic activity which limits the concentration of free haemoglobin that can be used to
about 57 g/dl.
Some of the adverse effects of free haemoglobin have been reduced by a variety of
modifications including polymerization and conjugation to increase the intravascular
retention time and the introduction of haemoglobin into cell-like structures, using stable,
porous membranes that allow molecules such as glucose to enter. Some products have
reached the stage of clinical trials.
Perfluorocarbon emulsions: perfluorocarbons are synthetic carbonfluorine

compounds. They dissolve gases including oxygen and carbon dioxide. They are not
metabolized in vivo and most are excreted unchanged via the lungs. A small amount
is taken up by the reticulo-endothelial system and excreted later. They are immiscible
in water and have to be emulsified. Initial emulsifiers caused numerous adverse
effects. Second-generation perfluorocarbons have reduced the complications, but high
doses can still interfere with coagulation, elevate liver enzymes and produce a febrile
response. They are in phase III trials as a blood substitute. u
FURTHER READING
Adams A P, Cashman J N. Recent Advances in Anaesthesia and Analgesia 21.
Duke J. Anesthesia Secrets. Philadelphia: Hanley & Belfus, 2000.
Goldstone J C, Pollard B J. Handbook of Clinical Anaesthesia. Edinburgh: Churchill

Livingstone, 1996.
Guidelines for the Clinical Use of Red Cell Transfusions. Br J Haematol 2001; 113:
2431.

Positioning the Surgical Patient
Jonathan Warwick

The correct positioning of a patient for surgery is a balance between optimizing surgical
exposure and minimizing complications for the patient. The surgeon may request a
particular position and it is often the role of the anaesthetist to ensure that this is
accomplished safely. The anaesthetist must consider the limits of position that may be
tolerated and ensure access to the airway, monitoring and vascular devices as far as
possible. In general, complications may arise from physiological consequences of the
position and the effects of direct pressure on soft tissue structures.
Supine position
Indications: the supine position is the standard for most surgical procedures. The
orthopaedic fracture table is a modification that enables traction to be maintained on a
lower limb and provides access for an image intensifier.
Physiological consequences: when an individual is upright, ventilation per unit lung

volume is greater in the lower part of the lung, because here the weight of the lung
makes the intrapleural pressurevolume curve steeper (see Figure 2). The apex of the
lung is on a flatter part of this curve, representing a relatively larger change in pressure
for a given change in lung volume, and hence a lower compliance. The lower part of the
lung is better perfused as a result of gravity.
When an individual is supine, ventilation and perfusion become more uniform and
the effects of gravity less marked. The differences between base and apex are then
replaced by differences between dependent and non-dependent parts of the lung.
Stroke volume and cardiac output may increase as a result of the increase in central
venous pressure. Baroreceptors sense an increase in arterial pressure, leading to a fall
in heart rate and systemic vascular resistance.
The physiological effects of a change of posture when anaesthetized depend on
additional factors:
pharmacological effects
circulating blood volume
method of ventilation.
The functional residual capacity (FRC) decreases by about 20% following induction,
though closing capacity remains unchanged. Anaesthetized patients are vasodilated
and have diminished compensatory cardiovascular reflexes. Therefore, all positioning
movements must be made slowly. The basic supine position is generally well tolerated
and has no additional physiological effects in healthy patients.
Pregnant patients may suffer from the supine hypotensive syndrome, where the
weight of the gravid uterus reduces venous return by compression of the inferior vena
cava (IVC). This can be avoided by a lateral tilt of the operating table, usually to the
left side.
Direct pressure complications: the eyes should be taped closed to prevent corneal
drying or injury from scratching. Limbs must be fully supported and moved with care to
prevent joint dislocation or even fracture. The arms can be secured in the drawsheet, or
by the use of padded arm supports.
Skin overlying all bony points is prone to pressure damage, especially the occiput,
elbows, knees, greater trochanter of the femur and sacrum. As little as 2 hours
of unrelieved pressure may result in a pressure sore; the duration of pressure is
considered to be more important than its intensity. The ankles should be placed in soft
foam-rubber boots to avoid pressure necrosis of the heel skin.
Injury to peripheral nerves (Figure 1) is often a consequence of the way in which
the patient is positioned during surgery. Nerve injury is most likely to occur with
the combination of muscle relaxation, an extreme position and prolonged surgery.
Peripheral nerves are damaged by local ischaemia caused by compression or
stretching. This produces segmental demyelination. Complete clinical recovery usually
occurs within 68 weeks, but may take several months. Severe damage may be
associated with permanent injury. Electromyography studies may aid the prognosis.
Supine position nerve injuries
Nerve injury Comments

Supraorbital Compression by catheter mount, trachael tube
connectors
Nerves to the eye Compression from face mask
Facial (VIIth) Compression by anaesthetists fingers against
ramus of mandible, face mask harness
Brachial plexus Stretching injury, especially when arm is abducted >
90, externally rotated, elbow extended and forearm
supinated
Ulnar Most common nerve injury occurring during
anaesthesia. Compression between the medial
epicondyle of the humerus and the edge of the
operating table. Pronation of the forearm may place
the nerve more at risk than supination
Radial Compression between the edge of the operating
table or armboard and the shaft of the humerus,
compression from a head-screen support
Pudendal Compression from the post of an orthopaedic
fracture table may cause pudendal nerve injury or
genital trauma
Sciatic Direct compression in thin patients undergoing
prolonged surgery on a hard table
Lateral (lateral decubitus) position

Indications:
thoracic surgery
lateral approach to the kidney
surgery to the hip.
Reference to the right or left lateral position indicates the side on which the patient
is lying.
Physiological consequences: when lying awake in the lateral position, ventilation to

the upper and lower lungs behaves in a similar fashion to the ventilation of lung apex
and base when upright. The lower lung lies on the steeper, more compliant part of
the intrapleural pressurevolume curve (see Figure 2, page 12). The weight of the
abdominal contents pushes the lower lung diaphragm higher than the diaphragm of the
upper lung, so that it is also able to generate a higher force of contraction. The lower
lung is therefore better ventilated than the upper lung. Perfusion of the lower lung is
also greater as a result of gravity.
Following anaesthesia, the distribution of blood flow remains unchanged but there
are significant changes to the distribution of ventilation. Muscle tone is greatly reduced
or absent and the FRC of each lung falls, especially in the lower lung as a result of the
weight of the mediastinum pushing down from above and the weight of the abdominal
contents below. This has the effect of moving the upper lung down to a more favourable
(i.e. steeper and more compliant) part of the intrapleural pressurevolume curve. The
lower lung moves down to a flatter, less compliant part of the curve. Therefore the upper
lung becomes the better ventilated, but because it receives less of the pulmonary blood
flow, ventilationperfusion mismatch increases.
To expose the flank during the lateral approach to the kidney, the lateral flexed
position over a support (kidney position) may be necessary. Significant hypotension
may result when the patient is positioned on the right side for a left kidney operation.
Reduced venous return occurs as a result of partial obstruction of the IVC from the
support. Hepatic encroachment on the IVC may also contribute. This problem is less
common when the patient is in the left lateral position.
Direct pressure complications: the pelvis and shoulders must be well supported to
prevent the patient from rolling backwards off the table, or forwards into the recovery
position. The lower leg should be flexed and the upper leg extended, with a pillow
between the two (Figure 2).
An axillary roll places the weight of the chest on to the ribcage and prevents direct
compression injury to the shoulder and axilla, thus avoiding deltoid muscle ischaemia or
neurovascular damage to the lower arm.
The lower leg is at risk from pressure damage, especially in obese patients.
Compartment syndrome, myoglobinuria and acute renal failure have been reported.
Nerve injuries that may result from the lateral position are listed in Figure 3.
c
b
a
d
2 The lateral position.

a Padded supports to prevent patient rolling over anteriorly next to iliac crests;
posteriorly next to lumbar spine.
b Lower leg flexed and pillow between knees.
c Heel supported.
d An axillary roll places the weight of the chest on to the ribcage.
Lateral position nerve injuries

Cervical spine Lateral flexion may stretch cervical spinal nerves
and make arthritic joint pain worse. May cause
Horners syndrome
Brachial plexus Stretching injury when the neck is extended and
in lateral flexion. May occur when the arm is
suspended from a bar or gutter and is inadequately
supported
Common peroneal Compression between the operating table and the
head of the fibula
Trendelenburg (head-down) position
Indications:
pelvic surgery
insertion of central venous lines.
Friedrich Trendelenburg first described the 45 supine head-down position in 1890. This
position facilitates access to the pelvis. Most head-down positions are now about 20
or less with acceptable results. The steep head-down position is now avoided because
it is unnecessary and has too many disadvantages. A corrugated or non-slip mattress
helps prevent patient movement.
Physiological consequences: there is a greater reduction in FRC than in the basic

supine position as a result of pressure of the abdominal contents on the diaphragm.
Usually ventilation is little impaired, especially in fit patients and for short periods. For
longer operations and in obese patients, there is increased work of breathing against
the weight of the abdominal contents, therefore controlled ventilation is preferable.
Central venous pressure rises, and cardiac output may increase. This may
precipitate acute heart failure in patients with poor cardiac reserve. The position is not
generally effective in improving the circulation during shock and can increase venous
pooling in the upper half of the body. A prolonged head-down position will cause
venous congestion and oedema in the head and neck.
Barrier pressure is the difference in intraluminal pressures either side of the
gastro-oesophageal junction. The pressure within the oesophagus is normally 1525
mm Hg higher than gastric pressure and gastro-oesophageal reflux is prevented.
Barrier pressure is maintained by the action of the smooth muscle cells of the lower
oesophageal sphincter and the skeletal muscle of the surrounding crural diaphragm.
The head-down position may raise intragastric pressure, reduce barrier pressure and
encourage reflux to occur.
There is an increase in intracranial and intraocular pressure. While inserting central
venous lines in patients with head injury, care should be taken to limit the head-down tilt
to the minimum necessary so as not to worsen cerebral perfusion pressure.
Direct pressure complications: injury to the brachial plexus was common when
the steep 45 head-down position was used and patient movement was prevented
by shoulder supports or wrist straps. Patient movement is prevented by the non-slip
mattress when lesser degrees of head-down tilt are used (e.g. 20). Brachial plexus
injury is now uncommon.
Reverse Trendelenburg (head-up) position
Indications:
operations on the head and neck; this position reduces venous pressure and helps
reduce bleeding
surgical access to the gall bladder and proximal gastrointestinal tract, especially
during laparoscopic surgery
operations on the shoulder joint.
Usually, 1520 head-up tilt is sufficient.
Physiological consequences: there is a small decrease in arterial pressure; but less

of a decrease in FRC than in the basic supine position because less pressure is exerted
on the diaphragm by the abdominal contents. There is a reduction in intraocular and
intracranial pressure, mainly as a result of improved venous drainage.
Any open vein or sinus above the level of the right atrium can cause venous air
embolism.
Direct pressure complications: injury to the brachial plexus may be caused by

excessive rotation and lateral flexion of the neck away from the operative site.
Lithotomy position
Indications:
urological procedures
operations on the perineum, anus and rectum.
The patient is positioned in the supine position, with both hips and knees flexed and
the thighs abducted. The ankles and feet may be supported by lithotomy poles using
stirrups or calf supports, or by strapping into padded boots. The position is usually
combined with some head-down tilt to aid surgical access.
Physiological consequences: the lithotomy position is generally well tolerated. There

is a reduction in vital capacity and FRC as a result of diaphragmatic splinting
from upward displacement of abdominal contents. This may cause difficulty with
spontaneous ventilation in obese patients and controlled ventilation may be preferable.
Care should be taken when the legs are lowered because this may reveal previously
unrecognized hypovolaemia and cause sudden hypotension.
Direct pressure complications: backache is common and may be reduced by

providing a support to maintain the normal lumbar lordosis. The sacrum must be
supported and should not hang free over the end of the table. Marked flexion of the
hips and knees may cause sacroiliac strain, and the legs must be moved together to
avoid pelvic asymmetry. Slippage of the lithotomy poles once the legs are positioned
can cause hip dislocation. Moving the thighs too far apart may strain the adductor
muscles.
Compartment syndrome in the lower leg may be initiated by pressure of the calf
muscles on the stirrup pole. Breaking or raising the lower end of the table when the
fingers have been inadvertently trapped in the gap has caused crush injury.
Anaesthesia should not be induced with the legs elevated because raised intra-
abdominal pressure may predispose to regurgitation, and turning the patient will be
difficult.
Nerve injuries that may occur with the lithotomy position are shown in Figure 4.
Lithotomy position nerve injuries

Sciatic Stretching as a result of maximum external rotation
of the flexed thigh
Common peroneal Compression between lithotomy pole and the head
of the fibula
Tibial Compression if the legs are supported by stirrups
behind the knees
Femoral Compression beneath the inguinal ligament when
the thighs are fully flexed on the abdomen
Obturator Compression at the obturator foramen when the
thighs are fully flexed on the abdomen
Saphenous Compression between the medial condyle of the
tibia and lithotomy post or stirrup
Prone position
Indications:
operations on the spine and posterior cranial fossa
operations on the buttocks and natal cleft
percutaneous extraction of renal calculi.
Physiological consequences: there is often an improvement in gas exchange in the

prone position. This may be as a result of the greater inspiratory pressures required to
maintain the tidal volume, which decreases atelectasis, increases FRC and improves
oxygenation. Pulmonary barotrauma caused by excessive inspiratory pressures should
be avoided by correct positioning of the pelvis and upper chest.
The pelvis and the upper chest must be supported so that the abdomen is not
compressed and the diaphragm can descend freely during respiration. This may be
particularly difficult to achieve in obese patients. Patients may be positioned by using
pillows, supporting the iliac crests with cushioned props, or by the use of a specialized
hollowed mattress. Controlled ventilation is preferable in most patients.
There are no significant cardiovascular changes. Pulmonary blood flow is essentially
unchanged from the supine position. Poor positioning and high inspiratory pressures
may decrease venous return. Patients with previous coronary artery bypass grafting
may be at risk from graft occlusion.
Direct pressure complications: turning the supine patient prone requires a team
of four people. Great care must be taken with the head and neck to avoid twisting
or hyperextension injury to the cervical spine. The face should rest on a cushioned
horseshoe with the weight of the head evenly distributed. The eyes are naturally
protected within their bony sockets, but exophthalmos or a flattened nasal bridge may
allow transmission of pressure to the globe. Prolonged compression may result in
central retinal vein thrombosis and blindness.
The tracheal tube must be securely fixed and its position checked after the turn.
Some experienced anaesthetists may use the laryngeal mask for airway maintenance
in prone patients, though the use of a reinforced tracheal tube is likely to be safer for
the trainee. Excessive pressure on the breasts may cause ischaemic damage to the
nipples, interstitial bleeding or rupture of breast implants. In men, the penis or scrotum
may become trapped and compressed.
Possible nerve injuries are shown in Figure 5.
Prone position nerve injuries

Cervical spinal cord Stretching injury caused by overextensio plane
Nerves to the eye Compression from face support
Facial (VIIth) Compression from face support
Brachial plexus Stretching injury caused by extreme
abduction of the arms. Limit abduction to 90
Ulnar Compression between the medial epicondyle of the
humerus and the mattress
Lateral cutaneous nerve Compression between iliac crest of the thigh and
the positioning prop. If used, props should be
angulated and positioned so that the patient is
unable to slip sideways
Anterior tibial Stretching injury caused by forced plantar flexion of
the foot
The sitting position
Indications:
operations on the posterior cranial fossa and cervical spine
dental chair anaesthesia.
The sitting position enables the surgeon to gain clear access, with optimal venous
drainage, low arterial pressure and reduced bleeding. CSF drainage is good and brain
swelling is minimized.
Dental chair anaesthesia in the sitting position is now uncommon.
Physiological consequences: the patient is anaesthetized in the standard supine

position and the neurosurgical pins and head frame are applied. On the operating table,
the patient is progressively sat upright with the neck flexed; the knees are slightly flexed
and the legs are lowered. The arms rest in the lap on a pillow, with the elbows flexed.
A small fall in systolic blood pressure of 20 mm Hg usually occurs; this can be
offset by prior volume loading with 500 ml of colloid solution. Occasionally, persistent
instability of blood pressure can occur that may cause the position to be abandoned
despite the use of vasopressors. Controlled ventilation is the method of choice,
to enable control of Pa CO2 and intracranial pressure. It maintains a higher mean
intrathoracic pressure and reduces the likelihood of air embolus.
Air embolus is the major complication. All patients must be considered to be at
risk throughout the procedure. For this reason, many neurosurgeons seldom use this
position. It is still used when insufficient access is provided by the alternative prone
or semi-prone positions.
Dysrhythmias, especially bradycardia, and blood pressure instability may occur
following surgical manipulation in the region of the brain stem. This is a result of direct
pressure effects on the autonomic control centres of the medulla.
Direct pressure complications: nerve injuries that may result from the sitting position
are shown in Figure 6.
The sitting position nerve injuries

Cervical spinal cord Stretching injury and spinal cord ischaemia following
excessive neck flexion. A two-finger breadth gap
between chin and chest is recommended
Brachial plexus Stretching injury if the arms are unsupported
humerus and the arm supports
Sciatic Stretching injury if thighs are flexed and knees
extended. Maintain adequate knee flexion

Premedication
Neal Evans
Neal Evans is Specialist Registrar in the Oxford School of Anaesthesia. He qualified

from the Royal London Hospital, and was previously a Research Fellow in ITU in
Cambridge, UK.

Anaesthesia at the Radcliffe Infirmary, Oxford, UK. He qualified from Charing Cross
Hospital, London, and trained in anaesthesia in London, UK, Toronto, Canada,
and Oxford, UK. His interests include neuroanaesthesia and medical education.
He organizes the Oxford Primary FRCA courses.
Premedication involves the prescription of drugs before the induction of anaesthesia

in order to alleviate the apprehension associated with surgery, to counteract the side-
effects of anaesthetic agents or to reduce the risks of pre-existing pathology (Figure
1). When choosing a premedicant drug the anaesthetist must consider which of its
properties are appropriate for the individual patient, the possible side-effects and its
potential effect on the proposed anaesthetic technique. The ideal premedicant is:
painless to administer
highly reliable and specific
of rapid onset and rapidly cleared
free of side-effects and interactions with other drugs.
Premedicant drugs entered anaesthetic practice in the late 19th century. Early
anaesthetic agents were delivered by open systems and induced unconsciousness
slowly. Ether caused an increase in pharyngeal and bronchial secretions, which
interfered with smooth gaseous induction. Chloroform caused marked vagal stimulation
of the heart leading to bradycardia. Atropine was first used in premedication in 1890.
Hyoscine, which combined anticholinergic effects with antiemesis and sedation, was
often combined with an opioid (e.g. papaveretum) to produce twilight sleep. Opioids
were prescribed to aid the induction of anaesthesia before the development of more
potent anaesthetic induction agents.
The routine use of drugs for premedication is now in decline. There are several
reasons for this.
Modern anaesthetic agents are potent and have a rapid, smooth onset.
The increased use of day-care surgery requires rapid patient recovery.
In-patients are often admitted on the day of surgery and the time available between
preoperative assessment and induction of anaesthesia is short.
Pressures of high patient turnover and staffing constraints can make premedication
difficult to deliver in practice.
Rationale of premedication
Reduction of anxiety and fear

Sedation
Amnesia
Antiemesis
Reduction in volume and acidity of gastric secretions
Attenuation of autonomic reflexes
Maintenance of cardiovascular stability
Reduction of airway secretions
Provision of analgesia
Anxiolysis, sedation and amnesia
The preoperative visit: anxiety is common in preoperative patients. As well as being

unpleasant, this anxiety is part of a stress response that may worsen coexisting
pathology such as hypertension or angina. A preoperative visit by the anaesthetist
is the most effective way to allay the fears and anxieties of forthcoming surgery.
This visit can be used to establish rapport with the patient, to discuss the proposed
anaesthetic technique in terms that they can understand and to address their worries
in a sympathetic manner. Older children will benefit from inclusion in preoperative
discussions and it is becoming usual for parents to stay with children during induction
of anaesthesia.
For some patients, the preoperative visit alone is insufficient to allay anxiety and
pharmacological methods are required. The nature of the surgical procedure, coexisting
pathology or the need for a rapid recovery from anaesthesia may dictate extreme
caution before the prescription of sedating premedication (Figure 2). Co-administration
of an opioid and a benzodiazepine has a potent respiratory depressant effect.
Relative contraindications to sedative premedication
Airway obstruction or airway surgery

Poor ventilatory reserve
Sleep apnoea
Intracranial pathology
Severe hepatic or renal disease
Obstetric anaesthesia
Day-case anaesthesia (delayed discharge)
Extremes of age
Benzodiazepines
Benzodiazepines are the most commonly used premedication. They are safe and have
a broad therapeutic index though they can cause unpredictable psychological effects
at the extremes of age. Those that are suitable premedicants can usually be given
by mouth about 1 hour before induction, have a short duration of action and produce
inactive metabolites (Figure 3).
Benzodiazepines are agonists of -aminobutyric acid (GABA) receptors within the
CNS. GABA is an important inhibitory neurotransmitter, which hyperpolarizes the
neuron by causing an influx of chloride ion. Benzodiazepines also produce sedation
and amnesia by their action on the limbic system. Both these effects are variable and
depend on the drug used and the dose given.
Temazepam is an effective anxiolytic and is available in elixir or tablet form. It has
a sufficiently short duration of action to allow its use in day-case surgery. Midazolam
is presented in 2 mg/ml or 5 mg/ml glass vials. Unlike the other benzodiazepines
it is water soluble at acid pH but becomes highly lipophilic at physiological pH. It
can be given orally or nasally, which makes it an attractive premedicant for children
in doses of 0.20.5 mg/kg. Lorazepam, 0.05 mg/kg (max. 4 mg), produces intense
anterograde amnesia within 30 minutes, often lasting over 3 hours. Amnesia may be
viewed as an advantageous property of a premedicant but some patients find the
sensation unpleasant.
Benzodiazepines commonly used as premedication
Drug Usual adult dose Half-life of parent Half-life of active

drug (hours) metabolites (hours)
Diazepam 510 mg p.o. 2448 410

Temazepam 1030 mg p.o. 410 None
Lorazepam 24 mg p.o. 1020 None
Midazolam 510 mg i.m. 13 None
0.5 mg/kg (maximum 20 mg)
p.o. in children
Other anxiolytics and sedatives

Phenothiazines are major tranquillizers that have sedative and anticholinergic actions.
They are histamine antagonists (via H1-receptors) and have antidopaminergic and
-adrenoceptor blocking properties. They may cause pallor and restlessness in the
presence of pain and hypotension. Trimeprazine elixir is sedating and is used for
children in doses of 1.52 mg/kg, up to 2 hours before surgery. It is not licensed for use
in children less than 2 years of age.
Droperidol is the only commonly used butyrophenone in current anaesthetic practice.

It has antiemetic and sedating properties. Antidopaminergic side-effects such as
dystonic reactions and agitation limit its routine use at sedating doses (e.g. 10 mg orally
for adults).
Antiemesis
Postoperative nausea and vomiting (PONV) is a common problem, which is distressing

for the patient. There are several risk factors:
gender (incidence is three times higher in women than in men)
patients undergoing operations on the ear, squint surgery, gynaecological
procedures and laparoscopy
previous history of PONV or motion sickness
use of morphine
anaesthetic technique (volatile anaesthetic maintenance is more emetic than
intravenous propofol maintenance).
The vomiting reflex is coordinated by the vomiting centre within the dorsolateral
reticular formation of the medulla. It receives multiple afferent pathways from peripheral
and central chemoreceptors, nociceptors, the vestibular system and the cerebral cortex.
The synapses in these pathways are predominantly muscarinic. The vomiting centre
also receives stimuli from the chemoreceptor trigger zone in the area postrema on the
floor of the fourth ventricle, but outside the bloodbrain barrier. This structure is rich
in dopamine (D 2) and serotonin (5-HT3) receptors. The antiemetics commonly used in
anaesthetic practice involve inhibition at one or more of these receptor sites.
Muscarinic antagonists: hyoscine (adults, 300 g; children 410 years, 75150

g orally) is a more effective antiemetic and is more sedating than atropine.
Antihistamines, including cyclizine, 50 mg orally, i.v. or i.m., and promethazine, children
25 years, 515 mg, 510 years, 1025 mg orally; adults, 2550 mg orally or intra-
muscularly, also have antiemetic properties, largely as a result of their antimuscarinic
activity. Antimuscarinics cause dry mouth, blurred vision, and bowel and bladder
dysfunction.
Dopamine antagonists are powerful antiemetics but extra-pyramidal side-effects,

such as dystonia, dyskinesia, tremor and oculogyric crisis are not uncommon.
Prochlorperazine, 12.5 mg i.m., is the most widely used phenothiazine because
it is less sedating and has fewer antidopaminergic and -blockade side-effects than
others of the same group.
Droperidol is an effective antiemetic at low dose, 0.6251.25 mg, reducing the risk
of unpleasant dopaminergic or psychological effects. It is usually given intravenously
at induction.
Metoclopramide, 0.1 mg/kg i.v., i.m. or orally, is a dopamine antagonist with
peripheral as well as central effects. Its prokinetic effects are more marked than its
antiemetic properties and comparative studies have raised doubt about its effectiveness
as a prophylactic antiemetic.
5-HT antagonists are powerful new antiemetics that are relatively free of side-effects.
The most widely used agent is ondansetron, 4 mg i.v., given immediately before or at
the end of surgery. Their relative expense has resulted in the cost-effectiveness of their
prophylactic use being questioned.
Non-pharmacological measures including acupunture and acupressure have been

explored. There is some evidence that these techniques are weakly effective.

The potential for lung damage from the aspiration of gastric contents increases with the
volume and the acidity of the aspirate. Risk of aspiration accompanies late pregnancy,
emergency or trauma surgery, symptomatic oesophageal reflux, and obesity.
Acid secretion by gastric parietal cells can be reduced by the use of
H 2 -histamine antagonists such as ranitidine,
150 mg p.o. Proton pump inhibitors such as omeprazole, 20 mg p.o., are more powerful
in reducing acid secretion but inhibit the metabolism of other drugs such as warfarin,
phenytoin and diazepam.
A 0.3 molar solution of sodium citrate, 30 ml, will raise gastric pH and is less
irritant to the airway should aspiration occur. The routine use of the prokinetic agent
metoclopramide, 10 mg, is common practice but of no proven value in the prevention of
gastric aspiration.
Parasympathetic stimulation can lead to hypotension, bradycardia or even asystole

mediated via the vagus nerve. Triggers include:
traction on the extraocular muscles during squint surgery
surgical dilatation of the cervix or of the anal sphincter
repeated doses of suxamethonium
laryngoscopy in children (especially on lifting the epiglottis with a straight-bladed
laryngoscope)
opioid analgesics, propofol and halothane.
Glycopyrronium, 0.2 mg i.v. at induction, provides prophylaxis without the discomfort
of a dry mouth before surgery. It does not penetrate the bloodbrain barrier and lacks
the central side-effects of atropine.
An increase in circulating catecholamines may be caused by several factors:
laryngoscopy and tracheal intubation
surgical stimulation and pain
drugs such as ketamine, cocaine and adrenaline (epinephrine) in local anaesthetics.
This increase may cause hypertension and increased myocardial oxygen demand. It
may result in myocardial ischaemia in susceptible patients. A balanced anaesthetic
technique reduces these risks, and -blocker premedication (atenolol, 50 mg p.o.) may
be of benefit.
There has been recent interest in the use of 2-adrenoceptor agonists such as
clonidine, 3 g/kg p.o., as premedicants. They reduce sympathetic activity, cause
sedation, a reduction in anaesthetic requirement (decreased minimum alveolar
concentration) and reduce pressor responses including that of laryngoscopy. However,
there appears to be a narrow therapeutic window with the potential for development of
hypotension and bradycardia.
Reduction in airway secretions
Antisialogogues are occasionally prescribed as premedicants though their use in

modern-day practice is uncommon. Glycopyrronium, 0.2 mg i.v. or i.m., may be used to
improve conditions before fibre-optic intubation.
Analgesia
Opioids (e.g. morphine, 0.10.2 mg/kg i.v. or i.m.) should be used to relieve acute
preoperative pain. However, in the absence of any preoperative distress and with the
development of new potent opioid analgesics with a rapid onset given at induction, such
as fentanyl, alfentanil and remifentanil, an opioid premedicant is seldom indicated.
Non-steroidal anti-inflammatory drugs decrease the requirement for opioid analgesia
during and after a surgical procedure. Typically, ibuprofen, 400 mg p.o., or diclofenac,
50100 mg p.o., p.r. or i.v., may be given. They should be avoided in patients with
a history of peptic ulceration or renal impairment and used with caution in asthmatic
patients. Other simple analgesics such as paracetamol, 1 g, can also be given p.o.
or p.r.
The concept of pre-emptive analgesia is that nociception can be modulated at
the level of the spinal cord by analgesia given before surgery, thereby reducing total
postoperative analgesic requirements. While this concept is attractive and has been
demonstrated in animal models, clinical studies have yet to prove its value.
Topical anaesthetics such as eutectic mixture of local anaesthetic (Emla cream) or
amethocaine gel applied to the site of venepuncture, reduce the fear of intravenous
anaesthetic induction in children and many adults.
FURTHER READING
Cot C J. Preoperative Preparation and Premedication. Br J Anaesth 1999; 83: 1628.
Kanto J, Watanabe H, Namiki A. Pharmacological Preparation for Anaesthesia. Acta

Anesthesiol Scand 1996; 40: 98290.
McQuay H J. Pre-emptive Analgesia: A Systemic Review of Clinical Studies. Ann Med

1995; 27: 24956.
White P F, Watcha M F. Postoperative Nausea and Vomiting: Prophylaxis versus

Treatment. Anesth Analg 1999; 89: 13379.

Principles of Anaesthetic
Vaporizers
Eileen Palayiwa
Eileen Palayiwa is a Clinical Scientist in the Clinical Measurement Department at

the Oxford Radcliffe Hospital. She graduated in physics from Oxford University and
obtained her PhD from Oxford Polytechnic. Her interests include evoked potential
monitoring and gas analysis.
Gases, liquids and vapours
Substances can exist in the solid, liquid or gaseous state. Below a certain temperature,
known as the critical temperature, it is possible to liquefy gases by compressing them.
When a gas is below this critical temperature it is referred to as a vapour.
Vapours consist of molecules that have left the surface of a liquid below the critical
temperature. Vapour molecules have had sufficient energy to break away from the
attraction of the molecules left behind in the liquid and are therefore the more energetic
molecules. Molecules leave the surface of the liquid and return to it randomly. When
the vapour is in equilibrium with the liquid, the number of molecules leaving the liquid
is equal to the number returning to it, and the vapour is said to be saturated. If there is
insufficient liquid for there to be a reservoir from which molecules can evaporate and to
which they can return, then the vapour is unsaturated and behaves as a gas.
The pressure of a vapour in equilibrium with a liquid is known as the saturated
vapour pressure (SVP).
Variation of SVP with temperature

As the temperature of the liquid increases, more molecules have sufficient energy
to escape from the surface and therefore the SVP rises. When the boiling point is
reached, all the molecules evaporate and the SVP is equal to atmospheric pressure.
Figure 1 shows the variation of SVP with temperature for halothane, enflurane and
isoflurane. Unsaturated vapours behave as gases so that the pressure is inversely
proportional to the volume (Boyles law).
Cooling due to vaporization

If molecules that have left the surface of a liquid are not allowed to return to it (e.g. if
they are swept away by a stream of fresh gas) then the liquid cools. This is because
the evaporating molecules are more energetic than those left behind, therefore there
is a net loss of energy from the liquid, which causes a drop in temperature. The latent
heat of vaporization is the heat required to convert a unit mass of liquid into its vapour
phase at a constant temperature. Cooling may be prevented or reduced if the liquid
is in contact with a surface that can supply heat by conduction. The amount of heat
that a body can supply at a given temperature depends on its specific heat and its
mass, or, in other words, on its thermal capacity. Heat is also supplied by conduction
from the surroundings and the rate at which this occurs is determined by the thermal
conductivity of the body.
The specific heat of a substance is defined as the amount of heat (or energy)
required to raise the temperature of a unit mass of the substance through 1 deg C.
The units of specific heat are joules per kilogram per Kelvin change in temperature
(J/(kg.K)).
The thermal capacity of a body is the heat required to raise its temperature through
1 deg C (this is also equivalent to the amount of energy the body loses when cooled
by 1 deg C). The units of thermal capacity are joules per kilogram (J/kg). The thermal
capacity of a body is equal to the product of its mass and specific heat.
The thermal conductivity of a material is the rate of heat transfer per unit area when
a temperature difference of 1 deg C is maintained across an insulated block of the
material 1 m thick. The units of thermal conductivity are Watts per metre per Kelvin
(W/(m.K)).
Values of specific heat, density and thermal conductivity for copper, aluminium,
glass and stainless steel are shown in Figure 2. It can be seen from this table that
copper has the highest thermal conductivity of these materials so that vaporizers made
of copper are the most efficient at conducting heat from the atmosphere to replace the
energy that the liquid agent loses due to evaporation. Copper has the lowest specific
heat of these substances; however, since it is much denser than aluminium or glass,
the thermal capacity of a given volume of copper is higher than that of either of these
materials. A given volume of stainless steel has the highest heat capacity of these
materials. In practice, most vaporizers are made of stainless steel because it is readily
available. However, copper is thermally more suitable because its much higher thermal
conductivity more than compensates for the lower heat capacity.
Anaesthetic vaporizers
The SVP of most anaesthetic agents at room temperature is too high for them to be
delivered to a patient without dilution (Figure 1). For example, the SVP of isoflurane
at 20C is 236.5 mm Hg (i.e. 31% v/v if atmospheric pressure is 760 mm Hg). In
general, concentrations below 2% v/v are required for maintenance of anaesthesia. An
anaesthetic vaporizer is a device that dilutes the vapour to give a known concentration
of the agent.
Fresh gas enters the vaporizer and is split into two portions (Figure 3). One portion
flows through an area known as the vaporizing chamber, where it comes into contact
with the anaesthetic vapour; the remainder of the gas bypasses this chamber. The
two flows then recombine and the vapour is diluted. By varying the flow rate in the two
paths the resultant vapour concentration can be varied. The concentration of agent
depends on the flow through the vaporizing chamber, the total fresh gas flow and the
saturated vapour pressure of the anaesthetic agent. The way in which the gas flow is
split between the bypass and vaporizing chamber depends on the relative resistance
of each pathway. If the total fresh gas flow (F) is split into a bypass flow (Fb) and a
vaporizing chamber flow (Fv) then:
Fv + Fb = F
The flow rate emerging from the vaporizing chamber (Fe) will be greater than that
entering it, due to the volume of vapour added:
Fe = Fv + Fe x SVP/100
where SVP is expressed as a percentage.
Therefore Fe = Fv/[1(SVP/100)]
The concentration (C) of the vapour in the gas emerging from the vaporizer will be
given by:
C = Fe x SVP/(Fb + Fe)
This calculation assumes that the gas emerging from the vaporizing chamber is fully
saturated with vapour. To ensure that this is the case, manufacturers increase the
surface area of liquid that the gas passes over by introducing wicks made of cloth
or metal into the vaporizing chamber. In many cases the gas is forced to take a long
pathway through the chamber, which also helps to ensure saturation.
Variation of saturated vapour pressure with temperature

400
350
pressure (mm Hg)
Saturated vapour
300
250
200
150
Halothane
100
Isoflurane
50 Enflurane
0
10 12 14 16 18 20 22 24 26 28 30 32
Temperature (C)
Physical properties of some common materials at 293K
Specific heat Thermal Density

(J/(kg.K)) conductivity (kg/m3)
(W/(m.K))
Copper 385 385 8930
Aluminium 913 201 2710
Glass 670 1 2600
Stainless steel 510 150 7930
An anaesthetic vaporizer
Gas Bypass
flow
Variable
resistances
Vaporizing chamber
Wicks
Liquid agent
Temperature compensation
As liquid evaporates from the vaporizing chamber the temperature drops, and unless
there is some means of compensating for this, the output of the vaporizer also drops.
The temperature drop, and hence the fall in output, is lower if the vaporizer has a large
heat capacity and can therefore supply energy to the liquid to compensate for that
which it has lost. For this reason most vaporizers contain a large mass of metal that
can also conduct heat from the surroundings into the liquid. In addition, most vaporizers
incorporate some kind of temperature compensation, which reduces the resistance of
the vaporizing chamber relative to that of the bypass as the temperature drops. As a
result, more gas flows through the vaporizing chamber so that the vapour concentration
is maintained.
Effect of intermittent positive-pressure ventilation (IPPV)

During IPPV, the pressure at the outlet of a vaporizer is not constant. When the
pressure is high, flow emerging from the vaporizer reduces and the pressure in the
vaporizing chamber builds up. As the pressure drops, the excess of vapour, which
has accumulated in the vaporizing chamber at this time, emerges not only from the
normal outlet of the vaporizing chamber but also from the inlet. This means that the
bypass gas contains vapour and therefore the concentration rises. Manufacturers have
compensated for this by introducing a long inlet tube into the vaporizing chamber. When
the pressure inside the vaporizing chamber drops, the vapour enters this tube, but its
volume is not enough to emerge into the bypass.
Effect of flow rate on vaporizer output

The vaporizer output is dependent on the resistance of the vaporizing chamber relative
to that of the bypass. With varying flows the vaporizer output remains constant only
if this does not change. In practice, this is difficult to achieve over the wide range of
flows used in anaesthetic practice. Only if laminar flow is maintained in each pathway
throughout the flow range will this be the case. Another factor influencing the output
at high flows is the increased cooling, which occurs as a result of the large amount of
evaporation taking place.
Figure 4 shows the variation of output with flow for a Penlon plenum enflurane
vaporizer. It can be seen that the output of this vaporizer at high settings drops as the
flow rate increases. However, at the lower settings more commonly in use, the output
remains reasonably constant. This indicates that the temperature compensator in the
Penlon plenum vaporizer (PPV) can adjust adequately for cooling due to evaporation
except at the highest dial settings and flow rates.
Effect of gas composition

The relative flow rates through the bypass and vaporizing chamber at a given dial
setting remain constant only if laminar flow is maintained in both pathways. As soon
as the flow in one pathway becomes turbulent, its resistance rises causing less gas to
flow through it, unless it is matched by a proportional rise in the resistance of the other
pathway.
Nitrous oxide has different physical characteristics from oxygen (Figure 5); in
particular, the ratio of viscosity to density, which determines the flow rate at which
turbulence sets in, is much lower. The effect that this has on the output of the vaporizer
depends on its design. In some vaporizers, output drops when the carrier gas contains
nitrous oxide whereas in others it increases.
Variation of output with flow for the Penlon plenum
vaporizer
6
5
Enflurane (vol %)
0
0 1 2 3 4 5 6 7 8 9 10 11
Flow rate (litre/minute)
Courtesy of Penlon Ltd.
Physical properties of oxygen and nitrous oxide
Gas Density Viscosity Kinematic

(kg/m3) (N.second/m2) viscosity (m2/second)
Oxygen 1.43 18.9 10.3 x 10-5

Nitrous oxide 1.96 13.5 6.9 x 10-5
Types of vaporizer
Vaporizers fall into two broad categories.
Drawover vaporizers in a drawover vaporizer, gas is pulled through as the patient
inspires (expiration is to atmosphere via a non-rebreathing valve). The flow rate of gas
through the vaporizer is therefore not constant and it is necessary for the vaporizer to
have a low resistance.
Plenum vaporizers in a plenum vaporizer, gas is driven through under positive
pressure. The term plenum is derived from the plenum system of ventilation where
gas is forced into the system. Plenum vaporizers may have a higher resistance than
drawover vaporizers though some vaporizers are designed to be used in either mode
(e.g. the Oxford miniature vaporizer).
Oxford miniature vaporizer

The Oxford miniature vaporizer (Figure 6) is designed as a low resistance drawover
vaporizer. It does not have any temperature compensation, but it has a water-filled
jacket to increase its heat capacity.

Concentration
regulator
Tubular slide valve
Wicks
Liquid agent
Base
6
Drager Vapor
The Drager Vapor (Figure 7) is constructed from a large block of copper and is
therefore thermally stable. It has a built-in thermometer so that the temperature of
the liquid agent may be read and the position of the concentration dial is adjusted
according to this temperature. In this vaporizer, the gas flow through the bypass and
the vaporizing chamber is controlled by a pair of needle valves, which are carefully
manufactured to ensure that gas flow is laminar in both pathways over a large range of
flow rates. There is therefore little variation of output with flow rate for this vaporizer.
Drager Vapor
3 0 16
2 5 20
2 0
24
1 5
28
Inlet
Outlet
Max
Min
7
PPV
In the PPV (Figure 8), when the control dial is in the zero position the vaporizing
chamber is isolated by means of a spring-loaded valve attached to the push rod, which
is aligned with the control knob. When the control knob zero lock button is pressed the
push rod opens the valve and as the control knob is rotated the vapour control orifice
opens to allow more gas to flow through the vaporizing chamber.
Temperature compensation is achieved by a moving needle valve within the bypass
orifice, which increases the bypass resistance as the temperature drops, thus forcing
more gas to flow through the vaporizing chamber. The movement of the valve is
controlled by a push rod attached to an ether-filled metal bellows unit. As the liquid
agent changes temperature, the ether in the bellows expands or contracts causing the
bellows to expand or contract linearly. Compensation for fluctuating back pressure is
achieved by the inclusion of a long narrow tube in the vaporizing chamber.
Penlon plenum vaporizer
Inlet Outlet Concentration

control dial
Bypass
orifice
Vapour
control
orifice
Zero Entry tube

lock Liquid level
port indicator
Liquid
level
Wick
Temperature compensator
8
Tec 6 vaporizer
The Tec 6 vaporizer (Figure 9) varies from most other conventional vaporizers because
it incorporates a heater element. This is necessary because desflurane concentrations
up to 18% v/v may be required. The concentration knob has an interlock system, which
means that it cannot be turned until the liquid agent has been heated to the correct
temperature. When the control dial is turned, an electronic signal opens the shut-off
valve. The pressure transducer measures the difference between the gas inlet pressure
and the regulated agent pressure. The agent pressure is controlled electronically by
opening or closing the pressure-regulating valve to balance the pressures. When the
pressures are correctly balanced the vaporizer functions correctly.
Calibration of vaporizers
Anaesthetic vaporizers are calibrated in the factory using a refractometer (an accurate
optical device) in a temperature-controlled room. In general, either oxygen or air at
a medium flow rate is used for the carrier gas. The output of a vaporizer may vary
under different conditions of temperature, flow or carrier gas this is not surprising,
considering the wide range of flow rates and concentrations over which a vaporizer is
used. It has been said that one should expect vaporizers to produce concentrations
only within 20% of their dial settings. While this is a wide margin, it is not at all unusual
for concentrations to differ by 10% of the dial setting and as conditions become more
extreme this difference may approach 20%. It is important that anaesthetists recognize
the problems faced by manufacturers when designing vaporizers and that they do not
always expect vapour concentration and dial setting to coincide.
Tec 6 vaporizer
Gas/agent
outlet
b Gas inlet pressure
Fresh
c d
gas
inlet e
Regulated agent pressure f

g
h Key
Fresh gas
Agent vapour
i Gas/agent vapour
j Electrical
connections
m l k
a Dial and rotary valve, b fixed restrictor, c pressure control

transducer, d pressure monitor transducer, e heater in vapour
control manifold, f vapour control manifold assembly,
g pressure-regulating valve, h shut-off valve, i sump assembly,
j agent, k level switch, l level sensor, m sump heaters
FURTHER READING
Hill D W. Physics Applied to Anaesthesia. 4th ed. London: Butterworths, 1980, 296
348.
Scurr C, Feldman S, Soni N. Scientific Foundations of Anaesthesia.
4th ed. Oxford: Heinemann Medical Books, 1990, 68797.

Recognition and Management
of Anaphylactic and
Anaphylactoid Reactions
Andrew McIndoe
Andrew Mclndoe is Consultant Anaesthetist and Senior Clinical Lecturer in the Sir
Humphry Davy Department of Anaesthesia, Bristol Royal Infirmary. He is also the
Director of Research and Education at the Bristol Medical Simulation Centre where he
has developed a specific interest in human factors and crisis management.
The term anaphylaxis was coined by Charles Richet in 1902 to describe the reaction
of dogs to a second, and often fatal, injection of foreign protein (sea anemone toxin).
The term was introduced to distinguish this later injection from the first prophylactic
injection that induced sensitization.
Anaphylaxis is now recognized to be an immediate hypersensitivity or type I immune

reaction mediated by immunoglobulin E (IgE) and resulting in mast cell degranulation
and basophil activation. It is not dose related and can occur in response to minute
exposure to an allergen. Typically, the severity of the response worsens on re-exposure
owing to progressive sensitization of the subject. The true incidence of anaphylaxis is
unknown but is estimated to be 1/600020,000 anaesthetics or 1/10,000 of the general
population/year. Women are more likely to suffer an anaphylactic reaction than men,
with a quoted increase in risk of 310:1. Intravenous administration of the antigen
is more likely to precipitate a severe generalized reaction. Cross-sensitivities with
non-steroidal anti-inflammatory drugs (NSAIDs) and muscle relaxants makes previous
exposure unnecessary. Up to 80% of neuromuscular blocking agent reactions are not
associated with known prior exposure.
Anaphylactoid reactions may present with a similar clinical picture, but do not result
from hypersensitivity and are not mediated by IgE. Drugs such as opioids can directly
stimulate mast cell degranulation with histamine release causing pruritus, rash and
hypotension. They should be managed as potential anaphylactic reactions because
confusion over the diagnosis merely delays effective treatment.
Pathophysiology
Primary exposure to an antigen results in the synthesis of specific IgE antibodies by

lymphocytes and plasma cells. The Fc portions of these antibodies are able to
fix themselves to the surface of tissue mast cells and circulating basophils. The
antigen binding sites are thus presented externally. Subsequent contact with antigen
causes IgE antibody:antigen cross-binding and triggers immediate degranulation of
the host mast cell or basophil. Release of histamine and serotonin results in an
acute inflammatory reaction, smooth muscle constriction, vasodilatation and increased
capillary permeability. The clinical picture depends on the mode of exposure.
Skin urticaria, flare and weal reaction (hence the use of skin prick testing).
Eyes conjunctivitis.
Mouth/airway perioral and laryngeal oedema, broncho-spasm.
Parenteral generalized cardiovascular collapse.
Eosinophils are mobilized by chemotaxis, attracted by histamine and other
substances, they produce histaminase, helping to terminate the reaction.
Anaphylaxis may present with a spectrum of clinical signs including hypotension,

tachycardia, dysrhythmias, dyspnoea, laryngeal oedema, bronchospasm, angio-
oedema, flushing, urticaria, conjunctivitis, rhinitis, abdominal pain and diarrhoea. It can
therefore mimic a variety of other conditions. Diagnosis is further complicated by a
variable time for exposure until symptoms develop, varying from a few seconds to
several hours. 5% of patients show a biphasic response with symptoms recurring from
172 hours after the initial attack. Many patients do not develop all the classic signs
(Figure 1).
Differential diagnoses are vasovagal faint with hypotension, bradycardia and pale,
sweaty skin and panic attack with hyperventilation, tachycardia and an erythematous
rash.
Percentage of patients presenting with classic signs of anaphylaxis
Signs Patients (%)

Cardiovascular collapse 88
Erythema 45
Bronchospasm 36
Angio-oedema 24
Rash 13
Urticaria 8.5
Management
The management of anaphylaxis is summarized in Figure 2.
Management of anaphylaxis
Condition
IgE mediated immediate hypersensitivity reaction to an antigen resulting in
histamine and serotonin release from mast cells and basophils
Presentation
Cardiovascular collapse
Erythema
Bronchospasm
Oedema
Rash
Immediate action
Remove trigger
100% oxygen
Elevate legs
Adrenaline (epinephrine) 500 g i.m. or 50 g increments i.v. titrated to effect
20 ml/kg i.v. fluid challenge
Follow-up action
Chlorphenamine (chlorpheniramine), 1020 mg i.v.
Hydrocortisone, 100300 mg i.v.
Arterial blood gases
Investigations
Plasma tryptase
Urinary methylhistamine
Also consider
Primary myocardial/cardiovascular problem
Latex sensitivity
Airway obstruction
Asthma
Panic attack
Immediate management
Check the airway, breathing and circulation. Stop the administration of or exposure
to any potential triggers, particularly intravenous agents. Muscle relaxants, antibiotics
and NSAIDs (and increasingly latex) are the most common triggers in an anaesthetic
environment. Outside the operating theatre, foods (especially nuts, fish, shellfish, eggs
and milk), insect venom, drugs (antibiotics, NSAIDs, contrast media, opioids) and latex
are the most common precipitants.
Call for help.
Maintain the airway and give 100% oxygen. Reassess airway patency frequently and
regularly, especially in known asthmatics and in those exposed to the allergen via the
airway or mouth. If in doubt and the reaction is severe, intubate early because it may be
impossible to do so later in the presence of increased oedema.
Cardiovascular collapse is most likely following parenteral exposure to the allergen.
Lay the patient flat with the legs elevated to increase central venous return.
If the patient has a continuous ECG monitor attached, give adrenaline (epinephrine)
in 50 g i.v. increments (0.5 ml of a 1:10,000 solution) at a rate of 100
g/minute until the blood pressure or bronchospasm improves. Alternatively,
give adrenaline (epinephrine) 0.51 mg i.m. as 0.51.0 ml of a 1:1000
solution (repeated after 10 minutes if necessary). Adrenaline (epinephrine)
stabilizes mast cell membranes, increases myocardial contractility, causes
bronchodilatation and reverses vasodilatation; it therefore treats both cause and effect.
Give intravenous fluid (colloid or suitable crystalloid), 20 ml/kg.
Latex allergy may take up to 30 minutes to manifest itself. Removal of all latex
triggers can then be a complex process. Allergen is more readily absorbed across
mucous membranes (e.g. from surgical gloves or a urinary catheter, which should be
removed immediately and hands should be re-washed to remove latex-impregnated
starch granules). Inhalation of aerosolized particles within the breathing circuit is
minimized by the use of an airway filter. Ensure that rubber corings are not introduced
intravenously (e.g. ampoule bungs and injection sets). Laryngeal mask airways are
made of silicone and do not contain latex. Diprivan syringe bungs are also latex free.
Subsequent management
Give an antihistamine (H1-blocker) such as chlorphenamine (chlorpheniramine,
Piriton), 1020 mg by slow i.v. or i.m. injection. Consider H2-antagonists, such as
ranitidine, 50 mg slow i.v. injection.
Give corticosteroids such as hydrocortisone, 100300 mg by slow i.v. or i.m.
injection, to inhibit later relapses.
Give a catecholamine infusion because cardiovascular instability may last for several
hours. Consider adrenaline (epinephrine) 0.050.1 g/kg/minute (e.g. 4 ml/hour of
1:10,000 for a 70 kg adult) or noradrenaline (norepinephrine) 0.050.1 g/kg/minute
(e.g. 4 ml/hour of a solution of 4 mg made up to 40 ml in 5% dextrose for a 70 kg
adult).
Check arterial blood gases for acidosis and consider giving bicarbonate, 0.51.0
mmol/kg (8.4% solution = 1 mmol/ml).
Check for the presence of airway oedema by letting down the tracheal cuff and
confirming a leak before extubation.
Consider bronchodilators for persistent bronchospasm (e.g. salbutamol, 5 mg by
nebulizer or 250 g slow i.v. injection, aminophylline 250500 mg slow i.v. injection).
Complications
Hospital mortality to anaesthetic drug-induced anaphylaxis is 4%, despite the presence

of good resuscitation facilities. Over half of those who die of anaphylaxis do so within
the first hour. The deaths are related to asphyxia, from severe bronchospasm or upper
airway obstruction, and from refractory hypotension.
The early use of adrenaline (epinephrine) is advisable but advice differs over the
safest and most appropriate mode of administration. Adrenaline (epinephrine) is best
administered by intramuscular injection (0.5 mg usually 0.5 ml of 1:1000 solution)
by first responders because it is a reliable means of achieving therapeutic plasma
concentrations quickly and safely. The subcutaneous route is slow and unpredictable
and is inappropriate during an acute life-threatening reaction. Anaesthetists often opt for
intravenous administration of a 1:10,000 solution in incremental doses (of 50100 g).
The intravenous route, while rapidly effective, can result in tachydysrhythmias. Cardiac
complications are more common in the presence of hypoxia, hypercapnoea, and in
patients taking tricyclic antidepressants or cocaine.
Patients taking -blockers are likely to suffer more severe reactions and may
be resistant to treatment with adrenaline (epinephrine). However, -blockers are
competitive antagonists and careful but continued titration of adrenaline (by sequential
doubling of the initial dose in severe cases) should achieve a clinical effect.
Late diagnosis may be complicated by severe compromise of the airway and
difficulty intubating the trachea.
Investigations
Investigations should be carried out when the patient has been stabilized.
Plasma tryptase: at least one 10 ml clotted blood sample should be taken 16 hours
after the start of the reaction to perform a tryptase assay. The specimen must be spun
down as soon as possible and the serum stored at 20oC, to stabilize the protein for
later analysis. Tryptase is the main protein released during mast cell degranulation
and is a specific marker of histamine release due to anaphylaxis or anaphylactoid
reaction. Normal basal levels of serum tryptase are less than 1 ng/ml. However, unlike
histamine, which is rapidly eliminated, tryptase levels remain elevated for up to 6 hours
after an anaphylactic reaction. It is not a protein that is produced by RBCs or WBCs
and is therefore not raised by haemolysis. Levels over 20 ng/ml may accompany an
anaphylactic reaction.
Elevated metabolites in the form of urinary methylhistamine may also be measured.

The value measured has to be corrected for urinary creatinine but levels in excess of
1520 ng/ml/mmol creatinine/litre are considered higher than normal, and may indicate
anaphylaxis.
Radio allergosorbent testing (RAST) is a means of searching for antigen-specific IgE

in the serum. Tests are limited to specific allergens. At present only a few anaesthetic
RASTs are available (e.g. suxamethonium). Fluoroimmunoassay is an alternative (CAP
System, Pharmacia).
Follow-up and prognosis
The anaesthetist should follow up the investigation, report reactions to the Committee
on Safety of Medicines via the yellow card reporting scheme, and arrange skin
prick testing in consultation with an immunologist. Having identified allergens, the
patient should be advised to wear an alert bracelet at all times. Those who have
suffered a severe reaction, especially anaphylaxis to allergens that are commonly
encountered in everyday life, may be advised on how to carry and when to administer
their own adrenaline (epinephrine). The Epipen syringe is preloaded with adrenaline
(epinephrine) and will deliver a fixed intramuscular injection of 300 g (0.3 ml of 1:1000)
for adults or 150 g for children.
Desensitization is a process that attempts to stimulate the production of IgG or
IgA antibodies that competitively bind to the antigen and help block the IgE antibody
antigen hypersensitivity reaction that precipitates anaphylaxis. It is not without risk
because it involves repeated inoculation with small doses of antigen.
FURTHER READING
Ewan P W. ABC of Allergies Anaphylaxis. BMJ 1998; 316: 14425.
Fisher M. Treatment of Acute Anaphylaxis. BMJ 1995; 311: 7313.
Project Team of the Resuscitation Council (UK). The Emergency Medical Treatment of
Anaphylactic Reactions. J Accident Emergency Med 1999; 16: 2437.

Recognition of Correct
Placement of Tracheal Tubes
Simon Berg
Simon Berg s Consultant Paediatric Anaesthetist at the Oxford Radcliffe Hospitals

NHS Trust, Oxford, UK. His special interests are anaesthesia for neonatal surgery and
paediatric strabismus surgery.
The technique of tracheal intubation is fundamental to anaesthetic practice. Critical

incident reporting indicates that oesophageal intubation is a relatively common problem.
Misplacement of a tracheal tube is not in itself harmful if the diagnosis is made promptly
and corrective action taken. However, tracheal tube misplacement still accounts for a
large proportion of anaesthetic deaths. It should be considered in any hypoxic intubated
patient. Failure to detect incorrect tube placement is equally common for trainees and
consultants. It is as likely with routine as with difficult intubation.
Methods of confirming correct tube placement
Clinical signs are often unhelpful in detecting tube misplacement and intubation should
be confirmed by:
direct visualization of the tube passing through the vocal cords
auscultation over both axillae, lung bases and the epi-gastrium
capnography
oesophageal detector device or colorimetric detector if capnography is not readily
available.
Visualization of larynx
The larynx is usually visualized and the tracheal tube is observed passing between
the vocal cords into the trachea. However, a view of the larynx is not always possible.
In routine laryngoscopy, an anaesthetist may become distracted at the moment of
intubation, allowing the tube to slide past into the oesophagus. Occasionally the
oesophagus may be mistakenly identified as the trachea or the tube may become
displaced during fixation. Direct visualization is thus not totally reliable and may even
delay a diagnosis of tube misplacement by promoting a false sense of security.
Repeat laryngoscopy is essential if a tube problem is suspected; oesophageal
intubation, extubation or a kinked tube can all be identified and remedial action taken.
Chest movement
Bilateral symmetrical chest wall expansion should occur coincident with inspiration. It
may be difficult to discern in the obese patient, in those with a rigid chest wall, or
in chronic lung disease (e.g. emphysema). Oesophageal ventilation may imitate chest
movement by expansion of the mediastinum, while gastric distension can simulate
diaphragmatic and lower chest wall ventilation, especially in infants.
Auscultation
The combination of auscultation over each axilla, lung base and epigastrium achieves
the most reliable results. Direct auscultation over the trachea may be of additional
benefit; more obvious breath sounds can be heard, which are less likely to be confused
with oesophageal ventilation.
Breath sounds over the chest wall do not always exclude oesophageal intubation.
Air ventilating the oesophagus can be transmitted through the lungs to resemble
convincing breath sounds. Conversely, breath sounds may be inaudible in the obese
patient.
Breathing circuit
The ability to ventilate the lungs via the reservoir bag together with its
typical compliance characteristics is a useful sign for the anaesthetist. In a
spontaneously breathing patient the bag should empty and refill synchronously with
the patients breathing pattern. However, small movements (cardiac oscillations) can be
demonstrated with oesophageal tube placement.
In contrast, it may be difficult to ventilate a morbidly obese patient via the
reservoir bag or to differentiate between oesophageal intubation and partial or complete
bronchospasm.
Fibre-optic laryngoscopy
The fibre-optic bronchoscope or laryngoscope can reliably confirm tracheal tube
placement by identification of the tracheal rings and carina under direct vision (Figure
1). The technique requires operator experience and the equipment must be readily
available.
1 View of the carina via a

fibrescope, confirming the correct
placement of the tracheal tube.
Oesophageal detector device

The Wee oesophageal detector device (ODD) consists of a 60 ml bladder syringe
connected to a catheter mount. This is attached to the tracheal tube following
intubation. The syringe freely aspirates gas from the patients lungs if the tube is in
the trachea (negative result). However, if this negative pressure is applied to a tube
within the oesophagus, the oesophageal wall collapses and no air can be aspirated
(positive result).
As a modification, the syringe has been replaced by a large rubber bulb (Ellicks
evacuator) to enable the device to be used one-handed (Figure 2). In this case the bulb
is first emptied and then failure to refill indicates oesophageal intubation.
The ODD is cheap, simple to construct, easy to use and reliable. It has been
validated in several studies with only a small incidence of false-positive results, possibly
related to endobronchial intubation or secretions blocking the lumen of the tracheal
tube; there are no reported false-negative results.
It has been used successfully with uncuffed tubes in older children but is unreliable
in those under 2 years of age.
2 Oesophageal detector device with

Ellick's evacuator modification.
Capnography
Capnography is the real-time detection of carbon dioxide in the breathing gases and its
display as a waveform that plots concentration versus time. Carbon dioxide is detected
by infrared spectroscopy. It is the gold standard for verifying tracheal intubation. The
guidelines of the Association of Anaesthetists state that during induction of anaesthesia,
capnography is 'essential to the safe conduct of anaesthesia'.
For carbon dioxide to be detected, it must be produced in the tissues, then
transported to the lungs, and finally exhaled in the expiratory gas. The capnograph is
therefore an important monitor that gives information about:
metabolic rate
pulmonary perfusion
alveolar ventilation.
If metabolic rate and pulmonary perfusion (or cardiac output) are constant, then
changes in the capnograph trace reflect the adequacy of alveolar ventilation.
Deceptively low values may result from a large leak around the tube. Gas arising
from the stomach and oesophagus usually contains only a trace of carbon dioxide,
but false-positive results occur if expired alveolar gas is introduced into the stomach
from mask ventilation. Significant concentrations of carbon dioxide have been reported
following ingestion of carbonated drinks ('cola complication'). In these circumstances,
capnography following oesophageal intubation initially resembles the normal waveform
for end-tidal carbon dioxide. This initial value rapidly diminishes towards zero as the
carbon dioxide is washed out. It has been suggested that the waveform should be
observed for a minimum of six breaths.
Colorimetric carbon dioxide detector

This small disposable device contains a pH-sensitive indicator that displays a colour
change (e.g. from purple to yellow) when exposed to carbon dioxide (Figure 3).
The colour change is rapid and the detector can be left in the breathing circuit for
several hours allowing continuous ventilatory monitoring. The device is about the same
size and weight as a heat/moisture exchange filter and requires no power source
for operation. This portability makes it useful during cardiopulmonary resuscitation or
in emergency situations when capnography may not be available. Reduced carbon
dioxide concentrations often present in these clinical situations, which may reduce its
sensitivity.
3 Colorimetric carbon dioxide detector.
Complications of oesophageal and endobronchial tube placement
Oesophageal intubation
Undetected oesophageal intubation is a major anaesthetic cause of permanent
neurological damage and death. There should be a high index of suspicion in any
situation in which hypoxia develops following intubation; the onset may be delayed if
preoxygenation has occurred. Difficulty in ventilation, poor or absent chest movement,
inaudible breath sounds and increasing abdominal distension should all alert the
anaesthetist to the possibility of tube misplacement. In practice, clinical signs are not
always obvious.
Progressive gastric distension may cause regurgitation and subsequent aspiration.
Splinting of the diaphragm impairs ventilation even after the patient has been correctly
intubated unless the stomach is actively decompressed using a nasogastric or
orogastric tube.
If there is any doubt as to correct tube placement, it is essential to remove the tube
and recommence mask ventilation.
Endobronchial intubation is more common in children owing to the smaller length of the
trachea. Flexion or extension of the neck can move the tube a significant amount within
the trachea (up to 5 cm in adults), leading to endobronchial intubation or inadvertent
extubation. The right main bronchus is more commonly intubated than the left side
because it arises at a straighter angle from the trachea.
One-lung ventilation causes hypoxaemia due to the shunt effect that failure to
ventilate the opposite lung produces. Progressive lung collapse of this unventilated side
occurs. There is a reduced uptake of volatile anaesthetic agent and bronchospasm is
a common occurrence, probably as a result of vagal stimulation from irritation of the
carina.
The diagnosis may be obvious with asymmetric chest movement and absent
breath sounds on one side of the chest, but clinical signs are often unreliable. With an
uncuffed tube, breath sounds can easily be transmitted to the non-ventilated lung. A
chest radiograph confirms the diagnosis and provides an estimate of the distance that
the tube needs to be withdrawn. Fibre-optic bronchoscopy can also be useful.
The chances of endobronchial intubation can be lessened by cutting tracheal tubes
to an appropriate size (e.g. 2224 cm in the adult) preceding intubation. The black
marker line present at the distal end of some tracheal tubes can also serve as a guide
to the length of the tube to be passed through the vocal cords.
FURTHER READING
Association of Anaesthetists of Great Britain and Northern Ireland. Recommendations
for Standards of Monitoring during Anaesthesia and Recovery. December 2000.
Holland R, Webb R K, Runciman W B. Oesophageal Intubation: An Analysis of 2000

Incident Reports. Anaesthesia 1993; 21: 60810.
Wee M Y. The Oesophageal Detector Device. Assessment of a New Method to

Distinguish Oesophageal from Tracheal Intubation. Anaesthesia 1988; 43: 279.

Regurgitation, Vomiting and
Aspiration
Polly Davies
Jonathan Warwick
Polly Davies is Specialist Registrar in Anaesthesia rotating within the Oxford Region.
She graduated from Bristol University and is currently based at Northampton General
Hospital, UK.

Regurgitation is the passive movement of gastric contents into the pharynx.

The lower oesophageal sphincter normally prevents regurgitation. The sphincter is
a physiological, rather than a distinct anatomical structure. Reflux is prevented
because the lower oesophageal pressure is greater than the gastric pressure. This is
referred to as the barrier pressure.
Vomiting is an active reflex usually occurring in the lighter planes of anaesthesia

(i.e. induction and emergence). It is the forceful ejection of the contents of the upper
gastrointestinal tract through the mouth. It is often secondary to stimulation from
inappropriate airway manipulation.
The afferent limb of the reflex arc is composed of fibres from the gastrointestinal
tract, the vestibular system, or from the chemoreceptor trigger zone in the brain stem.
The vomiting centre in the brain stem coordinates the reflex. The efferent limb involves
autonomic outflow to the gastro-intestinal tract and also produces widespread effects
such as pupillary dilation, sweating, salivation, vasoconstriction and tachycardia.
Pulmonary aspiration of gastric contents into the lungs is a serious, though infrequent,
complication of modern anaesthesia. Mendleson first described it in detail in 1946 in
66 obstetric patients. Aspiration occurs following gastro-oesophageal regurgitation or
vomiting when protective laryngeal reflexes are depressed or absent. Prevention of
pulmonary aspiration is by measures aimed at reducing the incidence of regurgitation
and vomiting.
Although silent regurgitation is thought to occur in up to 25% of patients under
anaesthesia, the incidence of significant pulmonary aspiration in the general surgical
population is much less at 16/10,000. For obstetric general anaesthesia the incidence
is doubled. The mortality following aspiration is about 5%.
Pathophysiology
The adverse effects of pulmonary aspiration occur by three mechanisms.

Particle related this could result in acute airway obstruction.
Acid related the traditional view is that patients are at risk if the gastric contents
consist of a critical volume of more than 25 ml and have a pH of less than 2.5;
there is little clinical evidence to support this. pH is the more critical factor for lung
injury sustained following aspiration though there may not be an exact cut-off value.
Significant morbidity can occur following inhalation of material with a very low pH even
in small volumes due to chemical pneumonitis, and following large volumes of neutral
fluid due to a near drowning effect.
Bacterial related aspirated fluid is not sterile and lung infection may result.
Damaged lung is also more prone to secondary infection.
Risk factors
Predisposing factors for pulmonary aspiration are shown in Figure 1. Vomiting and
regurgitation during induction of anaesthesia occur most often in emergency cases
with acute abdominal pathology or following trauma. Pain, fear, anxiety and opioid
administration all delay gastric emptying. These patients should be regarded as at high
risk and appropriate precautions taken. The interval between last oral intake and time
of injury in trauma patients is said to give a better guide to gastric emptying than the
duration of fasting. In practice this is unreliable and it is often best to assume patients
have a full stomach.
Risk factors for aspiration
Condition Examples
Full stomach Inadequate preoperative fasting

Gastrointestinal obstruction, bleeding or ileus
Trauma, burns, pain, anxiety
Pregnancy
Drugs (e.g. opioids)
Reduced lower Hiatus hernia

oesophageal Drugs (e.g. opioids, atropine)
sphincter function Pregnancy
Raised intra-abdominal pressure
Obesity
Lithotomy position
Material in oesophagus/ Achalasia, scleroderma

pharynx Strictures, carcinoma
Pharyngeal pouch
Depressed laryngeal Reduced consciousness

reflexes (e.g. general anaesthesia, drug or alcohol
intoxication, cerebrovascular accident, head injury,
seizures or postictal state)
Topical anaesthesia
Neurological disease (e.g. myasthenia, multiple
sclerosis, Parkinsons disease, GuillainBarr
syndrome)
Muscular dystrophies
Others Inexperienced anaesthetist

Night-time surgery
Emergency surgery
Extremes of age
Obstetrics
In the third trimester, the enlarged uterus increases intra-abdominal pressure and
therefore intra-gastric pressure. Before this, there is an increased risk of aspiration due
to the production of:
gastrin from the placenta, which increases gastric acid secretion
progesterone, which relaxes smooth muscle and reduces gastrointestinal motility.
Anatomical changes in late pregnancy may increase the incidence of airway
difficulties and thus of aspiration (e.g. increased body weight, large breasts, upper
airway oedema). Surgery often occurs out of hours as an emergency. Risks may
be increased further during labour from the effects of pain, anxiety and opioid
administration. Pregnant patients should be assumed to have a full stomach from the
end of the first trimester until at least 18 hours post-partum. Regional anaesthesia
should be used whenever possible to reduce the aspiration risks.
Prevention
Methods to prevent pulmonary aspiration are directed towards reducing the volume
and increasing the pH of the stomach contents. The technique of cricoid pressure and
induction of anaesthesia in the patient with a full stomach is elsewhere.
Fasting requirements
Traditionally, patients were fasted overnight before elective surgery. More recently it
has been shown that the administration of clear fluids (e.g. water, non-particulate juice)
up to 23 hours preoperatively does not increase residual gastric volume or alter pH.
This increases patient comfort and reduces dehydration and hypoglycaemia in infants.
An example of current fasting guidelines for elective, nonobstetric patients is shown
in Figure 2.
Fasting requirements are less straightforward for emergency surgery. It is often
necessary to provide anaesthesia to patients suspected of having a full stomach.
Delaying urgent surgery to reduce the possibility of aspiration is usually of no benefit
and may be detrimental. Patients requiring emergency surgery should be assumed to
have a full stomach, irrespective of the duration of fasting, because gastric emptying
is likely to be delayed. Following painful trauma, a significant gastric residue can be
present after 24 hours. It is not currently recommended that emergency patients be
allowed to drink clear fluids before surgery. Intravenous therapy should be used to
prevent dehydration. At present there is no consensus regarding fasting during labour.
Preoperative fasting guidelines for patients undergoing elective surgery
Length of fast
(hours)
Adults
Solid food 6
Clear fluid 23
Children
Solid food 6
Formula milk 4
Breast milk 3
Clear fluid 2
Regional anaesthesia
Avoiding general anaesthesia reduces the risk of pulmonary aspiration. Both the
proposed surgery and the patient must be amenable to the technique. The patient
should be fasted because an inadequate or failed regional block, or adverse reaction,
may make general anaesthesia necessary.
Gastric decompression
The insertion of a nasogastric tube to decompress the stomach may be useful. Liquid,
but not solid, gastric contents can be aspirated via the tube. It is not usually possible to
empty the stomach completely by this means, so the possibility of aspiration remains.
If a nasogastric tube has been passed before surgery, it should be aspirated before
induction. Effective cricoid pressure can be performed with the tube in situ.
Pharmacotherapy
Antacids: prophylactic administration of antacids to high-risk patients is recommended.
These drugs neutralize gastric acid and raise gastric luminal pH. Neutral pH aspirate
causes less lung damage than fluid of acidic pH. Antacids should be non-particulate to
reduce the potential for lung damage if inhaled. 0.3 M sodium citrate, 30 ml, is effective
in elevating the pH of gastric contents if given 1520 minutes preoperatively; it remains
effective for 13 hours. Antacids are used routinely in elective and emergency obstetric
anaesthesia, but less often in the general surgical population.
H2-receptor antagonists reduce the volume and acidity of gastric contents by the
inhibition of hydrochloric acid secretion from gastric parietal cells. Cimetidine, 400 mg
orally 90120 minutes before induction, and ranitidine, 150 mg orally 120 minutes
before induction, 50 mg intramuscularly or slow intravenous administration 45 minutes
before induction, are commonly used H2-antagonists. Ranitidine has a duration of
action of at least 8 hours; about twice as long as cimetidine. It is also associated
with fewer side-effects. Side-effects with cimetidine, though infrequent, include
sedation and confusion, and the potentiation of other drugs through inhibition of
hepatic enzymes. Hypotension, bradycardia and even cardiac arrest can follow rapid
intravenous injection of cimetidine, and also of ranitidine, though ranitidine has a much
lower incidence.
Prokinetics: metoclopramide, 10 mg orally 14 hours before surgery or intravenously
shortly before induction, acts centrally and peripherally to stimulate gastric emptying,
increases lower oesophageal sphincter pressure and is anti-emetic. Its central action is
due to its antidopaminergic properties whereas peripherally it stimulates acetylcholine
release, resulting in increased gastrointestinal motility.
Proton pump inhibitors: omeprazole, 40 mg orally at night and on the morning

of surgery, inhibits the proton pump in the parietal cells of the gastric mucosa,
resulting in prolonged suppression of acid secretion. It elevates gastric pH.
Combining omeprazole with metoclopramide reduces
gastric volume. It is seldom used in the UK despite proven effectiveness.
Anticholinergics (e.g. atropine, glycopyrollate) can decrease gastric acid secretion,

but have an adverse effect on barrier pressure by decreasing lower oesophageal
pressure. They are not used for aspiration prophylaxis.
If general anaesthesia is chosen, a cuffed tube in the trachea should secure the
patients airway. The airway should be assessed to predict whether this is likely to
be difficult. The laryngeal mask airway has become popular in modern anaesthetic
practice, however, it does not protect the airway from aspiration of gastric contents as
efficiently as a cuffed tube and should not be used routinely in patients at high risk.
Uncuffed tubes are used in children because the paediatric airway narrows at
the cricoid ring. Uncuffed tubes prevent tracheal mucosal damage by excessive cuff
pressure, and may allow passage of a slightly larger tube size permitting improved gas
flow. There is no precise age or size at which cuffed tubes are chosen, but use of
uncuffed tubes in children below 810 years is usual. The absence of a cuff may imply
the theoretical risk that aspiration can still occur, although satisfactory airway protection
still occurs in clinical practice.
Position:there is controversy regarding the optimum position for induction of

anaesthesia in the patient at risk of pulmonary aspiration. Some anaesthetists argue in
favour of a head-up (reverse Trendelenburg) or semi-sitting position, because this may
reduce the incidence of reflux in patients prone to passive regurgitation. Others favour
a head-down (Trendelenburg) position with the patient on their side, because this may
decrease the likelihood of aspiration should regurgitation occur.
Patient safety is paramount and therefore clinicians should induce anaesthesia in the
position in which they have the most experience and confidence. This will usually be a
rapid sequence induction in the supine position.
Rapid sequence induction: if the anaesthetist is confident that tracheal intubation

will be straightforward then an intravenous rapid sequence induction performed
with cricoid pressure is indicated. Aspiration is most likely to occur in the time
from loss of consciousness to intubation with a cuffed tracheal tube. Rapid sequence
induction reduces this time to a minimum.
Awake intubation: if a difficult intubation is anticipated consideration should be given

to securing the airway before induction. In modern practice this involves topical local
anaesthesia to the airway, and intubation via a flexible fibre-optic laryngoscope. A blind
nasal technique used to be popular, but the arrival of modern fibre-optic instruments
has allowed awake intubation to be performed under direct vision.
Inhalational (gaseous) induction may be indicated in a patient considered at risk

from aspiration, in whom conventional laryngoscopy and intubation is predicted to be
difficult and where awake intubation attempts may be hazardous (e.g. acute stridor,
maxillofacial trauma). There is a trade-off between taking steps to prevent aspiration
during induction, and maintaining and securing the airway. A senior anaesthetist should
manage these cases and patient safety is paramount.
Extubation should be performed with the patient awake and following the return of
upper airway protective reflexes. It is often safest to position the patient on their side
with head-down tilt to facilitate clearance of the upper airway using suction, should
regurgitation occur.
Diagnosis
Clinical signs and symptoms of aspiration are variable (Figure 3) and it is sometimes
difficult to make a definitive diagnosis. Silent aspiration may occur, and may not be
diagnosed until after surgery when the patient has returned to the ward. The initial and
most reliable sign of aspiration is hypoxia, which occurs following even mild cases.
Wheezing is also common. In severe cases an acute respiratory distress syndrome
can result. In such patients there is increased intrapulmonary shunting, ventilation
perfusion (V/Q) mismatch, increased lung water, increased airway resistance and
reduced lung compliance. Although aspiration classically affects the posterior aspect
of the right lower lobe, radiographic changes are variable, nonspecific and may be
absent, particularly in the first few hours. The most usual findings are irregular fluffy
den-sities, frequently bilaterally, collapse or pulmonary oedema (Figure 4).
Differential diagnoses include anaphylaxis, cardiac failure, pulmonary embolism, fat
embolism, sepsis and, in obstetric patients, amniotic fluid embolism.
Signs and symptoms of pulmonary aspiration
Symptoms Signs
Cough Stomach contents in oropharynx
Breathlessness Tachypnoea
Wheeze, crackles (mainly coarse)
Cyanosis
Tachycardia
Pulmonary oedema
Increased airway pressure
Radiographic changes
4 Typical radiographic appearance of

the chest in a patient with aspiration.
Management
If acute aspiration occurs the following procedure should be carried out.

Place the patient in a head-down position, with head turned to one side.
Suction material from the oropharynx.
Administer 100% oxygen.
Intubate the trachea if:
adequate oxygenation cannot be maintained with spontaneous ventilation
further tracheobronchial suction is required
the patient is unable to protect their own airway.
The decision to continue with surgery depends on the severity of the aspiration and
the urgency of surgery.
The management of established aspiration is largely supportive. Treatment is
described in Figure 5.
Management of established aspiration
Oxygen therapy
Guided by blood gas estimations or pulse oximetry
Ventilatory support
Spontaneous ventilation may be adequate in mild cases
Continuous positive airway pressure can be used for more severe cases, but
requires alert, cooperative patient at no further risk of aspiration
For severe cases, or those who cannot maintain a patent airway, mechanical
ventilation via a tracheal tube is indicated
Positive end-expiratory pressure is applied to increase functional residual
capacity of the lung and minimize intrapulmonary shunting
Removal of aspirate
Regular suctioning and physiotherapy are needed
Bronchoscopy is required in more severe cases
Bronchodilators
Given regularly by nebulizer
Antibiotics
No proven benefit from prophylactic use
Antibiotics often prescribed before identification of any pathogens
Fluid balance
Shifts of fluid from the circulation to the lungs can result in pulmonary
oedema
Central venous pressure and urine output monitoring help guide fluid
management
A positive fluid balance worsens gas exchange and should be avoided
Corticosteroid therapy
Routine use of corticosteroids is not indicated no current evidence has
shown benefit from their use
FURTHER READING
Engelhardt T, Webster N R. Pulmonary Aspiration of Gastric Contents in Anaesthesia.
Br J Anaesth 1999; 83: 41521.
Kallar S K, Everett L L. Potential Risks and Preventive Measures for Pulmonary
Aspiration: New Concepts in Perioperative Fasting Guidelines. Anaesth Analg 1993;
77: 17182.

Surgical Diathermy:
Mechanisms, Use and Abuse
Andrew D Farmery
Andrew D Farmery is Consultant Anaesthetist at the John Radcliffe Hospital, Oxford,

UK. He trained in London, Cambridge and Oxford. His interests are in bio-mathematical
modelling and clinical medical education.
The application of heat to wounds is evident in unearthed Neolithic skulls. Thermal

cautery to ulcers and tumours of the breast was described in a papyrus from about
3000 BC, and later described by Hippocrates in 300 BC. Electrical diathermy is at least
250 years old, predating the practice of anaesthesia by a century.
Diathermy (dia, through; thermy, heat) strictly applies to the uniform heating of
tissues by radiofrequency current or radiation. As a surgical tool, uniform heating is not
required, but rather discrete and destructive heating in a specific area. This application
is called 'electrosurgery' in the USA, and 'surgical diathermy' in the UK, but the term
diathermy has remained.
Basic electrical principles
Forcing current through a resistance liberates heat

The power to heat, cut or vaporize tissues is derived from passing an electrical current
through it. At any point in an electric circuit, the power dissipated is given by the
formula:
Power = Current2 x Resistance (P = I2 x R) 1
Current forced through regions of high resistance produces more heat than the same
current passed through regions of low resistance. Figure 1 shows how the current
density (and resistance) at the tip of a diathermy probe is many orders of magnitude
higher than the current density elsewhere in the circuit, namely the patients body and
the large dispersive electrode. This is analogous to a large crowd of people moving
along a wide walkway to gain access to a football stadium. The flow is ordered and
comfortable at the rear of the walkway, but when the same flow is forced through a
narrow turnstile, the power of the crowd will be liberated (destructively) at this high
resistance, high flow-density point.
Current density
1
Using high-frequency alternating current prevents electrocution
In Equation 1, both direct current (DC; e.g from a large battery) or alternating current
(AC; e.g. from the mains supply) produce the same amount of heat for the same
mean current. However, DC polarizes a tissue such that tissue connected to the anode
becomes positive, and that connected to the cathode, negative. This triggers ion
channel opening and depolarizes important excitable tissues such as nerves, striated
muscle and myocardium. The same is true of moderately low-frequency AC (e.g. 50
Hz), in which the tissue is alternately polarized and depolarized because the polarity of
the applied voltage changes sinusoidally. This can result in convulsions, tetanic muscle
twitch and ventricular fibrillation (i.e. electrocution).
High-frequency current is less prone to causing these phenomena because voltage-
sensitive ion channels in excitable tissues do not respond instantly to an applied
depolarizing voltage, but have a finite response time. An analogy is when the rudder of
a tanker is turned suddenly, there is a delay before it slowly starts to change direction.
If the rudder is turned from left to right with a low frequency, the tanker steers a course
veering from left to right sinusoidally. However, if the rudder is oscillated from left to
right with a high frequency, the ship steers a straight course because it does not have
enough time to respond to a rudder movement in one direction before being directed
to move in the opposite direction.
In the same way, a high-frequency AC voltage applied to the myocardium will neither
polarize nor depolarize the membrane, because the ion channels will not have time
to open or close before the polarity of the applied voltage is reversed and so the
tissue will continue to function normally. Electrosurgical generators typically operate at
frequencies of 0.54 MHz.
Surgical effects of diathermy
There are three main diathermy modes: desiccation, cutting and coagulation.
Desiccation
To cause desiccation (drying out), a low power current is passed through the tissues,
as in Figure 1. The aim is to increase tissue temperature at the site of contact with
the active electrode. Intracellular water is slowly driven off as steam and the tissue is
dried out. This produces a blanching of tissue. Because the current is of low power,
it is effective only in delicate tissues and small vessels (e.g. it is often used to blanch
the fallopian tube before surgical division in laparoscopic sterilization). When tissue has
been desiccated, its resistance to current flow becomes very high and current flow
effectively ceases, thus terminating the heating process. It is impossible to cut tissue in
this mode. The current waveform is not important in this application.
Cutting
In the cutting mode, the aim is to make a discrete cut through the tissue. Initial contact
with the electrode heats the tissue rapidly so that cells explode and their contents are
instantly vaporized. Heat is not conducted very far from the site of contact because
most of the liberated power is used to vaporize water (i.e. is consumed as latent heat
of vaporization). The heating effect is therefore concentrated and neighbouring tissue is
undamaged. Unlike desiccation, sparking is a key feature.
The vaporized desiccated tissue is a poor electrical conductor and therefore breaks
the circuit so that current flow ceases through this pathway. However, if the voltage (the
driving force for current) is high enough, air around the electrode is ionized. Ionized air
is a better conductor than desiccated tissue, and so current will now flow as a spark
jumps to the nearest region of moist tissue. Tissue heating is produced by:
current delivered by the spark (I2 x R)
radiant heat from the spark
collision of electrons bombarding the tissue.
This causes intense local heating, vaporization and thermal destruction. Cells are torn
apart. The current waveform used is a continuous radiofrequency sinewave (Figure
2a).
Coagulation
In coagulation mode (Figure 2b), the current waveform comprises short bursts of
radiofrequency sinewaves (about 1 MHz), with bursts occurring about 20,000 times
per second (burst frequency 20 kHz). The coagulation waveform can cause sparking
to tissues. However, the radiofrequency current is delivered in intermittent bursts and
therefore the ion cloud generated at each spark has a chance to disappear between
bursts. Therefore, with each current burst, ionization occurs afresh, and because this
is a random process sparking occurs more randomly and over a wider area than it
does in cutting mode. This reduces the concentration of the sparking power and allows
effective coagulation of vessels without tissue cutting. Peak voltages are much higher
in the coagulation mode than in the cut mode because the current is zero for most of
the time and so in order to deliver the same average power, the coagulation waveform
generator has to deliver more power in the short periods when current is switched on.
Monopolar and bipolar systems
Monopolar
The system described in Figure 1 is monopolar. Current is delivered via a pinpoint
active electrode, which then passes through the patient (in a low-density path)
to return via the dispersive electrode. This is the most widely used system
because it is most effective in producing cutting as well as coagulation.
Bipolar
In a bipolar system, current is delivered via one arm of a pair of insulated forceps. It
passes through any tissue grasped between the arms of the forceps and returns via the
opposite arm. With a bipolar system, only desiccation can be achieved. The system is
of limited power, and sparking does not occur. If the arms of the forceps are allowed
to make contact with each other directly, despite there being some tissue in the path,
current will be shorted-out, and diathermy will be less effective. Bipolar diathermy is
indicated where it is undesirable to pass current through the patients body to a distant
dispersive electrode; some examples are given below.
Narrow current conduits to extremities (e.g. testicle surgery) if a monopolar
system were used, with the dispersive electrode placed on the abdominal wall, current
would be forced to pass from the testicle along the vas deferens (the path of least
resistance) to the trunk. Because the vas deferens is a narrow tube, current density
would be high within it, and thermal injury might result.
Metal prostheses if a metal prosthesis lies between the dispersive and active
electrode, current preferentially passes through this low resistance route, producing
a high current density and heating in narrow points such as a cortical screw. This
may necrose bone or conduct heat to neighbouring soft tissue or vessels, sufficient
to perforate an artery.
Cardiac pacemakers the cable connecting a pacemaker generator box
(implanted in the anterior chest) to the electrode in the right ventricle and/or atrium
constitutes a low impedance pathway for radiofrequency current if it lies between the
active and dispersive diathermy electrodes. This may result in a high current density at
the point of pacemaker electrode insertion into the myocardium. Tissue desiccation may
occur at this point, increasing the resistance of the contact. The threshold potential
may increase, such that the pacing pulse fails to trigger the heart.
More sophisticated pacemakers are capable of detecting intrinsic cardiac activity
and withholding activation of the pacemaker. It is possible that stray radiofrequency
current may be detected by the pacemaker, and interpreted as intrinsic cardiac activity,
resulting in inappropriate inactivation of the pacemaker. For this reason, it is advisable,
if possible, to have the pacemaker programmed so that this function is disabled. The
safest precaution, however, is to avoid monopolar diathermy.
Patient safety
The principal issues are:

avoidance of inadvertent thermal burns from stray diathermy current
avoidance of inadvertent electrocution from stray 50 Hz mains current.
Isolated (unearthed) dispersive electrode system

Figure 3a shows a simple circuit in which neither live nor neutral terminals of the
radiofrequency current generator are connected to earth.
A fundamental law of electricity is that all the current leaving the live terminal
is returned to the neutral terminal. Therefore, if the patient makes contact with an
earthed object (e.g. lithotomy pole, drip stand or faulty low impedance ECG electrode)
none of the radiofrequency diathermy current should pass via this contact to earth
because such a stray current would not be able to return to the neutral terminal. All the
current should pass to the neutral terminal via the large dispersive electrode, thereby
eliminating the potential for burns. This might seem a safe system but it is possible
to burn patients inadvertently with isolated systems because of the phenomenon of
capacitive coupling. It is difficult to confine very high-frequency currents to wires,
and currents tend to pass out of the cables like a radio transmitter because a wire
and another conductor (e.g. earth) can behave like the two plates of a capacitor.
Capacitors can conduct high-frequency current, even though insulation and a few feet
of air separate the wire and earth. Radiofrequency leakage current flows only if there is
a route for it to return to the neutral terminal; Figure 3b shows how this might happen.
A certain amount of current from the active lead is leaked to earth via this capacitive
coupling. This can return to the patient via any small, grounded contact point and
potentially cause a burn at this site. From this point, the leakage current joins the main
current and returns to the neutral terminal via the dispersive electrode.
Early electrosurgical generators were not truly isolated. There was usually some
connection of the neutral terminal and dispersive electrode cable to earth because of
capacitive coupling between them, in a similar way to that described above. Figure 3c
shows how this allows current to flow to earth through grounded contact points and
complete the circuit to the neutral terminal via the virtual earth connection. The amount
of stray current passing through the grounded contact points depends on the relative
impedance of the pathways. Given that one cannot avoid some current passing to
ground, the best way to prevent this passing through unwanted pathways is to provide
a route to ground via the dispersive electrode which is more attractive than the
alternative routes. This is done by physically earthing the dispersive plate and making
the impedance of this connection as low as possible.
Earthed dispersive electrode system

Earthing the dispersive electrode overcomes both the virtual earth problem (Figure
3c) and the radiofrequency leakage problem (Figure 3b). Figure 3d shows how if
the dispersive electrode and neutral terminal are earthed, any radiofrequency leakage
current can return to the neutral terminal via a direct low impedance earth route that
bypasses the patient. However, earthing poses other problems.
Dispersive electrode detachment: the dispersive electrode is an attractive route

for ground-seeking radiofrequency current only if its impedance is many orders of
magnitude lower than unwanted stray routes. If the dispersive electrode becomes
detached or makes poor contact, all of the radiofrequency current can pass to earth
(and hence return to the neutral terminal) via unwanted grounded contact point, as
shown in Figure 3e, thus causing burns.
Mains electrocution: if the patient is exposed to a live mains voltage (e.g. via a
faulty monitor lead) the earthed dispersive electrode provides a low impedance pathway
for this dangerous 50 Hz current to pass through the patient to earth, thus causing
electrocution. This is because mains voltage is ground seeking. This problem can be
overcome by placing a capacitor in the circuit as in Figure 3f. This is capable of passing
radio-frequency current, but does not conduct low frequency (50 Hz) current. Even
though the patient is exposed to a live mains cable, no 50 Hz current will flow through
the patient to the ground.

Techniques of Cricoid Pressure
Richard Vanner
Richard Vanner is Consultant Anaesthetist and Clinical Director in a large District

General Hospital in the UK. He is a generalist with a specific interest in obstetric
anaesthesia.
In 1956, the Association of Anaesthetists had collected 1000 reports of anaesthetic

deaths; 110 from pulmonary aspiration of stomach contents. This often occurred during
induction of general anaesthesia especially when muscle-relaxant drugs were used.
Anaesthetic techniques were developed to prevent aspiration in patients at risk and
included:
emptying the stomach before induction
intravenous induction with head-up tilt position
inhalational induction in the lateral and head-down position.
In 1961, Sellick described cricoid pressure as a technique used to prevent
regurgitation of stomach contents during the induction of general anaesthesia. It was
brought into widespread practice in the UK by 1970 and largely replaced the other
techniques, despite no randomized controlled trials demonstrating its benefit. It has
become a routine part of anaesthetic practice for patients at risk of aspiration in
combination with pre-oxygenation, an intravenous induction and tracheal intubation.
All UK maternity units routinely apply cricoid pressure during induction of general
anaesthesia.
Before the introduction of cricoid pressure, the incidence of aspiration pneumonitis
in obstetric general anaesthetics was about 0.15%. If cricoid pressure prevents
aspiration, the number needed to treat to prevent one case of aspiration would be 666.
A controlled trial would be difficult because of the large numbers of
patients needed and the difficulty of obtaining ethical approval.
Indications
In a patient who has been prepared for elective surgery and has not eaten for 6
hours or drunk for 2 hours, regurgitation of stomach contents during the induction
of anaesthesia is unusual even when muscle-relaxant drugs are used, which relax
the upper oesophageal sphincter. In these patients, cricoid pressure is unnecessary,
because its benefits have to outweigh the risk of complications. However, cricoid
pressure is indicated if:
surgery is necessary before the patient is fasted
gastric emptying is delayed
the lower oesophageal sphincter is incompetent (e.g. in the last half of pregnancy
or in reflux oesophagitis). With a full stomach from any cause, distention of the fundus
causes reflex relaxation of the lower oesophageal sphincter.
Mechanism of action
Regurgitation is the flow of fluid from the oesophagus into the pharynx and is a
passive process. When patients are awake the upper oesophageal sphincter prevents
regurgitation. The pressure that this sphincter exerts is about 40 mm Hg and it relaxes
during swallowing and during sudden distension of the oesophagus (e.g. belching,
vomiting). The sphincter is mainly the cricopharyngeus muscle, a skeletal muscle,
which is attached to the lateral aspects of the cricoid cartilage and is positioned behind
it like a sling. The lumen of the hypopharynx within the cricopharyngeus is therefore
crescent shaped. The oesophagus begins below the level of the cricoid cartilage.
The upper oesophageal sphincter relaxes during intravenous induction with
thiopental (thiopentone), with heavy sedation, during deep sleep or following muscle-
relaxant drugs. In all of these situations the sphincter pressure is reduced to less than
10 mm Hg, which is low enough to allow regurgitation. Following thiopental
(thiopentone) the sphincter starts to relax just before loss of consciousness but is not
fully relaxed until 30 seconds later. Ketamine does not relax the upper oesophageal
sphincter, nor does an inhalational induction. Coughing during an inhalational induction
increases upper oesophageal sphincter pressure to over 100 mm Hg.
Cricoid pressure prevents regurgitation by replacing the function of the
upper oesophageal sphincter by compressing the hypopharynx against the
prevertebral fascia muscles and vertebrae behind. The convex cricoid is
pressed against the convex body of either the 5th or 6th cervical vertebrae.
Inevitably the cricoid cartilage is deviated slightly laterally (Figures 1 and 2).
Part of the crescent-shaped lumen is compressed against the vertebral body and
the rest of it is less well compressed against the longus colli muscle to one side.
A nasogastric tube is squeezed laterally towards the less well compressed part of
the lumen and makes the occlusion of the hypopharynx more complete and therefore
cricoid pressure more efficient.
A study of women undergoing emergency caesarean section under general
anaesthesia with muscle relaxation showed that gastric pressure is likely to be less
than 25 mm Hg in 99%. Oesophageal pressure can rise to equal gastric pressure
during gastro-oesophageal reflux as the lower oesophageal sphincter relaxes to create
a common cavity. A study of ten cadavers showed that 20 Newtons (N) of force applied
to the cricoid cartilage prevented the regurgitation of oesophageal fluid at a pressure
of 25 mm Hg in all cases and 30 N prevented regurgitation at a pressure of 40 mm
Hg in all cases. Therefore, 20 N of cricoid pressure is probably sufficient and 30 N
is more than enough to prevent regurgitation into the pharynx. Anaesthetic assistants
can be trained to apply the correct force by practising on weighing scales and by doing
this they can apply a range of forces between 5 N above or below the target force. A
reasonable recommendation is to apply 30 N (3 kg).
Correct technique
Although cricoid pressure is apparently a simple technique there is growing evidence
that incorrect application can cause serious problems during induction of anaesthesia.
The anaesthetic assistant should practise the correct forces on weighing scales. The
anaesthetist should be confident that the anaesthetic assistant knows the anatomical
landmarks of the cricoid cartilage. Although Sellick suggested that the patients head
should be extended, the author recommends that it should rest on a pillow because
intubation is easier and cricoid pressure is just as effective in this position. After pre-
oxygenation, but before intravenous induction, lightly applied cricoid pressure should be
started with a force of 10 N (1 kg), after loss of consciousness the force is increased
to 30 N (3 kg). Forces of 20 N or more are not tolerated by awake patients and may
cause them to retch and vomit. Normally the assistant applies cricoid pressure with
their dominant hand because this can be maintained more accurately and for longer
(35 minutes). There is no evidence that a bimanual technique, with the assistants
other hand supporting the patients neck, improves the view at laryngoscopy when the
correct forces are applied. The assistants other hand is best kept free to assist with a
difficult intubation if necessary.
Patients with small bowel obstruction should have a nasogastric tube inserted
preoperatively. This should be aspirated before induction and left in place during
induction. This does not make cricoid pressure less efficient and may improve it. As the
tube is not compressed, it is possible, by leaving it open to atmospheric pressure, to vent
liquid and gas remaining in the stomach, minimizing any increase in gastric pressure.
Sellick described the application of cricoid pressure with three fingers, thumb and
middle finger on each side of the cartilage with the pressure applied with the forefinger.
However, with the head on a pillow it is more comfortable to apply it with two fingers,
forefinger and thumb on each side of the cartilage. This gives flexibility to apply
upward and backward cricoid pressure, which improves the view at laryngoscopy if
this becomes necessary. As the cricoid inevitably moves slightly laterally during cricoid
pressure, it is better to ensure that it moves to the patients right rather than to the left
because this also makes intubation easier with a Macintosh laryngoscope.
Complications
Excess force applied to the awake patient has caused retching and death from
aspiration and ruptured oesophagus.
Difficult intubation can be caused by cricoid pressure if the force is applied to the
thyroid cartilage or if the larynx is pushed laterally to the left or if too much force is used,
which compresses the airway. When cricoid pressure is applied properly with a force
of 30 N (3 kg) the view at laryngoscopy is improved compared with the situation when
no cricoid pressure is used. However, if only the epiglottis can be seen, then the slight
lateral displacement of the larynx, which is inevitable, will make the passage of a gum
elastic bougie more difficult because this is normally passed in the midline.
The so-called cricoid yoke, a force transducer applied to the neck, is not ideal,
because it may not be applied accurately to the cricoid cartilage and may cause
tracheal compression or extreme lateral displacement of the larynx, resulting in difficulty
with tracheal intubation.
Difficult ventilation cricoid pressure can obstruct the airway and prevent
ventilation of the lungs with a face mask and Guedel airway. This is proportional to
the force applied; 30 N causes complete obstruction in 2% of patients and 40 N does
in 35%. Upward and backward cricoid pressure at a force of 30 N causes airway
obstruction in 56% possibly because it tilts the cricoid cartilage and opposes the vocal
cords. Following a failed intubation in a patient with a full stomach when the lungs
cannot be ventilated, the force of cricoid pressure should be reduced by half. If this
does not allow ventilation, cricoid pressure should be released completely to allow
ventilation, with laryngoscope and suction immediately available. Further airways that
may then be necessary (e.g. laryngeal mask, Combitube, cricothyrotomy cannula) are
all better placed without cricoid pressure applied.
1 Axial CT scan of the authors neck at the level

of the cricoid cartilage showing a nasogastric tube
filled with radio-opaque contrast media.
2 Cricoid pressure applied to the authors neck

showing the slight lateral displacement of the cricoid
and the lateral position of the nasogastric tube.
FURTHER READING
Brimaccombe J R, Berry A M. Cricoid Pressure. Can J Anaesthesia 1997; 44: 41425.

Sellick B A. Cricoid Pressure to Control Regurgitation of Stomach Contents during
Induction of Anaesthesia. Lancet 1961; 2: 4046.
Vanner R G, Pryle B J, ODwyer J P, Reynolds F. Upper Oesophageal Sphincter
Pressure and the Intravenous Induction of Anaesthesia. Anaesthesia 1992; 47: 3715.

Tracheal Intubation:
Management of Difficult and
Failed Intubation
Stuart W Benham
Stuart W Benham is Consultant in Anaesthetics and Intensive Care Medicine at the

John Radcliffe Hospital, Oxford, UK. He qualified from Glasgow University and trained
in anaesthetics and general medicine in the west of Scotland before finishing his
training in intensive care in Oxford. His research interests include acute renal failure on
the ICU and difficult airway training and research.
Securing the airway with a tracheal tube is a core skill for anaesthetists. The technique
may be required during anaesthesia, resuscitation or intensive care. The ability to
manage patients when laryngoscopy is predicted to be difficult, or when intubation
has previously failed, requires a methodical approach and a workable back-up plan.
Indications for tracheal intubation are given in Figure 1.
Patients with depressed conscious levels (e.g. following head injury, self-poisoning,
vascular accident, infections) need careful assessment. If there is any concern that
airway reflexes are diminished, the airway must be secured with a tracheal tube. A low
Glasgow Coma Score (e.g. GCS < 9) should not be relied on as the sole indication
of airway compromise.
Intermittent positive-pressure ventilation can be achieved by non-invasive means
without tracheal intubation. In the operating theatre this is often performed with the
laryngeal mask airway (LMA), and in the ICU with a secure fitting face mask with
head strapping.
Indications for tracheal intubation
Surgical indications
Shared airway surgery
Requirement for one lung ventilation
Prone or sitting position for surgery
Open abdominal or thoracic surgical procedures
Major head and neck surgery
Prolonged surgery
Emergency indications
Prevention of aspiration in unfasted patients requiring general anaesthesia
Impending airway obstruction (e.g. epiglottitis, airway burns)
Maxillofacial trauma (blood in the airway)
Depressed conscious level with poor airway reflexes
Ventilatory failure indications

For intermittent positive-pressure ventilation
Prevent aspiration of gastric contents
Advanced ventilation strategies (e.g. partial liquid ventilation, high frequency jet
ventilation)
Prone ventilation strategies
Ventilatory failure unresponsive to non-invasive positive- pressure ventilation
Management of difficult airway and failed intubation

The maintenance of alveolar ventilation is the most important aspect of difficult airway
management. Patients in whom intubation is difficult or has failed, and in whom
mask ventilation is also difficult are uncommon (about 1:10,000 routine anaesthetics).
The anaesthetic plan must not render an awake patient who can maintain a patent
airway into an unconscious patient with an unsafe and obstructed one. Preoperative
assessment aims to identify patients in whom laryngoscopy and/or airway maintenance
are likely to be difficult when consciousness is lost. Patients generally fall into one of
three categories:
anticipated difficult laryngoscopy
elective unanticipated difficult laryngoscopy
emergency unanticipated difficult laryngoscopy or failed intubation.
Anticipated difficult laryngoscopy

A comprehensive plan is required involving a primary plan and a secondary plan to be
used if the primary plan fails. Two common pitfalls are:
the operator is inexperienced in the technique chosen (e.g. flexible fibre-optic
laryngoscopy FFL)
the back-up plan involves staff, skills and equipment that are not readily available at
the time of induction (e.g. tracheostomy).
Anaesthetists have to develop plans with their own skill levels in mind, incorporating
available equipment and supporting staff. Patient safety is of paramount importance.
Generally, less invasive, atraumatic techniques should be preferred to surgical airway
control, especially in elective patients. However, the emergency anticipated difficult
airway (e.g. patients with severe maxillofacial trauma, or enlarging wound haematoma
and stridor following head and neck surgery) may require a surgical airway as the
primary plan.
Patients with bony abnormalities may have restricted mouth opening due to
temporo-mandibular joint disease, or a cervical spine with limited neck flexion or
extension (Figure 2). There is an expectation that the oropharynx and periglottic
regions will be normal. In these patients, direct laryngoscopy may be impossible,
but the normal oropharyngeal anatomy allows the passage of an FFL under general
anaesthesia and assisted ventilation should be possible. If the primary plan fails during
this elective surgery, the patient may be woken before implementing the secondary
plan.
2 Restricted neck extension in ankylosing

spondylitis.
Patients with obstruction in the supraglottic region include those with previous
major oral surgery or radiotherapy. If there is evidence of stridor, the patient should
be treated with extreme caution and one of the plans outlined below for periglottic or
infraglottic obstruction should be considered. Stridor implies 50% airway narrowing.
These patients may develop complete airway obstruction when anaesthetized and
a surgical airway should be included in the management plan. Depending on the
anaesthetists skill, two options for the non-stridulous patient are:
an awake fibre-optic endoscopy and intubation, before any relaxant or induction
agent is given
an inhalational induction and direct laryngoscopy to define the anatomical situation,
and the feasibility of passing a tracheal tube.
Patients with obstruction in the periglottic region (including obstructing laryngeal

tumours) require a thorough preoperative evaluation (e.g. CT, MRI) to assess the
degree of obstruction and clinical assessment of the degree of stridor. Indirect
laryngoscopy and flexible fibre-optic nasendoscopy are necessary to determine the
extent of the obstruction and the feasibility of passing a tracheal tube, which should be
performed by an experienced ENT surgeon. Non-stridulous lesions can be managed
similarly to lesions causing supraglottic obstruction. Stridulous lesions are the most
difficult to manage because neither awake fibre-optic endoscopy nor inhalational
induction guarantees success. The choice of technique depends on the degree of
stridor, the general condition of the patient and the experience of the anaesthetist.
Severe cases may best be managed by awake tracheostomy under local anaesthesia.
Depending on the level of the lesion, particularly with infraglottic obstruction, even
emergency tracheostomy may not be realistic. For the most severe lesions it may be
necessary to consider extracorporeal oxygenation as part of the secondary plan.
Elective unanticipated difficult laryngoscopy

Elective unanticipated difficult laryngoscopy is best managed using a stepwise
approach.
Reconfirm that assisted bag and mask ventilation is possible.
Consider repositioning the head and neck and the use of a bougie.
Avoid prolonged attempts at direct laryngoscopy. Change the length of laryngoscope
blade once and the type of blade once to achieve the optimum view.
Call for help and for the FFL if competent in its use.
Consider the use of the LMA or the intubating LMA (ILMA) for ventilation.
Consider using the LMA/ILMA as a conduit for intubation (see below).
Consider abandoning anaesthesia, and performing an awake intubation.
Emergency unanticipated difficult laryngoscopy and failed intubation

This is a failure to secure the airway with a tracheal tube following a rapid sequence
induction. Remember that it is failure of oxygenation, rather than a failure of intubation,
that accounts for morbidity and mortality. The same stepwise approach as that for
the elective unanticipated difficult laryngoscopy should be followed. All departments
of anaesthesia should have a failed intubation drill for these circumstances, and
clinicians should be familiar with their local protocols (see Anaesthesia and Intensive
Care Medicine 2:6: 221). It should be noted that in these situations the removal of
cricoid pressure may help ventilation attempts, especially through the LMA. The risks
of aspiration are small in comparison to the potential for morbidity and mortality caused
by hypoxia from failed ventilation.
Techniques to overcome difficult intubation
Many devices have been developed to improve the chances of securing the airway with
a tracheal tube. Some of those used by practising clinicians are described below.
Position and simple manoeuvres

Optimizing the patients position (flexion of the cervical spine and head extension at
the atlanto-occipital joint the sniffing the morning air position) is the first step to
improve the view at direct laryngoscopy. Simple manoeuvres such as external laryngeal
manipulation, especially backwards, upwards and rightwards pressure on the larynx
can improve the view by more closely aligning the visual axis with the laryngeal inlet.
Laryngoscopes
There is a range of curved and straight blades, as well as blades with movable hinged
tips (McCoy), that may improve the view at direct laryngoscopy (see Anaesthesia and
Intensive Care Medicine 1:1 34). Many experienced anaesthetists, however, tend
to use the same type of laryngoscope blade for all their patients. Skills in the use of
different blades are best acquired during routine intubations. The McCoy, or the angled
Belscope laryngoscope, may be able to convert a Cormack/Lehane grade 3 view to a
grade 2 view, though familiarization with the technique is required.
Simple props and aids
Gum elastic bougies should be used when:
direct laryngoscopy allows visualization of the epiglottis but not the larynx (a grade
3 view)
visualization of the larynx is possible but direct passage of the tracheal tube is
prevented by awkward oral anatomy or teeth
a reinforced or flexible tracheal tube cannot be directed into the visualized larynx.
Aintree intubation catheter (Cook ) (Figure 3) can be used like a gum elastic
bougie, or in combination with other airway and intubating devices such as the LMA or
FFL. It is sufficiently long and thin to allow a tracheal tube to be railroaded over it. It is
hollow and has a detachable tube connector/adaptor that allows ventilation during the
intubation process. An FFL can also be passed through it if required.
a Flexible fibre-optic
laryngoscope and Aintree
intubation catheter
passed through the
laryngeal mask airway
(LMA).
b Fibre-optic endoscopy
through the LMA with
the Aintree exchange
catheter.
a b
LMA and ILMA

Most anaesthetists use the LMA regularly for patients not requiring intubation. The
ability to insert an LMA to allow spontaneous or assisted ventilation is a core skill for
anaesthetists. It also provides a route guide for intubation, either blind or guided by an
FFL. The LMA may help to achieve ventilation in patients who are otherwise difficult to
intubate and ventilate.
The ILMA is modified to improve the chances of passing a tube blindly through the
mask into the trachea. There is an initial short learning curve for the operator, and the
clinician should practise using the ILMA in patients with normal airways before it is used
in those with difficult or abnormal ones.
The main limitation on both devices is that there has to be enough mouth opening to
permit inserting the device. Intubation can be blind, but both devices can be used with
an FFL to visualize laryngeal anatomy and aid intubation.
Railroading the tracheal tube

The need to railroad the tracheal tube over the guide is the final step in intubation. Two
manoeuvres to increase its success rate and minimize laryngeal trauma are choice of
tracheal tube and bevel direction.
The ILMA tube (softer tip) or reinforced tracheal tube (less acute bevel and softer
tip) has a higher chance of passing through the vocal cords (Figure 4).
The bevel of the standard tracheal tube is directed to lie in the right or left lateral
position as it reaches the vocal cords. It is then rotated 90o as it is pushed gently
through the cords. If this is unsuccessful, the tube is rotated through 360o continuously
with gentle pressure to slip through the cords. If still unsuccessful, direct laryngoscopy
can be performed to check the position of the route guide, and to lift the epiglottis to
facilitate tube railroading.
b c
a
4 Tracheal tube tips. a The intubating

laryngeal mask airway tube, b standard
tube, and c the flexometallic tube
FFL and intubation

FFL and intubation can be performed with the patient awake or anaesthetized. Awake
fibre-optic intubation performed by a competent endoscopist is safe (Figure 5). The
patient remains awake and self-ventilating with maintained pharyngeal muscle tone.
5 Awake fibre-optic intubation. Note

the use of propofol sedation and jaw
thrust.
Suggested procedure for awake fibre-optic intubation

1 Premedication of morphine, 0.10.15 mg/kg i.m., and hyoscine (scopolamine), 200
g i.m., 1 hour before procedure.
2 The patient should lie semi-reclined on a trolley in the anaesthetic room, facing the
anaesthetist.
3 Intravenous sedation should be administered cautiously. Target-controlled infusion
with propofol (plasma concentration 0.51.5 g/ml) is well tolerated.
4 Topical anaesthesia of the upper airway should be provided:
Nasal mucosa; mixture of 5% cocaine, 2 ml, and 8.4% bicarbonate, 2 ml, as topical
spray, with the patient taking deep breaths in with each spray. If the patient requires
orotracheal intubation the oropharynx can be anaesthetized with lidocaine (lignocaine)
spray or gel. Oropharyngeal route guides (e.g. Ovassapian or Berman airway) can
be used to aid orotracheal intubation. These allow the operator to pass the FFL and
tracheal tube through them. They prevent soft tissue collapse and are sized to guide
the FFL through the mouth, and emerge at the epiglottis, where it can be directed
into the larynx.
Spray as you go (SAYGO) with 4% lidocaine (lignocaine) through the working
channel of the FFL. Insertion of an epidural catheter through the working channel to
the tip of the scope, with the catheter end trimmed to produce one end-hole, can
facilitate accurate delivery of the local anaesthetic injection. Inject 1 ml solution with
45 ml air to help disperse the anaesthetic. Before the first attempt to pass the FFL,
and before each subsequent attempt, oropharyngeal suctioning with a Yankaur sucker
may be required.
Administer supplemental oxygen. This can be delivered conveniently via a flexible
suction catheter passed into the opposite nostril.
5 Allow adequate time (at least 30 seconds) after topicalization before the FFL is
advanced. Avoid passing the FFL blindly. If the view ahead becomes obscured, gently
withdraw the insertion cord until airway anatomy is again identified. Ask the patient to
take deep breaths when advancing towards the laryngeal inlet. This opens the airway
and abducts the vocal cords. If visualization of the larynx is difficult, performing a gentle
jaw thrust manoeuvre on the patient can help.
6 Once the scope has been advanced through the cords it should be advanced to just
proximal to the carina. A common error is to allow the FFL to withdraw, or even become
displaced from the trachea while the tube is railroaded into place. This happens more
often if the patient coughs at this time. The operator should attempt to keep the FFL in
the centre of the airspace at all times. This minimizes trauma to the delicate tracheal
mucosa and reduces the amount of blood in the airway.
7 Railroading the tracheal tube is described above. It is helpful for the assistant to
hold the FFL stationary allowing the operator to railroad the tube into place using both
hands.
8 A final useful check to estimate the distance from the end of the tracheal tube to
carina can be performed as follows. Once intubation has been performed, the FFL is
passed down just proximal to the carina. The assistant lightly pinches the FFL as it
enters the proximal end of the tracheal tube. The FFL is then withdrawn slowly until the
distal end of the tracheal tube comes into view. As soon as this is seen, the distance
from the assistants fingers to the tube connector of the tracheal tube is noted. This is
the distance from tip of tube to carina.
9 The breathing system with capnograph is connected. The patient may then be
anaesthetized and laid flat. Satisfactory ventilation is confirmed, and muscle relaxant
can be given if required.
Problems with flexible fibre-optic intubation: the FFL is an intubating tool, not
a ventilation device. Oxygenation and ventilation must be maintained throughout the
intubation procedure.
Blood and secretions in the airway a poor view is the endoscopists main
problem. Smaller FFLs have working channels that make suctioning of sticky secretions
or blood difficult; larger FFLs have proportionally larger suction channels. Repeated
insertion and withdrawal of the insertion cord may precipitate bleeding and should be
avoided.
Abnormal upper airway anatomy patients with oro-pharyngeal lesions or
previous reconstructive surgery may have abnormal upper airway anatomy. The
endoscopist should be familiar with the normal appearances through the FFL before
managing patients with abnormal anatomy. In all patients, keep the FFL in the centre
of the airspace and look for familiar structures. Often the larynx is identified only as a
small black hole, or what seems to be a fold in the mucosa. Identification is sometimes
suggested only by the image of small bubbles appearing from a dark crevice. It is
helpful to the operator if the patient is awake, semi-recumbent, and cooperating by
taking deep breaths.
Equipment problems the FFL should be checked and cleaned before use.
The tracheal tube should be loaded on the FFL before endoscopy; forgetting to do
this is a common mistake.
Ensure that the light is on and working with white balance and focus optimal before
commencing endoscopy.
Lubricating jelly should be applied to the outside of the scope, and the tracheal tube,
to facilitate easy nasal passage and tracheal intubation.
Difficulties in railroading the tracheal tube can sometimes result from a large
difference in the external diameter of the scope and internal diameter of the tracheal
tube. This may be overcome by use of the Aintree intubation catheter. The intubation
catheter can be railroaded over the scope, and then the tracheal tube railroaded over
this.
Lack of handeye coordination can be remedied by practice on simulators,
manikins and learning models such as an artificial bronchial tree or the Oxford hit-the-
hole box (Figure 6). It is indefensible to acquire these basic skills at the expense of the
patients mucosa.
6 The Oxford hit-the-hole training box.

An inability to recognize anatomy is easily addressed by experience gained from
instructional videos, clinical teaching and supervision. The case for using an FFL to
aid routine nasal intubation is robust. In addition to the excellent learning opportunity
afforded by routine use of the FFL, it assists in the selection of the best nostril and
largest airspace, and identifies vulnerable nasal pathology such as polyps.
Transtracheal access
The final route for rescuing an obstructed airway is direct transtracheal access.
This can be through the cricothyroid membrane, or through the upper trachea. Most
anaesthetists never need to resort to this. Elective procedures, such as cricothyroid
puncture used to inject local anaesthetic, or performing percutaneous tracheostomies
in the ICU, provide valuable experience in tracheal access. The ability to identify the
cricothyroid membrane and to insert a cricothyroid airway catheter rapidly may be a
life-saving procedure. See Anaesthesia and Intensive Care Medicine issue 2:7: 268 for
discussion of emergency tracheal access.
FURTHER READING
Latto I P, Vaughan R S, eds. Difficulties in Tracheal Intubation. 2nd ed. Philadelphia:
WB Saunders, 1997.
Popat M. Practical Fibreoptic Intubation. Oxford: Butterworth-Heinemann, 2001.

Anaesthesia
on CD-ROM
Airway Control
Oliver J Dyar
intubation:
obesity, pregnancy
intraoral masses
large goitre.



cartilages) visible
2
Airway patency
Aspiration risk

includes:
high-flow suction
two laryngoscopes
Magills forceps
required.




size 4.

Tracheal intubation
is not too tight.

4 Normal adults 30
5 Large adults 40
b
e
c
f
d g

a
b
c
d
e

Recovery

a b c

prongs.
a b c


Surgery
Michael W Platt

pain.

History

repair.

(pneumoperitoneum).




basal compression.


peritoneum.


these cases.
Recovery
home in 23 days.

FURTHER READING

Free Flap Surgery
Jane Quinlan
reconstruction.
Flap transfer
flap transfer are:
released
Primary ischaemia
vasoconstrictors
to blood flow.
include:

Physiology
8xxl
Vasodilatation


fluid management.
Crystalloids
Colloids
Blood
Dextran
1

Perfusion pressure
used.
Viscosity
delivery:
Br J Anaesth 57:

2
Monitoring

areas.


Induction

Maintenance


ventilation.
be added if needed.


Normothermia
Effective analgesia
Haematocrit 3035%
3
FURTHER READING
90421.

Michael OConnor
Ian Taylor

anaesthesia.



Units of pressure
approximately:
101 kPa
760 mm Hg
1035 cm H2O
1 bar
15 psi.

page 66).
glass.
Dial
Coil
Coil straightening
Pointer
Pressure
Pressure regulators
Pressure regulator
Regulated
low-pressure
chamber
Valve (a)
High-pressure
chamber
High pressure (P)

Flowmeters
Rotameters
viscosity
density.
Flowmeter
Turbulent flow
Laminar flow
Bobbin
4
measuring.
Accuracy is 2%.

altered.
Vaporizers
Safety
listed in Figure 5.

anaesthetic machine
to the wrong yoke
cylinder and yoke
hypoxic mixture
Bodok seal.
status Vaporizers
not tilted.
incidents
100%.
FURTHER READING
Apparatus, 1997.
1998.

Operating Theatre
J Duncan Young

Oxford.



Flow generator
Active process
Pressure
Cycling Time
Cycling Cycling
trigger Volume
EI IE Flow
Passive
process
Expiration


Flow
Time Time
Volume
Time Time

compliance.

Alveoli force
Resistance
inflow inflow
Pressure

compliance


normal lungs.
constant.
Ventilators may be:

Weight
Flow

P1
Inspiratory valve
Volume
P2
Time
Expiratory valve
Pressure
Time

maintained at
the expense of
Flow

P1 Time
flow resistor
A constant flow
Volume
P2 will deliver a
safety valve
constant tidal
volume
Time
Pressure
45 cm H2O.

circuits.
volume.

ventilation (IPPV)

breathing room air.

6
5
Volume (litres)
0 Time
Normal values

(Figure 10).

10 mBar
increases
down
Relative blood flow

the lung 2.5 100%
mBar
Volume
50%


V V
No ventilation
Q V/Q = 0 Q
Shunt
PAO2 PAO2
No PaO2
PaO2
flow
No perfusion
V/Q =
V
alveolus
Q
End
PAO2 PAO2
capillary PAO2
Q
O2
PaO2
PaO2 PAO2
O2 out = flow Q
so PaO2 will fall
10
of V/Q mismatching.


large tidal volumes
use of PEEP
diseased areas.

airway pressures.
venous return.

then improve.

output.


Adults:
used.
Children:
I:E ratio 1:2
Fi O2 0.5 (50% oxygen).
Safety issues

Ventilator checks
Ventilator checks

inspiratory phase
Apparatus, 1997.
11
FURTHER READING
Science, 1996.
1990.
1998.

Breathing Systems
Gordon W G French

be simple and safe
be easy to scavenge
be cheap.
unsafe.
as tuberculosis).


Valve screw top
Scavenging hood
Spring
Disc
Pathway of gas
when valve is open
Rebreathing systems

fresh gas flow
FGF
Lack FGF
FGF IPPV
23 x AMV

transfers

FGF

FGF
FGF
is used for IPPV.
adults or children.
b
e
g
c
f


FGF source
a Y-piece connector
a reservoir bag
litre/minute FGF.
CO2 + H2O H2CO3
Ideal circle set-up

pressure-limiting
(APL) valve

bag
One-way valves

4

Soda lime Baralyme
System checks
individual systems.
FURTHER READING

Duncan Parkhouse
Jonathan Warwick




is dependent on:
(the bio burden).

mucous membrane



infection
body fluids.
Cleaning
sterilization.
Manual cleaning
Mechanical cleaning
it.
by a rinse cycle.
does not disinfect.
Disinfection

pressure.

Washer disinfectors

recontamination.

by organic damaging
matter matter
Enveloped Non-
enveloped

0.20.35% (< 1 day)

6080%

compounds ( 7 days)

ppm average Cl2

phenolics
0.62%

ammonium
compounds
1
Sterilization
Steam

Steam sterilizer
times
Dry hot air

Ethylene oxide

Irradiation

Critical Incidents:
Joy E R Beamer
Jonathan Warwick


surgery.
Hypertension

after anaesthesia.
Hypoxaemia
Hypercapnia
Aortic clamping
Complications
Management
15 mg.
minutes.
Hypotension
Causes
Anaesthesia
histamine release.

trauma or burns

haemorrhage
head-up position
ischaemic tissues.

heart failure


Parkinsons disease
AIDS.
Other causes
Management
0.51.0 mg i.v.).
Massive haemorrhage

trauma
haemorrhage)
or coagulation.
Management
methods.
Blood loss (ml)

750 7501500 15002000 2000
Heart rate < 100 > 100 > 120 140

blood loss.
advance of surgery.
procedure
Arrhythmias
Management
mmol/kg/hour.
cardiac arrest.
is:
Hypertension
solvent abuse)
Anaesthetic factors
Hypoxaemia
Hypo/hypercapnia
Hypo/hypertension
Laryngoscopy
pressure lines)
Surgical factors
Catecholamines
Oculocardiac reflex
Embolism
Others
Limb reperfusion

infusion.



cardiac output.


metabolic acidosis
hyperkalaemia
Management
Immediate actions
Later actions
Future care
Leeds LS9 7TS
Tel: 0113 206 5274

Critical Incidents:
Orlando J Warner
Jonathan Warwick

Oxford.

surgery.
Aetiology
Error of judgement
Lack of experience
Lack of assistance
Lack of equipment
Equipment failure
involve:
Supraglottic
Tongue
Blood or secretions
Laryngeal
Laryngospasm
Tumour or oedema
Aspiration
Asthma
Anaphylaxis
Pneumothorax
Pulmonary oedema
arthritis)
from:
noisy airway

infection.

4
Optimum

intubating
position


(Figure 7).
a Macintosh size 4;
b Macintosh size 3;
c McCoy size 4;
d McCoy size 3;
e Belscope;
f Polio;
i Huffman prism.

catheter;


alveolar plateau.

breathing)
of aspiration.
Bronchospasm
Anaphylaxis
Pulmonary oedema
10
Failure to breathe

doses of drugs used
conscious.

block
Hypokalaemia
Hypothermia
Hypocarbia
Aminoglycosides
Calcium antagonists
Magnesium
Local anaesthetics
Lithium
Frusemide
11

Congenital
Acquired
Infections
Malignancy
Chronic disease
Liver disease
Renal failure
Hypothyroidism
12

circle system).
satisfactory.
include:
body temperature
CT head scan
Air embolism

13

present
is of benefit)
14
Pneumothorax
ventilated.
Signs Causes
Hyperresonance
Shock
affected side
15



John Moyle

I= E
R

cardiac arrhythmia
bone and fat.
5 mA Pain
Electrical safety
equipment sensibly.
described below.)



4
Safety standards
casing.

Alternating current
Direct current
Earth (ground)

Equipotentiality

John Moyle

anaesthetists.
Fire and explosion

is an explosion.
complete.
Fuel
2
Oxygen

Diethyl ether 1.9 48 2.0 82 1.5 24
Cyclopropane 2.4 10 2.5 60 1.6 30
Ethyl chloride 4.0 15 4.0 67 2.0 33
Enflurane 4.0 5.75 4.25
Halothane 4.75 3.25
Fluoroxene 4.0
Hydrogen 4.0 74 4.6 94 5.8 86
Methane 5.3 15 5.4 59 4.0 40
Sevoflurane 12 11

1

2
Ignition source

trapped beneath it.
Lasers
Precautions
are in use.


temperature (oC)

James Austin


analgesics)
is working.
Anaesthetic room

blade)
suction equipment
pressure monitor).
Monitoring

body temperature
stimulator)
required.
Induction methods

secure the airway

sequence induction
Risk of vomiting
Risk of arrhythmias

induction



neonates

dose (mg/kg)
patients
3
drugs
advised.
then be indicated.

inadequate.

previous allergy
myotonia
intubation:
suction available.
call for help
incident.

4%.
first instance.
output is quicker.
Historical note


3 Surgical
arrest
paralysis death
1
cannulation.

prilocaine 2.5%
as an oil/water
emulsion

per tube per tube

removed
paleness redness

< 1 year < 1 month
Further Reading


A full stomach
Hazards Management


the priority.

After head injury

when:
or less)
pressure.
Hazards Management

paralysis
pressure
required.
Hazards Management
in expert hands


airway
4
is safely secured.
FURTHER READING

James Austin



temperature control
monitoring
positioning.
impossible
production

is normal.
oxygen saturation.

response.


anaesthesia
is employed
available
anaesthetist

moving the patient.



Halothane 0.75 0.29
Enflurane 1.68 0.57
Sevoflurane 2.0 0.8

anaesthesia
Hypotension
Hypothermia
Hypothyroidism
Hypoxia
4
hyperpyrexia

technique.

documented.

Ian R Taylor
Michael OConnor


Cylinders
Cylinder body
test pressure
compressed gas
flammability status
pressure gases.
2 Cylinder label.

Oxygen E 680 13700 99.5

Air E 640 13700 21.0 (oxygen)
Storage
valve.
Testing
Filling

Mass of water
Cylinder valve
types of valve:
bull-nose valve
hand-wheel valve
star valve.
tare weight
cylinder owner
Cylinder use
Suction systems
laminar flow = Pr4

8L

misconnection.

contamination.
Vacuum pumps






100% saturation
Heated water bath

Heated Bernoulli
nebulizer and anvil
(adjustable)
0 25 34 44 50 75 100
lightweight
compact
disposable
about 2535 g/m3)
inexpensive.
single-patient use.

risk of scalding
droplets.
Water
droplets
Water
reservoir
High-pressure
gas
11
FURTHER READING
Livingstone, 1998.
Livingstone, 1995.
1998.

Delivery
Ian R Taylor
Michael OConnor


Medical gas
hospital.

Flexible pipeline
it carries.
5 Schrader probe.
Safety
gas outlet.

7.
Cylinder
Pipeline
Oxygen White 400
8).
Disc area (A)
Gas pressure (P)
F=PxA
Medical gases
Oxygen


carbon dioxide.
Dial
Coil
Coil straightening
Pointer
10
Pressure
11 Cylinder yoke.
Carbon dioxide
Air
flexible hose.
FURTHER READING
Livingstone, 1998.
Livingstone,1995.
1998.
Heinemann, 2000.

E Anne Thornberry

anaesthesia.
1.
Blood loss
Third-space losses
Adults
40 ml/kg/day
Children

K+ = 1 mmol/kg/day

Are they pyrexic?
Investigations


Dry mouth

Tachycardia
Tachypnoea
Oliguria
Drowsiness

Tachycardia
Anuria
Confusion/coma
3

a 70 kg male
10% 490 ml Thirst

Venoconstriction


Tachypnoea
Cool, clammy, pale
Anxious/aggressive
Oliguria

tachycardia
Tachypnoea
Anuria
Mental confusion
50% 2450 ml Coma
Fluid losses



Crystalloids


osmolality.
Colloids

Haemaccel 35,000 145 5.1 145 6.2

Gelofusine 35,000 154 0.4 154 0.4
Hetastarch 450,000 154 0 154 0
Dextran 70 70,000 150 0 150 0
in saline
Albumin 4.5% 70,000 150 2 120 0
endothelium.

reported.
gelatins.



volume

or
1530% As above
or
> 40% Transfuse

concentration

concentration
< 7 g/dl Transfuse

of age)

7

coagulation.
Blood substitutes

about 57 g/dl.

FURTHER READING

Livingstone, 1996.
2431.

Jonathan Warwick

Supine position

additional factors:
left side.

connectors
supinated
genital trauma

Indications:
thoracic surgery
surgery to the hip.
is lying.

c
b
a
d

c Heel supported.

Horners syndrome
supported
head of the fibula
Indications:
pelvic surgery

Indications:
reduce bleeding

embolism.

Lithotomy position
Indications:


muscles.
difficult.

of the flexed thigh
of the fibula
behind the knees
Prone position
Indications:


the foot
Indications:



Premedication
Neal Evans

Cambridge, UK.


reasons for this.

Sedation
Amnesia
Antiemesis

of anaesthesia.

Sleep apnoea
Extremes of age
Benzodiazepines


p.o. in children


for adults).
Antiemesis

use of morphine

dysfunction.

at induction.


gastric aspiration.

laryngoscope)
be of benefit.

Analgesia
or p.r.
FURTHER READING


1995; 27: 24956.


Vaporizers
Eileen Palayiwa



(J/(kg.K)).
(W/(m.K)).
of the agent.
Fv + Fb = F
given by:

400
350
pressure (mm Hg)
Saturated vapour
300
250
200
150
Halothane
100
Isoflurane
50 Enflurane
0
10 12 14 16 18 20 22 24 26 28 30 32
Temperature (C)

(W/(m.K))
Copper 385 385 8930
Glass 670 1 2600
Gas Bypass
flow
Variable
resistances
Vaporizing chamber
Wicks
Liquid agent
is maintained.



pathway.
vaporizer
6
5
Enflurane (vol %)
0
0 1 2 3 4 5 6 7 8 9 10 11

Oxygen 1.43 18.9 10.3 x 10-5

Nitrous oxide 1.96 13.5 6.9 x 10-5
Types of vaporizer


Concentration
regulator
Tubular slide valve
Wicks
Liquid agent
Base
6
Drager Vapor
Drager Vapor
3 0 16
2 5 20
2 0
24
1 5
28
Inlet
Outlet
Max
Min
7
PPV

control dial
Bypass
orifice
Vapour
control
orifice
Zero Entry tube

lock Liquid level
port indicator
Liquid
level
Wick
8
Tec 6 vaporizer
Tec 6 vaporizer
Gas/agent
outlet
Fresh
c d
gas
inlet e

g
h Key
Fresh gas
Agent vapour
i Gas/agent vapour
j Electrical
connections
m l k

FURTHER READING
348.

of Anaphylactic and
Andrew McIndoe

Pathophysiology


(Figure 1).
rash.
Signs Patients (%)

Erythema 45
Bronchospasm 36
Angio-oedema 24
Rash 13
Urticaria 8.5
Management
Condition
Presentation
Erythema
Bronchospasm
Oedema
Rash
Immediate action
Remove trigger
100% oxygen
Elevate legs
Follow-up action
Investigations
Plasma tryptase
Also consider
Latex sensitivity
Airway obstruction
Asthma
Panic attack
Call for help.
adult).
Complications

Investigations

anaphylaxis.

System, Pharmacia).
FURTHER READING

Simon Berg


be confirmed by:
capnography
available.
Chest movement
Auscultation
patient.
Breathing circuit
bronchospasm.
available.


(positive result).

Capnography
metabolic rate
pulmonary perfusion

sensitivity.
always obvious.
orogastric tube.
carina.
FURTHER READING



Aspiration
Polly Davies
Jonathan Warwick
Hospital, UK.



and vomiting.
Pathophysiology

Risk factors
Condition Examples

Pregnancy

Obesity
Lithotomy position

Pharyngeal pouch

Topical anaesthesia
syndrome)

Night-time surgery
Emergency surgery
Extremes of age
Obstetrics
Prevention
in Figure 2.
Length of fast
(hours)
Adults
Solid food 6
Clear fluid 23
Children
Solid food 6
Formula milk 4
Breast milk 3
Clear fluid 2
Pharmacotherapy
lower incidence.






Diagnosis
Symptoms Signs
Cyanosis
Tachycardia
Pulmonary oedema

Management

Oxygen therapy
Ventilatory support
Removal of aspirate
Bronchodilators
Antibiotics
Fluid balance
oedema
management
FURTHER READING
Br J Anaesth 1999; 83: 41521.
77: 17182.

Surgical Diathermy:
Andrew D Farmery



formula:
Current density
1
Desiccation
Cutting
2a).
Coagulation
Monopolar
Bipolar
Patient safety





Richard Vanner

anaesthesia.

included:
anaesthesia.
Indications
Mechanism of action
Correct technique
Complications


FURTHER READING


Failed Intubation
Stuart W Benham

head strapping.
Prolonged surgery

ventilation)

three categories:

laryngoscopy FFL)
primary plan.
plan.

spondylitis.
agent is given


approach.


Laryngoscopes
3 view)
intubation catheter
passed through the
(LMA).
catheter.
a b
LMA and ILMA


b c
a

FFL and intubation


thrust.

anaesthetist.
into the larynx.
may be required.
hands.
avoided.
this.
patients mucosa.

FURTHER READING
WB Saunders, 1997.

Anaesthesia
on CD-ROM
Airway Control
Oliver J Dyar
intubation:
obesity, pregnancy
intraoral masses
large goitre.



cartilages) visible
2
Airway patency
Aspiration risk

includes:
high-flow suction
two laryngoscopes
Magills forceps
required.




size 4.

Tracheal intubation
is not too tight.

4 Normal adults 30
5 Large adults 40
b
e
c
f
d g

a
b
c
d
e

Recovery

a b c

prongs.
a b c


Surgery
Michael W Platt

pain.

History

repair.

(pneumoperitoneum).




basal compression.


peritoneum.


these cases.
Recovery
home in 23 days.

FURTHER READING

Free Flap Surgery
Jane Quinlan
reconstruction.
Flap transfer
flap transfer are:
released
Primary ischaemia
vasoconstrictors
to blood flow.
include:

Physiology
8xxl
Vasodilatation


fluid management.
Crystalloids
Colloids
Blood
Dextran
1

Perfusion pressure
used.
Viscosity
delivery:
Br J Anaesth 57:

2
Monitoring

areas.


Induction

Maintenance


ventilation.
be added if needed.


Normothermia
Effective analgesia
Haematocrit 3035%
3
FURTHER READING
90421.

Michael OConnor
Ian Taylor

anaesthesia.



Units of pressure
approximately:
101 kPa
760 mm Hg
1035 cm H2O
1 bar
15 psi.

page 66).
glass.
Dial
Coil
Coil straightening
Pointer
Pressure
Pressure regulators
Pressure regulator
Regulated
low-pressure
chamber
Valve (a)
High-pressure
chamber
High pressure (P)

Flowmeters
Rotameters
viscosity
density.
Flowmeter
Turbulent flow
Laminar flow
Bobbin
4
measuring.
Accuracy is 2%.

altered.
Vaporizers
Safety
listed in Figure 5.

anaesthetic machine
to the wrong yoke
cylinder and yoke
hypoxic mixture
Bodok seal.
status Vaporizers
not tilted.
incidents
100%.
FURTHER READING
Apparatus, 1997.
1998.

Operating Theatre
J Duncan Young

Oxford.



Flow generator
Active process
Pressure
Cycling Time
Cycling Cycling
trigger Volume
EI IE Flow
Passive
process
Expiration


Flow
Time Time
Volume
Time Time

compliance.

Alveoli force
Resistance
inflow inflow
Pressure

compliance


normal lungs.
constant.
Ventilators may be:

Weight
Flow

P1
Inspiratory valve
Volume
P2
Time
Expiratory valve
Pressure
Time

maintained at
the expense of
Flow

P1 Time
flow resistor
A constant flow
Volume
P2 will deliver a
safety valve
constant tidal
volume
Time
Pressure
45 cm H2O.

circuits.
volume.

ventilation (IPPV)

breathing room air.

6
5
Volume (litres)
0 Time
Normal values

(Figure 10).

10 mBar
increases
down
Relative blood flow

the lung 2.5 100%
mBar
Volume
50%


V V
No ventilation
Q V/Q = 0 Q
Shunt
PAO2 PAO2
No PaO2
PaO2
flow
No perfusion
V/Q =
V
alveolus
Q
End
PAO2 PAO2
capillary PAO2
Q
O2
PaO2
PaO2 PAO2
O2 out = flow Q
so PaO2 will fall
10
of V/Q mismatching.


large tidal volumes
use of PEEP
diseased areas.

airway pressures.
venous return.

then improve.

output.


Adults:
used.
Children:
I:E ratio 1:2
Fi O2 0.5 (50% oxygen).
Safety issues

Ventilator checks
Ventilator checks

inspiratory phase
Apparatus, 1997.
11
FURTHER READING
Science, 1996.
1990.
1998.

Breathing Systems
Gordon W G French

be simple and safe
be easy to scavenge
be cheap.
unsafe.
as tuberculosis).


Valve screw top
Scavenging hood
Spring
Disc
Pathway of gas
when valve is open
Rebreathing systems

fresh gas flow
FGF
Lack FGF
FGF IPPV
23 x AMV

transfers

FGF

FGF
FGF
is used for IPPV.
adults or children.
b
e
g
c
f


FGF source
a Y-piece connector
a reservoir bag
litre/minute FGF.
CO2 + H2O H2CO3
Ideal circle set-up

pressure-limiting
(APL) valve

bag
One-way valves

4

Soda lime Baralyme
System checks
individual systems.
FURTHER READING

Duncan Parkhouse
Jonathan Warwick




is dependent on:
(the bio burden).

mucous membrane



infection
body fluids.
Cleaning
sterilization.
Manual cleaning
Mechanical cleaning
it.
by a rinse cycle.
does not disinfect.
Disinfection

pressure.

Washer disinfectors

recontamination.

by organic damaging
matter matter
Enveloped Non-
enveloped

0.20.35% (< 1 day)

6080%

compounds ( 7 days)

ppm average Cl2

phenolics
0.62%

ammonium
compounds
1
Sterilization
Steam

Steam sterilizer
times
Dry hot air

Ethylene oxide

Irradiation

Critical Incidents:
Joy E R Beamer
Jonathan Warwick


surgery.
Hypertension

after anaesthesia.
Hypoxaemia
Hypercapnia
Aortic clamping
Complications
Management
15 mg.
minutes.
Hypotension
Causes
Anaesthesia
histamine release.

trauma or burns

haemorrhage
head-up position
ischaemic tissues.

heart failure


Parkinsons disease
AIDS.
Other causes
Management
0.51.0 mg i.v.).
Massive haemorrhage

trauma
haemorrhage)
or coagulation.
Management
methods.
Blood loss (ml)

750 7501500 15002000 2000
Heart rate < 100 > 100 > 120 140

blood loss.
advance of surgery.
procedure
Arrhythmias
Management
mmol/kg/hour.
cardiac arrest.
is:
Hypertension
solvent abuse)
Anaesthetic factors
Hypoxaemia
Hypo/hypercapnia
Hypo/hypertension
Laryngoscopy
pressure lines)
Surgical factors
Catecholamines
Oculocardiac reflex
Embolism
Others
Limb reperfusion

infusion.



cardiac output.


metabolic acidosis
hyperkalaemia
Management
Immediate actions
Later actions
Future care
Leeds LS9 7TS
Tel: 0113 206 5274

Critical Incidents:
Orlando J Warner
Jonathan Warwick

Oxford.

surgery.
Aetiology
Error of judgement
Lack of experience
Lack of assistance
Lack of equipment
Equipment failure
involve:
Supraglottic
Tongue
Blood or secretions
Laryngeal
Laryngospasm
Tumour or oedema
Aspiration
Asthma
Anaphylaxis
Pneumothorax
Pulmonary oedema
arthritis)
from:
noisy airway

infection.

4
Optimum

intubating
position


(Figure 7).
a Macintosh size 4;
b Macintosh size 3;
c McCoy size 4;
d McCoy size 3;
e Belscope;
f Polio;
i Huffman prism.

catheter;


alveolar plateau.

breathing)
of aspiration.
Bronchospasm
Anaphylaxis
Pulmonary oedema
10
Failure to breathe

doses of drugs used
conscious.

block
Hypokalaemia
Hypothermia
Hypocarbia
Aminoglycosides
Calcium antagonists
Magnesium
Local anaesthetics
Lithium
Frusemide
11

Congenital
Acquired
Infections
Malignancy
Chronic disease
Liver disease
Renal failure
Hypothyroidism
12

circle system).
satisfactory.
include:
body temperature
CT head scan
Air embolism

13

present
is of benefit)
14
Pneumothorax
ventilated.
Signs Causes
Hyperresonance
Shock
affected side
15



John Moyle

I= E
R

cardiac arrhythmia
bone and fat.
5 mA Pain
Electrical safety
equipment sensibly.
described below.)



4
Safety standards
casing.

Alternating current
Direct current
Earth (ground)

Equipotentiality

John Moyle

anaesthetists.
Fire and explosion

is an explosion.
complete.
Fuel
2
Oxygen

Diethyl ether 1.9 48 2.0 82 1.5 24
Cyclopropane 2.4 10 2.5 60 1.6 30
Ethyl chloride 4.0 15 4.0 67 2.0 33
Enflurane 4.0 5.75 4.25
Halothane 4.75 3.25
Fluoroxene 4.0
Hydrogen 4.0 74 4.6 94 5.8 86
Methane 5.3 15 5.4 59 4.0 40
Sevoflurane 12 11

1

2
Ignition source

trapped beneath it.
Lasers
Precautions
are in use.


temperature (oC)

James Austin


analgesics)
is working.
Anaesthetic room

blade)
suction equipment
pressure monitor).
Monitoring

body temperature
stimulator)
required.
Induction methods

secure the airway

sequence induction
Risk of vomiting
Risk of arrhythmias

induction



neonates

dose (mg/kg)
patients
3
drugs
advised.
then be indicated.

inadequate.

previous allergy
myotonia
intubation:
suction available.
call for help
incident.

4%.
first instance.
output is quicker.
Historical note


3 Surgical
arrest
paralysis death
1
cannulation.

prilocaine 2.5%
as an oil/water
emulsion

per tube per tube

removed
paleness redness

< 1 year < 1 month
Further Reading


A full stomach
Hazards Management


the priority.

After head injury

when:
or less)
pressure.
Hazards Management

paralysis
pressure
required.
Hazards Management
in expert hands


airway
4
is safely secured.
FURTHER READING

James Austin



temperature control
monitoring
positioning.
impossible
production

is normal.
oxygen saturation.

response.


anaesthesia
is employed
available
anaesthetist

moving the patient.



Halothane 0.75 0.29
Enflurane 1.68 0.57
Sevoflurane 2.0 0.8

anaesthesia
Hypotension
Hypothermia
Hypothyroidism
Hypoxia
4
hyperpyrexia

technique.

documented.

Ian R Taylor
Michael OConnor


Cylinders
Cylinder body
test pressure
compressed gas
flammability status
pressure gases.
2 Cylinder label.

Oxygen E 680 13700 99.5

Air E 640 13700 21.0 (oxygen)
Storage
valve.
Testing
Filling

Mass of water
Cylinder valve
types of valve:
bull-nose valve
hand-wheel valve
star valve.
tare weight
cylinder owner
Cylinder use
Suction systems
laminar flow = Pr4

8L

misconnection.

contamination.
Vacuum pumps






100% saturation
Heated water bath

Heated Bernoulli
nebulizer and anvil
(adjustable)
0 25 34 44 50 75 100
lightweight
compact
disposable
about 2535 g/m3)
inexpensive.
single-patient use.

risk of scalding
droplets.
Water
droplets
Water
reservoir
High-pressure
gas
11
FURTHER READING
Livingstone, 1998.
Livingstone, 1995.
1998.

Delivery
Ian R Taylor
Michael OConnor


Medical gas
hospital.

Flexible pipeline
it carries.
5 Schrader probe.
Safety
gas outlet.

7.
Cylinder
Pipeline
Oxygen White 400
8).
Disc area (A)
Gas pressure (P)
F=PxA
Medical gases
Oxygen


carbon dioxide.
Dial
Coil
Coil straightening
Pointer
10
Pressure
11 Cylinder yoke.
Carbon dioxide
Air
flexible hose.
FURTHER READING
Livingstone, 1998.
Livingstone,1995.
1998.
Heinemann, 2000.

E Anne Thornberry

anaesthesia.
1.
Blood loss
Third-space losses
Adults
40 ml/kg/day
Children

K+ = 1 mmol/kg/day

Are they pyrexic?
Investigations


Dry mouth

Tachycardia
Tachypnoea
Oliguria
Drowsiness

Tachycardia
Anuria
Confusion/coma
3

a 70 kg male
10% 490 ml Thirst

Venoconstriction


Tachypnoea
Cool, clammy, pale
Anxious/aggressive
Oliguria

tachycardia
Tachypnoea
Anuria
Mental confusion
50% 2450 ml Coma
Fluid losses



Crystalloids


osmolality.
Colloids

Haemaccel 35,000 145 5.1 145 6.2

Gelofusine 35,000 154 0.4 154 0.4
Hetastarch 450,000 154 0 154 0
Dextran 70 70,000 150 0 150 0
in saline
Albumin 4.5% 70,000 150 2 120 0
endothelium.

reported.
gelatins.



volume

or
1530% As above
or
> 40% Transfuse

concentration

concentration
< 7 g/dl Transfuse

of age)

7

coagulation.
Blood substitutes

about 57 g/dl.

FURTHER READING

Livingstone, 1996.
2431.

Jonathan Warwick

Supine position

additional factors:
left side.

connectors
supinated
genital trauma

Indications:
thoracic surgery
surgery to the hip.
is lying.

c
b
a
d

c Heel supported.

Horners syndrome
supported
head of the fibula
Indications:
pelvic surgery

Indications:
reduce bleeding

embolism.

Lithotomy position
Indications:


muscles.
difficult.

of the flexed thigh
of the fibula
behind the knees
Prone position
Indications:


the foot
Indications:



Premedication
Neal Evans

Cambridge, UK.


reasons for this.

Sedation
Amnesia
Antiemesis

of anaesthesia.

Sleep apnoea
Extremes of age
Benzodiazepines


p.o. in children


for adults).
Antiemesis

use of morphine

dysfunction.

at induction.


gastric aspiration.

laryngoscope)
be of benefit.

Analgesia
or p.r.
FURTHER READING


1995; 27: 24956.


Vaporizers
Eileen Palayiwa



(J/(kg.K)).
(W/(m.K)).
of the agent.
Fv + Fb = F
given by:

400
350
pressure (mm Hg)
Saturated vapour
300
250
200
150
Halothane
100
Isoflurane
50 Enflurane
0
10 12 14 16 18 20 22 24 26 28 30 32
Temperature (C)

(W/(m.K))
Copper 385 385 8930
Glass 670 1 2600
Gas Bypass
flow
Variable
resistances
Vaporizing chamber
Wicks
Liquid agent
is maintained.



pathway.
vaporizer
6
5
Enflurane (vol %)
0
0 1 2 3 4 5 6 7 8 9 10 11

Oxygen 1.43 18.9 10.3 x 10-5

Nitrous oxide 1.96 13.5 6.9 x 10-5
Types of vaporizer


Concentration
regulator
Tubular slide valve
Wicks
Liquid agent
Base
6
Drager Vapor
Drager Vapor
3 0 16
2 5 20
2 0
24
1 5
28
Inlet
Outlet
Max
Min
7
PPV

control dial
Bypass
orifice
Vapour
control
orifice
Zero Entry tube

lock Liquid level
port indicator
Liquid
level
Wick
8
Tec 6 vaporizer
Tec 6 vaporizer
Gas/agent
outlet
Fresh
c d
gas
inlet e

g
h Key
Fresh gas
Agent vapour
i Gas/agent vapour
j Electrical
connections
m l k

FURTHER READING
348.

of Anaphylactic and
Andrew McIndoe

Pathophysiology


(Figure 1).
rash.
Signs Patients (%)

Erythema 45
Bronchospasm 36
Angio-oedema 24
Rash 13
Urticaria 8.5
Management
Condition
Presentation
Erythema
Bronchospasm
Oedema
Rash
Immediate action
Remove trigger
100% oxygen
Elevate legs
Follow-up action
Investigations
Plasma tryptase
Also consider
Latex sensitivity
Airway obstruction
Asthma
Panic attack
Call for help.
adult).
Complications

Investigations

anaphylaxis.

System, Pharmacia).
FURTHER READING

Simon Berg


be confirmed by:
capnography
available.
Chest movement
Auscultation
patient.
Breathing circuit
bronchospasm.
available.


(positive result).

Capnography
metabolic rate
pulmonary perfusion

sensitivity.
always obvious.
orogastric tube.
carina.
FURTHER READING



Aspiration
Polly Davies
Jonathan Warwick
Hospital, UK.



and vomiting.
Pathophysiology

Risk factors
Condition Examples

Pregnancy

Obesity
Lithotomy position

Pharyngeal pouch

Topical anaesthesia
syndrome)

Night-time surgery
Emergency surgery
Extremes of age
Obstetrics
Prevention
in Figure 2.
Length of fast
(hours)
Adults
Solid food 6
Clear fluid 23
Children
Solid food 6
Formula milk 4
Breast milk 3
Clear fluid 2
Pharmacotherapy
lower incidence.






Diagnosis
Symptoms Signs
Cyanosis
Tachycardia
Pulmonary oedema

Management

Oxygen therapy
Ventilatory support
Removal of aspirate
Bronchodilators
Antibiotics
Fluid balance
oedema
management
FURTHER READING
Br J Anaesth 1999; 83: 41521.
77: 17182.

Surgical Diathermy:
Andrew D Farmery



formula:
Current density
1
Desiccation
Cutting
2a).
Coagulation
Monopolar
Bipolar
Patient safety





Richard Vanner

anaesthesia.

included:
anaesthesia.
Indications
Mechanism of action
Correct technique
Complications


FURTHER READING


Failed Intubation
Stuart W Benham

head strapping.
Prolonged surgery

ventilation)

three categories:

laryngoscopy FFL)
primary plan.
plan.

spondylitis.
agent is given


approach.


Laryngoscopes
3 view)
intubation catheter
passed through the
(LMA).
catheter.
a b
LMA and ILMA


b c
a

FFL and intubation


thrust.

anaesthetist.
into the larynx.
may be required.
hands.
avoided.
this.
patients mucosa.

FURTHER READING
WB Saunders, 1997.

Clinical assessment
Anaesthesia
on CD-ROM
Assessment of Gastrointestinal
Problems
David James
David James is Consultant Anaesthetist at Guy's and St Thomas' Hospital Trust,

London. He graduated from St Bartholomew's Hospital, and trained in anaesthesia in
London. His interests are perioperative medicine and training.
Anaesthetists encounter patients with gastrointestinal problems in two contexts.

As critical care physicians caring for patients with gastro-intestinal problems that
occur as a cause of and a consequence of critical illness.
As perioperative physicians caring for patients undergoing elective and emergency
gastrointestinal surgery. The importance of this role was emphasized by the CEPOD
and NCEPOD reports, and is considered in this article.
Primary problems
Bleeding into a viscus may arise from the upper gastrointestinal tract. Bleeding
from duodenal ulcers, gastric erosions, gastric ulcers and oesophagitis accounts
for almost 75% of cases; other causes such as gastritis and oesophageal varices
are less common. Patients commonly present with haematemesis, melaena, with or
without pain, and varying degrees of shock. Physical examination aims to assess the
degree of shock and primary cause of the bleeding, which may be elucidated only by
upper gastrointestinal endoscopy or mesenteric angiography. Lower gastrointestinal
haemorrhage, most commonly encountered in the elderly, is often a result of colorectal
carcinoma, colonic polyps, ischaemic colitis, inflammatory bowel disease or diverticular
disease. The clinical presentation varies with the cause, often with few symptoms.
Perforation of a viscus is characterized by sudden onset of acute abdominal pain

and peritonitis, with the patient lying still with a rigid abdomen and absent bowel
sounds. Common causes include perforations of peptic ulcer, appendix or diverticulum.
Malignant and inflammatory bowel diseases may also present in this way. An erect plain
chest radiograph looking for free gas under the diaphragm may confirm the diagnosis.
Obstruction of a viscus is suggested by colicky abdominal pain, vomiting,

constipation and abdominal distension. Common causes include intra-abdominal
adhesions, hernias, inflammatory bowel disease and malignancies. Plain and contrast-
enhanced abdominal radiographs aid diagnosis.
Infarction of a viscus may be secondary to torsion or strangulation of a viscus,

thromboembolic occlusion of its arterial inflow or venous outflow or vasculitis. Pain and
peritonitis are common clinical features.
Inflammation of a viscus the history, onset of pain and site of maximal tenderness
help to determine the origin of the inflamed viscus. Common conditions include
appendicitis and diverticulitis. Crohns disease and Meckels diverticulitis are less
common causes. Other intra-abdominal structures can present in a similar way (e.g.
salpingitis, cholecystitis, adenitis, pancreatitis, cystitis, pyelonephritis).
Gastrointestinal emergencies may be complicated by hypovolaemic shock or

endotoxaemia/bacteraemia, culminating in the development of a systemic inflammatory
response syndrome and multi-organ dysfunction.
The urgency of the surgery is usually defined by the degree of acute systemic
disturbance. Surgery and anaesthesia for gastro-intestinal problems carry a high risk
of complications, principally affecting the respiratory, cardiovascular and renal systems.
The mortality rate for elective intra-abdominal procedures is up to 5%. Patients having
upper abdominal procedures have a higher risk of complications and are twice as likely
to die postoperatively as those having lower abdominal procedures. Factors increasing
the risk of an adverse postoperative outcome include the site of surgery, its urgency
and patient co-morbidities such as cardiac failure, physical status, those rated as ASA
III or IV, and age over 50 years. This emphasizes the need for careful preoperative
patient assessment, so that informed decisions can be made about the appropriateness
of surgery and what measures can be taken to achieve the best outcome for the
patient.
Secondary problems
Water and electrolyte depletion: the magnitude of any water and electrolyte
deficit reflects the duration of the primary problem and the site of the fluid loss.
Gastrointestinal fluid and electrolyte losses (Figure 1) may lead to severe hypovolaemia
and acidbase and electrolyte imbalances. Clinical estimation of the volume of fluid lost
is difficult and often underestimated.
Daily volume and electrolyte content of gastrointestinal secretions
Secretion Volume Na + K+ Cl HCO3

(litres) (mmol/litre) (mmol/litre) (mmol/litre) (mmol/litre)
Saliva 1.5 15 30 10 30
Gastric 2.0 50 15 120 0
Small bowel 3.0 140 10 100 30
Bile 0.6 140 5 100 35
Pancreatic 0.7 140 5 70 100
Total 7.8 725 112 764 226
Water extracellular volume deficit is a common problem before any gastrointestinal

surgery. It is caused by preoperative water deprivation, extracorporeal water losses
(e.g. vomiting, diarrhoea, fistulae, nasogastric suction), sequestration of water into
bowel lumen, bowel wall and peritoneum and preoperative bowel purgation. The clinical
features are outlined in Figure 2 and depend on the severity of the water deficit and
factors affecting cardiovascular reflexes (e.g. age).
Clinical features of water loss
Percentage body Clinical signs

weight lost as water
> 4% Thirst
Reduced skin turgor
Dry tongue
Reduced sweating
> 6% All above

Reduced peripheral venous filling
Oliguria
Apathy
Low central venous pressure
Haemoconcentration
Raised serum urea out of proportion to raised serum
creatinine (pre-renal pattern)
Low urinary sodium concentration (015 mmol/litre)
High urinary osmolality (8001400 mosmol/kg)
> 8% All above

Hypotension
Thready pulse
Cool peripheries
> 10% Coma

Shock
2
Electrolytes and acidbase significant loss of oral and pharyngeal secretions

predominantly affects water balance, with minimal effects on serum electrolyte
concentrations, whereas significant loss of gastric secretions can result in
hypochloraemic alkalosis (caused by loss of hydrochloric acid) with hypovolaemia
(caused by sodium and water loss) and hypokalaemia. In the early stages of this
problem, the urine is alkaline in an attempt to maintain a normal pH. As the condition
worsens, the kidneys attempt to preserve sodium ions, therefore hydrogen and
potassium ions are preferentially excreted, producing a paradoxically acid urine,
thereby exacerbating the alkalosis and the hypokalaemia. Hypocalcaemia can also
occur as a consequence of calcium lost in the vomitus and a reduction of the serum
concentration of ionized calcium owing to alkalosis (increased protein binding). Loss
of lower gastrointestinal secretions from massive diarrhoea, duodenal, jejunal and
pancreatic fistulae is more commonly associated with hypovolaemia and metabolic
hyperchloraemic (normal anion gap) acidosis, due to the loss of bicarbonate.
Hypomagnesaemia has been associated with loss of upper and lower gastrointestinal
secretions and malnutrition.
Abnormalities of serum phosphate can also be associated with gastrointestinal disease.

Hypophosphataemia may occur secondary to dietary deficiency and systemic alkalosis.
Haemorrhage: bleeding into the gastrointestinal tract sufficient to cause intravascular

volume depletion is a common cause of emergency hospital admission (Figure 3). It
is seldom possible to estimate the magnitude of gastrointestinal blood losses from the
patients history or by measuring overt blood losses. A better estimation is gained from
clinical assessment of the patients intravascular volume, bearing in mind that age and
co-morbidities significantly affect the clinical cardiovascular signs of hypovolaemia.
Clinical signs of hypovolaemia
Grade of Clinical signs1

hypovolaemia
1 10% IVBV lost HR normal

SAP normal
Urine output normal
Peripheral circulation 1 ml/kg/hour
Normal sensorium
2 20% IVBV lost HR 100120

SAP orthostatic hypotension
Urine output < 1 ml/kg/hour
Peripheral circulation cool and pale
Normal sensorium
3 30% IVBV lost HR 120140

SAP systolic pressure < 100
Urine output < 1 ml/kg/hour
Peripheral circulation cold, pale with slow capillary refill
Restless
4 > 40% IVBV lost HR > 140

SAP systolic pressure < 80
Urine output nil
Peripheral circulation cold and clammy with peripheral
cyanosis
Impaired consciousness
1
Typical signs in a young healthy adult with normal cardiovascular reflexes.
IVBV, intravascular blood volume; HR, heart rate (beats/minute); SAP, systemic arterial
pressure (mm Hg)
Pulmonary problems: respiratory dysfunction commonly arises from factors such as

diaphragmatic compression by an intra-abdominal process that decreases functional
residual capacity (FRC) and may lead to atelectasis. Pleural effusions, mediast-inal
emphysema, pneumothorax, and acute respiratory distress syndrome also occur.
Loss of muscle mass and weakness from malnutrition, accumulation of thick bronchial
secretions in dehydrated patients, and high metabolic demands resulting from sepsis
may cause functional and mechanical respiratory dysfunction. Such patients often
breathe shallowly, at higher than normal rates, and are often hypoxaemic. Chest
radiographs help to exclude pneumonia in these patients.
Aspiration of gastric contents can cause pulmonary damage including fulminant
aspiration pneumonitis. Fasting before anaesthesia reduces this risk (Figure 4). Some
clinical situations are always associated with an increased risk of aspiration:
reduced gastrointestinal motility secondary to metabolic causes (e.g. diabetes
mellitus, renal failure), peritonitis, head injury, trauma, pain, drugs (e.g. opioids)
gastrointestinal obstruction of pylorus or small bowel
reduced lower oesophageal function secondary to raised intra-abdominal pressure
(e.g. pregnancy, gastro-oesophageal reflux disease) and hiatus hernia.
The interval between the last oral intake and the injury is the fasting period. The
American Society of Anesthesiologists (ASA) has recommended preoperative fasting
times for healthy patients undergoing elective surgery (Figure 4).
Preoperative fasting times for healthy patients undergoing

elective surgery
Ingested material Minimum fast (hours)

Clear fluids 2
Breast milk 4
Formula milk 46
Non-human milk 6
Light meal 6
4
Sepsis is associated with the gastrointestinal tract; it divides broadly into primary
and secondary types. Primary acute intestinal infections (e.g. gastroenteritis) can be
confused with inflammatory bowel disease and are caused by a variety of pathogens.
Secondary acute intestinal infections cause inflammation of a viscus and are usually
associated with obstruction (e.g. appendicitis, diverticulitis) or another abnormality (e.g.
trauma, adenitis, peritonitis). The causative bacteria are usually the commensals (e.g.
Escherichia coli, enterococci, Streptococcus milleri, Bacterioides fragilis). Peritonitis
is often secondary to another intra-abdominal process (e.g. perforation of a viscus).
These infections are often polymicrobial, requiring broad-spectrum antibiotics until the
causative organism is isolated.
Patients with severe sepsis secondary to an intra-abdominal cause usually present with
abdominal symptoms (pain, vomiting, diarrhoea) and signs of peritonism (abdominal
tenderness, rigidity, guarding) together with signs of a systemic response to the
inflammatory process, the so-called systemic inflammatory response syndrome
characterized by fever, raised white cell count and insidious multiple organ dysfunction.
Nutritional deficiencies: malnutrition is commonly caused by failure to absorb multiple

nutritional components (protein, fat, carbohydrate, vitamins, minerals). It often occurs
in association with chronic disease states. In normal individuals, a 3040% weight
loss due to starvation may be fatal. During starvation, metabolic adaptation aims to
conserve essential tissues. Once glycogen stores are exhausted as a source of glucose
(in about 24 hours in normal individuals) protein and fat are broken down to provide
energy. Protein is initially catabolized, with the resultant urinary loss of urea, sodium,
potassium, magnesium and calcium, followed by fat as the chief source of energy once
the metabolic pathways are established with reduction of protein catabolism. Once fat
reserves are exhausted, protein catabolism begins. The physical result is a decrease
in basal metabolic rate due to decreasing lean body mass, decreased physical
activity and reduced thyroxine production. The co-existence of severe illness may
compound the rate of decline and cause fatality sooner. Starvation and malnutrition are
prevalent on surgical wards (notably following major abdominal surgery), in long-term
hospitalized patients and cancer patients. They occur through poor appetite, impairment
in digestion and absorption, and the increased metabolic demands of acute illness.
Nutritional support in malnourished patients undergoing major surgery reduces their
postoperative morbidity and mortality.
General assessment
Any clinician approaching a patient for the first time should rapidly assess the life-
threatening conditions that, if left unrecognized and unmanaged, can be lethal. When
problems associated with the airway, breathing and circulation are solved, a definitive
diagnosis can be sought and a management plan instigated.
Airway problems are uncommon unless consciousness is obtunded. Immediate

attempts to secure a patent, protected airway should ensue.
Breathing if vomiting is a significant feature, the risk of pulmonary aspiration of

gastric contents should be borne in mind; a nasogastric tube to drain fluid and gas
from the stomach may reduce this risk. Clinical features of respiratory dysfunction
(e.g. dyspnoea, tachypnoea, hypoxia) may occur for a variety of reasons, including
diaphragmatic splinting secondary to pain with or without abdominal distension causing
raised intra-abdominal pressure. Respiratory distress may be a sign of shock or sepsis.
Kussmauls respiration (tachypnoea with deep inspiratory excursions) is associated
with acidaemia from metabolic causes. Immediate steps should be taken to ensure
adequate oxygenation and ventilation, with interventions ranging from providing
supplemental oxygen to mechanical ventilation of the lungs.
Circulation hypotension is the most common circulatory problem asssociated with

gastrointestinal problems. Occult bleeding can occur in the gut lumen, peritoneal
cavity or retroperitoneum. Patients with septic shock are classically vasodilated
and warm, with hypotension and a fever, but many (particularly if presenting late)
are peripherally vasoconstricted and have a normal or even low body temperature.
Atrial fibrillation in the elderly patient with abdominal pain means that mesenteric
artery embolism should be considered in the differential diagnosis. Two large-bore
peripheral intravenous cannulae should be inserted and venous blood taken for a
full blood count, biochemistry (including amylase) and blood cross-match, and a
coagulation screen, blood cultures, pregnancy test and sickle screen if appropriate.
Suspected hypovolaemia should be treated by fluid resuscitation, septic shock with fluid
resuscitation and intravenous broad-spectrum antibiotics.
A portable ultrasound scan (if available) may confirm the cause of hypovolaemic shock
(e.g. a leaking aortic aneurysm, free intraperitoneal fluid, an ectopic pregnancy).
Anaesthetic assessment
Items of interest in the history include the presence and nature of pain, other
gastrointestinal symptoms (e.g. anorexia, dyspepsia, nausea, vomiting, haematemesis,
melaena, diarrhoea, constipation), previous abdominal surgery and recent drug
ingestion.
Physical examination should concentrate on the general appearance of the patient, in

particular their posture, pigment-ation, pallor and pattern of respiration. The following
should be specifically examined:
cardiovascular system particularly signs of intravascular and extracellular fluid
volume deficits
respiratory systems particularly signs of respiratory distress or areas of lung
collapse
signs of sepsis.
This is followed by a review of all appropriate investigations to help estimate the

magnitude of the secondary effects of the gastro-intestinal problem. Haematological,
blood chemistry, arterial blood gases and imaging techniques should be ordered only if
the result is likely to alter the management of the patient.
Preoperative management
When surgery is necessary and the secondary anaesthetic assessment is completed,
preoperative management should begin.
Analgesia: early judicious analgesia is advocated for the patient with acute abdominal
pain. If opioid analgesia is given as a dilute solution by slow intravenous injection,
the dose can be titrated against the patients pain. Adequate analgesia reduces the
patients suffering and may allow them to give a clearer history and be easier to
examine.
Anti-emetic and nasogastric tube: the ASA recommend physical and

pharmacological methods to reduce the risk of regurgitation and aspiration. They do not
recommend routine use of these agents in healthy, elective patients. Physical methods
involve nasogastric drainage of gastric contents. For most laparotomies a PVC/
polyurethane 16 FG Ryles or Salem tube is adequate.
Pharmacological methods include antacids, which neutralize acid in the stomach,

to reduce the risk of damage should aspiration occur. Particulate antacids are not
recommended. Sodium citrate solution administered shortly before induction is the
agent of choice in high-risk cases (e.g. pregnancy) but this results in an increase in
gastric volume. Additionally, antihistamines (e.g. ranitidine and proton-pump inhibitors
such as omeprazole) decrease acid secretion in the stomach and should be used
for high-risk patients. Ideally, they should be administered on the evening before
surgery (or early morning for an afternoon list) and a second dose given 2 hours
preoperatively. Gastric prokinetic agents (e.g. metoclopramide) increase gastric
emptying in healthy patients, but a clear benefit in trauma patients has not been
demonstrated. Anticholinergic agents do not have a significant effect and are not
routinely recommended.
Fluid and electrolyte replacement: signs of intravascular and extracellular volume

depletion require immediate correction with intravenous fluids, and the response to fluid
resuscitation should be monitored. Fluid and electrolyte deficits should be replaced
with an appropriate crystalloid solution; haemorrhage with clear colloid until red cells
are available for transfusion. Central venous pressure monitoring is often required to
manage fluid replacement in the elderly or those with cardiac disease.
Preoperative optimization of cardiovascular and respiratory function reduces mortality,

morbidity and length of stay in the ICU and hospital. High-risk patients include those
with severe cardiovascular and/or severe respiratory diseases; those having aortic
surgery, major surgery for malignancy or surgery for abdominal sepsis; and those with
haemodynamic instability due to an acute intra-abdominal catastrophe. It has been
suggested that haemodynamic monitoring should start in the preoperative period, using
a pulmonary artery catheter to assess fluid requirement and cardiac output. Patients in
studies by Boyd and colleagues were given blood if anaemic and oxygen if hypoxaemic
and subsequently colloid with or without an inotrope until a predetermined level of
pulmonary capillary wedge pressure and oxygen delivery were achieved. Such an
approach makes heavy demands on staff and resources. In emergencies, a balance
has to be struck between the benefits of optimization before surgery and commencing
surgery. If bleeding is the main problem, surgery may be part of the resuscitation
process, and time should not be wasted preoperatively.
Antibiotics are needed for localized infection or if clinical sepsis is thought to have an
intra-abdominal source (e.g. perforation of the colon in an elderly patient). Patients who
are septicaemic should start treatment with a broad-spectrum intravenous antibiotic
without waiting for the result of blood cultures. u
FURTHER READING
Boyd O, Grounds R M, Bennett E D. A Randomized Clinical Trial of the Effect of
Deliberate Perioperative Increase of Oxygen Delivery on Mortality in High-risk Surgical
Patients. J Am Med Assoc 1993; 270: 2699707.
Practice Guidelines for Preoperative Fasting and the use of Pharmacological Agents
for the Prevention of Pulmonary Aspiration: Application to Healthy Patients undergoing
Elective Procedures. Anaesthesiology 1999; 90: 896905.
Wilson J, Woods I, Fawcett J et al. Reducing the Risk of Major Elective Surgery:
Randomized Controlled Trial of Preoperative Optimization of Oxygen Delivery. Br Med J
1999; 318: 1099103.

Clinical Aspects of Hepatic
Problems
Elizabeth Sizer
Simon Cottam
Elizabeth Sizer is Specialist Registrar in Anaesthesia at King's College Hospital,

London, currently working in the Liver Unit. Her interests include liver transplantation,
liver intensive care and anaesthesia for hepatobiliary surgery.
Simon Cottam is Consultant Anaesthetist at King's College Hospital, London. His main
interests include intensive care and hepatobiliary anaesthesia.
Advanced liver disease is a classic example of multisystem failure resulting from a

single organ disease. Historically, even minor surgery on cirrhotic patients resulted in
high mortality. Liver transplantation has dramatically improved the prognosis for these
patients. It is important for clinicians to appreciate the multisystem sequelae of end-
stage liver disease, to assess risk and manage patients appropriately. Recognition of
severe disease is crucial; improved perioperative care has not significantly reduced
operative mortality. These patients should be referred for transplant assessment or, if
surgery for unrelated conditions is considered, should be managed in specialist centres.
Risk assessment
The ChildPugh classification of liver disease (Figure 1) was originally described to
assess operative risk in cirrhotic patients undergoing surgery for variceal bleeding. Its
use has extended to predict outcome in cirrhotic patients for all types of surgery.
Pughs modification of the Child classification of severity of liver

disease
Clinical and biochemical Points scored for increasing

measurements abnormality
1 2 3
Encephalopathy None Grade 12 Grade 34
Ascites None Slight Moderate
Bilirubin (mol/litre) < 35 3560 > 60
Prothrombin (seconds 14 410 > 10

prolonged)
Albumin (g/litre) > 35 2835 < 28
The points for the five variables are added to give a score ranging from
5 to 15. Patients with scores 56 are Grade A, 79 are Grade B and
1015 are Grade C. Grade A represents good risk with 5% mortality,
Grade B represents moderate risk with 10% mortality, Grade C
represents poor risk with mortality > 50%
1
Others have studied the effects of systems failure on outcome in patients with severe
liver disease (Figure 2). Optimizing treatable complications (e.g. ascites) may decrease
mortality significantly. Causes of death in these patients are sepsis, renal failure,
bleeding, hepatic failure and encephalopathy. Poor nutrition, portal hypertension with
ascites and encephalopathy herald poor prognosis for any surgery in these patients.
However, recent work suggests that cirrhotic patients with good function who are
well compensated (i.e. ChildPugh Grade A) are good candidates for certain types
of surgery (e.g. liver resection for hepatocellular carcinoma or portosystemic shunt
surgery).
Preoperative variable and mortality in cirrhotic patients
Variable Mortality if present (%)
Pulmonary failure 100

Cardiac failure 92
Gastrointestinal bleeding 86
More than two antibiotics 82
Second operation required 81
Renal failure 73
More than 2 units of blood required 69
Hepatic decompensation 66
Positive blood/urine culture 61
Albumin < 30 g/litre 58
Ascites 58
Less than 2 units of blood required 22
Extrahepatic effects of end-stage liver disease

Cardiovascular system: in end-stage liver disease the systemic circulation is
characterized by various pathological changes. Peripheral vasodilatation and shunting
(cutaneous, intrapul-monary, portopulmonary and pleural) result in increased cardiac
output. This can mimic the hyperdynamic picture of a septic state. Activation of the
reninaldosteroneangiotensin (RAA) system causes an increase in plasma and
extracellular fluid volume, though effective circulating volume is reduced. Cirrhotic
cardiomyopathy may be masked by the reduction in afterload, and is difficult to detect
by non-invasive preoperative investigations. Pulmonary hypertension is also seen
and is a rare cause (< 1%) of right ventricular failure. Cardiac arrhythmias also occur,
associated with cardiomyopathy or electrolyte abnormalities such as hypomagnesaemia
and hypokalaemia. The responsiveness to catecholamines is reduced.
Respiratory system: respiratory compromise may result from restrictive lung disease
caused by ascites or pleural effusions, the hepatopulmonary syndrome, pulmonary
hypertension, defects in alveolar oxygen diffusion or pulmonary manifestations of
systemic disease (e.g. 1-antitrypsin deficiency, autoimmune disease). Several factors
dispose the cirrhotic patient towards hypoxaemia: a rightward shift in the oxygen-
dissociation curve (due to decreased levels of 2,3-diphosphoglycerate (2,3-DPG)),
intrapulmonary shunting due to capillary vasodilatation and restrictive defects due to
large volume ascites and pleural effusions. These effects are compensated for by the
raised mixed venous oxygen saturation consequent on poor oxygen extraction and the
raised resting cardiac output. All patients with end-stage liver disease and a partial
pressure of oxygen (pO2) less than 9 kPa should be considered hypoxic. In patients
with the hepato-pulmonary syndrome (chronic liver disease, increased alveolararterial
gradient while breathing room air, and evidence of intrapulmonary vasodilatation)
transplantation is associated with a good outcome and improvement of hypoxia as
vascular remodelling occurs. By contrast, in patients who have porto-pulmonary
hypertension and an increase in pulmonary vascular resistance, transplantation does
not result in improvement. Severe pulmonary hypertension (mean pulmonary arterial
pressure > 50 mm Hg) is associated with right ventricular failure and sudden cardiac
death; mortality is 100% in this group. Preoperative therapy with prostacyclin and
nitric oxide may improve outcome in this group though treatment needs to continue
long term, suggesting that the benefit is obtained from vascular remodelling not just
a decrease in pulmonary pressures. Large volume ascites also increases the risk of
pulmonary aspiration.
Renal and endocrine system: some renal dysfunction is common in patients with
cirrhosis, portal hypertension and ascites. Compensatory mechanisms to restore mean
arterial pressure in cirrhotic patients result in activation of the RAA system with sodium
and water retention and the development of ascites. Non-osmotic hypersecretion
of vasopressin occurs due to the relative decrease in central blood volume due to
splanchnic pooling. As the severity of the disease progresses, disproportionate water
retention occurs and dilutional hyponatraemia results. At its most severe this can lead
to the hepatorenal syndrome. This represents severe renal vasoconstriction. Renal
angiography in this setting demonstrates absent cortical blood flow. Hepatorenal
syndrome is characterized by a rapid deterioration in renal function associated with low
urinary sodium excretion. Strategies to improve renal function in this setting include the
use of splanchnic vasopressors (e.g. terlipressin) with volume resuscitation, transjugular
intrahepatic portosystemic stent (TIPSS) placement to reduce portal hypertension,
and liver transplantation. Prognosis is poor for hepatorenal syndrome. Renal function
is difficult to assess in end-stage liver disease because reduced muscle mass and
hepatic synthesis of creatine reduce serum creatinine inappropriately. Creatinine
clearance overestimates glomerular filtration rate, and inulin or 51Cr EDTA clearance
remain the gold standard.
Endocrine dysfunction is common in end-stage liver disease, due to inappropriate

activation of some systems (RAA system, vasopressin release), abnormal responses
(insulin resistance), over-secretion of growth hormone and glucagon, and abnormal
metabolism (steroid hormones). This leads to clinical syndromes of insulin resistance
and impaired glucose metabolism, a shift towards lipid utilization as a preferred energy
substrate, and depletion of glycogen stores. Hypoglycaemia in cirrhosis is uncommon
and a poor sign. The abnormal metabolism of sex hormones leads to feminization,
gonadal atrophy and gynaecomastia in men, and amenorrhoea in women.
Gastrointestinal system: advanced cirrhosis is characterized by portal hypertension

and portosystemic shunting, typically resulting in oesophageal varices, which can
cause massive gastro-intestinal haemorrhage. Varices may also be present on
the anterior abdominal wall and may cause severe blood loss during laparotomy.
Ascites develops due to a combination of portal hypertension, poor synthetic function
with hypoalbuminaemia and the pathophysiological activation of the RAA system.
The volume of ascites may be such that intra-abdominal pressure exceeds renal
perfusion pressure causing deterioration in renal function. For this reason, draining
ascites (especially if intra-abdominal pressure is > 25 mm Hg) is regaining popularity,
especially in those resistant to diuretic treatment. Nutritional abnormalities are common
in these patients and associated with peripheral and hepatic insulin resistance and
a poor outcome. Glucose utilization is impaired and lipid utilization is increased in
fasting and fed conditions. Hypermetabolism seems to predate the malnutrition seen
with increasing severity of cirrhosis and in contrast to earlier regimens a high-protein,
high-calorie intake, taken little and often, seems to prevent the catabolic state without
increasing the incidence of hepatic encephalopathy.
Haematological system: the liver has a central role in the control of coagulation.
Impairment of haemostasis is common in liver disease, bleeding is a leading cause
of death in cirrhotic patients. The liver is the main site of synthesis of all coagulation
factors except von Willebrands factor. It is also the key site for clearance of activated
clotting factors and plasminogen activators; the coagulation state depends on the
balance of hepatic synthesis of clotting factors and clearance of activated clotting
factors, their inhibitors and fibrinolytic proteins. Failure of bile salt secretion results in
poor absorption of vitamin K and low levels of the vitamin K-dependent clotting factors
(II, VII, IX, X), but inactive prothrombin complexes are present in liver disease without
vitamin K deficiency suggesting an acquired defect in activation.
Many platelet abnormalities occur in patients with liver disease.
Thrombocytopenia may result from hypersplenism secondary to portal hypertension

in cirrhotic patients, bone marrow suppression, abnormalities in platelet metabolism or
autoimmune causes. In alcohol-related liver disease thrombocytopenia may result from
folic acid deficiency. Qualitative platelet dysfunction is also seen in liver disease, with
impaired aggregation and clot retraction.
CNS: hepatic encephalopathy is the decrease in conscious level seen in association

with severe liver disease. In the early stages a reversal of the sleepwake cycle is seen
with patients sleeping during the day. As encephalopathy advances, subtle changes in
intellectual function occur with confusion, memory loss and irritability being common.
Finally, changes in conscious level are observed. Work in liver failure shows intracranial
hypertension, brain oedema and herniation with altered perfusion. Encephalopathy can
be precipitated by a variety of factors including hypovolaemia, sepsis, gastrointestinal
haemorrhage and hypoglycaemia. The final common pathway in the aetiology of brain
oedema may be increased cerebral blood flow with consequent increased ammonia
uptake across the bloodbrain barrier. Hyperventilation and consequent alkalosis
increase the ammonia available to cross the bloodbrain barrier.
Immune system: patients with advanced cirrhosis are relatively immunocompromised.

Low complement levels, loss of effective white cell opsonization and dysfunctional
macrophage phagocytosis contribute to anergy, leading to high levels of bacteraemia.
Spontaneous bacterial peritonitis is common in end-stage liver disease. Increasingly,
Gram-positive bacteria, which may be multiresistant, are being cultured in these
patients. u

Laboratory Tests in Hepatic
and Renal Failure
Simon Cottam
Elizabeth Sizer
Simon Cottam is Consultant Anaesthetist at King's College Hospital, London. His main
interests include intensive care and hepatobiliary anaesthesia.
Elizabeth Sizer is Specialist Registrar in Anaesthesia at King's College Hospital,

London, currently working in the Liver Unit. Her interests include liver transplantation,
liver intensive care and anaesthesia for hepatobiliary surgery.
Laboratory tests of liver function are of little use unless combined with a thorough
history and examination. In this situation they may be used to pursue a diagnosis,
to assess degrees of acute or chronic liver failure, or as trends to map disease
progression or response to treatment. With the advent of automated serum multi-
channel analysis the most common indication for liver function testing is as a
screening test (often mistakenly performed to exclude a problem). Normal values for
tests are defined around 95% confidence intervals, therefore multiple tests commonly
produce false-positive results. True abnormal results usually represent liver dysfunction.
The most common profiles include bilirubin, aminotransferases, alkaline phosphatase
and -glutamyl transpeptidase (GGT).
True liver function tests

True liver function tests include tests of synthetic function such as estimation of serum
albumin, clotting factors or dynamic tests that estimate the livers capacity to metabolize
drugs or endogenous substances.
Albumin is the most abundant plasma protein and is largely synthesized by the liver. In
stable chronic liver disease, monitoring serum albumin is a valuable indicator of hepatic
synthetic function and as such is incorporated in many prognostic scoring systems
(e.g. the ChildPugh (see page 42) and Mayo End-stage Liver Disease (MELD) score).
Albumin has a long half-life of 20 days; this, combined with the possibility of regulation
of albumin synthesis in liver disease, can make interpretation of serum albumin levels
difficult in an acute situation. Peri-operative albumin levels may change as a result of
supplementation, changes in vascular permeability and in volume of distribution. In
these situations, measurement of albumin is an unreliable measure of liver function.
Prothrombin time (PT): in the acute situation, assessment of the coagulation factors
of the extrinsic cascade (with their much shorter half-lives) are a more reliable monitor
of liver failure than albumin. Failure of a prolonged PT to correct with parenteral vitamin
K supplementation defines hepatocellular failure, and is one of the most reliable
prognostic indicators of survival in acute liver failure. Inter-laboratory variations can
occur with different thromboplastin reagents. This may also occur when the PT is
expressed as the international normalized ratio (INR). Therefore, trends in prothrombin
time measured in a single laboratory are more useful than isolated values.
Blood lactate concentration reflects the balance between production and elimination.
Under normal conditions, the liver removes 4060% of lactate. Hypoperfusion, hypoxia
and severe ischaemic damage convert the liver from a lactate-consuming to a lactate-
producing system. In acute liver failure, hyperlactacidaemia may be used as a marker
of hepatic injury and the accompanying multiple organ failure. Assuming adequate
oxygen delivery, blood lactate levels have been shown to correlate with survival in
paracetamol-induced liver failure.
Dynamic tests of liver function

Dynamic tests measure the ability of the liver to clear or metab-olize an infused
substance.
Formation of monoethyleneglycine (MEGX): this lidocaine (lignocaine) metabolite

can be measured 1530 minutes after injection of lidocaine (lignocaine), 1 mg/
kg. Theoretically, it can be used to quantify the hepatic cytochrome P450 family
metabolism. However, lidocaine (lignocaine) is a flow-limited rather than capacity-
limited drug. Although MEGX measurements have been shown to correlate with
survival in chronic liver disease, they probably reveal more about liver blood flow than
functional capacity. Inevitably there is a delay while assay results are obtained.
Indocyanine green (ICG) clearance: the elimination of injected ICG, 0.5 mg/kg,
has been used to assess liver function. Interest in this method was fuelled by the
introduction of a bedside non-invasive monitor of ICG clearance. ICG has a high
hepatic extraction ratio and measurements reflect changes in liver blood flow. Reports
suggest it is useful for assessing donor livers for transplantation and following liver
resection.
Conventional tests of liver dysfunction

Bilirubin is the by-product of haem metabolism. Unconjugated bilirubin is water
insoluble and transported bound to serum albumin. Hepatic conjugation produces a
water-soluble compound, normally excreted in the bile. Total bilirubin levels therefore
represent the balance between production metabolism and excretion. Excessive
production may result from disease processes resulting in increased red cell turnover
leading to unconjugated hyperbilirubinaemia. Conjugated hyperbilirubinaemia results
from leakage of bilirubin into the blood directly from the hepatocytes or distal to the
liver in the case of biliary obstruction. Conjugated bilirubin released into the blood
stream tends to be excreted and can be measured in the urine, however, because
some of the conjugated bilirubin can covalently bind to serum albumin, bilirubin is not
always detected in the urine. The presence of bilirubin in the urine (as tested by a
Diazo impregnated test strip) is sensitive and may detect liver dysfunction before overt
jaundice is detected.
Aminotransferases: aspartate aminotransferase (AST) and alanine aminotransferase

(ALT) are released into the blood stream as a result of cell damage or necrosis. AST
is a sensitive but nonspecific marker of hepatocellular damage. AST can be released
from a number of damaged organs including liver, heart muscle, kidney, pancreas and
red blood cells. ALT is slightly more specific for liver damage with less extrahepatic
production, but may be elevated in conditions such as myositis. High (> 1000 IU/litre)
levels of AST usually represent hepatitis of viral, drug or ischaemic origin. Intermediate
levels (200400 IU/litre) may be seen in acute alcoholic hepatitis with more severe
clinical dysfunction. Absolute levels of transaminases do not correlate with outcome.
Glutathione-S-transferase (GST): one problem with AST and ALT as measures of

hepatocellular damage and necrosis is that these enzymes are not uniformly distributed
throughout the liver, being predominantly concentrated in periportal hepatocytes.
Centrilobular hepatocytes are most prone to hypoxia and are relatively deficient in AST
and ALT, this may explain some of the difficulties when correlating absolute values
of transaminases with outcome. GST is more evenly distributed throughout the liver.
In addition, its relatively small molecular weight encourages rapid release following
hepatocellular damage. A short half-life of 90 minutes means that acute changes can
be tracked rapidly but that peak effects may be missed, depending on the sampling
time after injury. GST is increasingly used as a sensitive marker for changes in
hepatocellular function following surgery and anaesthesia.
Alkaline phosphatase (AP): this family of enzymes is located in liver, bone, placenta
and intestine. In healthy individuals, circulating AP is derived from bone or liver. In
pregnancy, AP is often twice the upper range of normal. Elevations also occur in
peri-pubertal children. The wide distribution of the enzyme can cause confusion in
the assessment of liver function, and extrahepatic elevation may occur as a result of
hyperthyroidism, cardiac failure, hypernephroma and Pagets bone disease. In the liver,
AP is located in the microvilli of the biliary canaliculi and on the sinusoidal surface of the
hepatocyte. Classically, AP levels in liver disease are elevated when there is intra- or
extrahepatic obstruction to biliary drainage or due to space-occupying lesions such as
tumours. The raised levels in the blood seem to be due to increased synthesis in the
canalicular membrane rather than failure of excretion. The diversity of AP families makes
isoenzyme determination desirable, but this assay is not widely available and other
markers of biliary obstruction, such as GGT, are often monitored.
GGT is a membrane-bound glycoprotein found in cells with a high secretory or

absorptive activity (e.g. liver, kidney, pancreas intestine, prostate). 90% of patients
with hepatobiliary disease have raised GGT, but specificity is low. Its main value is in
combination with AP to convey additional liver specificity. Raised levels of GGT have
been associated with obesity, alcohol use and raised cholesterol levels. In non-drinking,
obese individuals the most common cause of raised GGT is a fatty liver.
Tests of renal failure

In perioperative care, laboratory tests are commonly requested to aid in the diagnosis
and management of acute renal failure. This brief review concentrates on tests
of function rather than those requested to confirm or refute a specific diagnosis.
Classically, renal impairment (Figure 1) is classified as:
pre-renal (poor perfusion), often correctable with volume resuscitation
renal (intrinsic renal disease)
post-renal (obstruction).
Urinary measurements in pre-renal and renal failure
Indices Pre-renal Renal

Urinary sodium < 20 (low) > 40 (high)
(mmol/litre)
Urine osmolarity > 500 < 350 (low)

(mosmol/litre) (high serum +100)
Urine/plasma urea > 8 (high) < 3 (low)
Specific gravity High Fixed

1.020 1.0101.020
1
Post-renal failure is common and is often excluded by ultrasound. Clinical acumen

is vital for the detection of hypovolaemia and low cardiac output states. Laboratory
examination of the urine can sometimes be useful in the differentiation of pre-renal and
true renal failure.
Measuring urinary biochemical indices has limitations because typical values are
seldom present and concomitant diuretic therapy often confuses estimates of urinary
sodium in pre-renal failure. Hepatorenal failure mimics pre-renal failure with extremely
low urinary sodium levels, but fails to respond to volume loading.
Urine analysis is an important, but often neglected, investigation. A normal urine

analysis in the presence of impending acute failure supports the presence of pre-
renal or obstructive patterns. Abnormal results may help to discriminate tubular and
glomerular problems. Red blood cells suggest the presence of glomerular or vascular
inflammatory disease. Urine protein excretion can occur as a result of glomerular
damage (increased loss) or tubular failure of absorption.
Blood urea is often measured automatically when concentrations of sodium and

potassium are requested. There is a common misconception that plasma urea usefully
relates to glomerular filtration rate (GFR), however it is altered by diet, fever, gastro-
intestinal haemorrhage, renal blood flow, urine flow rates and in liver disease. Some
laboratories no longer offer it as a routine assay. It still has a place in assessing the
effect of compliance or alterations to diet in patients with stable chronic renal failure or
in assessing the need for, or effects of, renal replacement therapy.
GFR, classically measured by inulin clearance, would be the ideal measurement

to detect alterations in renal function, but in early renal disease, GFR is normal or
increased. Inulin clearance is seldom measured in clinical practice and the serum
creatinine and the creatinine clearance are used as estimates of GFR.
Serum creatinine is the most commonly used indirect estimate of GFR. The
exponential rise in serum creatinine with falling GFR limits its use in assessing patients
with low clearances. With low concentrations of creatinine, cross-reaction in the
assay may overestimate the creatinine concentration and consequently underestimate
creatinine clearance. Also, creatinine secretion by the tubules occurs and creatinine
production is determined by muscle mass. Wasted patients have low levels of
creatinine, which underestimate deterioration in renal function. Serum creatinine is also
affected by age as muscle mass falls.
Attempts to correct for age and muscle mass have resulted in formulae that attempt to
compensate for these changes.
Creatinine clearance =
1.22 x (140age) x Weight
Serum creatinine (mol/litre)
Creatinine clearance can be calculated by combining a timed urine collection with

estimations of plasma and urine creatinine concentration.
Creatinine clearance =
Urine concentration (mol/litre) x Urine volume (ml/minute)
Serum concentration (mol/litre)

Measuring creatinine clearance removes some of the problems associated with the use
of isolated creatinine values, but it necessitates a 24-hour urine collection and assumes
that serum creatinine is constant over 24 hours.
Measuring GFR using radioactive indicators: labelled chromium ethylenediamine

tetraacetic acid (51Cr EDTA) is the most widely used indicator. Clearance of this agent is
almost identical to inulin even down to a GFR of 315 ml/minute. Following a single
injection of 2 MBq 51Cr EDTA, clearance can be calculated by serial blood sampling
over 5 hours. u
FURTHER READING
Bircher J, Benhamou J-P, McIntyre N, Rizzetto M, Rodes J, eds. Oxford Textbook of
Clinical Hepatology. Oxford: Oxford University Press, 1999.
Davison A M, Cameron J S, Grunfield J-P, Kerr D N S, Ritz E, Winearls C G, eds.

Oxford Textbook of Clinical Nephrology. Oxford: Oxford University Press, 1998.

Clinical measurement
Anaesthesia
on CD-ROM
Cardiac Output Measurement
Robin Berry
Jeremy A Langton
Robin Berry is Specialist Registrar in Anaesthetics with the Royal Air Force, currently
based at Derriford Hospital, Plymouth. He qualified from Nottingham University Medical
School. He is interested in the transport of the critically ill as part of his military role.
Jeremy A Langton is Consultant Anaesthetist at Derriford Hospital, Plymouth. He

qualified from Guy's Hospital, London and trained in anaesthesia in London and
Leicester. His research interests include airway reflexes and anaesthesia.
The cardiac output is the volume of blood in litres pumped by the left ventricle per
minute and is the product of heart rate and stroke volume. It changes with heart rate
as well as with preload, afterload and contractility (the three determinants of stroke
volume).
Cardiac output is measured primarily because it is thought to reflect the adequacy of
global blood flow. However, poor tissue perfusion and cellular hypoxia can exist despite
normal blood oxygen content and cardiac output. Therefore, the clinician must be
wary of relying on absolute values and should concentrate on trends and their
physiological effect on the patient. Numerical data should be evaluated frequently
in the context of clinical and laboratory findings rather than relying on accepted
normal values. The values obtained should also be considered in the context of the
patients age, sex, weight, pre-morbid condition and current disease process. Cardiac
output measurements are used to determine myocardial performance, oxygen delivery,
derived variables (e.g. systemic vascular resistance), to calculate shunt, and as a
measure of therapeutic intervention.
In laboratory animals, cannulation of the aorta and pulmonary artery allows direct
measurement of output with flowmeters, but such invasive practices are unacceptable
in human medicine. The essence of clinical cardiac output measurement is to quantify
end-organ perfusion and therefore clinical examination should be the cornerstone of
good practice. Level of consciousness, unprovoked urine output and examination of
the skin for colour, temperature and capillary refill are good indicators of circulating
volume and the adequacy of cardiac output. Blood pressure measurement provides a
poor guide to pump function, and may be maintained despite a failing myocardium by
increased systemic vascular resistance. In critical illness or its recovery phase, simple
assessment of organ function may be difficult to interpret owing to the disease process,
associated medical interventions and the combined effects on normal physiology.
The ideal method of measuring cardiac output would be non-invasive, continuous,
accurate over the range of cardiovascular function encountered in intensive care,
operator independent and labour free. In the absence of this ideal method, the
gold standard for cardiac output measurement in intensive care remains the indirect
thermodilution technique using the highly invasive, balloon-tipped, flow-directed,
pulmonary artery catheter. Earlier methods employed the Fick principle and dye dilution,
based on the theory of volume displacement.
The Fick method
The Fick principle states that the total uptake or release of a substance by an organ is
the product of the blood flow through that organ and the arteriovenous concentration
difference of the substance in question. Applying the Fick principle to cardiac output
measurement, the pulmonary blood flow over 1 minute may be determined by
measuring the arteriovenous concentration difference of oxygen across the lungs and
the rate of oxygen uptake. In the absence of intracardiac or intrapulmonary shunts, the
pulmonary blood flow is equal to systemic blood flow and thus cardiac output.
The Fick principle will not give a dynamic measure of output and the procedure is
time-consuming, with blood sampling and the need for steady-state haemodynamic,
respiratory and metabolic conditions over the period of measurement. For these
reasons, and the development of the pulmonary artery catheter, the Fick method has
remained largely a laboratory tool, despite its accuracy, especially in low-output states.
Indicator dilution methods
An indicator mixed into a flowing volume of blood can be used to determine the position
of that volume in time and space, provided that the following conditions are met:
the indicator remains in the system between the points of injection and
measurement
complete mixing of the indicator and the blood occurs
blood flow is constant during the measurement phase.
Dye dilution
Classically, the non-toxic dye, indocyanine green is injected into the pulmonary artery
and its transit time through the systemic circulation monitored by aspirating peripheral
arterial blood through a densitometer. A washout curve is then plotted on semi-
logarithmic paper to describe the changing concentration of dye from injection through
to steady state. The cardiac output can be derived from this curve, by dividing
the dose of dye injected by the area under the washout curve. Recirculation of
the dye distorts the timeconcentration curve and therefore the downslope to point
zero has to be extrapolated from the primary curve and an exponential decay
assumed (Figure 1). Furthermore, steady-state conditions are assumed over the
40-second measurement period. Errors may occur in the mixing and administration of
the dye, which is photosensitive and unstable with time. The technique is invalidated
by intracardiac shunts owing to inadequate mixing and severe valve regurgitation and
shock, because the first-pass curve is so prolonged that recirculation occurs before the
downstroke is fully inscribed. For these reasons, as well as the elevation of the baseline
concentration with repeated injection and the need for referenced controls, this method
has been superseded by thermodilution.
Indicator dilution curve

1
Log concentration of dye
2
Area under
the curve
3
4
Transit time
Injection Time
1 Primary curve
2 Recirculation peak
3 Extrapolation of primary decay curve
4 Elevation of baseline secondary to circulation of dye
5 Appearance time
Source: Hinds CJ, Watson D. Intensive Care. Philadelphia:
WB Saunders, 1997.
Thermodilution
Heat can also be used as a detectable indicator in the blood and has the advantage
of rapid dissipation into the tissues and consequently no recirculation peak or elevation
of the indicator baseline. As a result, cardiac output measurements can be repeated at
frequent intervals and thermodilution is therefore the established method of measuring
cardiac output.
Using a pulmonary artery catheter, a 10 ml bolus of ice-cold saline is injected into
the right atrium and the ensuing temperature change recorded by a thermistor at the
catheter tip located in the pulmonary artery. A plot of temperature against time gives a
washout curve, from which cardiac output can be calculated using a modification of the
StewartHamilton conservation of heat equation:
Q = V x Di x Si[Tb Ti] x 60
dT x t x Db x Sb x 1000
where: V = volume of injectate; Di and Db = densities of injectate and patients blood; Si

and Sb = specific heats; Ti and Tb = temperatures; dT = mean temperature change; t
= duration of temperature change in seconds. To convert cardiac output to litres/minute
a scaling factor of 60/1000 is used.
In current practice, a microprocessor system measures the area under the curve and
calculates cardiac output. The manufacturers of the sensors add correction factors to
account for the mixture of cold indicator with warm residual fluid in the catheter injection
lumen and heat transfer from the catheter walls to the cold indicator.
Sources of error include any circumstances that affect the temperature versus time
graph. For example, intracardiac shunts and severe tricuspid and mitral regurgitation.
The presence of thrombus on the thermistor can delay cooling and rewarming, and
therefore overestimate the area under the curve.
Distal migration of the catheter can lead to disproportionate blood flow with
variability in the volume of cold bolus reaching the thermistor.
The volume, temperature and rate of delivery of the injectate are important variables.
For example, the cold saline bolus has been associated with bradycardias and
supraventricular tachyarrhythmias.
Alteration in ventricular performance owing to an arrhythmia also affects the thermal
dilution washout curve.
It is possible to lose the thermal indicator, especially in low cardiac output states
if the baseline temperature is variable, for example during large-volume transfusion
or rewarming following cardiopulmonary bypass. The temperature of pulmonary artery
blood changes with respiration, owing to the different contributions of blood from the
superior and inferior venae cavae at different stages of the respiratory cycle, which is
exacerbated by mechanical ventilation.
Modified pulmonary artery catheter: this apparatus was developed to address the
intermittent nature of the thermodilution method. A thermal filament placed in the right
atrium and ventricle gives 15 W pulses, which are recorded by a thermistor at the
catheter tip to generate washout curves and continuous cardiac output measurements.
Since bolus injections are not required, this system avoids what can be a considerable
volume load to the patient with the attendant risk of infection. Described as a continuous
output monitor, this apparatus has a lag time of about 10 minutes. It has the potential
to detect changes in myocardial function more rapidly than traditional thermodilution,
but it does not give beat-to-beat output data. Concerns about thermal damage to the
myocardium and red blood cells appear unfounded, but this technique suffers from
many of the limitations of the bolus method.
Future developments: although the pulmonary artery catheter is well established,

derangements in the normal physiological function of the heart and lungs make errors
in interpretation likely. Furthermore, it is an invasive tool and is associated with risks
regarding initial central venous access, floating the catheter and its residence in
the right heart and pulmonary circulation. As a result of these problems, there is a
reluctance to initiate early invasive monitoring, which may delay appropriate therapeutic
intervention. For these reasons, and the desire to obtain continuous cardiac output
data, a number of non-invasive or minimally invasive monitors have been developed,
though they have not received universal acceptance.
Oesophageal probes have been developed to determine cardiac output from
measurements of blood velocity. Doppler devices derive flow in the descending aorta
from integrals of the systolic velocity versus time curve, the aortic cross-sectional
area and the heart rate. Transoesophageal echocardiography generates outputs from
flow through the mitral valve, multiplied by the calculated valve area, a computation
constant and the heart rate. These devices have the advantage of giving anatomical
information about ventricular function, but they require constant repositioning. There are
also questions about their safety, related to bleeding and unrecognized oesophageal
rupture. The greatest restriction to their use, however, is that the patient has to be
intubated, ventilated and sedated to tolerate the probe which offsets the benefits of
avoiding invasive vascular monitoring.
Recently, transpulmonary thermodilution with pulse contour analysis has been
advocated as a minimally invasive means of continuous (30 seconds) cardiac output
measurement. Left ventricular stroke volume is computed by measuring the area under
the systolic part of the arterial pressure waveform (Figure 2) and dividing by aortic
impedance. When multiplied by the heart rate, this gives the cardiac output. Initial
studies suggested that cannulation of a central artery was necessary for accurate
measurement, however, the radial artery has been found to be satisfactory. Before
using pulse contour analysis, cardiac output has to be measured by an alternative
method to derive the aortic impedance used in the pulse contour equation. Traditionally,
thermodilution using a pulmonary artery catheter would have been used, but now a
less invasive transcardiopulmonary method is applied. A cold fluid bolus (0.2 ml/kg) is
injected into the right atrium via a central venous line and a temperature washout curve
recorded by a thermistor located in a peripheral artery. When the aortic impedance is
known, further cardiac outputs are recorded continuously by pulse contour analysis,
with calibration by thermodilution as required. Under steady-state conditions, this can
be as infrequent as 8 hourly, but when changes in systemic vascular resistance are
anticipated, calibration should be more frequent.
The technique uses central venous and peripheral arterial lines, and its advocates
suggest that it is no more invasive than standard intensive care monitoring. It
is not affected by the respiratory cycle, because the washout curve is at least
20 seconds long, but it is subject to thermal baseline drifts, with inadequate volumes
of injectate or too warm a solution giving inaccurate dilution curves. Errors can also
be generated by air in the manometer lines, giving dampened arterial waveforms and
therefore inaccurate pulse contour analysis.
Cardiac output
Arterial pressure
Time
Cardiac output is calculated continuously by integrating the area below
the systolic portion of the arterial pressure curve
FURTHER READING
Bartlett R H. Alice in Intensiveland. Chest 1995; 108: 112939.
Hinds C J, Watson D. Intensive Care. Philadelphia: WB Saunders, 1997.

Measurement of Pressure:
Direct and Indirect Methods of
Measuring Blood Pressure and
Pulmonary Artery Pressure
Balraj L Appadu
Mahesh Prabhu
Balraj L Appadu is Consultant Anaesthetist at the Peterborough Hospitals Trust,

UK. He qualified from Saint Etienne University, France where he trained in internal
medicine and haematology. He trained in anaesthetics in Ashford, London, Southend
and Leicester. His research interests include basic sciences, receptor pharmacology
and intensive care.
Mahesh Prabhu is Specialist Registrar at Peterborough Hospitals Trust, UK. He

qualified from Bombay University, India, and trained at Bedford and Cambridge, UK. His
interests include basic sciences, cardiothoracic anaesthesia and day surgery.
Pressure is defined as force per unit area. In clinical practice, the units commonly used
to measure pressure are mm Hg and kPa. The SI unit of pressure is Newton per square
metre (N/m2) or Pascal (Pa).
Instruments used for measuring pressure
Liquid manometers
There are two types of liquid manometers (Figure 1).
In the closed mercury manometer (e.g. barometer) there is a virtual vacuum
(Torricellian vacuum) above the mercury, such that the height of the mercury column
indicates absolute pressure.
In the open mercury manometer (e.g. sphygmomanometer), the tube is opened at
both ends and thus the height of the fluid column indicates the amount by which the
pressure exceeds atmospheric or gauge pressure. The force exerted by a column of
fluid is equal to:
height x density x acceleration due to gravity.
Thus, pressure is independent of the width of the fluid column and of the shape of
the liquid column. In single tube manometers, pressure is defined by the height of the
fluid column as measured from the meniscus in the reservoir. One source of error is
that the level of the meniscus in the reservoir falls as fluid is forced up the tube so that
a fixed graduated scale does not accurately reflect the true difference between the
two menisci. This error can be minimized either by making the cross-sectional area of
the reservoir large compared with the cross-sectional area of the tube or shortening
the scale length to allow for the fall in reservoir level. Another potential source of error
is caused by the surface tension of the liquid. Most liquids have a meniscus that is
concave upwards, and surface tension causes the position of the meniscus to appear
to be higher than it is. However, in mercury manometers, the meniscus is concave
downwards and this causes a negative error in the reading.
Liquid manometers
Mercury manometer giving measurement for
absolute pressure
Torricellian vacuum
P
h
P P
Mercury manometer giving gauge pressure

A A
P
P
h
P, applied pressure; A, atmospheric pressure; h, measured pressure 1
Mechanical pressure gauges

Aneroid gauge is used to sense and measure small pressures (Figure 2). Expansion
of a small metal bellows is detected by a lever mechanism, which amplifies the
movement and drives a pointer on a scale.
Bourdon gauge is used for measuring high pressure. It consists of a coiled tube,
flattened in cross-section. One end of the coil is anchored to the case and connected
to the pressure source, while the other end is closed and attached to a mechanism
that drives a pointer across a dial. Application of pressure causes the cross-section
to become more circular, thus causing the coiled tube to straighten and, with one end
fixed, the pointer moves across the dial.
HIGH
Aneroid pressure
gauge RE
SU
ES
PR
LOW
P, pressure P 2
Measuring blood pressure
Indirect measurement of arterial pressure

Most indirect methods of measuring blood pressure are based on the occlusion of a
major artery by a cuff. In clinical practice, systolic and diastolic end points are detected
by auscultation of the Korotkoff sounds. The systolic point is marked by the sudden
appearance of tapping sounds (phase I) synchronous with the heart beat. The sounds
then become quieter (phase II) and as the cuff pressure decreases further the sounds
become louder with a tapping quality (phase III), then the sounds become muffled
(phase IV) and disappear (phase V). Errors may occur related to the site of the
measurement, because arterial blood pressure is not identical in every artery. Pulse
pressure is greater in peripheral arteries because the velocity of the pulse wave
increases as it travels from the heart to the artery. Blood pressure may also differ in the
limbs. Indirect methods are intermittent, with systolic and diastolic readings reflecting
conditions in the artery at two instants at which they are measured. The end point
of diastolic blood pressure measurement is also the subject of controversy; there is a
difference of 510 mm Hg between Korotkoff phases IV and V. This is not important
in clinical practice but may affect epidemiological studies. A short or narrow cuff may
cause readings to be too high, while a wide cuff gives a low reading. The cuff should
cover about two-thirds of the length of the upper arm, or its width should be 20%
greater than the diameter of the arm. Zero and calibration errors in aneroid manometers
also occur.
Oscillometric measurement of blood pressure depends on the principle that blood

pressure can be estimated by analysing the pressure oscillations in the cuff as it is
slowly deflated. Most instruments use a single pressure cuff applied to the arm, which
is inflated to about 30 mm Hg above systolic blood pressure. During slow deflation,
each pulse wave leads to a pressure transient in the cuff, which is transmitted to the
connecting tube, where a transducer detects it. Above systolic blood pressure, the
transients are small and, at the systolic point, they quickly increase in magnitude. As
the cuff pressure decreases, the transients reach a peak amplitude and then decrease.
The mean arterial pressure is the lowest cuff pressure where the peak amplitude is
maintained and at diastolic blood pressure is the point where the transients abruptly
decrease in amplitude.
This oscillometric principle is used in the Dinamap (a non-invasive, automatic
method of measuring blood pressure) where at each pressure plateau point, successive
pulses are compared and accepted only if their amplitude is similar. With this device,
systolic blood pressure shows good correlation with direct pressure measurement with
a bias towards overestimation at low blood pressure and underestimation at high blood
pressures. Newer devices operate in a similar fashion, but cuff deflation is continuous,
rather than in steps, leading to shorter measurement time. However, all these devices
rely heavily on a regular cardiac cycle with no great difference between successive pulses.
Continuous non-invasive blood pressure measurement is based on the Penaz

technique, which makes use of the principle that the force exerted by a body may
be measured by determining the counterforce needed to stop the original force from
causing physical disruption. This principle works only if the counterforce can be
measured accurately and the detection does not need to be linear because it should be
capable of detecting the null condition only.
A small cuff is placed round a finger and can be inflated or deflated at high speed.
Inside the cuff is a light-emitting diode, which transilluminates the finger, and on the
other side is a photodiode that detects light intensity after it has passed through the
finger (using the same principle as a pulse oximeter). The detected light intensity is
a crude measure of the blood volume in the finger, but is a precise indicator of any
change in volume. The system inflates the cuff rapidly to above systolic blood pressure
and then deflates. As soon as the optical detector senses the pulse wave, the pressure
in the cuff is increased such that flow is decreased to maintain a constant volume
of blood in the finger, thus maintaining a constant signal. The pressure waveform
applied to the finger by the cuff closely mirrors the pressure waveform within the
arteries. This device not only measures systolic and diastolic blood pressure but also
reproduces the actual arterial waveform. These devices are highly accurate in the
normal or vasodilated finger but less effective in patients with poor peripheral perfusion
or in hypotensive patients. They show marked variability between patients, and small
differences in the positioning and tightness of the cuff produce significant differences in
recorded blood pressures.
Direct methods of monitoring blood pressure

Continuous monitoring of arterial blood pressure using intra-arterial cannulation,
pressure transduction and display is particularly useful during cardiovascular
instability, massive fluid shifts, drug-induced manipulation of blood pressure and
when non-invasive blood pressure measurement is inaccurate (e.g. with obesity,
cardiopulmonary bypass, arrhythmias). Intra-arterial cannulation also allows repeated
sampling of arterial blood for blood gas analysis.
The ability to provide a continuous, accurate, beat-to-beat reproduction of the
arterial waveform depends on a structured pressure transducer system. The lumen
of the vessel is connected to the pressure transducer by a fluid-filled catheter. The
components of the system include a short, parallel-sided, Teflon or polyurethane
cannula inserted into one of the peripheral arteries; a catheter (a short length of
narrow-bore, stiff, non-compliant tubing containing saline or heparinized saline); a
flush system to prevent occlusion of the cannula with clots by flushing with saline at
the rate of 14 ml/hour; and a pressure transducer. A transducer is any device that
converts energy from one form to another. Most physiological pressure measurements
are made by sensing the movement of a flexible diaphragm, which can be converted
into an electrical signal for processing and display. The most common method of
pressure transduction uses a strain gauge (an electrically conductive elastic material
that responds reversibly to deformation by a change in its electrical resistance). Silicon
strain gauges are more sensitive, but they are affected by temperature and are non-
linear. In a silicon strain gauge, a thin slice of silicon crystal is bonded on to the back
of the diaphragm. The movement of the diaphragm causes a change in the resistance
of the crystal, which can be converted into an output signal using a Wheatstone bridge
circuit. The movement of the diaphragm may also be sensed optically by reflecting
a beam of light off the silver back of the diaphragm on to a photoelectric cell, which
measures changes in electrical output. These transducers have a high-frequency
response and eliminate the risk of microshock.
The sensing element of the diaphragm may rely on capacitance. The diaphragm
forms one plate of the capacitor, the second plate being fixed. The capacitor is part of a
bridge circuit that is energized by an alternating current source. The impedance of the
transducer changes with the displacement of the plates of the capacitor. The output is
an alternating signal with an amplitude that varies with pressure. Inductance may also
be used, in which case the diaphragm moves a soft iron core between the primary and
secondary coils of a transformer. An alternating current energizes the primary coil. The
movement of the soft iron core modulates the voltage in the secondary coil. The voltage
is then rectified, filtered and amplified.
Pulmonary artery catheter pressure measurements
Pulmonary artery catheterization was introduced into clinical practice in the early 1970s
for the treatment of patients with cardiac diseases. While many physicians believe that
a pulmonary artery catheter is useful in guiding intravascular volume expansion and
pharmacological intervention in selected critically ill patients, its use is controversial.
The balloon-tipped, flow-directed, pulmonary artery catheter (SwanGanz) is
commonly used to measure pulmonary artery pressure and pulmonary capillary
wedge pressure (PCWP) or pulmonary artery occlusion pressure (PAOP) as a means
of assessing left ventricular filling pressures. It also allows the measurement of
cardiac output by a thermodilution technique and the measurement of mixed venous
oxyhaemoglobin saturation. A pulmonary artery catheter should be inserted by a
physician who knows about the complications, and is capable of interpreting and
using the data obtained (Figure 3). Figure 4 gives normal values for pulmonary artery
measurement.
PCWP or PAOP reflect mean left atrial pressure, which reflects left ventricular
end-diastolic filling, which reflects left ventricular preload. However, preload is the
stretch placed on the left ventricle by the end-diastolic volume. Assuming changes in
left ventricular end-diastolic pressure are predictive of changes in left ventricular end-
diastolic volume implies that the compliance of the left ventricle is constant, which
may not always be the case. Therefore PCWP is not a perfect reflection of left heart
preload, because changes in the myocardium may alter left ventricular compliance (i.e.
during myocardial ischaemia). Other factors that may adversely affect the accuracy of
PCWP measurements include significant mitral valve stenosis and pulmonary venous
resistance (as may be seen in patients with chronic obstructive airways disease).
The insertion path of a balloon-tipped, flow-directed,

pulmonary artery catheter with its waveform
characteristics Balloon deflated
Venous entry site Balloon inflated
Pulmonary artery
catheter Pulmonary capillary
wedge pressure
Pulmonary
Right atrial pressure artery
pressure
Right
ventricular
pressure
Typical 25
pressure Spontaneous
20
waveforms ventilation
end-expiration
Pressure
(mm Hg)
15
10
5 I E
RA = 5 RV = 22/4 PA = 21/10 PAOP = 9
0
Typical pressure waveforms of a pulmonary artery (PA) catheter as it travels
through the right atrium (RA), right ventricle (RV), and PA where it is wedged
to give the pulmonary capillary wedge pressure (PCWP) or pulmonary
artery occlusion pressure (PAOP). I, inspiration; E, expiration. The diastolic
PA pressure is usually significantly higher than RV diastolic pressure and the
PAOP is necessarily lower than PA diastolic pressure. To record otherwise
suggests that blood is flowing from the left heart to the right heart. It is
essential to read the PAOP at the end-expiration
Normal values of physiological measurement obtained using a pulmonary

artery catheter
Value Normal range

Right atrial pressure (RAP) 28 mm Hg
Right ventricular pressure Systolic: 2030 mm Hg; diastolic RAP less
or equal to RAP
Pulmonary artery pressure Systolic: 2030 mm Hg;
(PAP) diastolic: 515 mm Hg
Pulmonary capillary wedge 212 mm Hg; must be
pressure (pulmonary artery less than diastolic PAP
occlusion pressure)
Cardiac output 46 litres/minute (adult)
Mixed venous oxyhaemoglobin 6575%
saturation
FURTHER READING
French Society of Anaesthesia and Intensive Care. Arterial Catheterisation and Invasive
Measurements of Blood Pressure in Anaesthesia and Intensive Care in Adults. Ann Fr
Anesth Reanim 1995; 14(5): 44453.
Gardner I R. Direct Blood Pressure MeasurementDynamic Response Requirements.


Principles of Cardiac
Pacemakers and Defibrillators
Richard Griffiths
Richard Griffiths is Consultant Anaesthetist at Peterborough District Hospital. He

qualified from St Thomas Hospital and trained in anaesthesia in Nottingham, Leicester
and San Francisco, USA. His main interests are vascular anaesthesia and medical
education.
A patient presenting for surgery with a permanent cardiac pacemaker is a common

occurrence. The anaesthetist must be familiar with the type of pacemaker that has been
inserted and the potential malfunctions that can occur during surgery. Over 1 million
pacemakers have been implanted worldwide and in 1994 the estimated new implant
rate was 295/1 million population.
The pacemaker system
The system consists of a generator and one or two leads. The pulse generator has
three basic components, a power source, an electrical impulse former and a timer. The
early pacemakers had a fixed rate, but most new devices are demand units. The life
of the battery is 815 years, and the units are checked regularly for battery life and
performance. The circuitry and battery are contained in a titanium or stainless-steel
box attached to a block that contains the electrode connections through which the
pacemaker leads interface with the generator circuit.
The leads are non-thrombogenic, resistant to fracture and have to be insulated. The
wire is made of metal alloy covered by an insulating layer of silicone or polyurethane.
The pacing lead can be connected to the epicardial or endocardial surface of the heart.
The endocardial surface is used if the unit is inserted via a subcostal approach or if
inserted at the time of cardiac surgery. The epicardial surface is most commonly used
and is reached transvenously either through the internal jugular or subclavian veins.
The femoral and antecubital veins have also been used. Electrical impulses are formed
in the pulse generator and are transmitted to the myocardium by the lead, resulting in
mechanical contraction of the heart (Figure 1).
The distal end of the pacing lead is attached to the myo-cardium. The lead can
be anchored by passive or active fixation. Passive fixing is achieved using a system
of fins, which become entangled in the myocardium. Active fixation is used in patients
with dilated right ventricles and involves insertion of the lead into the myocardium with
a screw mechanism.
Cathodal stimulation is used in permanent pacing systems because the thresholds
are lower and the risk of induced arrhythmias is reduced. The electrode has a small
surface area to enhance current density and thus reduce the stimulation threshold.
Permanent pacing systems are able to cause myocardial contraction (capture) and can
sense the intrinsic electrical activity. The minimum stimulation needed to cause capture
is the pacing threshold. The voltage is set at twice the threshold level to ensure reliable
capture. The sensing threshold is the voltage at which the pacemaker is able to detect
the intrinsic signal in the chamber being sensed. The current returning via blood to the
anode completes the circuit. The anode is just proximal to the tip in a bipolar system
and is part of the pacemaker unit in a unipolar system.
1 Chest radiograph showing the leads and

generator unit of a dual-chamber system.
Types of pacemakers
In the 1960s, pacemakers were introduced to treat bradycardias, but now they can also
be used to treat tachycardias. Pacemakers can pace both cardiac chambers to improve
the physiological performance of the heart. They can also respond to the patients
activity and enable heart rate to alter with exercise. A common nomenclature has been
described by the NASPE (North American Society of Pacing and Electrophysiology)
and BPEG (British Pacing and Electrophysiology Group) known as the NBG pacemaker
code (Figure 2).
In fixed-rate modes, the pacemaker paces but does not sense the myocardium.
The NBG codes for these pacemakers are VOO, AOO or DOO. Fixed-rate pacing can
interfere with the intrinsic cardiac rhythm and may lead to other arrhythmias. Owing
to the risk of spontaneous cardiac activity, demand units have superseded fixed-rate
pacemakers.
Demand mode pacemakers sense the electrical activity of the atria (P wave) or
the ventricle (R wave). When spontaneous ventricular activity is sensed, the output
of the pacemaker is suppressed (R wave inhibited) or the unit is made to discharge
instantly (R wave triggered) so that the impulse will occur within the safe period of
the QRS complex.
Most pacemakers are on-demand units with a single pacing lead passing to the right
ventricle. In cases where there is sinus node disease and normal atrioventricular (AV)
conduction, the lead may be located in the right atrium to maintain the normal sequence
of atrial and ventricular depolarization.
The NASPE/BPEG Generic (NBG) Pacemaker Code
Letter position I II III IV V

Category Chamber paced Chamber sensed Response to Programmability Anti-tachycardia
sensing rate modulation functions
O = none O = none O = none O = none O = none

A = atrium A = atrium T = triggered P = simple programmable P = pacing
V = ventricle V = ventricle I = inhibited M = multiprogrammable S = shock
D = dual D = dual D = dual C = communicating D = dual
R = reverse R = rate modulation
The code is a five-letter system in which the first three letters describe the basic anti-bradycardia functions and the last
two letters describe programmability and anti-tachycardia functions. Clinically the first three letters are often used alone
if the last two letters have no function (e.g. fixed-rate modes are VOO, AOO or DOO)
Atrial only: the NBG codes for these pacemakers are AAI or AAT. The atrium is paced
and sensed, and is either inhibited or triggered. These modes are used for sinus node
dysfunction when the AV conduction system is normal.
Ventricular only: the NBG codes for these pacemakers are VVI or VVT. The ventricle
is sensed and paced, and either inhibited or triggered. However, there is no AV
synchrony and these modes are not used for patients who rely on coordinated atrial
contraction to improve end-diastolic filling of the left ventricle. A single ventricular lead
is shown in Figure 3.
Dual chamber pacemakers have pacing electrodes in both the right atrium and
ventricle (Figure 3). They are designated VAT, VDD, DVI or DDD. AV synchronous
pacing is provided with VAT and VDD modes, and the ventricle is paced after sensing
atrial activity. These modes are useful in patients with abnormal sinus node function
who have an intact AV conduction system. Atrial synchronous pacemakers enable the
heart rate to increasein response to an increase in sinus rate during exercise. These
modes also maintain the physiological relationship between the atria and ventricles.
Position of leads in single and dual pacemaker

systems
In the single chamber system, the lead is implanted in the ventricle only (V).
In the dual system, one lead is implanted in the ventricle (V) and the other in
the atrium (A)
3
Rate-responsive pacemakers can sense other stimuli as well as atrial and ventricular
activity and can increase the basic pacemaker rate. Dual-chamber pacemakers
are unable to increase heart rate during exercise in patients with severe sinus node
disease, because the node fails to respond to stimuli. There may also be a need to
increase heart rate and cardiac output during physiological stimuli other than exercise.
Various sensors are used to detect muscle activity, movement and an increase in
minute ventilation, temperature and mixed venous oxygen saturation. Rate-responsive
modes include VVIR, DVIR and DDDR. Most modern implanted pacemakers have
some programmable features.
Implantable cardioverter defibrillators are used in patients who have sustained

ventricular tachycardia (VT) and syncope caused by VT. They are described according
to a separate NASPE/BPEG code the defibrillator code (Figure 4). The typical code
is VVEV. Early models could deliver countershocks only, but now the pacemakers can
cardiovert episodes of VT with anti-tachycardia pacing.
The NASPE/BPEG Defibrillator Code
Letter position I II III IV
Category Shock chambe Anti-tachycardia pacing Tachycardia detection Anti-bradycardia

chamber pacing
O = none O = none E = electrogram A = atrium

A = atrium A = atrium H = haemodynamic V = ventricle
V = ventricle V = ventricle O = none D = dual
D = dual D = dual
4
Surgery for patients with a pacemaker
The two primary concerns during anaesthesia in patients with a pacemaker are whether
the unit will continue to function and the consequences of using diathermy.
Full preoperative assessment must be undertaken. Of particular note in the history is
the initial indication for pacemaker insertion and an assessment of the present function
of the unit. The type and mode of pacemaker can be obtained from the patients
pacemaker identity card. The date of the most recent check should be noted with
specific reference to the state of the battery. The ECG should be examined for evidence
of sensing, pacing and capture (Figure 5). If the intrinsic heart rate is greater than the
preset rate of the pacemaker, applying a magnet over the unit can check the correct
functioning of the unit. This converts the unit to an asynchronous mode and captured
beats should appear on the ECG. A chest radiograph should be taken to confirm the
position of the leads. The potassium level should be determined because hypokalaemia
increases the resting membrane potential and may lead to loss of capture. Acute
hyperkalaemia decreases the resting membrane potential and thus increases
ventricular irritability.
ECGs of patients with pacemakers
Patient with an AAI pacemaker
AP AP AP AS AS AS AS
Patient with a VVI pacemaker
VP VP VS VP VP VS
AP, atrium paced; AS atrium sensed; VP, ventricle paced;

VS, ventricle sensed
The anaesthetic technique should avoid suxamethonium because muscle fasciculations
can inhibit demand pacemakers (myopotential inhibition). The pacemaker senses
skeletal muscle electrical activity, which can be caused by mechanical ventilation and
myoclonic movements from induction agents (e.g. etomidate). Normothermia should
be maintained because shivering can also change the performance of demand pace-
makers. Evidence of mechanical, as well as electrical, heart function is provided
by looking at the pulsemeter that accompanies a pulse oximeter. Mechanical and
electrical function should be checked after any patient movement and also at the start
of mechanical ventilation. An external converter magnet should be available in the
operating room. This should not be placed over the pacemaker routinely because it
may adversely affect a programmable unit; however, it may prove invaluable if the unit
has to be converted to an asynchronous mode because of interference from diathermy.
Atropine and isoprenaline should also be readily available in the event of pacemaker
failure. Ventricular fibrillation is managed conventionally in pacemaker patients, but the
paddles must not be placed directly over the pulse generator. The stimulation threshold
may alter following defibrillation, therefore equipment must be available for temporary
pacing or for non-invasive transcutaneous pacing.
Interference from diathermy

Current pacemakers are well shielded and are less likely to be affected by
electrodiathermy than older types. Monopolar diathermy involves the passage of radio-
frequency alternating current between an active electrode and a return electrode (the
ground pad). The electrical artefact from the diathermy may be sensed as an intrinsic
myocardial potential resulting in inhibition of the pacemaker. In some units, if the
electrical interference continues, the unit can revert to a fixed rate until the interference
ceases. To ensure that interference is minimized, the ground pad of the diathermy
unit should be positioned close to the site of surgery and as far away as possible
from the pacemaker unit and leads. Diathermy must also be used in short bursts.
Current flow between the two elements of the diathermy unit should not cross the
pacemaker system. Bipolar diathermy should be considered if interference continues
with monopolar diathermy.
Pacemakers and unusual environments

MRI is contraindicated in pacemaker patients. If an MRI scan is absolutely necessary
the pacemaker can be removed before the scan and reimplanted afterwards.
Lithotripsy is a safe procedure in patients with permanent pacemakers. The pulses
from the lithotripsy should be timed with the electrical activity of the heart. Care must
be taken when the pacemaker has been placed in the upper abdomen, because direct
impulses should not be sent through the unit.
Other methods of cardiac pacing

Non-invasive transcutaneous pacing is useful following cardiac arrest and can buy
time before a transvenous system can be inserted. Electrode patches are placed on the
anterior and posterior aspects of the chest. The anterior patch should be the cathode
and be placed along the left costal margin. It is important to avoid placing the electrode
patches over a muscle mass, because it will be stimulated by the applied current. The
anode should be placed posteriorly, inferior to the left scapula. Pacing is done with the
lowest effective power output; this is usually 80 mA.
Temporary transvenous pacing: through central venous access, a temporary pacing

wire can be inserted and connected to an external pulse generator. These devices can
operate in either asynchronous (fixed rate) or in synchronous (demand rate) mode.
Defibrillators are used to deliver electrical energy to the myocardium, which

depolarizes a critical mass of the muscle to allow a stable heart rhythm to be restored.
In the defibrillator, direct current (DC) is stored and released in a controlled fashion.
DC is preferred to alternating current (AC) because it is more effective and causes
less damage to the myocardium. DC is also less likely than AC to cause arrhythmias.
The electrical charge is stored in a capacitor. The electrical energy delivered from the
defibrillator depends on the charge and the potential. When charged, the electrical
energy is discharged across the patients chest as a current pulse. The pulse is applied
via two paddles, which are placed on the sternum and the left mid-axillary line at the
5th to 6th rib space. In order to ensure that most of the applied charge depolarizes the
myocardium, the transthoracic impedance of the patient should be low. The impedance
can be reduced by applying firm pressure and by the use of conductive gel pads.
Defibrillators can also be used to correct atrial fibrillation. Less energy is applied and
the charge is synchronized so that it is delivered during the R wave of the cardiac cycle.
Internal defibrillators are also used when the chest is open during cardiac surgery. The
electrodes are applied directly to the heart and less energy is used.
FURTHER READING
Bernstein A D, Camm A J, Fletcher J D et al. The NASPE/BPEG Generic Pacemaker
Code for Antibradycardia and Adaptive-rate Pacing and Antitachycardia Devices.
Pacing Clin Electrophysiol 1987; 10: 7948.
Bernstein A D, Camm A J, Fletcher J D et al. North American Society of Pacing and
Electrophysiology Policy Statement: The NASPE/BREG Defibrillator Code. Pacing Clin
Electrophysiol 1993; 16: 177680.
Bourke M E. The Patient with a Pacemaker or Related Device. Can J Anaesth 1996;
43: R24R32.
Rozkovec A. Basic Principles of Permanent Cardiac Pacing. Br J Hosp Med 1996; 55:
317.
ACKNOWLEDGEMENT
The author would like to acknowledge the support of Medtronics for help with the
figures.

Principles of Pressure
Transducers, Resonance,
Damping and Frequency
Response
Mark R Stoker
Jeremy A Langton
Mark R Stoker is Specialist Registrar in Anaesthetics, Anglia Anaesthesia Training

Scheme, at Norfolk and Norwich Hospital, Norwich, UK. He qualified from Oxford
University and trained in anaesthetics in High Wycombe, Oxford, Cambridge and
Peterborough.
Jeremy A Langton is Consultant Anaesthetist at Derriford Hospital, Plymouth. He

qualified from Guys Hospital, London, and trained in anaesthesia in London and
Leicester. His research interests include airway reflexes and anaesthesia.
The types of pressure of most clinical importance to anaesthetists are those

within the blood vessels, such as the central veins, systemic arteries, intracardiac
chambers, pulmonary arteries and the pulmonary capillary wedge pressure. Pressures
of additional clinical significance are those generated within enclosed spaces such as
the skull (intracranial pressure) or limb compartments and CSF pressure.
All body pressures are composed of a static and a dynamic component.
The static component (hydrostatic pressure) is related to the weight of
fluid supported above the reference point and to any externally applied or
internally generated pressure. Internally generated pressure within the skull or limb
compartments is most commonly caused by tissue swelling within the confines of an
enclosed space.
The dynamic component of pressure is related to kinetic energy generated by the
interaction of contractile cardiac activity with the blood vessel walls, to which is added
changes in flow resulting from fluctuations in intrathoracic pressure with respiration.
These cause blood flow and rapidly travelling pressure waves within the circulatory
tree. Pressure waves within blood vessels are progressive and mechanical, in that they
carry energy associated with their oscillation through the bloodstream. The dynamic
component of intracranial and intracompartmental pressure waves is also associated
principally with the flow of blood through vessels and is transmitted throughout the
enclosed space.
Methods of direct pressure measurement
Accurate recording of in vivo pressure waveforms involves the conversion of the

biological pressure wave into an electrical signal by a transducer. The resultant
electrical signal can then be amplified, processed and displayed electronically. Two
alternative transducer arrangements are used clinically for measuring biological
pressure waveforms (Figure 1).
A miniaturized sensor on the tip of a catheter can be placed in the patient at the
point of measurement.
A fluid-filled pathway (manometer) can be used to link a catheter or cannula to a
transducer placed some distance away from the site of measurement.
Although catheter tip sensor systems are the most accurate, their disadvantages
are that they are more expensive because of their greater complexity, they are prone to
fibrin deposition if used within the circulation, and they cannot be recalibrated once in
situ. Therefore, manometric transducer systems are in more widespread clinical use.
1
a Disposable manometric pressure
monitoring set. Photograph courtesy
of BD UK Ltd. b Intracranial pressure
transducer connected to a monitor. A
miniaturized strain gauge is situated at
the tip of the fine white catheter. The
natural frequency of the transducer is
over 10 kHz. Photograph courtesy of
Codman/Johnson & Johnson.
A variety of methods is used to convert pressure changes into an electrical signal,

the most common of which is the strain gauge. A strain gauge consists of a fine metal
wire bonded to a diaphragm. Pressure changes distort the diaphragm and stretch the
wire, thus altering its electrical resistance. Piezo-resistive strain gauges measure the
change in the electrical resistance of silicon when exposed to pressure. A Wheatstone
bridge is used to detect the change in electrical resistance (Figure 2). Strain gauges
have been miniaturized to allow their use on the tip of catheters to measure intracranial
pressure. Other catheter tip transducer systems use pressure-induced changes in the
intensity of light travelling along a fibreoptic pathway to measure intracranial pressure.
Strain gauge transducer and Wheatstone bridge
Resistors R2 and R4 are strain gauges incorporated A

into a Wheatstone bridge circuit with conventional
resistors R1 and R3. A potential difference is applied R1 R3
between points C and D. The bridge is adjusted so
that it is balanced when no strain is applied, and no
potential difference is measured between points A
and B. When strain is applied to gauge R4, the
bridge becomes unbalanced, and a potential C D
difference proportional to the strain is measured
between points A and B. Gauge R2 may be placed
close to R4 without strain being applied to
compensate for changes in resistance due to
temperature. Alternatively, the two gauges may be
sandwiched back to back so that applied strain B
causes an increase in resistance within one gauge,
which is matched by a fall in resistance in its partner. R2 R4
This amplifies the magnitude of the potential
difference between points A and B, and increases
the sensitivity of the transducer.
Setting up a pressure transducer

Setting up a transducer system correctly is crucial to its accuracy. Manometric sets
must be carefully primed with sterile flush solution at room temperature without
pressurization of the solution bag, to avoid micro and macro air bubble formation within
the fluid pathway. A manometric transducer should be positioned at mid-heart level.
Each 10 cm height difference from this point equates to a hydrostatic error of 7.4 mm
Hg from the true pressure reading.
All pressure transducers require zero balancing to atmospheric pressure before use,
and at regular intervals thereafter, to compensate for drift. This may be impossible for
catheter tip sensors once in situ. The electronic monitoring equipment, to which the
transducer system is connected, must also be suitably calibrated.
Resonance
Resonance occurs when the frequency of the in vivo driving oscillations matches the
natural frequency of the driven transducer system, and oscillations of large amplitude
are induced (Figure 3). This results in significant error by overshooting of the peaks and
troughs in the actual pressure waveform, with an overestimation of the systolic pressure
and underestimation of the diastolic pressure.
The natural or resonant frequency is the frequency at which the undamped
transducer system oscillates freely with maximal amplitude. The natural frequency
of a transducer system is proportional to the square root of the stiffness of the
diaphragmand is inversely proportional to the square root of the mass of the oscillating
fluid and diaphragm (Figure 3). The mass of oscillating fluid is proportional to the length
and radius of the fluid pathway and density of fluid.
The resonant frequency of the system can therefore be raised by including a short,
stiff, parallel-sided catheter joined to short, stiff, narrow-bore, interconnecting tubing,
together with a transducer with a stiff diaphragm. Increasing tubing length from 30 to
150 cm can reduce resonant frequency by over 50% and from 15 to 150 cm may
decrease resonant frequency from 30 to 7 Hz, leading to an overestimation of systolic
blood pressure by up to 17%.
Resonance
No damping
Amplitude of induced oscillations
Damped
X Y Z f0d f0u
Frequency of driving oscillations
As the frequency of driving oscillations increases, the amplitude of induced

oscillations rises to a maximum at the natural or resonant frequency of the
transducer system (f0u). If the system is damped by absorbing some of the
energy of the induced oscillations, the maximal amplitude attained is
reduced. Damping also reduces the resonant frequency of the transducer
system (from f0u to f0d), and extends the flat range of the system from
XY to XZ. The resonant frequency of a manometric transducer system
is calculated as:
1 stiffness of diaphragm
Resonant frequency =
2 mass of oscillating fluid and diaphragm
3
Damping
Damping is the process whereby some of the energy of the driven oscillations within
the transducer system is absorbed, thus reducing their amplitude. Damping also
reduces the resonant frequency of a transducer system (Figure 3), but this relationship
is complex. Damping in the correctly functioning manometric system arises mainly
from viscous drag in the fluid pathway, tubing connections and stopcocks. Damping
increases by the third power of any decrease in the diameter of the tubing (33%
narrower tubing increases damping by 135%); a far greater change than the rise in
resonant frequency. As a consequence, the diameter of interconnecting tubing has the
greatest effect on system performance.
Excessive damping, sufficient to obtund the shape of the pressure waveform,
commonly results from compressible large air bubbles, a blood clot, soft compliant
connector tubing, numerous connections and stopcocks, and catheter kinks within the
system.
The damping factor is an index of the tendency of a transducer system to resist
oscillation.
Critical damping corresponds to a damping factor of 1, and represents the amount
of damping required such that when a stepwise change in pressure is applied, the
system returns to rest in the shortest possible time without overshooting the baseline
(Figure 4).
In contrast, optimal damping is the amount of damping necessary to maximize the
frequency response or flat range of the system and corresponds to a damping factor of
0.7 (Figure 4). At this level, overshoot of the baseline is limited and the response of the
pressure transducer accurately reflects the actual pressure change up to two-thirds of
the natural frequency of the system in a close to linear fashion.
Excessive damping with factors greater than 1 causes a significant delay between
the input arriving at the transducer and an output being generated. This is called phase
shift (Figure 4) and is measured in degrees. Distortion of the output by phase shift is
minimal with a damping factor of 0.7.
Damping of a manometric transducer system
a In an underdamped transducer
system, where the damping factor
is < 0.7, significant overshoot and X X
subsequent oscillation occurs
when a stepwise pressure change
from X to Y is imposed at time t.
This results in a significant
overestimation of the magnitude of Y Y
the pressure change.
b In an optimally damped system,
where the damping factor is 0.7,
t t
overshoot is limited to 67% of the
initial pressure change and no Time Time
oscillation occurs.
a Damping factor < 0.7 b Damping factor = 0.7 (optimal)
c In a critically damped system,
(significant overshoot error)
where the damping factor is 1.0,
the change in pressure is
measured accurately with no
overshoot.
d In an excessively damped
system with a damping factor X X
> 1.0, the full magnitude of the
pressure change may not be
registered.
With increasing degrees of

damping, the system is Y Y
progressively slower to respond to
the applied change in pressure,
and the increasing delay in the t t
transducer output is termed phase Time Time
shift
c Damping factor = 1.0 (critical) d Damping factor > 1.0
(excessive with marked phase shift)
Waveforms
By means of Fourier analysis, it is possible to split complex waveforms mathematically

into a summation of simple sine waves or ascending harmonics, each of which has an
increasing frequency and decreasing amplitude (Figure 5). Summation of the first eight
to ten harmonics of an arterial blood pressure waveform gives a reasonably accurate
representation of its shape. This number of harmonics is required to track accurately
the initial steep rate of rise in the pressure waveform corresponding to left ventricular
ejection.
Fourier analysis of the arterial pressure waveform

Amplitude
3 Hz
+
0
12 Hz
1.5 Hz
Time
The first or fundamental harmonic (1.5 Hz) together with the second (3 Hz)
and eighth (12 Hz) harmonics of a single blood pressure beat waveform
are shown, for a heart rate of 90 beats/minute. Progressively higher
harmonics display decreasing amplitude. As a consequence, only the first
810 harmonics need to be summed to reproduce the shape of the
arterial pressure waveform accurately
5
Minimum bandwidth
Minimum bandwidth is the minimum frequency range over which measurement by a
transducer system is sufficiently accurate to reproduce the first eight harmonics of
the in vivo pressure signal, resulting in an accurate electronic representation of the
shape of the pressure waveform. For the measurement of arterial blood pressure,
this is equal to eight times the fundamental frequency of the expected heart rate. At
90 beats/minute (fundamental frequency of 1.5 Hz), the minimum bandwidth would be
12 Hz, with the first eight harmonics comprising sine waves with frequencies of 1.5, 3,
4.5, 6, 7.5, 9, 10.5 and 12 Hz. At a heart rate of 120 beats/minute (2 Hz), minimum
bandwidth would be 16 Hz. Progressively higher harmonics display rapidly decreasing
amplitude, contribute less to the shape of the transduced waveform and are eventually
lost within the noise of the measuring system. Accurate reproduction of the amplitude
of the pressure waveform, rather than its shape, requires accurate measurement of only
the first five harmonics of the fundamental frequency.
Frequency response
The frequency response or flat range of a transducer system is the highest frequency
to which the system can be exposed before it registers significant overshoot. Accurate
measurement to a limit of 10% greater than the actual pressure is generally acceptable.
The frequency response must be equal to, or greater than, the minimum bandwidth.
The frequency response of the measuring system depends on its resonant frequency
and the amount of damping.
The ideal measuring system has a resonant frequency much higher than the
frequencies to be measured; frequencies up to 1020% of the resonant frequency are
accurately reproduced and no damping is required. This is because initial resonance
occurs at a frequency much higher than the necessary bandwidth for accurate
waveform reproduction. Catheter tip sensors are the closest available systems to this
ideal. For the more commonly used manometric systems, the total measuring chain
(consisting of catheter or cannula, tubing, stopcocks and transducer) has a much
lower resonant frequency, and damping is therefore vital for increasing accuracy.
Optimally damped systems can reproduce frequencies up to 67% of the resonant
frequency accurately. Continuing the calculations introduced above, an optimally
damped transducer system with a resonant frequency of 30 Hz or more will accurately
reproduce the shape of the arterial pressure waveform.
FURTHER READING
Billiet E, Colardyn F. Pressure Measurement Evaluation and Accuracy Validation: the
Gabarith Test. Intensive Care Med 1998; 24:13236.
Runciman W B, Ludbrook G L. The Measurement of Systemic

Arterial Blood Pressure. In: Prys-Roberts C, Brown B R, eds. International Practice of
Anaesthesia. Oxford: Butterworth-Heinemann, 1996.

Co-morbidity
Anaesthesia
on CD-ROM
Anaesthesia for the Obese
Patient
David W Noble
Fiona McCallum
David W Noble is Consultant in Anaesthesia and Intensive Care at Aberdeen

Royal Infirmary. He trained in Aberdeen and Edinburgh. He is interested in the
pharmacological and immunological aspects of anaesthesia and intensive care.
Fiona McCallum is Specialist Registrar in Anaesthetics at Grampian University

Hospitals NHS Trust. She qualified from Edinburgh University and worked in Stirling
and Elgin before moving to Aberdeen. She is interested in medical education.
The incidence of obesity, with its attendant health risks, continues to rise. Consequently,
increasing numbers of obese patients are presenting for surgery and their perioperative
care presents a significant challenge to the anaesthetist. In 1997, in Britain, 13% of men
and 16% of women were considered to be obese. Obesity is defined according to the
body mass index (BMI) or with reference to the ideal body weight (IBW) (Figure 1).
BMI = weight (kg)/[height (m)] 2
IBW (kg) = height (cm) 100 (men) or 105 (women).
Classification of obesity
Body mass Percentage above

index ideal body weight
Overweight > 26 30
Obese > 30 40
Morbidly obese > 40 100
Pathophysiological effects of obesity
The pathophysiological effects of obesity are wide ranging and are greatest in the
morbidly obese, though they occur in all obese individuals.
Cardiovascular system
Cardiac structure and function: cardiac output and blood volume are increased
in obesity to meet the increased metabolic demands of a greater body mass.
Chamber dilatation and ventricular hypertrophy occur to reduce wall stress and can
progress to ventricular dysfunction and cardiac failure a condition known as obesity
cardiomyopathy (Figure 2). Cor pulmonate may also develop (Figure 3). These changes
are related to the severity of obesity and are improved by weight loss.
Development of cardiomyopathy in obese patients
Excessive adipose tissue
Increased circulating blood volume
Increased stroke volume plus cardiac output
Left ventricular enlargement
Increased left ventricular wall stress
Exacerbated
Left ventricular hypertrophy
if hypertensive
Left ventricular dysfunction
Left ventricular failure
Development of cor pulmonale in obese patients
Excessive adipose tissue
Sleep apnoea/obesity hypoventilation syndrome
Hypoxia/respiratory acidosis
Pulmonary arterial hypertension
Right ventricular hypertrophy plus enlargement
Right ventricular failure
Hypertension is present in 60% of obese individuals and is severe in 10%. The

aetiology remains unclear, but weight loss reduces blood pressure.
Coronary artery disease: the role of obesity as a risk factor for coronary disease
is difficult to evaluate because of the association between obesity and hypertension,
diabetes mellitus and hypercholesterolaemia, which are all coronary risk factors. There
is an association between central obesity and an early age of onset of obesity, and the
development of coronary artery disease.
Cardiac arrhythmias may occur secondary to chamber dilatation, ischaemic heart

disease or fatty infiltration of the conducting system.
Respiratory system
The increased metabolic demands of obesity also require an increased minute
ventilation to meet the increase in oxygen consumption and carbon dioxide production.
The work of breathing is further increased because of the reduction in chest wall and
lung compliance. Obese patients tend to take rapid shallow breaths, leading to greater
mismatching of ventilation and perfusion. There is a reduction in functional residual
capacity (FRC) because the increased adipose tissue in the chest wall and abdomen
limits diaphragmatic excursion. If the FRC falls below closing volume, small airway
closure occurs resulting in intrapulmonary shunting and hypoxaemia. This situation
may occur in obese individuals under normal circumstances and is exacerbated
by increasing age, the supine position and general anaesthesia (Figure 4). As a
result of the above mechanisms, obese patients may become chronically hypoxic
and develop secondary polycythaemia, pulmonary hypertension and ultimately right
ventricular failure.
Relationship between functional residual capacity and closing volume
Normal young adult Patients in whom FRC is reduced

because of obesity, supine position,
general anaesthesia or
abdominal pain
Tidal
volume
FRC Tidal
CV volume CV
FRC
FRC, functional residual capacity; CV, closing volume
Obesity hypoventilation syndrome occurs in 410% of morbidly obese patients. It

is characterized by chronic hypoxia and its sequelae, in association with a decreased
responsiveness to carbon dioxide, and results in hypoventilation and hypercapnia.
Airway problems: excess adipose tissue in the soft tissues of the head and neck
makes airway problems more likely, and intubation is difficult in 13% of this pateint
population. Obesity also predisposes to the development of the sleep apnoea
syndrome, which is characterized by upper airway obstruction and hypoxic episodes
when the conscious level is reduced (e.g. during sleep). Classically, these patients have
a history of heavy snoring, periods of apnoea during sleep and daytime somnolence
because of disturbed sleep at night.
Gastrointestinal system
Hiatus hernia and gastro-oesophageal reflux are more common in obese individuals.
Fasting, obese patients have higher residual gastric volumes of lower pH than the
non-obese. Liver disease, mainly in the form of cholelithiasis, and fatty infiltration are
more common in obese individuals, but hepatitis, fibrosis and cirrhosis can also occur.
Obesity is a recognized risk factor for the development of hepatitis following volatile
anaesthesia.
Endocrine system
Endocrine disturbances such as hypothyroidism and Cushings syndrome may have a
causal role in obesity. The most important consequence of obesity for the endocrine
system is the development of diabetes mellitus.
Common to all patients, preoperative assessment comprises the history, physical
examination and preoperative investigations, as well as discussing with the patient the
proposed anaesthetic technique and perioperative care plan. The following aspects of
the history and examination are of particular importance in obese patients.
Evaluation of the severity of any cardiorespiratory compromise.
Careful airway assessment to decide safe airway management.
Assessment of acid aspiration risk (this also influences airway management).
Confirmation of the presence of conditions associated with obesity (e.g. diabetes).
Examination of potential sites for venous access, which may be problematic.
Examination of the spine if epidural or spinal anaesthesia is contemplated.
Establishment of a rapport and providing relevant information to the patient.
Preoperative investigations depend on the findings of the history and examination,
and the intended surgery, but the following investigations may be helpful in obese
patients:
urinalysis to screen for diabetes
full blood count to identify polycythaemia
urea and electrolytes, which may be altered by antihypertensive or diuretic drug
therapy
ECG which may show ventricular hypertrophy, arrhythmias or ischaemic changes
chest radiography, which is useful for determining heart size, signs of pulmonary
oedema and as preoperative baseline
pulmonary function tests to reveal any restrictive defects; any obstructive component
should prompt a trial of bronchodilator therapy
arterial blood gases to confirm hypoxia and hypercapnia; the response to oxygen
therapy should be elicited if the patient is hypoxic on air
echocardiography and exercise testing which may help to assess the severity of
cardiac compromise
specialist opinions for optimization of medical therapy before elective surgery.
Pharmacological considerations: the changes in blood volume, cardiac output,

adipose tissue and total body water content that occur in obesity can alter drug
pharmacokinetics.
Intravenous agents propofol kinetics appear unaltered though recovery from
thiopental (thiopentone) and benzo-diazepines may be prolonged.
Volatile anaesthetics there is little evidence that recovery is prolonged in obesity
despite the lipophilicity of these agents. Toxicity from metabolic products may be
reduced by using relatively insoluble and minimally biotransformed anaesthetics (e.g.
isoflurane, desflurane).
Muscle relaxants pseudocholinesterase activity is increased, but doses of
suxamethonium, less than 1 mg/kg, have been shown to provide adequate vocal cord
paralysis. The dose and duration of action of atracurium is unaltered. Vecuronium has
a prolonged duration of action and the dose should be calculated according to lean
body weight.
Opioids the doses of alfentanil and remifentanil should be calculated according to
lean body weight. Although this restriction does not apply to other opioids, careful dose
titration of all opioids is warranted because of their respiratory depressant effect.
Regional anaesthesia avoids the problems associated with general anaesthesia in

obesity but is not without problems. Landmarks may be difficult to define and long
needles may be required. For spinal or epidural anaesthesia the sitting position aids
location of the midline and a nerve stimulator can aid needle placement for other
blocks. Smaller volumes of local anaesthetic solutions should be used for spinal and
epidural blocks, because spread is greater in obese patients. A final consideration,
if a regional technique alone is planned, is the ability of the patient to tolerate the
position required for surgery. Some obese patients are unable to lie flat because
of respiratory compromise, which may be exacerbated by a regional block affecting
thoracic segments. A combination of regional and general anaesthesia may be the
optimal technique.
Pre-medication: H2-antagonists or proton pump inhibitors combined with a prokinetic

agent can be prescribed because of the risk of acid aspiration. An anxiolytic can be
given, but heavily sedative or opioid premedication should be used with caution and
perhaps avoided in the morbidly obese. The oral route is preferable to the intramuscular
or subcutaneous routes because absorption from these sites is unpredictable.
Induction and airway management

Tracheal intubation and controlled ventilation are required for all but the shortest
procedures in carefully selected patients. During the preoperative assessment, a
decision should be made regarding the need for an awake fibre-optic intubation, but
difficult intubation equipment and a range of face masks, laryngoscope blades, bougies
and other airway adjuncts must always be available immediately. For difficult cases,
two anaesthetists and an experienced assistant should be present. Careful positioning
of the patients head and shoulders will make airway management and intubation
easier, and a rapid-sequence induction technique should be used because of the risk
of acid aspiration. Adequate pre-oxygenation is essential because the combination
of increased oxygen consumption and a reduced oxygen reservoir can cause a
precipitous fall in oxygen saturation once apnoea occurs. Suxamethonium remains
the muscle relaxant of choice because of its rapid onset and offset of action. The
choice of induction agent depends on individual circumstances (e.g. cardiorespiratory
disease) and obesity per se does not influence drug selection. All the commonly used
anaesthetic agents have been used successfully in obese patients.
Maintenance and intraoperative care

A balanced anaesthetic technique with muscle relaxation and controlled ventilation,
combined with regional anaesthesia is appropriate for many patients. As with induction
agents, the choice of agent used to maintain anaesthesia depends on the patients
co-morbidities, the duration of surgery and whether elective ventilation is planned
postoperatively. Some important aspects of intraoperative care in obese patients are
described below.
Operating table the table must be wide enough for the safe positioning of the
patient and strong enough to take the patients weight.
Staff adequate numbers of staff must be present for patient transfer. The patient
should be anaesthetized on the operating table so that only one transfer is required
with the patient anaesthetized.
Monitoring the correct size of blood pressure cuff is required for the accurate
measurement of blood pressure. Arterial cannulation is often desirable for serial blood
gas analysis during and after surgery as well as for arterial pressure monitoring.
Capnography must be available for induction to confirm correct tracheal tube
placement. Central venous monitoring may be necessary for venous access and will
aid fluid management, particularly in those with cardiac compromise. The use of an
ultrasound probe is recommended to aid placement. Pulse oximetry is an essential tool
for rapid detection of hypoxaemia during and after surgery.
Controlled ventilation is almost always required to ensure adequate gas exchange,
often with a combination of high-inspired oxygen concentration and the application
of positive end expiratory pressure. High inflation pressures may be unavoidable
particularly if the lithotomy or Trendelenburg positions are used.
Blood loss is likely to be greater in the obese because surgery is technically
more difficult. Adequate venous access must be secured and the threshold for cross-
matching of blood may need to be reduced.
End of surgery if extubation at the end of surgery is intended, it should not
be attempted until residual neuro-muscular blockade has been reversed, the patient
is awake, cooperative, has a good cough, and an acceptable respiratory pattern and
oxygen saturation.
Postoperative complications are more common in obese patients, therefore transfer to
a high dependency unit or ICU should be considered. Some patients undergoing minor
surgery may be nursed safely on the general ward.
Respiratory complications: basal lung collapse during anaesthesia and resulting

hypoxia is common, and is exacerbated by
the respiratory depressant effects of residual anaesthetic agent and/or opioid therapy
in the postoperative period, as well as the effects of surgery. Collapsed lung segments
also act as a focus of infection.
Hypoxia can also occur as a result of airway obstruction if the conscious level is
reduced (e.g. in patients with obstructive sleep apnoea receiving opioids).
Respiratory complications may be minimized by:
humidified oxygen therapy with pulse oximetry
adequate balanced analgesia
aggressive physiotherapy and early mobilization
using continuous positive airway pressure in patients at risk of airway obstruction
during sleep or sedation
nursing patients upright or in the lateral decubitus position is preferable to a
recumbent position.
Thromboembolic complications are more common in obese patients. Adequate

prophylaxis for deep venous thrombosis is mandatory and early mobilization should
be encouraged.
Wound infections: longer incisions, greater wound retraction and the poor blood
supply to adipose tissue make wound infections more common in the obese.
Postoperative analgesia
Adequate analgesia allows deep breathing and coughing, facilitates chest
physiotherapy and aids early mobilization, which reduces the incidence of postoperative
complications. In obese patients, various options for postoperative analgesia, either
alone or in combination, are available.
Parenteral opioids are administered intravenously, most commonly using a patient-

controlled analgesia device. Standard dosing regimens are adequate for obese
patients. Careful monitoring of respiratory parameters and conscious level is necessary
in obese patients and supplemental oxygen is essential.
Epidural analgesia using low-dose local anaesthetic solutions, alone or in combination

with opioids, is the best method of providing analgesia following thoraco-abdominal
surgery in obese patients, provided the epidural can be sited successfully. It may also
be useful following pelvic or lower limb surgery.
Local anaesthetic techniques: local anaesthetic blocks performed for surgery will
last for a variable length of time into the postoperative period. By using a catheter
technique, useful analgesia can be extended.
Supplementary analgesics: though seldom sufficient alone, the use of regular

paracetamol and non-steroidal anti-inflammatory drugs (if not contraindicated) has an
additive effect with opioid or epidural analgesia. A balanced approach to analgesia may
be particularly helpful in obese patients.
FURTHER READING
Adams J P, Murphy P G. Obesity in Anaesthesia and Intensive Care.
Br J Anaesth 2000; 85: 91108.
Craig D B. Postoperative Recovery of Pulmonary Function. Anesthesia and Analgesia

1981; 60: 4052.
Oberg B, Poulsen T D. Obesity An Anaesthetic Challenge. Acta Anaesthesiol Scand

1996; 40: 191200.
Rosenbaum M, Leibel R L, Hirsch J. Obesity. New Engl J Med 1997; 337: 396407.

Hepatitis and HIV Infections
Rick Keays
Neil Soni
Rick Keays is Consultant Intensivist at the Chelsea and Westminster Hospital, London, UK
Neil Soni is Consultant at the Chelsea and Westminster Hospital, London, UK.
Blood-borne viral infections have implications for anaesthesia and intensive care
because of their potential for transmission and as disease entities.
Hepatitis
Recently, there has been an explosion in the understanding and diagnostic

subcategorization of viral hepatitis. The terminology has changed from either serum or
epidemic hepatitis to a recognition of the many causative agents of hepatitis acquired
either from faecal contamination (hepatitis A and E) or parenterally via body fluids
(hepatitis B, C, D and G). Many hepatologists were aware that hepatotropic agents
were responsible for the hepatitis seen in patients in whom neither hepatitis A or B
could be identified and an increasing alphabet is now filling the gap formerly known
as non-A, non-B hepatitis.
Hepatitis A virus (HAV)

HAV is a small RNA virus that causes acute hepatitis only. It is a common cause of
both sporadic and epidemic hepatitis and is spread by the faeco-oral route. Symptoms
appear about 2 weeks after infection, with an associated rise in transaminase levels
and excretion of viral particles in the faeces. At the same time, anti-HAV and IgM
anti-HAV antibodies appear; the former persist for life and the latter disappear within
312 months of infection. HAV antigen is present in the stools in the late prodrome
and early symptomatic phase of the infection, and its presence in serum indicates viral
shedding. The features of acute hepatitis and the presence of IgM anti-HAV and HAV
antigenaemia are usually diagnostic. The disease is self-limiting and seldom leads to
fulminant hepatic failure. It is possible to become infected with HAV after transfusion,
if the donor was in the viraemic phase of the illness. This risk is estimated to occur
with 1/1 million units of blood and its rarity is explained by the absence of a chronic
carrier state with HAV.
Treatment: vaccines are available, but are not wholly effective in controlling outbreaks.
They are not recommended for children under 2 years of age, but can be given to
pregnant women because the virus is inactivated.
Hepatitis B virus (HBV)

HBV is a DNA virus and has the smallest genome of any DNA virus infecting humans. It
has four gene regions: the S or envelope region (HBsAg), the C or nucleocapsid region
(HBcAg and HBeAg), the P region (DNA polymerase), and a fourth region which is a
transactivator of HBV replication (HBxAg). Genotypic variants exist with a geographical
distribution similar to human ethnic distribution. In the UK, the prevalence is about 0.1%.
As many as 1013 viral particles can be found in 1 ml of infected blood; this compares
with 101104 particles in HIV-infected blood. HBV can survive in dry blood for up to 1
week. Trans-fusion-transmitted HBV has, however, been dramatically reduced since the
introduction of third-generation screening tests in the mid-1970s.
Symptoms usually appear about 2 months after infection, with a concomitant rise
in alanine aminotransferase (ALT) in the acute phase. HBsAg, HBeAg and HBV-DNA
are all detectable in the blood slightly before the appearance of jaundice and other
symptoms. Also, at this time, anti-HBc and IgM-anti HBc become evident, denoting
acute infection. A month later, antibodies to HBe appear, resulting in clearance of
HBeAg and a gradual reduction in HBV-DNA levels. Some months after this, HBsAg
clears from the blood and anti-HBsAg antibodies become detectable. In 1025%
of patients, a chronic carrier state develops and there is persistence of HBV-DNA,
indicating continuing viral replication, and HBsAg and HBeAg, which if found together
indicate continuing viral replication with a high level of infectivity and active liver
disease. The development of anti-HBe antibodies, which can occur at any time, implies
disease resolution and quiescence of liver disease. However, in the face of increasing
host immune activation, the virus can mutate to different forms that replicate, though
they may not produce HbeAg. These forms are infective and can cause severe liver
disease.
Treatment: vaccination is effective in eradicating HBV from the population. However,

there are genetic variants of the HBsAg epitope cluster, which results in poor
binding of some polyclonal and monoclonal antibodies. These variants are capable of
transmission and of causing liver disease, and may be best dealt with by administering
polyvalent (multiple antigen) vaccines.
In patients with chronic disease, 1015% develop cirrhosis and 10% develop
hepatocellular carcinoma. Interferon- is effective in achieving sustained response
rates in 3040% of patients with chronic hepatitis B and for those who do not respond,
nucleoside analogues may be promising adjuncts. In un-immunized individuals,
percutaneous exposure leads to seroconversion in 12% (if infected blood is only HBsAg
positive) rising to 30% if infected blood is also HBeAg positive. In such cases, the
exposed individual should be given hepatitis B immunoglobulin and the recombinant
DNA vaccine as soon as possible.
Seroconversion rates are high, therefore it is extremely important that healthcare
workers are properly immunized, but vaccine failure can occur in as many as 12%.
Achieving a protective titre of antibody will sometimes last up to 9 years, though
boosters are recommended more regularly than this.
Hepatitis delta virus (HDV)

HDV is a small defective RNA virus, which has some similarity to satellite viruses that
infect higher plants. It causes liver disease only in those already infected with HBV
(superinfection) or where HBV is transmitted simultaneously (co-infection). In the acute
phase, the disease has a high mortality and, in the chronic phase, there is a high risk of
developing cirrhosis. HBV is the helper virus and provides surface antigen for the delta
particle envelope, without which it is non-infectious.
Diagnosis depends on the circumstances. In cases of co-infection, anti-HDV may
never become detectable or is detectable only in the convalescent serum sample,
whereas in superinfection anti-HDV may rise to high titres. The level of IgM anti-HDV is
also useful for diagnosis, but it tends to be present at low levels in some patients with
chronic delta hepatitis. HDV-RNA can be detected in the serum of infected patients, but
its disappearance does not mean the disease has been eradicated.
Treatment: interferon therapy has transient effects. The virus replicates by RNA control
without the need for protein enzymic assistance and this ribozymic activity is attracting
interest as a potential target for therapy.
Hepatitis C virus (HCV)

HCV was identified a decade ago and appeared to be responsible for most non-A,
non-B post-transfusion viral hepatitis. It is an RNA virus that causes both acute,
though seldom fulminant, hepatitis and chronic hepatitis. There is an 85% chance of
the infection becoming chronic with the attendant risks of developing cirrhosis (20%)
and hepatocellular carcinoma (15%). In addition, there is an increased chance of
developing a variety of non-hepatic autoimmune conditions. Its prevalence worldwide is
about 1%, though it is less in the UK.
Exclusion of blood donors with known risk factors for HIV, or with raised
transaminases or antibodies to hepatitis B core antigen has reduced the incidence of
transfusion-related non-A, non-B hepatitis. However, the real breakthrough came with
the introduction of a test for antibodies to HCV. It is now estimated that the risk of
developing HCV is about 1/103,000 transfusions. Although transfusion is an uncommon
cause of HCV infection, once a patient is infected the likelihood of complications is
high. For percutaneous exposure, the seroconversion rate is as high as 610%, which
represents a risk 1033 times greater than for HIV, but 1020 times less than for
HBV. This correlates very closely with the average measured viral loads encountered
in these three diseases.
The variants of HCV seem to be distributed on geographical grounds and depend on
the type of exposure that an individual has encountered. Type 3 occurs more commonly
in intravenous drug users, whereas types 4, 5 and 6 seem to have some geographical
concentration. HCV-RNA can be detected in the serum about 1 month after exposure to
the virus and symptoms and transaminasaemia develop 1 or 2 weeks later. Symptoms
are usually mild in the acute stage and may not include jaundice. It seldom progresses
to a fulminating hepatitis. Anti-HCV is detected only after symptoms have appeared,
generally 424 weeks later, and is of little use in establishing the diagnosis of
acute HCV. The clinical disease may be related to different genotypes, for example
hepatocellular carcinoma may be linked with subtype 1b, which is also more resistant
to interferon therapy.
Treatment: response rates for chronic HCV infection treated with interferon are low
(1025%), especially in Europe and the USA, which may be explained by a higher
prevalence of HCV-1b. Post-exposure immunoglobulin is not useful and there is no
available vaccine against HCV. In the USA, the Food and Drug Administration has
recently approved the combination of interferon and ribavirin, which several studies
have shown leads to a sustained response in 4050% of patients.
Hepatitis E virus (HEV)

HEV is similar to HAV in that it is contracted enterally in sporadic or epidemic outbreaks.
It leads to an acute illness with no chronic carrier state, but mortality is increased in
pregnant women in endemic regions. Diagnosis is usually made on the clinical and
laboratory features of acute hepatitis, in the absence of serological markers for other
forms of viral hepatitis, and a history of recent travel to endemic areas. Viral RNA
can be detected with molecular amplification techniques and assays for antibody to
the virus are available.
Hepatitis G virus (HGV, GBV-C)

Even with the discovery of HCV, it was appreciated that there remained a subgroup
of transfusion-related hepatitis that was non-A to non-E related. Two separate centres
discovered the viral sequence; one from a surgeon (initials GB) and one from a
West African individual. Three related sequences are known as GBV-A, GBV-B and
GBV-C, of which the first two are thought not to be pathogenic to humans whereas
the immunoassay industry is holding out hopes for the latter. This somewhat confusing
nomenclature rests under the canopy of HGV. It is doubtful whether HGV is especially
hepatotropic or causes any particular disease. The prevalence of HGV viraemia, at
least among donors in the USA, is about 12%, whereas in Africa it is at least 12%.
Thus, the virus can be transmitted by blood transfusion and this raises some ethical
considerations because molecular techniques have demonstrated the presence of a
viral sequence that can be transmitted. For example, is it right knowingly to infect
others and will the repeated transmission of this virus lead to pathogenicity? In 10% of
individuals, seroconversion will follow percutaneous exposure to infected blood.
Other viruses
The potential for transmitting other viruses during transfusion also exists. Those
capable of manifesting hepatitic features include cytomegalovirus, EpsteinBarr virus
and herpes simplex virus usually with other accompanying systemic symptomatology.
With regard to hepatotropic viruses, considerable efforts are being applied to
characterize a new transfusion-transmitted virus (TTV) and time will tell whether this
yields a new letter for the hepatitis alphabet.
Anaesthesia and intensive care

In the absence of chronic liver disease, with the associated alterations in drug handling,
there are no extra implications for anaesthesia. Standard precautions should always be
adopted. It is important to obtain evidence of the extent of hepatic synthetic dysfunction,
generally by measuring the international normalized ratio. This may preclude neuraxial
local anaesthetic techniques and suggest extra vulnerability to ischaemic hepatitis if
the hepatic blood flow decreases. Managing acute and end-stage chronic liver failure is
complex because multiple organ systems are involved and transplantation is often the
only realistic option.
Human immunodeficiency virus (HIV)
HIV was first described in 1981, through the emergence of Pneumocystis pneumonia
associated with candidiasis in otherwise healthy homosexual men. The retrovirus was
identified as being a Lentiviridae. There are two main types, HIV-1 and HIV-2, but they
also demonstrate significant genetic variation and there are subgroups of each virus.
The viral genome has a propensity for change and evolution. As with other blood-borne
viral infections, the patient develops viraemia following an initial inoculum, with a rapid
increase in the viral load. The immune response then becomes established over a
variable period of time and this has an impact on the viral load, which may stabilize
or decrease (Figure 1).
Acute HIV infection
HIV antibody
CD4+
Counts
Viral load;
rapid progress
Viral load
P24 antigen
0 1 2 3 4 5 6 7 8 9 10 11
Weeks
1
Transmission
It has been estimated that 5692% of all infection is transmitted during the acute phase
of infection when the viral load is high and the host is unaware of the infection. The
virus is probably present in a range of body fluids, but those considered to be of high
risk are blood, semen, vaginal secretions, peritoneal fluid, CSF and other cavity fluids.
Less risk is associated with faeces, nasal secretions, saliva and urine, provided they are
not contaminated with blood. There are several levels of screening for donated blood
for transfusion, which start with donor selection. In the UK, blood is tested for HIV-1
and HIV-2 antibodies. In some countries it is also screened for HIV p24 antigen. A
needlestick injury is associated with a 0.3% chance of seroconversion. Hollow needle
injuries are more risky than solid needle injuries, because a larger inoculum is likely.
Presentation
Acute infection occurs after initial exposure, when there is a phase of viral replication
and initiation of a host immune response. In this response phase, the patient may have
a viral-type illness, which is non-specific and probably corresponds to seroconversion.
This response varies between individuals but, in one study, 89% of patients
experienced symptoms and signs including fever, fatigue, skin rash, myalgia, headache,
pharyngitis, lymphadenopathy, arthralgia, oral ulcers, weight loss, nausea, vomiting
and diarrhoea. Patients commonly present with opportunistic infections. These may be
typical of an immunocompromised patient (e.g. Pneumocystis pneumonia, disseminated
Cryptococcus, toxoplasmosis, widespread candidiasis) or may be more general (e.g.
tuberculosis, pneumococcal pneumonia). Multi-resistant tuberculosis is a transmissible
problem and precautions should be taken to minimize the risk of spread if the diagnosis
is considered. Gastrointestinal disturbance is extremely common and may be infective,
though a non-specific enteropathy is also seen (Figure 2). Neurological complications,
often infective, are common. Non-infective presentation includes Kaposis sarcoma.
Clinical syndromes associated with HIV1
Gastrointestinal
Weight loss and malnutrition
Diarrhoea bacterial, viral, fungal
Parasitic (Cryptosporidium, Giardia, Entamoeba histolytica)
HIV enteropathy
Hepatic viral hepatitis B, C or D, tuberculosis, fungal Cryptococcus,
Candida, histoplasmosis)
Kaposis sarcoma, lymphoma
Ocular
Non-infective conjunctivitis, keratitis, haemorrhage, cotton wool spots
Infective conjunctivitis, keratitis, retinitis, uveitis
Respiratory
Any bacterial infection, Pneumocystis carinii, cytomegalovirus,
cryptococcosis, coccidiomycosis, histoplasmosis
Tuberculosis including Mycoplasma avium type
Kaposis sarcoma, non-Hodgkins lymphoma
Bone marrow
Peripheral blood cytopenias, anaemia, thrombocytopenia, granulocytopenia
Rheumatological
Arthralgia, Reiters syndrome, psoriatic arthritis, vasculitis
Cardiac
Pericardial effusions, non-specific impairment of left ventricular function,
myocarditis
Neurological
Brain HIV-related meningo-encephalitides, infections including herpes,
varicella, cytomegalovirus
Toxoplasmosis, Cryptococcus, Nocardia, tuberculosis, syphilis, Kaposis
sarcoma, lymphoma
Spinal cord vacuolar myelopathy, infection
Peripheral neurology, polyneuropathy, demyelination, neuralgic amyotrophy
Psychological
Any of the neurological causes above
HIV encephalopathy
Renal
HIV nephropathy (glomerular disease)
Oral problems
Candidiasis, herpes simplex, varicella zoster
Gingivitis, periodontitis
Kaposis sarcoma
1
The list is not comprehensive, but indicates the range of problems.
Laboratory testing
Antibodies to HIV-1 can be demonstrated using enzyme-linked immunosorbent assay
or Western blot techniques. In the acute phase, HIV-1 and HIV-2 antibodies are at best
weakly positive or non-reactive and this will be misinterpreted as a negative result. HIV-
1 RNA or viral p24 antigen should be tested; levels of 13 x 10 6 RNA particles/ml may
be seen. A false-positive rate of 25% has been reported, therefore all tests should
be repeated. This should be confirmed when seroconversion occurs later. During the
acute phase, the CD4 count often falls and is followed by an expansion of the CD8
population, thereby altering the CD4:CD8 ratio at about day 16 of the acute illness. The
expansion of the CD8 cytotoxic T cell subgroup is probably associated with antiviral
activity.
Treatment
After the initial infection, the viraemia and the immune response equilibrate at a set-
point. At this stage, there is a relationship between the viral load and prognosis. Those
with a high persistent load do less well than those with a low load. Early aggressive
treatment to reduce the load may lead to a better prognosis. It is hypothesized that, in
the acute phase, when there is rapid proliferation of the virus, highly active antiretroviral
therapy (HAART) may reduce the viral load and minimize damage to the CD4 T-helper
lymphocytes. It may also reduce the emergence of resistance.
Nucleoside reverse transcriptase inhibitors (NRTI) (e.g. zidovudine, lamivudine)

were used as monotherapy, with limited effect in suppressing HIV except materno-fetal
transmission, but some patients have become resistant to them. Side-effects
include gastrointestinal problems (e.g. diarrhoea, vomiting), pancreatitis and peripheral
neuropathy.
Non-nucleoside reverse transcriptase inhibitors (NNRTI) (e.g. nevirapine,

efavirenz) bind only to HIV-1 reverse transcriptase.
Protease inhibitors (e.g. saquinavir, ritonavir, indinavir, nelfinavir) are particularly

effective when used in conjunction with NRTI. HIV-1 protease is an essential enzyme
for viral replication and acts at the point at which virions become mature. Treatment
results in the release of immature non-infectious viruses, which can be eliminated. Viral
load is reduced, often to levels that are undetectable. It acts on maturing virus particles,
therefore it does not have any impact on cells. CD4 that are already infected will be
destroyed, but it does prevent spread of infection. The use of dual therapy seems to
improve CD4 counts and to reduce viral load. Protease inhibitors have led to a dramatic
alteration in the pattern and natural history of HIV, with decreased hospital admissions
and fewer opportunistic infections. However, even with imperceptible viral load, an
infective risk still exists. Protease inhibitors are metabolized by the P450 system and
tend to either inhibit or induce cytochrome P450 isoenzymes. They therefore have the
potential for drug interaction. They have a range of side-effects (Figure 3).
Side-effects of protease inhibitors
Onset of diabetes mellitus and insulin resistance, type II diabetes

Fatty deposition in neck buffalo hump
Peripheral lipodystrophy, hyperlipidaemia
Gastrointestinal problems (nausea, vomiting, diarrhoea)
Elevations of creatine phosphokinase, hepatic transaminases (occurs with
saquinavir)
Circumoral and peripheral paraesthesia (occurs with ritonavir)
Hepatitis with elevations of transaminases and bilirubin (occurs with
indinavir)
Mitochondrial toxicities (non-specific)
Anaesthesia
The problems that HIV poses for anaesthesia relate to the general problems of the
disease and drug therapy. There are also non-specific considerations relating to dealing
with a potentially infective condition. General problems include the chronic health status
of the patient, who may be malnourished and wasted, and may have haematological,
hepatic or renal problems. Local manifestations of the disease can cause technical
difficulties. Chronic respiratory problems may alter oxygenation, in particular those
who have had Pneumocystis pneumonia and are taking prophylaxis. Airway problems
are common, from infection or from Kaposis sarcoma. The implications of using an
epidural should be discussed because of possible neurological involvement and the
increasing number of HIV-positive women of child-bearing age. There is no evidence to
suggest that complications following epidural are any higher in this population. This is
important because caesarean section may reduce vertical transmission of HIV. There
are inadequate data to make any statement about using blood patches if dural puncture
occurs.
The side-effects of the drugs used to treat HIV may add to anaesthetic
considerations.
Pain control in HIV patients is also a problem. This may be associated with the
disease or the opportunistic infections, or be drug related.
Contaminating equipment is another problem when dealing with potentially infective
patients. A sensible and hygienic approach to cleaning and sterilizing devices such as
filters on anaesthetic circuits all help to reduce the risk of transmission; these measures
should be universal.
Intensive care
The management of patients with HIV in the ICU should be the same as for other
patients. Difficulties encountered include trying to maintain HAART, particularly if the
gut is non-functional.
Presentation with HIV-related disease is also common. Primary presentation with
Pneumocystis carinii is less common than it used to be. When it does present, it may
be in undiagnosed patients. Neurological and gastroenterological presentation is also
common. Rapid diagnosis is important. Prognosis is determined by the condition,
the chronic health status of the patient and their immune system, and appropriate
treatment. Prognosis appears to be worse in patients who fail to respond to appropriate
treatment in the first few days. For example, Pneumocystis carinii pneumonia that is
unresponsive after 45 days of aggressive treatment has a poor prognosis. The pattern
of presentation is undoubtedly changing with the advent of HAART, but it is too early to
anticipate the long-term effects on ICU admission.
Healthcare workers and HIV

The risk of contracting HIV infection at work is perceived to be low. Sensible
precautions, such as wearing gloves, attention to hygiene and avoidance of sharps
injuries by careful practice are all advocated. Exposure to fluids or blood that might be
infected constitute an exposure. Specialist advice should be sought immediately after
exposure and it is likely that post-exposure prophylaxis would be implemented, within
12 hours. This should always be done with guidance from an HIV specialist. Currently
it consists of a combination of two NRTI drugs (zidovudine and lamivudine) added
to a protease inhibitor (e.g. indinavir). The side-effects of indinavir can be daunting
and include gastrointestinal upset, headache, fatigue, paraesthesia or hypaesthesia,
myalgia, nephrolithiasis, hyperbilirubinaemia and change in liver function (Figure 3).
The risk of an HIV-infected healthcare worker transmitting the disease to a patient is
considered to be very low, provided the healthcare worker does not carry out exposure
prone procedures. These are procedures where the healthcare worker is at risk of
injury with sharp instruments within an open body cavity and where the operator's
hands may not be visible. If injured, the patient will be exposed to blood. A health
worker infected with HIV should seek appropriate medical and occupational health
advice.
FURTHER READING
Poon S H, Rosenberg E S. Clinical and Laboratory Implications of Acute HIV-1
Infection. Clin Microbiol Newsletter 2000; 22: 5.

Pacemakers and Anaesthesia
Caroline Bateman
Brian Keogh
Caroline Bateman is Senior Clinical Fellow in Cardiothoracic Anaesthesia at the Royal

Brompton Hospital, London UK. Her interests include cardiothoracic anaesthesia and
intensive care.
Brian Keogh is Consultant Anaesthetist at the Royal Brompton Hospital, London, UK.
His interests include cardiothoracic anaesthesia and severe acute pulmonary failure.
The first permanent transvenous pacemaker was implanted in 1962. It weighed about
250 g and was expected to last for less than 2 years. Since then, advances in
microprocessor technology and the introduction of lithium power sources have resulted
in the development of more complex and reliable pacing systems. As a result, the
number of patients with pacemakers inserted to treat bradycardia and tachyarrhythmias
has increased. Implantable cardioverter defibrillators (ICD) were first used in 1980; they
provide a method of treatment for patients with ventricular arrhythmias that are not
managed or amenable to anti-arrhythmic agents, ablative techniques or surgery.
Many patients present for surgery with a pacemaker or ICD implanted and
anaesthetists need to understand the problems that can be encountered with all types
of pacing device.
Pacemaker insertion
Indications: guidelines specifying the indications for insertion of a permanent

pacemaker have been published but are likely to expand with increasing sophistication
of the devices. Current indications for permanent pacing include symptomatic complete
heart block, prolonged sinus arrest associated syncope, carotid sinus syndrome and
malignant vasovagal syncope. Asymptomatic second degree and complete heart block
remain controversial indications, as does pacing for cardiomyopathy and congestive
cardiac failure.
In general, the pacemaker should aim to mimic normal physiological conditions.
The ventricle should be paced if there is actual or potential atrioventricular (AV) block.
The atrium should be sensed and paced unless there are contraindications such as
chronic or repetitive atrial flutter or fibrillation. Rate-responsive pacemakers respond
to the increased physiological demands of exercise in active patients, but may be
unnecessary in inactive patients or in those with a normal chronotropic response.
Anaesthesia: pacemakers are often inserted under local anaesthesia but if general
anaesthesia is required the technique and monitoring should be tailored to the
individual. A temporary wire may be inserted and external defibrillator pads used.
Insertion of ICD: patients requiring insertion of an ICD are likely to have severe
underlying cardiac dysfunction. Cardiac function should be optimized preoperatively.
Invasive monitoring, external defibrillator pads and an emergency method of pacing
are required.
Management of a patient with a pacemaker
The general condition of the patient has the most important influence on the anaesthetic
management. Co-morbid conditions should be addressed with further investigation
and treatment as necessary. The original indication for pacemaker insertion should
be sought and any recurrence or development of new cardiac symptoms noted and
investigated.
Information about the type of pacemaker, its mode and rate of pacing, and the
cardiologist and centre responsible for insertion are included on the pacemaker
registration card, carried by the patient, and on the notes in the cardiology unit. A code
on the card indicates the symptoms, ECG abnormalities and aetiology of the condition
that precipitated pacemaker insertion. If the card is unavailable, the information can
be obtained from the British Pacing and Electrophysiology Group National Database
(website http://ccad3.biomed.gla.ac.uk/bpeg).
Pacemakers should be checked annually (including a battery check) or every 6
months for devices implanted more than 6 years previously. An up-to-date pacing check
in a patient without new cardiological symptoms should ensure effective pacemaker
function and an additional preoperative pacemaker check is not required.
A thorough examination of the cardiovascular system is required and the position
of the pacing box must be confirmed. Usually, the box is in the pectoral region, though
abdominal sites are used. Investigations should be performed as indicated by the
patients condition and the type of surgery. Electrolyte abnormalities, particularly of
potassium, should be corrected. ECG can help determine the type of pacing by the
position of the pacing spike. All patients should have a chest radiograph so that the
position, number and integrity of the leads may be determined.
The patient should be monitored in a manner appropriate to the underlying condition
and the type of surgery being performed. ECG monitoring is essential and mechanical
methods of verifying pacing capture include pulse palpation, pulse oximetry and direct
arterial pressure monitoring (if this is indicated by the patients condition). Central
venous cannulation may be appropriate, but should be performed with caution if the
leads have been placed within the past month because they may be dislodged.
The presence of a pacemaker has little influence on the choice of anaesthetic
drugs. However, there are reports of demand pacemakers being inhibited as a result
of suxamethonium-induced fasciculations being interpreted as myocardial activity.
Conditions likely to precipitate arrhythmias (e.g. hypercarbia, electrolyte disturbances)
must be avoided.
The risk of developing bacterial endocarditis as a result of the implanted lead is
small and prophylactic antibiotics are not recommended unless there is some other
indication for their use.
Emergency drugs (e.g. atropine, isoprenaline) and alternative methods of pacing
must be available in case of pacemaker failure. Transvenous wires with an external
pulse generator or transcutaneous pacing, which uses electrodes attached to the skin,
may be useful. Transoesophageal atrial pacing is also an effective and simple pacing
method that can be used in anaesthetized patients, but requires an intact AV pathway;
the system consists of a pacing oesophageal stethoscope, which paces the left atrium,
the structure closest to the oesophagus.
Reprogramming, particularly an increase in heart rate, should always be considered in
patients with haemodynamic compromise or critical illness. Following exposure of the
pacemaker to possible interference or damage, it is necessary to perform a pacing
check.
Specific problems
Electromagnetic interference advances in the design of protective circuits in
the pacemakers have reduced, but not eliminated, the risk of damage from external
electrical sources. The most common source of electromagnetic interference is surgical
diathermy. Risks are reduced by the use of bipolar diathermy, application of diathermy
in short bursts and, in monopolar systems, positioning of the ground plate as far away
as possible from the pulse generator and leads. If difficulties are anticipated, it may
prove necessary to reprogramme the pacemaker to a fixed rate mode preoperatively.
Diathermy also interferes with ECG monitoring and alternative methods of monitoring
the pulse should be used (e.g. direct palpation, pulse oximetry). At one time, magnets
were used to convert the pacemaker to a fixed rate mode intra-operatively, but this is
no longer recommended because the combination of diathermy and the magnet may
induce a programme change (so called phantom reprogramming). The use of magnetic
instrument pads during surgery can also cause phantom reprogramming.
Cardioversion or defibrillation may damage the circuitry inside the pulse
generator. If the lead is damaged, the current can pass down the lead and may burn
the myocardium, causing a threshold increase and loss of capture. If defibrillation is
necessary, the current path should be perpendicular to the lead and as far away from
the pulse generator as possible.
Mobile telephones there have been reports of interference with certain types
of mobile telephones. The ringing phase is the most vulnerable time especially if the
phone is in a pocket near the pulse generator.
Transcutaneous electrical nerve stimulators (TENS) and peripheral nerve
stimulators can cause a tachycardia or inhibit a DDD or rate-responsive pacemaker and
it is recommended that these are reprogrammed to simpler modes.
MRI a pacemaker is a relative contraindication to MRI. If MRI is essential, the
pacemaker must be turned off or explanted before the examination (provided that the
patient is not pacemaker-dependent). Scans can be performed with a pacemaker in situ
but require multidisciplinary support and specialist expertise.
Ionizing radiation can damage the internal circuits in the pulse generator. Therefore
a paced patient undergoing radiotherapy treatment should have the function of the
pacemaker checked following treatment.
Lithotripsy treatment of renal calculi uses high-energy shock waves. In a patient
with a pacemaker the shock wave must be carefully timed with the ECG and the focal
point of the delivery probe must be kept at least 15 cm away from the pulse generator. If
the pulse generator is positioned in the abdomen it is important to avoid passing a direct
impulse through it. Rate-responsive and DDD pacemakers should be programmed to a
simpler mode for the treatment and the function checked following treatment.
Management of a patient with an ICD
Patients presenting for surgery who have an ICD must have the anti-tachycardia and
other functions disabled before surgery. Diathermy must not be used in the presence of
an active ICD unit because of the risk of damage. External defibrillation facilities must
be available and if defibrillation is required then the paddles or pads should be placed at
a right angle to the plane of the defibrillating/pacing lead.
Passing the defibrillator current through the pulse generator will damage it
permanently. The ground plate for the diathermy unit must be placed as far away from
the surgical site and the ICD as possible, and this distance should be at least 15 cm.
Central venous cannulation using the Seldinger technique can be arrhythmogenic and
back-up defibrillation facilities must be available. Care must be taken with recently
placed leads because of the risk of dislodgment. Following surgery, the device can be
reactivated and the function checked.
FURTHER READING
Clarke M, Sutton R, Ward D et al. Recommendations for Pacemaker Prescription for
Symptomatic Bradycardia. Report of a
Working Party of the British Pacing and Electrophysiology Group.Br Heart J 1991;
66: 18591.
Levine P A, Balady G J, Lazar H L, Belott P H, Roberts A J. Electrocautery and

Pacemakers: Management of the Paced
Patient Subject to Electrocautery. Ann Thorac Surg 1986; 41: 31317.
Mehta Y, Swaminathan M, Juneja R, Saxena A, Trehan N. Non Cardiac Surgery and

Pacemaker Cardioverter Defibrillator
Management. J Cardiothorac Vasc Anesth 1998; 12: 2214.
Zaiden J R. Implantable Cardioverter Defibrillators. J Cardiothorac Vasc Anesth 1999;

13: 47583.

Repeat Anaesthesia:
Hepatic Injury
Olga Siemaszko
Hamish A McLure
Olga Siemaszko is Specialist Registrar in Anaesthesia working on the North West

Thames Rotation. She qualified from St Bartholomews Hospital, London. Her interest
is chronic pain management.
Hamish A McLure is Consultant at the Royal Marsden Hospital. He qualified from the
University of Manchester. His interests are intensive care and regional anaesthesia.
Hepatic injury following repeat anaesthesia is a rare complication that may be

precipitated by many of the commonly used volatile anaesthetic agents. Halothane is
the most common culprit, causing either a mild dysfunction or a more severe fulminant
liver injury. Similar immune-mediated reactions may occur with enflurane, isoflurane
and desflurane. There are no investigations that can accurately predict who will be
affected, therefore those with a history of recent halothane anaesthesia or unexplained
fever or jaundice after a previous anaesthetic should avoid repeat volatile anaesthesia.
No cases of propofol-induced liver failure in adults have been published, therefore total
intravenous anaesthesia may be suitable for these patients.
Postoperative hepatic injury has profound effects on the future conduct of
anaesthesia. The injury ranges from asymptomatic derangement of liver enzymes
to fatal liver failure. The major precipitants are non-anaesthetic such as sepsis,
hypotension, hypoxaemia, transfusion-related viral infection (hepatitis B, hepatitis C,
cytomegalovirus, herpes virus), transfusion reaction, surgical trauma to the liver or
biliary tract, prolonged nutritional deficiency, or a combination of factors in patients with
pre-existing liver dysfunction.
Aside from the usual measures to minimize physiological stress by careful attention
to oxygenation, blood pressure and fluid status, there is little the anaesthetist can do to
prevent recurrent hepatic injury during repeat anaesthesia.
Pre-operative assessment: comfort may be gained from the knowledge that a patient
has survived a previous anaesthetic. If the patients previous anaesthetic charts are
available, valuable information may be gathered regarding difficulties with the airway
or drug reactions. Vigilance must be maintained, even if the patients last anaesthetic
was uneventful, because new and significant pathology may have emerged since then.
Also, postoperative complications may not have been recorded in the anaesthetic chart
or in the medical case notes.
Halothane hepatitis
Halothane was introduced into clinical practice in 1956. Compared with other
inhalational agents of the time, it was potent, non-irritant and non-flammable with
minimal toxicity, and it rapidly gained widespread popularity. However, within2 years,
reports describing cases of massive hepatic necrosis after halothane anaesthesia were
published.
Incidence
In 1969, the National Halothane Study was published in the USA. In this retrospective
study, the incidence of fatal hepatic necrosis was investigated in 856,000 patients
undergoing general anaesthesia. Fatal hepatic necrosis occurred in 7/255,000 of the
patients who received halothane. The study could not show a definite link between
halothane and hepatic injury, but confirmed that fatal liver disease following halothane
anaesthesia was uncommon. Subsequent studies have demonstrated an increased
incidence of hepatitis of about 1/6000 halothane anaesthetics, and there is now a
wealth of data describing the patterns of hepatic damage after halothane.
Characteristically, but not exclusively, halothane hepatitis develops in patients who
have had repeat halothane anaesthesia over a short period of time. It may have
been required for dressing changes, diagnostic radiology, or as part of multi-stage
procedures for the treatment of trauma, burns or complications of previous surgery.
The peak incidence occurs in those aged 5060 years, and 70% of affected patients
are over the age of 40 years. Children seldom develop halothane hepatitis (1/82,000).
Obese patients appear more at risk, possibly because of increased halothane
metabolism, or prolonged duration of exposure as halothane that has accumulated
in adipose tissue is metabolized and excreted. Despite equal exposure to halothane,
women are at greater risk than men (about 2:1). Drugs that induce cytochrome P450
(e.g. isoniazid, dexamethasone, phenobarbital (phenobarbitone)) increase the degree
of hepatic injury.
Pathology
Two forms of hepatic injury after halothane anaesthesia have been described:
a common (2030%), but mild, form in which there is a transient rise in liver
enzymes
a rare fulminant form with massive hepatic necrosis.
These are thought to be separate processes initiated by different metabolic pathways,
and not varying severities of the same pathological mechanism. Halothane is
metabolized in the liver by an oxidative pathway when the oxygen tension is high and
by a reductive pathway when the oxygen tension is low (Figure 1); both may occur
during uneventful anaesthesia.
Oxidative and reductive pathways of halothane

metabolism
Oxidative F Br Reductive
F C C H
e
O2 F Cl
Br
Cytochrome Cytochrome
P450 P450
F Br F
F C C OH F C C H
F Cl F Cl
H+

F
HBr
F O F H F H
F C C F C C H C C
F Cl F Cl F Cl
H2O
CTF CDF
HCl
F O
F C C
F OH
TFAA
The main products of oxidative metabolism are HBr and trifluoroacetic

acid (TFAA). The main products of reductive metabolism are bromine,
fluorine, 2-chloro-1,1,1-trifluoroethane (CTF), 2-chloro-1,1-
difluoroethylene (CDF).
Source: Br J Anaesth 1991; 67: 88
Reductive halothane metabolism occurs when there is an imbalance between liver

perfusion and oxygen demand, resulting in relative hepatocyte hypoxia. Under these
conditions, the mixed function oxidase, P450, favours a reductive metabolic pathway
with the formation of 2-chloro-1,1,1-trifluoroethane or 2-chloro-1,1-difluoroethylene.
These byproducts have not been shown to be directly hepatotoxic. However, liver
damage by free radical intermediates has been proposed. This type of hepatic injury
is more common if halothane anaesthesia is associated with hypotension and hypoxia.
The clinical features of this short, self-limiting illness are non-specific and include
lethargy, fever, nausea and jaundice. Biochemical tests show an elevation of alanine
and aspartate aminotransferase.
Oxidative halothane metabolism is more common than reduction metabolism and

proceeds via a trifluoroacetyl (TFA) halide, which is not thought to be hepatotoxic.
However, TFA halide may bind covalently to liver microsomal proteins. In susceptible
patients, this TFAprotein complex acts as a hapten against which anti-TFA antibodies
are formed.
On repeated exposure to halothane, a hypersensitivity response mediated by
anti-TFA antibodies occurs and liver damage ensues. Typically, liver failure develops
within 15 days of the last exposure to halothane. The clinical picture is similar to viral
hepatitis or drug-induced hepatic damage, but as there are no pathognomonic features
the diagnosis is often made by exclusion. Histologically, the pattern is predominantly
centrilobular necrosis, but may range from multifocal necrosis to panlobular massive
necrosis.
Treatment is essentially supportive, with transfer to a specialist unit when severe.
Fulminant disease has a mortality of up to 50%.
Immunological effects: features supporting an immunological basis for the hepatic

injury include the clinical picture of hepatitis with fever, rash, arthralgia and eosinophilia
in patients with a history of atopy, drug allergy or adverse reactions to halothane. In
addition, there is a clear association with prior exposure to halothane and worsening
response with subsequent halothane anaesthetics. In up to 70% of patients with
halothane hepatitis, an enzyme-linked immunosorbent assay may be used to detect
antibodies to TFA proteins. Proponents have suggested that free radicals from the
reductive pathway may initiate the hepatic damage, which is then exacerbated by an
immunological response.
Prevention
Halothane should be avoided in patients who have been exposed to halothane recently,
or who have a history of halothane hepatitis. The Committee on Safety of Medicines
(CSM) advises that halothane should be avoided if a patient has had an adverse
reaction following a halothane anaesthetic, previous exposure within 3 months or a
history of unexplained jaundice or pyrexia after exposure to halothane.
Hepatitis associated with other volatile agents
The use of halothane has declined with the introduction of newer volatile
agents (enflurane, isoflurane, desflurane, sevoflurane). Isoflurane and desflurane are
oxidatively metabolized producing an identical TFA hapten to that seen with halothane.
The metabolite of enflurane is immunologically similar though not structurally identical.
Consequently, enflurane, isoflurane and desflurane have the potential to produce
hepatic injury by an immune response directed at TFA haptens or similar structures.
The incidence of hepatotoxicity correlates with the degree of cytochrome P450-
mediated metabolism, which is 20% for halothane, compared with 2%, 0.2% and 0.02%
for enflurane, isoflurane and desflurane, respectively.
Enflurane hepatitis is uncommon with an incidence of 1/800,000. Isoflurane hepatitis
is less common and a literature review revealed only one case report of desflurane-
associated hepatitis. Isoflurane does not undergo reductive metabolism (nor does
enflurane), free radicals are not produced and hepatic perfusion is maintained to a
greater degree than with halothane, contributing to the low incidence of isoflurane-
induced hepatotoxicty. With both enflurane and isoflurane hepatitis, the initial exposure
has been reported to be to a different agent than that believed to be precipitating the
hepatic damage, indicating possible cross-reactivity. Consequently, the CSM guidelines
regarding patients who sustain a hepatic injury after one halogenated agent indicate
that it is probably best to avoid all others.
Sevoflurane is metabolized to a similar degree to enflurane but does not form
trifluoroacetic acid. A mild elevation of liver enzymes after repeat sevoflurane
anaesthesia has been shown, but there have been no cases of fulminant hepatic
necrosis.
FURTHER READING
Bottinger L, Dalen E, Hallen B. Halothane Induced Liver Damage:
Analysis of the Material Reported to the Swedish Adverse Drug Reaction Committee
196673. Acta Anaesthesiol Scand 1976; 20: 406.
Bunker J, Forrest W, Mosteller F, Vandam L. National Halothane Study. A Study of
the Possible Association between Halothane Anesthesia and Post-operative Hepatic
Necrosis. Washington DC: US Government Printing Office, 1969.
Inman W, Mushin W. Jaundice after Repeated Exposure to Halothane: An Analysis of
Reports to the Committee on Safety of Medicines. BMJ 1974; 896: 510.
Ray D, Drummond G. Halothane Hepatitis. Br J Anaesth 1991; 67: 8499

Day case
Anaesthesia
on CD-ROM
Assessment of Recovery in Day
Surgery
Alexander P L Goodwin
Alexander P L Goodwin is Consultant in Anaesthesia and Intensive Care at the Royal

United Hospital, Bath, UK. He qualified from St Thomass Hospital Medical School,
London, and, after serving in the Royal Navy for 7 years, completed his anaesthetic
training in Cambridge and Oxford. His research interests include morbidity in day
surgery and analgesic pharmacology.
Surgical procedures of increasing complexity and duration can now be undertaken

in day surgery units. For example, cholecystectomy and prostatectomy are now
acceptable day case procedures. These procedures are appropriate for day surgery
only if the clinician can ensure that the patient will return home safely, having recovered
from the effects of anaesthesia and surgery. The assessment of recovery is therefore
an important part of the patients hospital stay. Recovery includes return of normal
physiological and psychomotor function together with a minimal level of morbidity
associated with anaesthesia and surgery.
Phases of patient recovery
Recovery is a continuous process, the beginning of which overlaps with the end of the
surgical procedure. Patients are not fully recovered until they have returned to their
preoperative physiological and psychomotor state. The process may last for days, but it
can be divided into distinct phases.
Early recovery (first-stage recovery) end of anaesthesia until the patient has
recovered protective reflexes and motor function. This occurs in the recovery unit or
post-anaesthesia care unit.
Intermediate recovery (second-stage recovery) patients are fit enough to be
transferred to the day surgery ward and then home. Patients are considered to have
achieved street fitness.
Late recovery (third-stage recovery) full recovery and physiological recovery.
The patient can return to work. Late recovery occurs in the patients home.
Tests of recovery
Clinical
Day case anaesthetists may use their experience and knowledge to decide when a
patient is fit for discharge. However, if clinicians are to delegate this decision, a well-
designed scoring system is a useful tool for those assuming this responsibility. In
some countries, time dictates how long patients remain in recovery areas. However,
time-based recovery is inappropriate because of inter-patient variation and advances
in surgery and anaesthesia that allow patients to move from one recovery phase
to another more quickly than previously laid down or expected. Thus, criteria-based
recovery has been introduced. In this system, the patient dictates the speed at which he
or she progresses from one recovery stage to another.
Tests of early recovery involve recording the time at which specific events occur:
eyes open
date of birth recalled
orientation
able to obey commands
stable vital signs
recovered protective reflexes.
Scoring systems involve the evaluation of a number of patient factors. For first-stage
recovery the Steward Score (Figure 1) and Modified Aldrete Scoring System (Figure 2)
are used to determine when patients are ready for discharge from the recovery room;
for second-stage recovery the Excitement Score or the Post-anaesthesia Discharge
Scoring System (PADS; Figure 3) is used.
Scoring systems cannot be used to determine the patients suitability for discharge
home because they fail adequately to address pain, nausea, vomiting, surgical
complications and patient ambulation. Discharge criteria have therefore been laid down
to assist in the evaluation of a patients street fitness following day surgery. Street
fitness is an ill-defined term, which implies that the patient has recovered the ability to
make everyday decisions under everyday circumstances. However, decision-making is
not amenable to objective testing. Each day surgery unit has discharge criteria tailored
to the population served by the hospital (Figure 4). One criterion that is often devalued
is that the patient should feel confident about leaving hospital. In the authors hospital,
this criterion is considered most important.
The patient must be discharged by the person who administered anaesthesia and
the person who performed surgery, or by their designates. Written instructions for
the postoperative period at home should be provided, including a contact telephone
number. Owing to anxiety, extraneous noise and the amnesic effects of some drugs,
patients may not assimilate verbal information, therefore written instructions are
necessary. The patient must be accompanied by a responsible adult who will escort
them home and ensure that they are not alone for at least the first 24 postoperative
hours. Patients should avoid alcohol and refrain from driving for at least 48 hours.
Recently, the need to void urine and tolerate oral fluids before discharge has been
questioned. In one study, the mandatory drinkers had a higher incidence of nausea and
a longer discharge time. No patient in either group required admission. Eliminating the
requirement to tolerate oral fluids may shorten the stay in the day surgery unit. Waiting
for the patient to pass urine may also delay discharge. There is some evidence that
patients who are not considered to be at high risk of developing urinary retention can
be discharged safely without developing urinary problems at home. Risk factors for
postoperative urinary retention are:
history of postoperative urinary retention
spinal/epidural anaesthesia
pelvic surgery
urological surgery
perioperative catheterization.
Removing the requirement to tolerate oral fluids and void urine and separating the pain
and nausea/vomiting scores has led to a modified version of PADS (Figure 3).
The use of guidelines together with common sense should prevent the premature
discharge of patients who later experience postoperative complications requiring their
readmission to hospital.
Steward Score1
Consciousness
Awake 2
Responding to stimuli 1
Not responding 0
Airway
Coughing on command or crying 2
Maintaining a good airway 1
Airway needs maintenance 0
Movement
Moving limbs purposefully 2
Non-purposeful movement 1
Not moving 0
1
Six points are required for discharge.
Modified Aldrete Scoring System1
Activity: able to move, voluntarily or on command

Four extremities 2
Two extremities 1
No extremities 0
Respiration
Able to breathe deeply and cough freely 2
Dyspnoea, shallow or limited breathing 1
Apnoea 0
Circulation
Blood pressure within 20 mm Hg of preoperative level 2
Blood pressure within 2050 mm Hg of preoperative level 1
Blood pressure 50 mm Hg of preoperative level 0
Consciousness
Fully awake 2
Arousable on calling 1
Unresponsive 0
Oxygen saturation
Saturation > 92% 2
Needs oxygen to maintain saturation > 90% 1
Saturation < 90% with oxygen 0
1
Nine or more points are required for recovery to be confirmed.
Post-anaesthesia Discharge Scoring System for assessing home readiness1
Vital signs
Vital signs must be stable and consistent with age and preoperative baseline
Blood pressure and pulse within 20% of baseline 2
Activity level
Patient must be able to ambulate at preoperative level
Steady gait, no dizziness, or meets preoperative level 2
Requires assistance 1
Unable to ambulate 0
Nausea and vomiting

Minimal: successfully treated with oral medication 2
Moderate: successfully treated with intramuscular medication 1
Severe: continues after repeated treatment 0
Pain
The patient should have minimal or no pain before discharge
The level of pain that the patient has should be acceptable to the patient
Pain should be controlled by oral analgesia
The location, type and intensity of pain should be consistent with
the anticipated postoperative discomfort
Acceptable 2
Unacceptable 1
Surgical bleeding
Postoperative bleeding should be consistent with the expected blood
loss for the procedure
Minimal: does not require dressing change 2
Moderate: up to two dressing changes required 1
Severe: more than three dressing changes required 0
1
Nine points are required for discharge.
3
Guidelines for safe discharge after day surgery
Vital signs must have been stable for at least 1 hour
The patient must be able to:

orientate themselves in person, place and time
keep oral fluids down
void urine
dress
walk without assistance
The patient must not have

more than minimal nausea and vomiting
excessive pain
bleeding
Psychomotor tests
Most psychomotor tests are complex and difficult to use routinely (Figure 5). To
assess psychomotor function accurately requires tests to measure sensory, motor,
physiological and central processing. This is difficult in the conventional setting.
When testing any individuals psychomotor function the following precautions must be
taken.
Each individual acts as his/her own control.
Time of day may affect performance.
The hormonal effects of the menstrual cycle must be taken into account.
Practice or learning effects must be reduced, either by allowing sufficient learning
time before collecting results, or by having a control group not undergoing anaesthesia.
The ideal psychomotor test has the following qualities:
quick and simple to perform
no learning effect
uses inexpensive equipment
needs an unskilled operator
is sensitive to the residual effects of all drugs used in anaesthesia
has sufficiently reproducible results that firm conclusions may be drawn from
individual measurements.
Despite the number of available tests, none has been validated by follow-up studies
to provide adequate criteria to guide discharge in the day surgery environment.
Lockwood has suggested that a psychomotor test suite comprising body sway,
inspection time, critical flicker fusion, digital symbol substitution and a picture recall test
should be used to study recovery from anaesthesia. It is unlikely that additional tests
would reveal an effect not shown by this suite of tests.
Psychomotor testing therefore allows comparison between anaesthetic regimens. If
one anaesthetic regimen leads to a swifter return to baseline psychomotor function
then it would be valid to assume that the higher intellectual functions also return more
quickly. At present, there is no place for these psychomotor tests in routine clinical
practice.
Examples of psychomotor tests
Paper and pencil tests (measure the number of correct entries in a specific
time)
Trieger dot test
Perceptual speed tests
P deletion tests
Digit symbol substitution test (most sensitive paper and pencil test)
Other tests
Maddox wing test (measures imbalance of extraocular muscles)
Reaction time tests
Peg board tests
Flicker fusion tests (tests central integrity)
Tapping board tests
Driving simulators
Balance tests (measure postural sway)
Following regional anaesthesia

In the UK, the use of regional anaesthesia (spinal and epidural blocks) is uncommon.
The perceived problems are concerns over post-dural puncture headache, urinary
retention and the local anaesthetic agents available. However, if regional anaesthesia
is used, it is important to ensure that the motor, sensory and autonomic blocks have
receded before allowing patients to ambulate. Suitable criteria to judge if this has
occurred are:
normal perianal sensation
plantar flexion of foot
proprioception in big toe
normal blood pressure on standing and sitting.
Ability to walk to the lavatory to pass water may be a suitable test of recovery from
regional anaesthesia.
Patients, who have had a more peripheral nerve block (e.g. brachial plexus block)
do not need to wait for the return of full sensation before discharge. They may be
sent home with the anaesthetized area protected, with precise written and verbal
instructions, and a 24-hour contact number.
Causes of prolonged recovery following regional and general anaesthesia are given
in Figure 6.
Causes of prolonged recovery following regional and general anaesthesia
Pain
Nausea and vomiting
Haemorrhage
Cardiovascular or pulmonary dysfunction
Wound drains
Needing observation
Lack of escort or inadequate home conditions
Safety and legal considerations
Following day case surgery, a patient may leave the clinicians care under the residual
effects of anaesthetic drugs. It is an offence for a person to drive while under the
influence of drugs. Operating machinery under the influence of these drugs may lead
to an accident causing injury and/or damage to property. The effects of alcohol may
be potentiated.
If not warned about these potential problems, the patient and anybody injured as a
result of the patients actions may hold the anaesthetist responsible. Patients must be
warned of the danger and the fact documented.
Driving after anaesthesia

In 1972, Ogg found that 73% of car owners drove within 24 hours of outpatient
anaesthesia. In 1996, the author found that no patients drove within 12 hours of surgery,
but that 3.5% drove within 24 hours of general anaesthesia. The patients who drove
within 24 hours had all been warned not to drive for at least 24 hours but were
convinced that they were safe to drive. Safe driving requires an effective response to
multiple secondary tasks. The primary task of control can be undertaken with impaired
cerebral functioning, but the ability to react to the unexpected is crucial. A higher level
of coordination is required to control a motorcycle or bicycle because the rider also has
to balance. Previous research into the effects of anaesthesia on the ability to drive has
involved single anaesthetic agents in volunteers not undergoing surgery.
A survey of motor insurers found that generally they would accept the medical
advice given to the patient. However, one company commented that in the event of a
claim, if the advice given was shown to be wrong, they might seek reparation from the
hospital or individual concerned.
In the UK, 24 hours is the most common period of abstinence advised and is the
time considered appropriate by the Medical Advisor to the Driver and Vehicle Licensing
Agency. Recently, it has been suggested that the residual effects of anaesthesia and
surgery extend into the second and third postoperative days. This may be a result
of the residual effects of anaesthetic agents on higher cerebral centres or caused by
the increased metabolic demands induced by the endocrine response to surgery. It
is the authors practice to advise patients not to drive for 48 hours following general
anaesthesia.
FURTHER READING
Klepper I D, Sanders L D, Rosen M, eds. Ambulatory Anaesthesia and Sedation.
Oxford: Blackwell Scientific Publications, 1991.
Kortilla K. Recovery from Outpatient Anaesthesia. Anaesthesia 1995:

50 (suppl): 228.
Lockwood G G. Methods of Assessment and Recovery. In: Whitwam J G, ed. Day-

Case Anaesthesia and Sedation. Oxford: Blackwell Scientific Publications.
Marshall S I, Chung F. Discharge Criteria and Complications after Ambulatory Surgery.

Anesth Analg 1999; 88: 50817.
Millar J M. Recovery from Anaesthesia. In: Anaesthesia Rounds. Abingdon: The

Medicine Group, 1996.
Rudkin G E. Patient Recovery and Discharge. In: Millar J M,

Rudkin G E, Hitchcock M M, eds. Practical Anaesthesia and Analgesia for Day
Surgery. Oxford: BIOS, 1997.

Clinical Service and Audit:
Working Clinical Systems
Kerri Houghton
Kerri Houghton is Consultant Anaesthetist and Director of Day Surgery in the

Department of Anaesthesia, Torbay Hospital, Torquay, Devon, UK.
Day surgery environment

In response to the Royal College of Surgeons Working Party Report (1992) and the
Audit Commission (1992) advice on day surgery, day surgery rates have increased and
new facilities have been developed. Different day surgery services have evolved with
different styles of management: premises vary from modifications of existing facilities,
to free-standing units; operational policies vary from the proactive to the non-existent;
and case mix is variable and not always true day case. Where day surgery is not
actively and continuously monitored and audited, good facilities can remain under-
utilized or unpopular, or become inappropriately used. Some purpose-designed facilities
still treat in-patients, thereby defeating much of the purpose of the original development
and making audit more difficult. Many units still lack good information systems and
have difficulty defining, auditing and controlling their activity, yet the success of their
parent hospital in managing surgical beds is largely dependent on the good use of their
day surgery facilities.
Information to enable audit to track the success of a day surgery clinical service
closely parallels that required for management in this setting, and systems should
be contemporaneous and accessible to busy clinicians, though they seldom are. The
information generated should enable analysis of:
the success and viability of the day surgery facility as a whole
the quality of the day surgery practice within the facility.
If the clinical process fails and the patient is admitted, then not only has the patients
experience fallen short of what he/she and the clinicians expected, but also the savings
have not been made. If operating lists are under-used, fewer patients are treated. If
patients fare badly at home, clinicians are discouraged from undertaking day surgery
or at least extending their practice. Information should be available to enable rapid
identification of activity, and recognition and anticipation of both clinical and managerial
problems on a daily basis. Such information can be used to drive true audit and
continuous quality improvement.
Use of clinical systems

The need for clinical information systems that help patients and provide sound data to
support clinical and managerial decisions is well recognized. The Audit Commission
has stated that information is one of the most important resources that a hospital holds.
In order for a clinical service to evolve, data about individual patients must be grouped
and abstracted, and then related to data about staffing facilities and other resources.
It has been shown that clinical practice is seldom altered by evidence-based medicine.
This must be due, at least in part, to the difficulties in obtaining relevant information.
Clinicians require different types of information, which is gained from diverse
sources. In the context of daily practice, a high-quality clinical database can be used
to provide accurate information for clinical practice, audit and administration. Clinicians
perceive most health service information systems as offering no obvious benefits for
patient care or themselves.
Service, audit and systems
Essential features of a computerized day surgery system

Patient information should be available for every stage of the process from pre-
assessment and booking, through anaesthesia and surgery, to recovery, discharge
and follow-up. Ideally, the patient record should be held on an on-line computerized
management information and audit system, and should be instantly retrievable. It should
be perceived as being easy to use and helpful by all staff, and be capable of being
integrated with other systems to provide the comprehensive Electronic Patient Record
(EPR) of the future. Alternatively, the ideal features of a day unit system should be
embedded in a total EPR solution. The ability to cross-reference data easily, from a
user-friendly and virtually instantaneous database, without the need to use complicated
report packages, is particularly helpful in this environment. It should also be possible to
identify omissions and inconsistencies in data entry readily. Clinical coding in hospitals
is known to be fraught with difficulties. If surgical teams enter the diagnosis and
procedures performed directly on to a system that already holds the relevant clinical
codes, the coding can be automated. Sample parallel manual and automatic coding
checks should be undertaken intermittently to validate coding and should demonstrate a
high level of accuracy and completeness.
Any computerized system should also facilitate management processes in a fast
throughput environment, and provide features such as:
individualized surgical diaries
direct booking on to operating lists in a manner that complies with the National
Booked Admissions Project objectives
a pre-assessment module to record clinical and booking details, decisions and alerts
automatic generation of reminders for patients who have not confirmed their
attendance
automated communications with primary care workers
automated generation of operating lists and, subsequently, the individual operating
record
automated coding
extensive and flexible reporting.
As large numbers of patients pass through day surgery units, there is a potential wealth
of clinical information waiting to be gathered; information relating to the unit as a whole,
and to individual patients and clinicians.
The day surgery process the need for information

The essential criteria for successful day surgery are well understood.
Operations should be appropriate.
Suitable patients should be identified.
The work should be undertaken by experienced surgeons and anaesthetists.
Additional criteria for success include:
well-informed patients
good dedicated facilities
first-rate organization
good liaison with primary care workers
follow-up and audit.
As more patients and procedures are perceived as treatable on a day-stay basis,
successful application of these criteria becomes increasingly important. The ideal
process through which patients pass for their treatment should therefore incorporate:
good identification of appropriate procedures by the referring surgeon (i.e.
those without the expectation of excessive postoperative pain, bleeding or other
complications)
elimination of patients identified as unsuitable on medical or social grounds through
a comprehensive pre-assessment process, now normally nurse-based and supported
by anaesthetists
efficient (and ideally integrated) booking and pre-assessment to minimize steps in
the process, align urgency with the date of surgery and maximize use of operating
time
information for patients and carers about pre- and post-operative expectations.
Measures of all of these process functions can be developed and easily audited. For
example, numbers of patients who do not attend on the expected day of surgery are
likely to be higher when negotiated booking and pre-assessment are not performed.
Poor pre-assessment, or none at all, results in a higher rate of cancellation on the day
of surgery. Poor selection of either surgical procedure or inadequate pre-assessment
results in higher unplanned admission rates. Poor discharge processes are likely to
produce higher re-admission rates, callout of primary care services or difficulties at
home. Poor booking processes can result in under-utilized operating time and wasted
resources.
Standard management reports

Any day surgery facility should be capable of producing standard reports easily.
Simple, automated, daily reports showing cases performed, those who do not
attend, cancellations and unplanned admissions can point to specific difficulties.
At a minimum, monthly reports should be generated (Figure 1). This data can be
used to shape the service by determining:
the correct number of lists for each specialty or surgeon
the impact of pre-assessment
the need for in-patient beds
clinical complications.
Only when data of this quality are widely available will it be possible to compare general
and specific practice in different units.
Suggested items for standard monthly reports
Total activity of the unit

Number of cases per specialty
Pre-assessments performed and numbers accepted/rejected
Numbers and procedures for each referring consultant
Numbers and procedures for each operating surgeon
Numbers, procedures and codes by specialty
Cancellations on the day of surgery and reasons
Non-attendance rates
Unplanned admissions with reasons
Sessions/lists used and utilization per session
Qualitative data
Information should not only ensure a successful, viable unit, but also help to promote
safe clinical practice and a good experience for the patient. Data to promote safe
clinical practice should be available through monthly reports as described above.
Clinical complications and other important aspects of patient feedback require some
direct information gathering. Clinical outcome measures and patient feedback are both
desirable and increasingly sought by purchasers, and should include patient satisfaction
as well as clinical outcome and complications. The increase in day surgery has been
a cause of concern for all clinicians, including GPs, who are anxious about quality of
care for their patients and a possible rise in night calls at a time when the availability of
district nursing services is decreasing.
One system allowing access to qualitative data, which was first designed for use in
the pioneering Norfolk and Norwich Day Surgery Unit (Daynamics Calcius Systems
Ltd), incorporates all the functions described above. The system is also used in the
authors unit, in which an additional module was developed for audit. The responses to
our structured postoperative telephone questionnaire, which patients receive the day
after surgery, are entered directly on to the system, thereby linking the follow-up with
the entire patient episode. This addition represents a significant advance in clinical audit
by allowing rapid identification of clinical problems, and their relationship to procedures
within the unit, answering many questions on a daily basis. Reasons for analysing
patient responses through a postoperative telephone call are summarized in Figure 2.
The format of the questionnaire is simple and contained on one screen. The enquiry is
kept simple because telephone calls are time-consuming and complexity can impede
decision making. The questions chosen (Figure 3) are directed at identifying;
postoperative symptomatology
recourse to primary care services
patient expectation
patient satisfaction
readmission rates (i.e. readmitted after discharge).
Analyses of responses from telephone questionnaires carried out by other units have
been published but, inevitably, if a manual collection process is used, a research worker
is required to gather the data over a long period. It is preferable to be able to look at
large numbers of variables in a short time, in order to trawl for problem (or successful)
areas of practice without having to set up complex reports each time (Figure 4). It
should be possible for a clinician with minimal computer expertise to run reports such
as these virtually instantaneously and the data should be easily importable into a
standard data-handling package for further analysis if required (Figure 5).
Despite the efficiency of entering patient responses directly, the generation of hard
copies of the patient feedback telephone calls makes daily review by a doctor or senior
nurse easier. Patients concerns can then be responded to, compliments passed on
to the individual staff concerned (which appears to have a positive impact on staff
attitudes and practice) and complications immediately identified.
Specific clinical issues that have been identified and followed up in the authors
unit through this process include patients readmitted with retention or bleeding
postoperatively, a low-risk patient suffering a pulmonary embolus the day after
arthroscopic knee surgery (subsequently confirmed), and a non-epileptic child who
had two possible convulsive episodes the day after surgery; the child was referred for
further investigation and possible drug causes were investigated and reported. Patient
complaints about waiting times have persuaded some surgeons to pilot an appointment
system for operating lists. It is highly unlikely that these incidents would have been
picked up without the follow-up.
Improvements in clinical practice have been made through education of clinicians,
particularly in relation to performance of local anaesthetic techniques and postoperative
analgesia. Clearly, a further, later follow-up for all patients would be desirable.
Rationale for the postoperative telephone call
To provide a clinical service to patients

To detect and remedy areas of practice that are unsuccessful
To obtain patient feedback for audit purposes
To reassure hospital clinicians that their practice is safe and encourage more
referrals
To provide some outcome measures for clinicians, managers and
purchasers
To promote a good image for the day surgery facility
Example of a telephone follow-up questionnaire1
In general, how did you feel?

very good
good
reasonable
not so good
bad
Was this
better than expected
much as expected
worse than expected?
Did you experience any

dizziness
drowsiness
feverishness
pain2
nausea2
vomiting2
bleeding?
Have you had to contact anyone since discharge (unplanned)? Was it GP/
District Nurse/Practice Nurse/A & E Dept/Day Unit/SHO on-call?
Is further help required?

From whom?
Overall were you

very satisfied
satisfied
dissatisfied?
Did you like the unit?

Did you like being a day case?
Did you have trouble parking?
General comments (entered free hand)
1
Failure to contact the patient is also recorded.
2
Quantified if present.
Examples of useful practical monitoring
Complete breakdown of workload by specialty, surgeon, and age/sex of

patient over any chosen period
Individual clinicians personal records including their own patients feedback
Seniority of surgeons and anaesthetists working in the unit
Procedures producing most postoperative difficulties
Patients experience of individual postoperative symptoms, by severity
(graded), specialty, procedure, surgeon, anaesthetist, time of day, ASA grade
and anaesthetic type
Unplanned admissions by reason, surgeon, anaesthetist, and procedure
Factors contributing to unplanned admissions, such as patient selection,
pre-assessment, experience of surgeon, surgical technique, experience
of anaesthetist, anaesthetic technique, timing of session (a.m./p.m.), and
nursing factors
Success rates in contacting patients postoperatively
Patient satisfaction across all specialties, adults and children
Primary care callouts
Readmissions from home overnight
Analysis of cancellations and rebooking workload for clerical staff
Examples of specific reports or audits
Nausea and vomiting rates in children under 14 years undergoing squint

surgery
Patient satisfaction and unplanned admissions following the introduction of
new lists or procedures to the unit
Unplanned admission rates and reasons in gynaecological laparoscopy and
inguinal hernia repair
Comparison of individual anaesthetists techniques in laparoscopic surgery
Procedures producing severe pain identified at patient feedback
Success in contacting patients after discharge
Satisfaction of carers with transfer of the service for special needs patients
undergoing dental treatment in the new day surgery unit
Use of laryngeal mask airways and endotracheal tubes
Profile of unit work for identification of specialist registrar training
requirements
Analysis of patient comments/complaints
Review of workload on some operating lists (leading to an increase in cases
booked)
Compliance with unit policy for senior operators and anaesthetists
Identification of numbers of intraocular lenses following both extracapsular
extraction and phaco-emulsification to obtain accurate costings for the lists
Review of paediatric activity
Potential for future anaesthetic and surgical practice

Ideally, any patients electronic record should include an anaesthetic record-keeping
system to allow specific techniques, perioperative events, and drugs and their doses to
be linked to postoperative follow-up.
Computer-aided drawing tools for surgical operating records could, potentially, allow
data collection of the site and frequency of pathological lesions and their treatment.
The concept of being able to set up automatic reports to allow re-runs of previous
audits is attractive and should be striven for.
Using the data to inform clinical practice

Clearly, the data collection described is not clinical research and, if these data are
to become true audit information, audit criteria must be defined and performance
measured against them. Nevertheless, important information can be gained and may
provide pointers for more structured research projects. It becomes possible to gain a
picture of what is really happening to patients. The patients have not been subject to
double-blind, controlled trials; they have been treated in a real hospital by identifiable
clinicians under real conditions. Such information is now essential to produce a realistic
clinical governance agenda for day surgery.
Presenting results of surveys and audits at local surgical and anaesthetic audit
meetings, to individuals and other groups (e.g. GPs) informs local practice. The
information can be sensitive and requires diplomatic handling. It is wise to insist that
clinicians who request data for audits gain prior permission from all colleagues whose
work is involved, and that no clinical data are presented in identifiable form without the
permission of the individual. Information should be provided to managers only with the
permission of the clinician, though anonymized monthly activity reports are generally
less contentious. Increasingly, however, clinicians will have to be accountable for their
own information on outcomes and wide variations in practice will have to be justified.
FURTHER READING
Allery L A, Owen P A, Robling M R. Why General Practitioners and Consultants
Change their Practice: a Critical Incident Study. BMJ 1997; 314: 8704.
Anderson C. Measuring What Works in Health Care. Science 1994; 263: 10801.
Audit Commission. All in a Days Work. London: HMSO, 1992.
Audit Commission. For Your Information: a Study of Information Management and
Systems in the Acute Hospital. London: HMSO, 1995
Black N. Developing High Quality Clinical Databases. BMJ 1997; 315: 3812.
Celliott P. Making Clinical Information Work. BMJ 1994; 308: 8023.
Commission on the Provision of Surgical Services. Guidelines for Day Case Surgery.
London: Royal College of Surgeons of England, 1992.
Jackson I J B, Paton R H, Hawkshaw D. Telephone Follow-up the Day after Day
Surgery. One-Day Surg 1997; 6: 57.
Kinn S, Lee N, Millman A. Using Computers in Clinical Audit. BMJ 1995; 311: 73942.
Ralphs D N L, Shiu S. A Dedicated Computer System for Day Surgery Units. The
Health Business Summary April 1994.
Smith R. What Clinical Information Do Doctors Need? BMJ 1996; 313: 10628.
Wyatt J C. Hospital Information Management: the Need for Clinical Leadership. BMJ
1995; 311: 17580.
Acknowledgement
The author would like to acknowledge the expertise and cooperation of Stephen
Shiu, Calcius Systems Ltd, and Zeneca Pharma and GlaxoWellcome for
support to enable further development of audit in the authors unit.

Design Requirements of Day
Care Units
Mark Hitchcock
Inge Falk van Rooyen
Mark Hitchcock is Consultant Anaesthetist and Director of Day Surgery at

Addenbrooke's NHS Trust, Cambridge, UK. He qualified from St Bartholomew's
Hospital, London, and trained in anaesthetics in Cambridge and Bristol, UK.
Inge Falk van Rooyen is Specialist Registrar in Anaesthesia at the Norfolk and
Norwich Hospital, East Anglia, UK. After qualifying from Stellenbosch University, South
Africa, she specialized in anaesthesia. Her main interests are day stay anaesthesia
and teaching.
The efficient design of day care units is important to optimize costs and maintain quality
of care and patient safety while processing large numbers of patients.
The rules that preclude the treatment of adults and children alongside each other
significantly influence the provision of day surgery services for children. The design of
the day care unit will reflect the level of need for paediatric care in the community by
providing a dedicated childrens unit, dedicated childrens sessions within the adult unit,
or accepting the fact that the use of the unit by children will be limited.
Basic design considerations
The day care unit must allow direct flow lines for patients and supplies, in order to
avoid cross-infection and to maintain sterility. The layout must ensure that preoperative
and postoperative patients do not meet. To maximize the efficient use of resources,
the level of double handling of patients and supplies must be minimized, and careful
consideration must be given to staff traffic patterns. The plan of a typical day care unit
Basic day unit design
1
Traffic patterns
In the USA, which has led the field in day surgery, there is a fixed prototype design
for day care units. Each unit is divided into three zones. The front third is a non-sterile
reception area for the public and houses the administration centre. The sterile area,
containing the operating theatres, is situated in the back third of the building, and the
middle section comprises patient preparation and recovery areas, storage facilities and
staff lounges. The central section is accessible from both the sterile and non-sterile
sides of the building along one or two corridors, one of which may be sterile.
Within the unit, the traffic pattern flows from front to back. Patients and staff enter
through reception, staff move to the facilities in the central section, while patients
complete the administrative procedures, and can remain with their escorts before
moving into the central section for preoperative preparation. After surgery, patients are
taken to the recovery area and monitored until they are safe to be discharged. They
pass back through reception, where they can be collected by their escort.
Technology
An integrated management system, networked to the main hospital, provides an
efficient method of processing patients on a daily basis, and produces statistical
information, which can be used as an audit tool to ascertain patterns, manage
productivity and resources. Such a system should improve legibility and accuracy of
information and allow efficient management of supplies and a reduction in storage
requirements in the unit.
General requirements
The decor should create a sense of relaxation and use finishes that are easy to clean
and maintain. Floors should be on a single level, and should be non-slippery and
hardwearing. Wherever possible, natural daylight should be used. Fire precautions
should ensure that the building can be evacuated quickly and easily.
Specific requirements
Location/site selection and entrance

The main requirement is the need for easy access for patients, staff and services.
Ideally, the unit should be freestanding, and of single-storey construction with dedicated
car parking. Siting the unit on in-patient hospital sites allows direct access to support
services without compromising independence. An easily identifiable main entrance is
essential. There should be entrances for secondary supplies off the street. It should be
possible for patients to be dropped off and collected by their escort at the entrance,
which may be covered by a canopy to offer weather protection.
Reception area
The reception area is the non-sterile area of the unit where the administrative centre
is located. It should contain a reception desk with information technology facilities and
allow good visibility over the waiting area and any play facilities for children. The design
of the desk should accommodate disabled patients.
The main waiting area should be informal, perhaps containing a fish tank
and reading material, and should provide space for people using walking aids or
wheelchairs. Sufficient lavatories should be provided including some with disabled
access; one per ten users is recommended.
Patient preparation, second- and third-stage recovery area

The design of the patient preparation area and the second- and third-stage recovery
area should incorporate administrative facilities.
Patients trolleys may be separated by curtains hung from suspended tracks, and
should allow adequate space for changing. A bedside cabinet should be provided for
storage of valuables and a chair provided for the escort.
Male and female patients can be separated most easily by grouping those of the
same gender together, according to the numbers of each on the operating list. This
obviates the need to duplicate the facilities, and allows most efficient use of the ward
area.
Trolleys are preferred to beds because they are more economical, occupy less
space and avoid the need to transfer immobile patients from one platform to another.
The use of thick mattresses makes them comfortable, while a 90o adjustable backrest
promotes their use for first- and second-stage recovery. A mobile resuscitation trolley
is needed.
The provision of hand basins (two per ten trolleys) and face mirrors allows patients
to check their appearance before discharge. There should be a separate consulting/
examination room to provide privacy if required. This can also be used for pre-
assessment or teaching.
Anaesthetic room and operating theatre(s)

Ideally, there should be a separate anaesthetic room that is large enough to allow free
access around the patients trolley to permit the use of local or general anaesthesia.
The room should contain a full suite of equipment to the level provided in a standard
theatre suite. The alternative of anaesthetizing patients in theatre is less efficient
because it requires the anaesthetists time to prepare the patient, and causes delay
while the theatre is cleaned. However, the cost involved in providing and equipping this
second room may be prohibitive. Alternatively, a single anaesthetic room may serve two
theatres, depending on list allocation.
The operating theatre should be large enough to accommodate the usual surgical
equipment. It should also provide a good operating light, air-conditioning, piped services
and scavenging facilities as well as scrub-up and lay-up facilities of a comparable
standard to in-hospital theatres. Scrub facilities and sterile services may be designed to
serve two theatres if interposed between them.
First-stage recovery area

The first-stage recovery area should have direct access to the theatres to allow access
in the case of emergencies and to shorten transfer times. Piped services and the full
range of monitoring and resuscitation equipment are mandatory. A minimum of two bed
spaces per theatre should be accommodated to ensure rapid turnover times.
Ancillary services
Ancillary services must be provided in the most efficient manner.
The delivery of sterile supplies and the removal of dirty utility needs to be effected
directly through secondary entrances to prevent disruption to the flow of patients within
the unit.
It is important to situate the kitchen in the second-stage recovery area, where it
can serve the needs of postoperative patients and offer their escorts light refreshments
and beverages. Ideally, a well-stocked vending machine should be available within the
waiting area.
Sufficient accessible storage facilities must be incorporated in the design of the unit;
the need for them is often under-estimated.
The staff of the unit should have a private rest area incorporating kitchen facilities
and pleasant changing rooms with personal lockers. Consideration has to be given to
the ratio of female to male staff and this should be reflected in the area assigned to
each changing room.
FURTHER READING
Commission on the Provision of Surgical Services. Guidelines for Day Case Surgery.
London: The Royal College of Surgeons of England, 1992. Department of Health and
Social Security. Health Building Note 52. London: HMSO, 1992.
Kanich D G, Byrd J R. How to Increase Efficiency in the Operating Room. Surg Clin
N Am 1996; 76: 16172.

General and Regional
Anaesthesia for Day Case
Surgery
Peter Davies
Peter Davies is Consultant Anaesthetist and Lead Clinician in Day Surgery at Derriford
Hospital, Plymouth, UK.
Day case patients are discharged soon after surgery and thus need complication-free
anaesthesia and surgery provided by senior staff. Although unexpected overnight
admission (Figure 1) following day care surgery is often required for surgical reasons,
it may also result from anaesthetic causes such as pain, postoperative nausea and
vomiting (PONV) and delayed recovery. Attention to detail is therefore vital when
selecting an appropriate anaesthetic technique for each patient.
Much day case surgery and anaesthesia is viewed as routine or simple, but it has
to be performed to a high standard, therefore senior staff should perform day case
anaesthesia. If complications arise when the patient has been discharged, they have to
contact their GP or return to hospital. Following day surgery, 540% of patients contact
their GP, usually for wound problems, but sometimes because of pain or PONV. With
the increase in pressure on in-patient beds, many operations are now performed almost
exclusively as day case procedures, therefore trainees in anaesthesia will have to gain
supervised experience in the day surgery unit.
Reasons for unexpected overnight admission
Surgical reasons
Longer operation than planned
Bleeding
Urinary retention
Surgical complications
Social reasons
Failure of escort
Changed social circumstances
Anaesthetic reasons
Pain
Nausea and vomiting
Drowsiness
Anaesthetic complications
Premedication
Anxiolytic premedication
Anxiolytic premedication is seldom prescribed in day case patients because it is thought
to delay discharge, though the few studies investigating it have demonstrated no
increase in overnight admission or delayed discharge.
A patient who has had adequate preoperative counselling and preparation is
less likely to be anxious. The simplest treatments for anxiety include reducing the
waiting time for that particular patient by reorganizing the list and providing a relaxing
environment with entertainment such as magazines or television.
If this is inadequate, temazepam, 20 mg p.o., is a suitable regimen. In children,
midazolam, 0.5 mg/kg p.o., is an effective anxiolytic, if required. Most children also
have local anaesthetic cream applied to prospective cannulation sites if intravenous
induction is to be used.
Antacid therapy
There is an increase in volume and acidity of gastric contents in day case patients,
and many advocate the routine use of an H2-receptor blocker and metoclopramide.
However, there is no evidence of an increased incidence of regurgitation and aspiration,
therefore their routine use is unnecessary. For full effect, they must be taken the night
before, and on the morning of, surgery.
In patients with a high risk of aspiration (e.g. those with gastro-oesophageal reflux or
obesity), it may be necessary to prescribe the drugs and give detailed instruction at the
pre-assessment clinic for them to be taken at home the night before surgery.
Perioperative analgesic drugs

Perioperative analgesic drugs can be given orally, rectally or intravenously. Oral
absorption may be affected by anxiety and the rectal route may not be popular with the
patient. It is important to obtain specific oral consent for rectal medications given under
general anaesthesia or sedation.
The mean time to peak plasma levels of diclofenac is 120 minutes orally (enteric-
coated oral form) and 60 minutes rectally. Slow-release oral preparations are available,
but they do not reach a steady state until several doses have been given. Intravenous
drugs can be given but have their own problems. Diclofenac must be given by infusion
over 20 minutes to avoid venous sequelae. The quickest-acting drug with the least
complications is probably diclofenac, 1 mg/kg p.r. This can be self-administered by the
patient preoperatively or given just after induction of anaesthesia.
Parenteral ketorolac has few local effects, but its data sheet in the UK limits the
initial dose to 10 mg. Most of the studies into the effect of this drug used doses of
3090 mg.
Tramadol is an opioid drug that is meant to be devoid of central side-effects, but it
increases the incidence of PONV.
General anaesthesia
There has been an increase in the availability of short-acting agents for induction and
maintenance of anaesthesia and although all of these drugs appear more expensive
initially, there is increasing evidence of a reduced overall cost to health services and
society. Few studies have examined the overall implications of different anaesthetic
regimens, or surgical treatments, on total costs to the hospital, the patient or society.
Early return to work, less use of expensive primary care resources, reduced overnight
admission and less PONV could provide cogent arguments for the use of total
intravenous anaesthesia with propofol, for all day case patients, despite the increase
in total propofol costs to the hospital. This would help patients who are more worried
about PONV than postoperative pain, as well as managers of day case units who
are concerned about increased overnight admissions and surgeons who do not want
in-patient beds filled with day case patients. Anaesthetists should provide high-quality
symptom-free anaesthesia using multimodal postoperative analgesia.
Day case anaesthetic agents

Until recently, induction and maintenance of anaesthesia would have been discussed
separately, but with the advent of total intravenous anaesthesia (TIVA), and volatile
induction and maintenance anaesthesia (VIMA), the distinctions are blurred. Face
masks and needles are still used with VIMA because it is safer to induce with a cannula
in situ. Coughing and breathholding occur in 515% of inductions, though less often
in more experienced hands.
The qualities of an ideal day case anaesthetic agent are listed in Figure 2.
Qualities of an ideal anaesthetic agent
Fast predictable onset

Fast predictable elimination
Easily titratable depth of anaesthesia
No active metabolites
No accumulation
Stable in solution in water/volatile liquid at room temperature
No pain on injection/non-irritant on inhalation
Good side-effect profile
No PONV
2
Propofol is the most widely used induction agent in ambulatory surgery and, when
used as part of TIVA, produces smooth induction with a rapid return to clear-
headedness. Propofol induction and maintenance anaesthesia, without nitrous oxide,
using combination analgesic therapy is the treatment of choice for most patients
undergoing day case anaesthesia. It has a low incidence of PONV. Its side-effect of
pain on injection can be ameliorated by injection into larger forearm veins and the
addition of 1% lidocaine (lignocaine), 2 ml.
The advent of target-controlled infusions (TCI) of propofol has made training in
TIVA easier. Studies have shown TIVA- nave anaesthetists find it easier to learn TCI
compared with manually controlled infusions, but in experienced hands, the outcome
of the two methods is similar. Figure 3 gives typical dose requirements for TCI and
manually controlled propofol. The rate of infusion of propofol affects the speed of
induction and the total dose required. With a rate of 600 ml/hour,induction takes up
to 90 seconds requiring 1.96 mg/kg, whereas 1200 ml/hour takes about 60 seconds
requiring 2.6 mg/kg, an increase of about 40 mg for a 70 kg patient.
Typical doses of propofol for manually controlled infusion and target-

controlled infusion
Manually Target
controlled controlled
Induction 1.52.5 mg/kg 48 g/ml
Maintenance 12,10, 8 mg/kg/hour1 35 g/ml
1
The maintenance dose manually without nitrous oxide is 12 mg/kg/hour for 10 minutes,
followed by 10 mg/kg/hour for 10 minutes with a maintenance thereafter of 8 mg/kg/hour.
Sevoflurane and desflurane have blood gas partition coefficients of 0.67 and 0.42,
respectively, and are thus rapid acting with a short duration of action. Both drugs have
demonstrated faster early recovery than older agents (e.g. isoflurane, propofol), but
time to discharge is not reduced. The higher incidence of PONV with these volatile
agents may account for this. Desflurane alone has demonstrated time to home
readiness more than three times longer than propofol and, even when combined with
ondansetron, desflurane does not lead to earlier discharge. Desflurane is unsuitable for
gaseous induction of anaesthesia owing to its pungent odour and irritant airway effects.
Sevoflurane produces rapid smooth induction of anaesthesia, and rapid offset with few
side-effects except for PONV.
Isoflurane is widely used for maintenance of anaesthesia, despite higher incidences of

PONV compared with propofol. Like desflurane, it is unsuitable for gaseous induction.
The main reasons for continuing with isoflurane in the ambulatory setting are cost,
familiarity with volatile anaesthesia and lack of equipment.
Opiates: despite the increased risk of PONV associated with the use of opiate
drugs, they are used in most general anaesthetics as part of a balanced anaesthetic
technique. The shorter-acting drugs (fentanyl, alfentanil, remifentanil) are in widespread
use because they are cardiostable, non-allergenic and have a short duration of action.
The older opiates (morphine, pethidine) provide good longer-lasting analgesia, but are
associated with an increased incidence of PONV. These drugs are useful for treating
severe postoperative pain when shorter-acting agents and other analgesic modalities
have been tried.
Remifentanil is a relatively new esterase metabolized opiate, which has many of
the requirements of the ideal ambulatory surgery anaesthetic agent. As more complex
procedures are being performed in the ambulatory setting, the availability of a drug that
can produce deep anaesthesia for a short period of time combined with haemodynamic
stability and rapid recovery is of great benefit (e.g. for wisdom teeth extraction or anal
surgery). In ventilated patients, it is given in doses of 1 g/kg followed by infusion
ranging from 0.10.75 g/kg/minute (usually 0.250.5) when combined with expired
isoflurane 0.8%, or propofol, 100 g/kg/minute. A reduced induction dose of propofol,
11.5 mg/kg, is generally required. The time to wake-up is short owing to the context
sensitive half-time of 3 minutes, but it is the quality of wakening which is impressive,
with reduced coughing and breathholding. Fast recovery has been shown in studies
demonstrating better psychomotor tests at 30, 60 and 90 minutes compared with
alfentanil use.
In spontaneously breathing patients, it has been difficult to find a dose of remifentanil
that produces anaesthesia but allows adequate respiration. Doses of remifentanil,
0.0250.05 g/kg/minute, with expired isoflurane 0.81.3% or propofol, 120140 g/kg/
minute, provided maintenance of anaesthesia. In studies, the induction boluses of drugs
have produced periods of apnoea, which makes dose selection difficult.
In some studies, remifentanil has been shown to produce a significant incidence of
PONV but, owing to its rapid elimination, this effect is short lived. The short action of
remifentanil means that any analgesic opiate effect wears off rapidly after termination
of the drug, which may limit its usefulness in operations with significant postoperative
pain
PONV
PONV is one of the main symptoms causing distress to day case patients and
unexpected admission. The risk factors for PONV are listed in Figure 4.
Every day unit should have an action plan for patients at risk of PONV (Figure 5).
Airway maintenance
Risk factors for postoperative nausea and vomiting (PONV)
Female gender
Ambulatory surgery
Opiates
Starvation
Gynaecological, ENT or ophthalmic surgery
Early in menstrual cycle
Previous PONV
Motion sickness
Nitrous oxide
Non-smoker
Action plan for postoperative nausea and vomiting (PONV)
All patients or high-risk patients

Total intravenous anaesthesia, no nitrous oxide
Triple analgesic therapy (non-steroidal anti-inflammatory drugs, opiates,
local anaesthetics)
Hydration
Early treatment of postoperative pain
Early treatment of PONV with 5-HT3 antagonist
The advent of the laryngeal mask in 1988 revolutionized anaesthetic practice (Figure
6), particularly in ambulatory surgery. The laryngeal mask is less likely to cause sore
throat compared with a tracheal tube and, in gynaecological laparoscopy, it decreases
total operation time, which may allow more patients to be treated on an operating list,
thus reducing overall costs.
In paediatric tonsillectomy, airway contamination is reduced when an armoured
laryngeal mask airway is used compared with an uncuffed tracheal tube. Desaturations
and surgical time are reduced in grommet insertion when compared with a face mask,
and coughing and breathholding are reduced in cataract patients when compared with
intubation. In short procedures, the laryngeal mask and spontaneous respiration avoid
some of the problems of muscle relaxants. Though it has a short duration of action,
suxamethonium causes muscle pains. None of the currently available non-depolarizing
muscle relaxants can be given with certainty of easy intubation at 2 minutes and easy
reversal after 10 minutes.
Much has been made of the dangers of unintubated spontan-eously breathing
laparoscopy. With careful selection of patients, modern drugs and monitoring, this is
a safe procedure. Complications arose in the past because of inadequate airways,
unmonitored end tidal carbon dioxide concentrations and halothane anaesthesia,
which all increase the likelihood of cardiac arrhythmias. Although in current use for
ventilated gynaecological laparoscopy, ventilation through the laryngeal mask airway
will occur against the increased intra-abdominal pressure which may overcome the
laryngeal mask leak pressure of about 20 cm H2O and cause increased intragastric
air insufflation, perhaps resulting in an increased risk of regurgitation. Guidelines for
laryngeal mask airway laparoscopy are given in Figure 7.
Uses of the laryngeal mask airway
Gynaecological laparoscopy
Tonsillectomy (adults and children)
Dental extractions
Intranasal surgery
Head and neck procedures
Shoulder operations
Ocular surgery
Guidelines for laryngeal mask airway laparoscopy
Elective gynaecological surgery only

Body mass index < 31
No symptoms of reflux
Short procedures (< 30 minutes)
Full monitoring
Spontaneous breathing
2 litres of gas
Trendelenburg tilt as needed
Propofol infusion
7
Regional anaesthesia alone or combined with general anaesthesia or sedation should
be standard practice for many ambulatory patients because it provides optimum
operating conditions for the patient and the surgeon, with minimal side-effects. Regional
anaesthesia alone is particularly suitable for less fit patients who would otherwise
need overnight admission for general anaesthesia. Regional techniques provide good
postoperative pain relief for patients and may allow the addition of more complex
procedures to the routine mix of day case operations.
Regional anaesthesia for day case surgery has not been undertaken with great
enthusiasm in the UK for various reasons, including the incidence of post-dural
puncture headache in young people following early ambulation. Also nerve and plexus
blocks take time and skill to set up and have a high failure rate. The advantages and
disadvantages of regional anaesthesia compared with general anaesthesia are listed
in Figure 8.
In the UK, much health authority funding has been used to increase the range and
complexity of day case surgery, which requires long-lasting postoperative pain relief.
The addition of drugs to local anaesthetics, and the manipulation of local anaesthetic
drug concentrations and baricity have allowed a more predictable onset and offset
of motor block, often providing prolonged analgesia, without delayed discharge. Many
operations can be performed under local or regional anaesthesia. Plexus blocks
and other regional techniques can also be performed with sedation or general
anaesthesia to provide good postoperative analgesia. This reduces the benefit of
avoiding sedative drugs in terms of PONV and recovery, but allows patients who
would not otherwise tolerate regional anaesthesia the best of both worlds. Some
advantages and disadvantages of local anaesthetic techniques in common day case
surgical operations are given in Figure 9.
Comparison of regional and general anaesthesia
Prolonged analgesia Prolonged motor block
Reduced postoperative Post-dural puncture
nausea and vomiting headache
Reduced confusion Slow onset
High failure rate
General anaesthesia
Fast Postoperative nausea and
No failures vomiting
Confusion
Regional techniques for some common day case procedures

Surgical procedure Regional technique Advantages Disadvantages
Hernia repair Field block Good postoperative pain relief Needs supplementation
Speed
Low failure rate
Spinal Speed Post-dural puncture headache

Llittle supplementation Urinary retention
Delayed mobilization
Cataract extraction Peribulbar block Reduces confusion and Ocular complications

discharge time
Knee surgery 3-in-1 block Good analgesia Failed blocks
Spinal Speed Post-dural puncture headache

Little supplementation Urinary retention
Delayed mobilization
Foot surgery Popliteal block, ankle blocks Good analgesia Failed blocks
Hand surgery Biers block, brachial Analgesia Failed plexus blocks

plexus blocks Minimal systemic disturbance
9
Spinal anaesthesia
The advent of 2627 G pencil-point spinal needles has reduced the incidence of
post-dural puncture headache from over 10% to about 1.5% for ambulatory patients.
Few direct comparisons between spinal and general anaesthetic techniques have been
conducted in the ambulatory setting, but time to fitness for discharge is longer after
spinal anaesthesia compared with general anaesthesia, and is related to time to return
of motor and bladder function.
Concerns regarding the neurotoxicity of high concentrations of lidocaine (lignocaine)
have led to questions about its use in spinal anaesthesia. It has been widely used
because of its fast onset and short duration of action, but it has been suggested that
spinal bupivacaine should be used instead. Much research has been directed towards
elucidating the optimum dose, concentration and baricity of bupivacaine to provide an
adequate spinal block for surgery to proceed, but a short enough duration of action to
allow timely discharge home. The optimum drug for knee arthroscopy is bupivacaine,
7.5 mg, which provides 100% success and street fitness after only about 3 hours
(Figure 10). Clonidine, adrenaline (epinephrine) and fentanyl have been studied as
additives to spinal local anaesthetics; the addition of fentanyl, 20 g, can increase the
length of postoperative analgesia, but not delay discharge.
Choice of spinal anaesthesia for knee arthroscopy
Drug Dose (mg) Time to discharge Successful

(minutes) block (%)
2% lidocaine (lignocaine)1 40 178 91
60 216 91
80 214 97
Hyperbaric 5 181 73
0.5% bupivacaine 7.5 202 100
diluted to 3 ml2 10 260 100
1
Urmey et al Anesthesiology 1995; 83: 52834
2
Ben David et al Anesth Analg 1996; 83: 71620
10
Major orthopaedic surgical techniques are being performed regularly as day case
procedures. Arthroscopic shoulder surgery, and ligament reconstruction in the knee are
operations with a high incidence of postoperative pain unless regional anaesthesia is
used as part of the perioperative technique. Interscalene or suprascapular nerve block
in the upper limb and 3-in-1 femoral block in lower limb procedures can produce long-
lasting pain relief. Prolonged motor block is seen after these procedures and, in many
UK orthopaedic centres, the discharge criteria after knee surgery include production of
an adequate quadriceps contraction. Adequate physiotherapist-led instruction for the
patient is needed regarding ambulation and protection of the blocked limb (Figure 11).
Postoperative instructions following local anaesthetic block
Local anaesthetic block Postoperative instructions

Spinal Needs full ambulation and ability to pass urine
Biers block No discharge for 30 minutes after release of tourniquet

Brachial plexus block Sling for limb, protection of numb, weak limb
Return if no full return of power and sensation in 18 hours
Take analgesics as soon as the first pain is felt
Lower limb nerve block Teach ambulation with crutches, protection of numb, weak limb
Return if no full return of power and sensation in 18 hours
Inguinal field block Discharge early so patient reaches home before block wears off
11
FURTHER READING
Liu S S. Optimizing Spinal Anesthesia for Ambulatory Surgery. Regional Anesthesia
1997; 22 (6): 50010.
Rowe W L. Economics and Anaesthesia. Anaesthesia 1998; 53: 7828.
White P F. Role of Rapid Short-acting Anesthetics, Analgesics and Muscle Relaxants in
Ambulatory Anesthesia. Acta Anesth Scand 1997; 41: 2236.
Web site of the Society of Ambulatory Anesthesia (SAMBA)www.sambahq.org. (search

for 'core curriculum').

Postoperative Analgesia for
Day Case Surgery
Anna Johnson
Anna Johnson is Consultant Paediatric Anaesthetist at Derriford Hospital, Plymouth,

UK. She qualified from St Andrews University and Manchester Medical School and
trained in anaesthesia at University College, the Hammersmith Hospital and Great
Ormond Street Hospital, London. She is dedicated to raising the standards and quality
of paediatric anaesthesia in the district general hospital and is especially interested in
providing good paediatric pain control.
A significant proportion of surgical procedures are performed as day cases and,

owing to economic pressures, this is continuing to increase. However, inadequate
postoperative analgesia is a major problem resulting in patient dissatisfaction, delays in
discharge and in the resumption of normal activities.
Analgesia needs to be maintained throughout the recovery period and to allow
comfortable mobilization. Many studies suggest that, despite good analgesia at
discharge, patients suffer pain once they are home; this has recently been highlighted
as a major problem in children. The provision of good postoperative analgesia needs
careful planning, which should begin in the preoperative period.
Explanation is of paramount importance, because allaying anxieties can decrease the
severity of postoperative pain. A verbal description of the analgesia to be provided
should be reinforced with concise written information. If local anaesthesia is planned,
it is necessary to explain how this will feel on wakening, the duration of its action and
any side-effects. Consent for suppository administration and neural blockade should
be obtained.
Patients need to be educated about how to express any postoperative pain they
may feel and how it may be treated. Regular, pre-emptive analgesia is a particularly
important concept, which must be explained to the patient. In paediatric day case
surgery, it is important to communicate appropriately with both the parent and child.
Preoperative analgesics, usually oral or rectal non-steroidal anti-inflammatory drugs
(NSAIDs), may be given though the usefulness of preoperative pre-emptive analgesia
is debatable.
Peroperative management
Analgesic strategies should be aimed at enabling the patient to be pain free on
regaining consciousness. This can be achieved using a balanced approach with a
combination of NSAIDs, local anaesthesia and, if necessary, small amounts of short-
acting opiates.
NSAIDs (Figure 1): paracetamol acts synergistically with other NSAIDs, so both should
be given. In children, paracetamol, 3040 mg/kg p.r. or 20 mg/kg p.o., is the accepted
loading dose, followed by regular dosing of up to 90 mg/kg/day. Diclofenac is also
available as topical eye drops, which are effective as analgesia following strabismus
surgery.
Side-effects concerns have been raised over the side-effects of NSAIDs. They
inhibit platelet function and should not be used in patients with pre-existing coagulation
defects or those undergoing extensive tissue dissection. NSAIDs are commonly given
for adenotonsillectomy, but should be withheld if there is excess blood loss or if there
is any evidence of a coagulopathy.
No increase in gastrointestinal side-effects is seen with short-term use (up to 3 days)
of NSAIDs, provided that the patient has no history of gastrointestinal irritation.
NSAIDs should be avoided if there are any signs of renal impairment or if other
nephrotoxic drugs are being administered. The renal tubules are protected from the
effects of dehydration by mechanisms utilizing prostaglandins, so it is important to keep
patients well hydrated.
Of adults with asthma, 510% are sensitive to NSAIDs, therefore it is worth checking
specifically if such individuals have taken NSAIDs previously without problems; if in
doubt, NSAIDs should not be given. In children with asthma, NSAIDs seldom cause
respiratory complications, but they should be avoided if nasal polyps are present or if
the child has had recent repeated hospital admissions, especially if they have required
intensive care.
NSAIDs commonly administered peroperatively
Drug Route of administration Dose (mg/kg)

Diclofenac Oral or rectal 1
Ibuprofen Oral 5
Ketorolac Intravenous 0.5
Local anaesthesia can be used in a number of ways to provide excellent analgesia

with few side-effects and often obviates the need for opiates (Figure 2). However,
care must be taken not to delay early ambulation and patients must be advised about
any possible interference with motor function. If sensation is impaired at discharge,
warnings should be given especially about touching or drinking hot liquids, which may
cause inadvertent scalds.
In laparoscopic cholecystectomy, 20 ml of 0.5% bupivacaine may be administered
into the hepatodiaphragmatic space. Bupivacaine is generally preferred to lidocaine
(lignocaine), because of its longer duration of action, which can be prolonged by
the addition of 1:200,000 adrenaline (epinephrine). Ropivacaine has recently been
introduced and has a similar duration of action, but causes less motor blockade.
Spinal and epidural anaesthesia are seldom used in the UK, but are commonly used
in day case procedures in other countries.
Opioids: if possible, opioids should be avoided because of the increased incidence

of nausea and vomiting but, if their use is necessary, the shorter-acting opioids are
preferred.
Remifentanil and alfentanil are so short-acting that they provide little postoperative
analgesia.
Fentanyl, 12 g/kg provides 3060 minutes of analgesia allowing time for NSAIDs
to become effective. Fentanyl is the drug of choice in treating significant postoperative
pain in the early stages of recovery and should be given in small boluses of 0.20.4
g/kg.
Morphine causes increased nausea and vomiting especially if administered
intravenously. However, doses of 0.1 mg/kg are used intramuscularly, for example, in
day case adenotonsillectomy.
Codeine phosphate may be given by the intramuscular, rectal or oral routes, and it
may be useful for more painful procedures.
Tramadol combines an opioid action with a central adrenergic effect, but has a
significant incidence of postoperative nausea and vomiting.
Examples of the use of local anaesthesia
Technique Type of local anaesthetic Surgical procedures Comments
Topical Emla Myringotomy Emla for myringotomies

4% lidocaine (lignocaine) gel Circumcision 4% lidocaine (lignocaine) gel for
circumcision which can be continued on
discharge
Laparoscopic sterilization 4% lidocaine (lignocaine) gel can be applied

to clips
Infiltration 0.25% bupivacaine All surface wounds Pre-incisional wound infiltration probably
12% lidocaine (lignocaine) offers no benefit
Laparoscopic sterilization Mesosalpingeal infiltration
Intra-articular 0.5% bupivacaine Arthroscopy and arthroscopic Usually 2530 ml are used for knee
surgery arthroscopy
Nerve blocks 0.250.5% bupivacaine Upper limb surgery No adrenaline (epinephrine) for digital nerve
12% lidocaine (lignocaine) blocks
Lower limb surgery
Hernia repair Inadvertent femoral nerve block may
Orchidopexy result in leg weakness
Circumcision No adrenaline (epinephrine) for dorsal nerve
blocks
Otoplasty Great auricular nerve block decreases
vomiting
Eye surgery
Plexus blocks 0.250.5% bupivacaine Upper limb surgery

12% lidocaine (lignocaine) Lower limb surgery
Caudal epidural 0.125% bupivacaine Surgery below the umbilicus Ketamine (preservative-free), 0.5 mg/kg, or
block 0.75% ropivacaine clonidine,12 g/kg, prolongs the block
Intravenous regional 0.5% prilocaine Upper limb surgery Limited postoperative analgesia
2
In the immediate postoperative period, it is important to establish good analgesia
before discharge. Small amounts of intravenous fentanyl may be given until analgesia
is achieved. Most patients can tolerate oral medication shortly after surgery. A large
variety of soluble oral analgesics are available, enabling rapid absorption and action.
Most day case units have a drug discharge policy with combinations of paracetamol,
NSAIDs and codeine preparations as regular oral analgesics continued for at least 3
days postoperatively (Figure 3). If paracetamol and codeine (or its derivatives) are used
as a combined preparation, the patient should be warned not to take other medications
containing paracetamol. Also, higher doses of codeine may cause constipation. The
discharge drugs should be given to the patient with both verbal and written instructions
emphasizing the importance of regular pre-emptive analgesia. Controlled or slow-
release preparations may be beneficial, especially at maintaining analgesia overnight.
Patients need to know who to contact in the event of any problems. Postoperative
follow-up, either by a community nurse or by telephone, increases patient satisfaction
and can help improve postoperative analgesia. The adequacy of the analgesia provided
should be regularly assessed and audited.
Non-pharmacological techniques of improving patient comfort may help.
Psychological strategies such as relaxation and distraction therapy and physical
strategies such as the application of heat or cold, massage, exercise or rest have been
used in combination with pharmacological methods. Acupuncture and transcutaneous
electric nerve stimulation and other similar techniques have also been studied but their
clinical efficacy is yet to be proven.
Postoperative oral analgesia
Expected severity Analgesic regimen

of pain
Mild Paracetamol, 15 mg/kg (up to a maximum of 1 g) 6 hourly
Moderate Paracetamol, 15 mg/kg (up to a maximum of 1 g) 6 hourly plus

NSAID (e.g. ibuprofen, 510 mg/kg 8 hourly, or diclofenac, 1
mg/kg 8 hourly)
More severe Paracetamol and codeine combination

(e.g. Co-codamol, 2 tablets 6 hourly1,
Co-dydramol, 2 tablets 6 hourly2,,
Co-proxamol, 2 tablets 6 hourly3 plus NSAID (e.g. ibuprofen,
510 mg/kg 8 hourly, or diclofenac, 1 mg/kg 8 hourly)
1
Co-codamol tablet is paracetamol, 500 mg, with codeine, 8 or 30 mg.
2
Co-dydramol tablet is paracetamol, 500 mg, with dihydrocodeine, 10 mg.
3
Co-proxamol tablet is paracetamol, 500 mg, with dextropropoxaphene, 32.5 mg.
FURTHER READING
ennan L J. Modern Day-case Anaesthesia for Children. Br J Anaesth 1999; 83 (1):
91103.
Joshi G P. Pain Management after Ambulatory Surgery. Ambulatory Surg 1999; 7:
312.
Peng P W H, Chan V W S, Chung F F T. Regional Anaesthesia in Ambulatory Surgery.
Ambulatory Surg 1997; 5: 13343.
Whitwam J G, ed. Day-Case Anaesthesia and Sedation. Oxford: Blackwell Scientific
Publications, 1994.
Web site of the Society of Ambulatory Anaesthesia (SAMBA) www.sambahq.org.

Search for 'core curriculum'.

Selection Criteria and
Preoperative Evaluation for
Day Surgery
Stuart Collins
Stuart Collins is Consultant Anaesthetist and Lead Clinician of the Day Surgery
Unit at Musgrove Park Hospital, Taunton, UK. He qualified in Nottingham and trained
in anaesthesia in Bristol and Oxford. His main interests include total intravenous
anaesthesia for day surgery and quality assurance.
Day surgery has expanded rapidly in recent years and it is estimated that soon 6070%
of all elective surgery will be performed as day cases. Correct patient selection and
preoperative evaluation are important to minimize morbidity and unplanned overnight
stays, and to maintain patient satisfaction.
Assessment should identify patients who are suitable for day surgery, prepare them for
their operation and enable any preoperative testing to be performed. Questionnaires
or structured telephone calls can be used, but many units now use a nurse-led clinic
under clinical guidance with a standardized questionnaire and predetermined selection
criteria (Figure 1). It is important to establish that the patient is in the optimum condition
for the planned procedure.
Pre-assessment questionnaire
Suitable for day surgery? Yes No If no inform: GP Consultant Patient
Name: Date of assessment: Proposed date of operation:

Consultant: Proposed operation:
Unit no.: Patient Tel. no. Home: Work:
Date of birth:
Next of kin: Telephone no.: Relationship:
Have you had any serious illness in the past?
Previous admissions to hospital (date, problem, type of operation, type of anaesthetic)
Have you or any of your relatives ever had a problem with a general anaesthetic?
Yes / No Action taken
Medications currently being taken. include all prescriptions, aspirin and the pill
BMI Blood pressure Weight Height Pulse
Investigations ordered
Do you have haemophilia, anaemia or another blood disorder? Yes / No

Do you have diabetes? Yes / No
Do you have kidney disease or kidney failure? Yes / No
Have you ever had liver disease, hepatitis or been jaundiced? Yes / No
Have you had a heart attack? Yes / No
Do you get angina or chest pain at rest or with minimal exercise? Yes / No
Do you have a pacemaker? Yes / No
Have you had heart disease, rheumatic fever or high blood pressure? Yes / No
Do you get breathless walking, climbing one flight of stairs or lying flat? Yes / No
Do you have asthma, bronchitis, or chest disease? Yes / No
Have you ever had a convulsion, fit, blackout, or do you have epilepsy? Yes / No
Do you get swollen ankles? Yes / No
Do you have a hiatus hernia? Yes / No
Do you get indigestion or heartburn? Yes / No
Have you ever had a stroke? Yes / No
Do you have arthritis or muscle disease? Yes / No
Have you had any corticosteroid drugs in the past? If so when? Yes / No
If female, are you or could you be pregnant? Yes / No
Do you smoke or have you smoked in the last 6 months? Yes / No
If you smoke, how many a day? Yes / No
Do you drink alcohol? If yes, how many units per week? Yes / No
Urinalysis Yes / No
Check list
Starve Yes / N/A Suture and wound care Yes / N/A
Shave Yes / N/A Drains and dressings Yes / N/A
24-hour postop information Yes / N/A Pain control Yes / N/A
Stairs after discharge? Yes / N/A Information leaflet received/given Yes / N/A
Transport home discussed? Yes / N/A
Name of person collecting: Tel. no.

Name of 24-hour carer: Tel. no.
I have understood the information given to me at my pre-anaesthetic assessment and I have also received information about my operation.
Signature of patient: Date:
All the above information is correct to the best of my knowledge and understood by the patient:
Assessment nurse signature: Date:
Anaesthetists comments:
1
Selection criteria
The boundaries in day surgery are continually being pushed back and recent studies
suggest that significant associated morbidity is low, even in patients with controlled
systemic disease. Selection criteria help to establish consistency and agreement among
medical staff. The appropriateness of the selection criteria should be reviewed regularly
by auditing cancellation rates, patient morbidity and patient satisfaction. Determining
suitability solely on the American Society of Anesthesiologists (ASA) classification is
unhelpful.
Social factors the patient must be prepared to have the procedure performed as
a day case, live close to the hospital, and have a responsible, able, adult carer at home
with them for 24 hours postoperatively.
Surgical factors the proposed surgery must have a low incidence of
postoperative complications and any pain should be controllable by local anaesthetic
techniques and analgesics administered orally or rectally. The duration of surgery does
not affect the likelihood of same-day discharge, provided longer cases are listed early in
the day. A stand-alone unit is different from an integrated unit with facilities for overnight
stay, and the patients and surgical procedures should be selected accordingly.
Medical factors it is difficult to agree on absolute medical contraindications
to day surgery because significant postoperative morbidity is uncommon. However,
certain medical conditions are associated with an increased risk and render the patient
unsuitable for general anaesthesia (Figure 2). With invasive procedures, it is essential
that the patients physical condition is matched to the planned procedure. It is important
to consider whether treating the patient as an in-patient would lessen the risks or
change the anaesthetic approach.
Medical contraindications for day case anaesthesia
Morbid obesity
Body mass index > 35 kg/m2 or weight > 125 kg
Cardiovascular disease
Poorly controlled angina, arrhythmia or cardiac failure
Hypertension > 180/100 mm Hg
Significant valvular or congenital heart disease
Myocardial infarction or stroke within 6 months
Respiratory disease/airway
Poorly controlled asthma or chronic obstructive pulmonary disease (patients taking oral
corticosteroids, with poor exercise tolerance or with a peak expiratory flow rate < 200
litres/minute are unlikely to be suitable)1
Severe restrictive lung disease (e.g. kyphoscoliosis)
Previous failed intubation
Significant obstructive sleep apnoea
Metabolic/endocrine/haematological
Poorly controlled diabetes or insulin dependent1
Active liver disease
Anaemia (haemoglobin < 10 g/dl)1
Haemophilia/anticoagulation1
Cholinesterase deficiency1
Hypo- or hyperkalaemia (acceptable range 36 mmol/litre)
Renal disease
Patients requiring renal support1
Neuromuscular disease
Myasthenia gravis
Significant multiple sclerosis
Malignant hyperpyrexia susceptibility
Poorly controlled epilepsy
Parkinsons disease interfering with daily activity
Significant motor neuron disease
Acute substance abuse
1
Patients might be suitable discuss with lead clinician.
Cardiovascular disease
Patients with well-controlled cardiovascular disease should not be denied the
opportunity to have their surgery in the ambulatory setting. However, patients with
poorly controlled angina, congestive cardiac failure, symptomatic valvular disease,
uncontrolled arrhythmias or recent myocardial infarction or stroke (within 6 months) are
unsuitable for elective surgery. Minor surgical procedures are categorized as being of
low risk for significant cardiac events. Hypertension is associated with an increased
risk of developing perioperative cardiac events and should be treated before surgery. A
reasonable upper limit for blood pressure is 180/100 mm Hg. It is important to explain
to the patient, and their GP, the reasons for controlling hypertension perioperatively
so that treatment is initiated. In general, cardiac medication should be taken as usual
on the day of surgery.
Respiratory disease
Asthma, chronic obstructive pulmonary disease and smoking all predict adverse
perioperative events, but patients with well-controlled disease are likely to be suitable
for day surgery. A regional anaesthetic technique can be considered for the more
seriously affected. Patients with poorly controlled disease, marked exercise limitation or
a recent exacerbation of their condition should have their surgery postponed. Smokers
should be encouraged to stop smoking.
Diabetes
Diabetes may be associated with cardiovascular and renal disease or autonomic
dysfunction. Diabetes is a predictor of adverse intraoperative and postoperative events,
but patients with good diabetic control and a good understanding of their disease
should be allowed day surgery. Patients with Type 2 diabetes are, in general, more
suitable for day surgery than those with Type 1 diabetes; however, well-motivated
patients taking insulin can be considered if their procedure is of short duration and
carried out early in the morning. Many Type 1 diabetics understand their insulin
requirements better than their anaesthetist does. Hypoglycaemic agents are best
avoided until the procedure is completed and the patient has resumed eating and
drinking.
Obesity
Obesity is often associated with cardiac disease, diminished respiratory reserve and
gastro-oesophageal reflux. A body mass index greater than 35 kg/m2 is associated with
perioperative anaesthetic and surgical problems, and is often used as a cut-off point for
patient suitability. Obese patients can be anaesthetized in a day case setting, but they
should be encouraged to lose weight before agreeing to any elective procedure in any
setting. The patient trolleys and operating tables in the day unit have a maximum safe
weight limit. Antacid prophylaxis can be prescribed for symptomatic reflux.
Renal and hepatic disease

Patients on renal support or those with active liver disease are usually unsuitable for
day surgery.
Patients with myasthenia gravis, motor neuron disease, hereditary dystrophies
or a susceptibility to malignant hyperpyrexia are generally unsuitable for general
anaesthesia in the day unit. Patients with poorly controlled epilepsy are unsuitable, but
well-controlled epileptics can have day surgery, provided appropriate drugs are chosen.
Although not strictly a neuromuscular disease, pseudocholinesterase deficiency is a
relative contraindication to day surgery.
Musculoskeletal disease
Patients with severe degenerative neck disease, predicted difficult airway, or previous
failed intubation are probably best anaesthetized in the main hospital, depending on the
facilities of the day unit. Patients with significant obstructive sleep apnoea should be
observed overnight in hospital.
Haematological disease
Patients with bleeding diatheses may be suitable for day surgery if the deficient factors
are corrected preoperatively and the surgery is not too invasive. The opinion of a
haematologist should be sought.
Medication
Corticosteroids: patients taking corticosteroid supplements are usually able to
undergo day surgery because the stress response to minor surgery has not been found
to cause problems. Oral supplementation can also be prescribed. However, patients
taking higher doses of corticosteroids require individual medical review.
Oral contraception and hormone replacement therapy are associated with a slightly
increased risk of thromboembolic events, but patients are not advised to stop their
medication before surgery because the risk of unwanted pregnancy is felt to be greater.
Their continued use in patients undergoing lower limb surgery or requiring tourniquet
use is more contentious and, if they are continued, the use of subcutaneous heparin
would seem prudent.
Warfarin: if the patient needs to stop taking warfarin before surgery, but has a
significant risk of thromboembolic events, admission and anticoagulation therapy with
heparin are required.
Monoamine oxidase inhibitor use does not preclude day surgery, but suitable
anaesthetic drugs should be selected carefully.
Age
Old age should not be a barrier to day surgery. The patients physiological age is more
important than their chronological age; however, they must be assessed carefully for
social and physiological factors. The lower age limit for day surgery depends on many
factors and should be set locally.
Investigations
In general, patients are over-investigated for day surgery, and the cost:benefit ratio
is not always apparent. Preoperative testing should be performed only if indicated by
the medical history or by physical examination and if an abnormal test would affect
patient management.
Blood tests: full blood counts are usually performed to detect anaemia and therefore
should be reserved for patients with a history of heavy bleeding, dyspnoea, renal
disease or if they appear unduly pale. Urea and electrolyte assays are usually
performed to detect abnormalities in potassium or to detect abnormalities in renal
function, and should be reserved for hypertensive and diabetic patients, patients taking
diuretics and those with a history of renal disease. A blood sugar level should be
performed if indicated by urinalysis. Clotting studies may be indicated if there is a
history of excessive bleeding or hepatic disease.
Radiographs: chest radiographs are seldom required. A radiograph of the cervical

spine may be indicated in patients with rheumatoid disease or Downs syndrome.
ECG: the usefulness of a preoperative ECG in day surgery is controversial. Up to 30%

of ECGs are abnormal in patients over 60 years old, but in only 20% of patients does
this lead to a change in management. Patients over the age of 60 or with a history of
chest pain, dyspnoea, diabetes or hypertension, should be considered for an ECG. A
preoperative ECG can provide a useful baseline.
FURTHER READING
Chung F, Mezei G, Tong D. Pre-existing Medical Conditions as Predictors of Adverse
Events in Day-case Surgery. Br J Anaesth1999; 83 (2): 26270.
Collier J, ed. Drugs in the Peroperative Period. Drugs and Therapeutics Bulletin 1999;
37: 912.
Millar J M, Rudkin G E, Hitchcock M. Practical Anaesthesia and Analgesia for Day

Surgery. Oxford: BIOS, 1998.
Twersky R S. Patient and Procedure Selection for Adult Ambulatory Surgery. Anesth
Analg 1998; 86 March Suppl: 13946.
Warner M A, Shields S E, Chute C G. Major Morbidity and Mortality within 1 Month of

Ambulatory Surgery and Anesthesia. JAMA1993; 270: 143741.

Dental/maxillofacial
Anaesthesia
on CD-ROM
Anaesthesia and Dental
Trauma
Harry Owen
Harry Owen is Associate Professor in Anaesthesia and Intensive Care at Flinders

University of South Australia and Honorary Consultant at Flinders Medical Centre. He
graduated from Bristol University and trained in anaesthesia in Bristol, Melbourne and
Glasgow. His research focuses on use of new technologies, including simulation, to
improve undergraduate education and postgraduate training.
Dental trauma is unpleasant for the patient and the anaesthetist. Dental trauma caused
by the straight Magill blade was well known and Macintosh claimed an advantage of
his curved blade was a reduced risk of trauma to teeth. The incidence of dental trauma
in anaesthesia is 0.010.7%. In malpractice claims, anaesthetic-related dental trauma
is the most common injury accounting for up to 33% of claims filed in the UK, the USA
and Australia. In Australia, the average cost of settling a claim for dental damage is
A$2,400 (range A$10012,800) but the total costs incurred in managing these claims
are far higher.
The most common technique of tracheal intubation involves using a laryngoscope to

lift the base of the tongue and epiglottis. The pattern of dental trauma, shown in Figure
1, confirms reports that a common mistake is to use the laryngoscope blade as a lever
with the upper teeth as the fulcrum. The left upper central incisor is the tooth most at
risk.
Pattern of dental trauma in patients examined by a

dentist after anaesthesia
In the early 1960s, Dr William Haddon launched a movement to base injury-prevention

programmes on sounder scientific concepts. Haddon developed a generic approach
to the analysis, control and management of injury, which can be applied to all types of
hazards associated with energy transfer. Haddon divided accidents into three phases,
pre-event (factors that determine whether an accident occurs), the event itself and
post-event (everything that determines the consequences of the injuries received).
Combining the phases and factors (humans involved, equipment and environment)
yields a matrix, that can be used to determine where best to apply strategies to
prevent or control injury (see Figure 2). Applying this to the problem of dental trauma in
anaesthesia reveals three broad strategies:
risk avoidance dont let the event happen
damage control if damage occurs, minimize its consequences
insurance have someone else pay for the damage.
Haddons Matrix applied to dental trauma during anaesthesia
Phases Factors
Human Equipment Patient factors
Pre-event Good intubation Appropriate range of Good dental hygiene

technique intubation equipment readily Normal oral anatomy
Aware of risk factors available in hospital No drug therapy or diseases
for dental damage Dental protection devices contributing to dental
Dental history and readily available problems
examination undertaken Knows what dental treatment
and understood has been undertaken
Know when and how to Elective procedure
use different intubation
techniques
Event Careful and appropriate Use devices to protect teeth No loose teeth
use of equipment Use laryngoscope blades No malaligned or prominent
Good assistance designed to reduce teeth
contact with teeth No isolated teeth
Use warning devices on No heavily restored teeth
laryngoscope blades No dental prostheses
Intubating without a Normal airway anatomy
laryngoscope and no risk factors for
difficult intubation
No urgency
Post-event Know how to manage Materials to splint Able and willing to cooperate
situation teeth safely readily with treatment
Dental help readily available
available
Preventing dental trauma is the ideal approach, but the perceived costs of managing
occasional dental trauma have to be balanced by the inevitable increased costs to
reduce the incidence of dental trauma. A logical approach to reduce dental trauma is to
consider intubation strategies for each patient, based on the history, examination and
planned procedure.
The primary objective of intubation is patient safety and oxygenation must always be
prioritized above dental protection. However, if two alternatives are equally suitable, the
most tooth-friendly technique should be preferred. It is important to warn patients of
the risk of dental damage associated with intubation. If risk factors for dental damage
are present an alternative to direct laryngoscopy should be considered.
Patient factors
The preoperative assessment must include a dental history and an oral examination
and the findings should be noted.
Condition of teeth
Major restorations and caries reduce the strength of teeth and make them more likely
to break even when small forces are applied to them. Periodontal disease affects the
supporting structures of the tooth and increases the risk of dislodgement. Malaligned
teeth are more likely to be exposed to unusual forces. An isolated tooth does not have
the support of its neighbours and may also have the same condition that led them to be
lost so is more likely to be dislodged.
Patients age
The neonate may not have teeth on view, but delicate tooth structures are just under
the gum and can easily be damaged. Infants and young children may have loose
deciduous teeth that are easily dislodged. Force applied to a deciduous tooth can also
damage the underlying developing permanent tooth. Occasionally, severe caries is
seen in adolescents and young adults though this age group generally has healthy
teeth. In older patients, dental prostheses are more common.
Dental prostheses
Bridges, particularly to replace upper incisors, are most at risk of damage. They
are designed to sustain the forces associated with mastication and do not tolerate
forces applied in other directions. Crowns can be weaker than normal teeth. While
the porcelain jacket is strong, the supporting post may give way under pressure.
Veneers may sheer off if lateral forces are applied. Composite resins are being used
increasingly to restore teeth and may be used to repair chipped teeth or as a veneer.
Resin restorations can be difficult to detect but forces applied through the laryngoscope
can fracture this material. Devitalized teeth as a result of trauma or root canal treatment
become more brittle than healthy teeth and are more likely to break when loaded.
Difficulty with intubation

Difficulty with intubation is an important risk factor because it may lead to additional or
unusual forces being applied to oral structures including teeth. Earlier use of a bougie
or flexible-tip layngoscope or an alternative method of intubation should always be
considered when risk factors for difficult intubation are observed.
Emergency surgery
Urgent cases have an increased risk of dental damage possibly because of the
necessary haste and because a laryngoscope is usually used. It is probably prudent to
explain this to the patient.
Drug therapy and co-morbidities

Many conditions and drug treatments have dental implications, which is why taking
an accurate history is important. Any drug or disease that results in a dry mouth
(xerostomia) increases the risk of dental pathology. For example a patient taking
methadone as part of a drug rehabilitation programme has an increased risk of dental
disease. All opioids reduce salivary flow and promote dental disease. While a patient is
abusing narcotic drugs it is likely that dental hygiene is not attended to, making dental
pathology even more likely. Methadone is presented in a sugary syrup and this also
promotes caries. Also, if the patient has acquired HIV or AIDS, problems may arise
from HIV periodontitis and xerostomia from the disease and/or drug treatment.
Intubation alternatives
There are several alternative intubation techniques that may reduce the risk of dental
trauma.
Flangeless or reduced-flange laryngoscope blades: the most extreme example

of this is the Bizzarri-Guiffrida blade which has no flange at all, but this makes it more
difficult to use. The Bellscope blade is shaped to reduce the risk of contact between
teeth and flange.
Warning devices: a number of prototype systems that warn when pressure is being
applied to teeth have been described.
Lightwand intubation: the malleable wand of the Trachlight and the need for very
little mouth opening should reduce the incidence of dental trauma from intubation.
The intubating laryngeal mask airway (LMA): the Fastrach could reduce the risk
of teeth being broken, but loose teeth could still be subluxed during insertion and
manipulation of the LMA.
Fibre-optic intubation is used routinely in some centres but the cost limits its routine
use in most hospitals.
Dont intubate: the growing range of airway management systems (e.g. the LMA
Proseal) may provide an acceptable alternative to intubation in some patients.
However, objects put in the mouth to protect the device (e.g. a Guedel airway) may
increase the risk of dental damage. A real bite block sits between the molars which are
designed to tolerate high forces. Anything put between the incisors increases the risk of
subluxation of the upper incisors.
Mouthguards: there is no good evidence that using a generic mouthguard protects

teeth from damage during laryngoscopy. In one study, when the mouthguards were
removed they sometimes had teeth embedded in them. Custom mouthguards may be
useful, especially if there are anterior bridges, but they need to be fabricated in advance
of the procedure and may make intubation more difficult. u
FURTHER READING
Chen J-J, Susetio L, Chao C-C. Oral Complications Associated with Endotracheal
General Anaesthesia. Anaesthesiol Sin 1990; 28: 1639.
Gaiser R R, Castro A D. The Level of Anesthesia Resident Training does not Affect the
Risk of Dental Injury. Anesthesia Analgesia 1998; 87: 2557.
Owen H, Waddell-Smith I. Dental Trauma associated with Anaesthesia. Anaesth Intens

Care 2000; 28: 13545.

Anaesthesia for Facial Trauma
Joy E Curran
Joy E Curran is Consultant Anaesthetist at the Queen Victoria Hospital, East

Grinstead, West Sussex, UK. She is currently College Tutor and is the South East
Thames Lead Consultant for flexible training. She qualified from St Thomas Hospital,
London, and trained as an anaesthetist at St Bartholomews, St Georges and Kings
College Hospitals, London. Her main interests are in anaesthesia for head and neck
Facial trauma has particular importance for anaesthetists because it directly involves
the upper airway. Trauma to the face can also affect the vital structures involved in
four of the five senses, the underlying brain, the soft tissues (with implications for the
cosmetic result) and the bony skeleton.
The main cause of facial injury in developed countries was road traffic accidents (RTAs)
until the later half of the 20th century when assault became the most common cause.
Sports injuries and falls (especially in those under 5 years of age) are the second
most common cause. Industrial accidents have decreased as safety regulations have
become more stringent, but like gunshot and missile injuries they can cause complex
fractures with gross comminution and soft tissue loss.
Many patients with facial trauma following RTAs and assaults have ingested alcohol
and/or social drugs. Young men account for 75% of facial trauma patients.
Types of injury
Figure 1 shows the relative strength of the bones of the skull and face. Facial fractures
follow the lines of weakness of the facial bones. Guerin in 1866 and Le Fort in 1901
described these in their classic papers. Facial fractures are still known by the Le Fort
classification (Figure 2). A patient may have multiple levels of fracture.
Fractures of the Facial Skeleton
Initial management
Other injuries
About 15% of severely traumatized patients also have maxillofacial injuries. 510%
of patients with blunt trauma to the head and face have an associated cervical spine
injury; cervical spine immobilization is essential until this is excluded. A survey of
patients with Le Fort fractures in the late 1980s found that 26.5% presented with either
airway obstruction or decreased respiration requiring immediate airway and ventilatory
control. The head injury that often accompanies facial injury affects the need for airway
control.
Early management
The immediate and early management of all trauma patients must follow the ABC of
resuscitation. Of the facial injuries, the eye should be treated first, then the soft tissues
(within the first 12 hours) and finally reconstruction of the facial skeleton (this can wait
for a semi-elective theatre slot).
Airway problems
Minor airway problems become major ones in the presence of decreased
consciousness, examples are:
blood, which can be considerable
vomit, teeth, dentures, bony fragments
the anterior insertion of the tongue can be disrupted in bilateral mandibular fractures
allowing the tongue to fall back.
All of these can be compensated for in the awake patient but can cause rapid loss of
the airway once consciousness is lost or diminished. Conscious patients tend to place
themselves in the best position for their airway.
Problems with the airway that need immediate control occur with extensive disruption
as a result of missile or industrial injuries; they are uncommon following RTAs or
assaults. Infrequently, a bleed from a mandibular fracture into the floor of the mouth and
base of the tongue can obstruct the oropharynx. Haemorrhage may be closed within
the maxilla causing significant swelling over a few hours (resulting in typically tense
shiny cheeks; Figure 3), or open, in which case there can be a large blood loss from the
pterygonal venous plexus or maxillary artery.
3 The classic moon-face appearance of a patient

with multiple fractures of the mid-facial skeleton.
Tramlines can be seen caused by CSF leak
(arrows).
Airway control
In the emergency situation, a straightforward route to securing the airway is required.
This should be via an oral tracheal tube or a surgical airway (tracheostomy or
cricothyroidotomy under local anaesthesia). Retrograde passage of a guide (e.g. an
epidural catheter) via the cricothyroid membrane in severe disruption is potentially
useful. The main problems are:
blood and debris preventing a good view (ensure effective suctioning with a wide
bore, blunt ended sucker; induction in the lateral or prone position will allow blood to
drain)
distorted anatomy
cervical spine immobilization (removing the hard collar and using manual in-line
stabilization allows better oral access; a gum-elastic bougie is useful and must be to
hand)
full stomach needing cricoid pressure (if this makes the view impossible, release it)
associated head injury may make the patient uncooperative (protect the brain from
further damage by avoiding hypoxia, hypotension and hypercapnia).
Good assistance is crucial and fibre-optics not very useful. The classic rapid sequence
induction is the best choice, but if lying on their back being pre-oxygenated for 3
minutes will cause the patient to drown in their own blood then think again (Figure 4).
Local anaesthesia works poorly on surfaces covered with blood or clot therefore awake
intubation is difficult. A surgical airway under local anaesthesia might be possible, if
the patient is cooperative and able to lie on his back. Cricothyroidotomy is quicker and
requires less expertise than a formal tracheostomy. Each case should be considered on
its merits, bearing in mind ones own expertise. Always have a backup plan should the
first plan fail.
Haemorrhage control
Bleeding from the soft tissues of the face can be packed and explored later. A
maxillofacial surgeon is the best person to carry this out and to suture facial lacerations
under local anaesthesia. A steady flow of blood from the nose and mouth with profound
cheek swelling is probably the result of a closed injury to the middle third. Bleeding from
a base of skull fracture should be excluded by palpating the pharyngeal wall for tears
and fractures. The anterior and posterior nasal spaces can then be packed (Figure 5).
Occasionally a tear of the terminal branches of the maxillary artery can result in life-
threatening haemorrhage. This requires a good nasal pack. Careful application is
essential because this is not well tolerated by an awake patient and when incorrectly
placed can cause partial obstruction of the airway.
4 Intubation with a bougie.
Fractures of the Facial Skeleton.
A fracture of the body of the mandible occasionally causes complete rupture of the
inferior alveolar artery. Normally, the artery goes into spasm, but if it fails to do so,
copious haemorrhage can occur. This is an emergency, which requires immediate
reduction of the fracture followed by the bone segments being held in rough alignment
by wires around the adjacent teeth. A laceration to the tongue can cause profuse
haemorrhage that is hard to control. Bleeding from the ear can be caused by a fracture
of the base of the skull or a fracture of the condylar head, which has been forced
backwards and torn the external auditory meatus.
After securing the airway, follow the BCDE priorities of basic life support (Figure 6).
Ensure good ventilation, check the chest and obtain a radiograph of the chest and
the cervical spine and pelvis if appropriate. It is rare to get circulatory shock from
maxillofacial injuries, therefore if it is present look elsewhere for the loss. Monitor the
neurological deficit, initially by using the AVPU scale (Figure 7) together with pupillary
reactions. Then the Glasgow Coma Score (see Anaesthesia and Intensive Care
Medicine 3:4: 132) should be measured at frequent intervals.
Priorities for basic life support
A Airway with spine control

B Breathing and ventilation
C Circulation and control of haemorrhage
D Assessment of disability and neurological deficit
E Exposure and environmental control
6
Monitoring neurological deficit using AVPU scale
A responds appropriately and is aware

V responds to verbal stimuli
P responds to painful stimuli
U does not respond unconscious
7
Soft tissue injuries

Soft tissue swelling can occur rapidly or insidiously. It is at its maximum 1012 hours
after injury. Therefore, patients who have suffered more than a single isolated fracture
should be kept under close observation for this time.
Lacerations to the soft tissue should be thoroughly cleaned and sutured under local
anaesthesia within 24 hours. Fractures to the facial skeleton can be treated later if the
patients underlying condition is poor or an experienced surgeon is unavailable. This
may involve reopening wounds, but most facial fractures are reduced and plated via the
oral mucosa; only upper facial injuries require skin incisions.
Pain control
In general, even extensive trauma to the face does not cause a large amount of pain.
One exception is a mobile fracture of the body of the mandible, which can give a lot
of discomfort and be a cause of restlessness. Minor analgesics such as paracetamol
and a non-steroidal anti-inflammatory drug (NSAID) usually suffice. In general, avoid
excessive sedation in case there is occult head injury.
Preventing infection
There is widespread use of prophylactic broad-spectrum antibiotics; usually amoxicillin
(amoxycillin) with metronidazole or augmentin. Although they do not penetrate the CSF
well, neurosurgical opinion is that if there is a breach in the CSF then antibiotics that
are in the oral and pharyngeal tissues will penetrate sufficiently. However, retrospective
studies indicate that prophylactic antibiotics do not significantly affect the incidence of
meningitis in patients with a CSF leak.
Dural tears
A dural tear is possible with all Le Fort II and III mid-face fractures. Normally the CSF
leak stops after a few days. Its detection is possible clinically from the observation
of tramlines on the face or the halo effect on bedding; this can be seen in the patient
in Figure 3. These are caused by CSF not coagulating and blood that does. Testing
glucose and protein levels is of little clinical help. Definitive diagnosis is by high
resolution CT or MRI.
There is a small risk (about 1%) of meningitis, at the time of injury and also years later,
if the cribriform plate is involved. If the posterior wall of the frontal sinus has been
fractured, a late presentation of a mucocele may occur, which requires neurosurgical
input. Most cases of CSF rhinorrhoea stop spontaneously and virtually all stop after the
fractures have been reduced.
Late management
Delaying definitive treatment for facial fractures allows resolution of head injury,
treatment of other more life-threatening conditions, soft tissue swelling to diminish and
an experienced surgeon to be present.
Particular areas for preoperative anaesthetic assessment are the mechanism of trauma;
any possibility of head, cervical spine or other injury, and any history of drug or alcohol
abuse.
Airway assessment
In mandibular fractures, trismus caused by pain is likely to limit mouth opening. This
usually disappears on induction. Fragments of bone in the temporomandibular joint
can prevent mouth opening even after induction. The mobility of early fractures tends
to make laryngoscopy easier than normal. Check for teeth that have been loosened or
broken in the impact of the trauma and be aware that missing teeth could have been
inhaled.
Intubation
Before commencing induction it is essential to discuss the operative plan with the
surgeon. In most patients with mid-facial fractures intraoperative dental occlusion is
required and an oral tracheal tube prevents this. For surgery to the zygoma and orbital
floor an oral south-facing tracheal tube is probably best. Panfacial fractures involve the
structural bones and the smaller bones of the nasal complex, which means that access
to the nose as well as occlusion is required.
There is debate regarding the nasal route of tracheal intubation in the presence of
a base of skull fracture or the Le Fort II and III fractures. Two cases of intracranial
placement of a nasal tracheal tube have been reported in the literature. Only two,
retrospective, studies have looked at outcome for this group of patients, but they did
not show any increase in the incidence of meningitis when the nasal route was used for
intubation.
If surgery cannot be carried out with an oral tube, the three main options are: formal
tracheostomy; nasal intubation (using fibre-optic guidance); and submental intubation.
Submental intubation involves passing the tracheal tube through the floor of the
mouth. Figure 8 lists the advantages and disadvantages of each approach. Unless
postoperative ventilation for more than 2448 hours is likely to be required the author
favours using the nasal route.
In complex cases the position of the tracheal tube may need to be changed
intraoperatively. The author usually starts with an oral tube and then the surgeon places
a nasal tube through to the pharynx after fixation of the small bones in the mid-zone,
the author then re-intubates with the nasal tube.
Maintenance
For maintenance of anaesthesia, a total intravenous technique using propofol and a
short-acting opiate (alfentanil or remifentanil) has a number of advantages. It allows
rapid awakening, with early return of glottic reflexes, immediate assessment of
conscious level in the patient with head injuries, and cooperation with eye testing after
zygomatic and orbital floor work. It is also less emetogenic than the volatile agents.
Deliberate hypotension is of limited benefit in most cases and may harm the patient with
a head injury.
The general principles of a head-up tilt, carbon dioxide control and rehydration
should be borne in mind. Most of these injuries cause little pain and so large doses of
opiates are unnecessary. The surgeon will often use local anaesthetic with adrenaline
(epinephrine), which is helpful. A rectal or intravenous NSAID is useful and intravenous
or intramuscular tramadol is a good analgesic because it causes less respiratory
depression and sedation.
Comparison of tracheostomy, nasal intubation and submental intubation
Tracheostomy
Avoids controversial nasal route Most invasive of the techniques
Allows dental occlusion intra- and postoperatively Extra procedure
Better for long-term ventilation Risks of haemorrhage, tracheal damage
stenosis, tracheomalacia and infection
Nasal intubation
Allows dental occlusion intraoperatively A fibre-optic scope is preferable
Avoids an extra surgical procedure Poor for prolonged postoperative ventilation
and weaning
Avoids a surgical scar The nose must be patent
Risks of nasal haemorrhage, sinusitis and
unproven possibility of an increase in the
infective complication of meningitis
Submental intubation
Technically easy Many surgeons are unfamiliar with the
technique
Allows dental occlusion intra- and postoperatively Not good in prolonged ventilation and
weaning
Low complication rate If an armoured tube is used re-intubation
may be necessary, because the connector
Cosmetically acceptable scar does not detach from the tube
Most patients can be extubated at the end of surgery. This should be awake if the
stomach is full or if re-intubation would be difficult. A deep extubation is less likely to
lead to laryngospasm and coughing. Airway problems at extubation are as common as
at intubation. If a nasal tube has been used, it can be left in the nose and pharynx until
the patient is fully awake to maintain a clear airway and splint any nasal haemorrhage
until the airway is safe.
Postoperative care
Good recovery facilities are important. Patients must be observed for further soft
tissue swelling, eye signs may need checking and the Glasgow Coma Score should be
monitored if there was any suggestion of head injury. For moderate and severe facial
injuries, high dependency facilities are required for 1012 hours postoperatively. u
FURTHER READING
Banks P, Brown A. Fractures of the Facial Skeleton. Oxford: Butterworth-Heinemann,
2000.
Patel H, ed. Anaesthesia for Burns, Maxillofacial and Plastic Surgery. London: Edward
Arnold, 1993.
Skinner D, Driscoll P, Earlam R, eds. ABC of Major Trauma. London: British Medical
Journal, 1991.

Anaesthesia for Maxillofacial
Surgery
S Fadheel
H Drewery
S Fadheel is Specialist Registrar in anaesthetics at the North Thames School of

Anaesthesia East. He qualified from the University of Baghdad, Iraq, and trained in
anaesthesia in Iraq and the UK. His interests include management of the difficult airway
and day stay anaesthesia.
H Drewery is Consultant Anaesthetist at The Royal London Hospital.
Maxillofacial surgery encompasses a range of hospital-based procedures of the head,

neck and mouth that overlap with ENT, plastic, general surgical and neurosurgical
operations. In the UK, most maxillofacial surgeons are qualified as dental and medical
practitioners. Because of the wide range of maxillofacial procedures, the patients
encountered range from the very young to the elderly.
Dental procedures include exodontia and removal or biopsy of orocutaneous lesions.

The most common maxillofacial surgical operation is dental extraction. In the UK, most
dental extractions are carried out under local anaesthesia in high street dental clinics,
only the more complicated cases are referred for hospital care.
Facial injuries or trauma involve skin, soft tissues and/or bony fractures. Most
trauma patients can be operated on in a planned manner though some require urgent
intervention, for example if the airway is compromised or if scalp lacerations threaten to
cause large blood losses.
Corrective (orthognathic) procedures for facial bone deformities are sometimes

carried out for aesthetic reasons but more commonly for orthodontic ones. Most
patients are young children and adults.
Excision of benign or malignant tumours necessitates long, extensive operations,

sometimes involving pedicle or free-flap techniques.
Tracheostomies are often carried out by maxillofacial surgeons.
General procedures such as thyroidectomy, parathyroidectomy and excision of parotid

glands occasionally come under the maxillofacial remit.
General considerations
The presence of an experienced anaesthetist is essential because the incidence of a
difficult airway and/or intubation is high.
Routine monitoring for general anaesthesia should include inspired oxygen

concentration, oxygen saturation, ECG, capnography, agent monitoring, non-invasive
blood pressure and temperature. For extensive procedures, invasive monitoring should
be considered, such as invasive blood pressure, central venous pressure and urinary
catheterization.
Intravenous access is mandatory, even for minor non-invasive procedures.
Generally, nasal intubation is preferred for intra-oral procedures. However, simple

extractions can be carried out safely with an orotracheal tube or a laryngeal mask
airway (LMA).
The surgical field interferes with the airway therefore LMAs, tracheal tubes and
tracheostomy tubes should be well secured and observed for position and patency.
A mouth or throat pack is often placed to prevent blood and debris falling down the
trachea and oesophagus; however, great care must be taken to document this and
fail-safe mechanisms should be developed to ensure their removal before extubation.
Orogastric or nasogastric tubes are required for extensive operations.
Head and neck operations often require a head-up tilt position and normotension;
occasionally, the surgeon requires controlled induced hypotension. Discussion with the
surgeon regarding the extent of the procedure and airway maintenance is necessary
before starting any anaesthetic.
Postoperative admission to a high dependency unit or ICU should be considered for

patients undergoing extensive prolonged operations.
Concomitant head injury, cervical spine instability and a full stomach should be
considered to be present in trauma patients until proved otherwise.
Inhalational or intravenous induction of anaesthesia is suitable for most patients.

Inhalational induction is preferred for children and also whenever a difficult airway
and/or intubation are anticipated. Some patients require awake fibre-optic intubation.
Inhalational agents or intravenous propofol are suitable for maintenance of anaesthesia.
Remifentanil, either with propofol or with an inhalational agent, is sometimes an
extremely favourable option. Spontaneous ventilation may be a suitable technique,
but controlled ventilation with or without muscle relaxation is preferred for longer
procedures. Dexamethasone is commonly administered to reduce surgical oedema.
Paracetamol, non-steroidal anti-inflammatory drugs (NSAIDs; e.g. diclofenac,
ibuprofen) and opioids (e.g. fentanyl, alfentanil, remifentanil, morphine, codeine) may
be used for intraoperative analgesia. Local anaesthetic infiltration may also be used for
procedures carried out under general anaesthesia as an adjunct to other analgesics.
Extubation may be carried out in the lateral position under deep anaesthesia, or when
the patient is awake (especially after difficult intubation). Consideration should be
given to extubating difficult airways over a tube exchange catheter with the facility to
insufflate oxygen if necessary. Recovery in the post-tonsillectomy position is preferred.
Postoperatively, patients are generally nursed with some head-up tilt once they have
regained consciousness, which helps to control bleeding, reduce swelling and minimize
venous engorgement in free flaps.
Postoperative analgesia is best provided as a combination of residual local

anaesthesia, together with simple analgesics and the addition of opioids when
necessary, either by patient-controlled or nurse-controlled analgesia. Care should
be given to patients who have had a free-flap procedure to treat opioid-induced
constipation, which can lead to venous engorgement and possible flap failure.
Anaesthesia for dental procedures

In the UK, general dental practitioners working in dental clinics are not permitted
to perform dental procedures under general anaesthesia or sedation in children.
Therefore, all children requiring such treatment must be treated in hospital. Since
1 January 2002, general anaesthesia for adults requiring dental extraction can be
performed only in hospital. Before a patient is offered a general anaesthetic for dental
extraction a thorough and clear explanation of the risks involved and the alternative
methods of pain control available must be given to them (see page 239). However,
certain groups of patient require general anaesthesia:
children, commonly those less than 10 years of age, who will not tolerate the dental
chair and local injections
patients with special needs
adults who cannot tolerate local anaesthesia (e.g. needle-phobia, multiple impacted
wisdom teeth, failed local anaesthesia, previous allergy to local anaesthesia).
Dental extraction in children

Extraction of decidual teeth is usually easy and quick and can be performed as an
outpatient procedure. The child should be prepared and fasted as for any general
anaesthetic. The anaesthetic technique should allow rapid recovery and discharge
from hospital. Premedicant analgesia (e.g. oral paracetamol) before induction is helpful.
Local anaesthetic cream (Emla or Ametop) can be applied for older children who
may agree to intravenous cannulation and induction. Occasionally, sedation with oral
midazolam may be used as premedication. However, most children choose inhalational
induction. Each child needs to be assessed as to which monitors will be tolerated
before induction; most will accept a pulse oximeter. Sevoflurane is particularly suitable
for both induction and maintenance of anaesthesia. Once anaesthesia is deep enough,
intravenous access is secured and the remaining monitors attached. For intravenous
induction, propofol is useful for its rapid recovery and anti-emetic properties, though
pain associated with the injection is possibly more evident with children.
Airway management depends on the extent of the procedure. A nasal mask for
extraction of incisor teeth alone or easily accessible molars, can be used with or without
a nasal airway. Usually the surgeon uses a mouth pack, and a mouth prop on the
opposite side of the mouth to the proposed extractions. Jaw thrust may be needed
to maintain airway patency but a fastidious surgeon ensures that the lower jaw is
always supported. The reinforced LMA (RLMA) is preferred for multiple extractions or
if surgical difficulty is anticipated. The RLMA can easily be moved from one side of the
mouth to the other as the operator moves and usually provides an unobstructed airway.
Additionally, the inflated cuff probably prevents airway and stomach soiling by blood
better than a tracheal tube (Figure 1). Some anaesthetists prefer tracheal intubation.
1 This child is having multiple

extractions under general
anaesthesia.
Note the reinforced laryngeal
mask airway (RLMA) and gauze
pack. The anaesthetists hand can
steady the head and the surgeon
holds up the lower jaw. The LMA
is removed while inflated and the
child still deeply anaesthetized.
Intraoperatively, NSAIDs or paracetamol administered as a suppository provide some

postoperative analgesia. Additionally, local anaesthetics can be infiltrated, especially if
large back molars are being extracted. It is rare to require opioids, but rectal codeine
phosphate may be the most suitable.
When the procedure is finished, the child is placed on his side. The LMA is removed
with the cuff inflated, or extubation is performed, preferably under deep anaesthesia.
Recovery is initially best in the post-tonsillectomy position, but once the child is awake
he or she should be sat up. Further postoperative analgesia (e.g. paracetamol and/or
ibuprofen) may be prescribed to take home.
Children who are unsuitable to be treated as outpatients for medical reasons, should be
assessed for treatment as a day case or in-patient.
Dental extraction in adults

Dental extraction in adults is usually performed as a day case procedure either under
general anaesthesia or sedation. Patient preparation and monitoring for sedation,
is the same as for general anaesthesia. Midazolam in small incremental doses is
most commonly used together with local anaesthetic infiltration, though propofol in
subanaesthetic doses is an alternative in experienced hands. Supplemental oxygen
via nasal cannulas is given, and jaw support may be needed to maintain the airway.
An alternative is inhalational sedation using up to 70% nitrous oxide in oxygen or
sevoflurane in oxygen followed by local anaesthetic infiltration. Many patients are willing
to try sedation rather than general anaesthesia once the technique has been explained
carefully.
Some adults may request or require general anaesthesia. Intra-venous induction is

most commonly performed although many of these patients are needle phobic. The
airway can be maintained on LMA or by tracheal intubation, the choice depends on the
anticipated ease of extraction and whether or not the surgeon is familiar with working
around an LMA. If nasal intubation is to be performed, nasal bleeding can be reduced
by using a nasal vasoconstrictor preparation (Otrivine) or by warming the tracheal
tube. Local anaesthetic infiltration intraoperatively by the dentist is recommended.
Intravenous NSAIDs (e.g. diclofenac) with suitable opioids are also used for analgesia.
Dexamethasone is optional, but may have an anti-emetic effect. The LMA or tracheal
tube is removed with the patient in the lateral position under deep anaesthesia or
awake if preferred, bearing in mind that blood pressure surges associated with
awake extubation with a nasal tracheal tube in place can lead to bleeding. NSAIDs,
paracetamol or occasionally opioids are given for postoperative analgesia. Tramadol
may be useful if the extractions are difficult and painful and the patient wishes to go
home.
Anaesthesia for orthognathic surgery

Patients requiring orthognathic surgery are either children with congenital or familial
facial bone and soft tissue deformities, or adults who have sustained previous facial
trauma or infection, or have unresolved childhood deformities.
Cleft lip and palate
Cleft lip and palate are the most common congenital maxillo-facial deformities. They
can occur in isolation or as part of a syndrome (e.g. Pierre Robin syndrome, Treacher
Collins syndrome, Stickler syndrome). Other bony deformities such as maxillary
dysostosis can also be isolated, or part of a syndrome (e.g. Goldenhar's syndrome).
Cleft lip is usually corrected in infancy. A specialized paediatric anaesthetist should
be involved and difficult intubation should be anticipated. Inhalational induction, oral
tracheal intubation with spontaneous or controlled ventilation, is a standard technique.
Paracetamol, NSAIDs and local anaesthesia are used intraoperatively for analgesia.
Opioids may be added if required. Extubation is best achieved after full awakening and
paracetamol supplied for postoperative analgesia, with codeine if necessary.
In adults, bone deformities are usually corrected in specialized centres with surgery
often involving osteotomies based on the Le Fort classification. Invasive monitoring and
intravenous fluid and blood transfusion may be required. Inhalational or intravenous
induction, followed by nasal tracheal intubation and inhalational maintenance is
common practice. Fibre-optic intubation may be needed, particularly if fixed trismus
follows disturbance of the mandibular condyles after childhood infection or trauma.
Analgesia is achieved intraoperatively with opioids, local anaesthesia and NSAIDs. A
nasogastric tube is useful to empty the stomach of blood, and can be removed at the
end of the case. Bi-maxillary osteotomies may be extensive and lead to considerable
blood loss. Extubation can be awake or deep depending on the surgical procedure
and the pre-existing deformity. Postoperatively, patient- controlled analgesia may be
needed in conjunction with simple analgesics.
Anaesthesia for maxillofacial tumours

Benign or malignant tumours, cysts and abscesses can develop in most oral and facial
zones. Tumours and cysts are usually scheduled for elective operations, but abscesses
and biopsies may require more urgent intervention. Patients requiring biopsies can
usually be fasted adequately before induction of anaesthesia. A difficult airway should
be anticipated and a plan for intubation prepared.
Patients with oral cancers can be elderly, with a high incidence of excessive alcohol
or cigarette consumption. Operations for such malignant tumours may be extensive,
requiring prosthetic implants, bone grafts (from the iliac crest, ribs, radius or scapula)
or flaps (local or free transfer) and can be prolonged (some procedures last more than
12 hours; Figure 2). Before induction of anaesthesia, the airway should be assessed
to plan for possible intubation difficulties, paying particular attention to the position of
the tumour in relation to the airway. Other investigation results such as nasendoscopy
(performed by the surgeons) or CT scans should be sought if appropriate.
2 This patient has had several

intra-oral tumour resections and
a scapular flap forms the base of
the mouth. A pedicle flap is also
present. Intubation was achieved
on three separate occasions using
an awake fibre-optic technique.
The mode of induction of anaesthesia depends on the degree of anticipated difficulty.

Intravenous or inhalational induction, asleep or awake fibre-optic intubation are all
suitable. Usually a nasal tracheal tube is required. If tracheal intubation is deemed
impossible, then tracheostomy should be performed in the awake patient with local
anaesthetic infiltration, or in the asleep patient by inhalational anaesthesia with a
facemask or LMA. A nasogastric tube is required for postoperative feeding following
extensive resections. Ventilation for long operations has to be controlled and muscle
relaxants may be used as needed unless contraindicated (e.g. dissection for motor
nerves with the use of nerve stimulator). For maintenance of anaesthesia, inhalational
or intravenous agents are suitable. Opioid analgesia is required in most patients.
A tracheostomy may be performed at the beginning or at the end of the operation
particularly if resections have been extensive and swallowing dysfunction is anticipated
postoperatively. Invasive monitoring is required. The surgeon may request controlled
hypotension, dexamethasone, antibiotics and anticoagulation. Postoperative sedation
and possibly ventilation in the ICU should be planned for extensive long procedures
or if free-flap vasculature is dependent on patient position, when a still head is
advantageous. In cases where a tracheostomy is not performed and the patient is
not going to ICU postoperatively, extubation should be performed as appropriate with
provision for dealing with any subsequent difficulties should they arise. Postoperative
analgesia is usually achieved with NSAIDs and opioids.
Patients with oral tumours may require repeated anaesthetics, testing the
anaesthetists skill with airway management. Even the technique of awake fibre-optic
intubation may progressively prove to be difficult in these patients. u
FURTHER READING
Department of Health. A Conscious Decision. A Review of the Use of General
Anaesthesia and Conscious Sedation in Primary Dental Care. London: Department of
Health, July 2000.
Miller R D. Anaesthesia. Philadelphia: Churchill Livingstone, 2000.
Patel H. Anaesthesia for Burns, Maxillofacial and Plastic Surgery. London: Edward
Arnold, 1993.
Prys-Roberts C, Brown B R Jr. International Practice of Anaesthesia. Oxford:


Blind Nasal Intubation
Adrian J England
Adrian J England is Consultant Anaesthetist and Honorary Senior Lecturer at the

Royal Free NHS Trust, London, UK.
Magill and Rowbotham pioneered blind nasal intubation in the 1920s as an alternative
to oral intubation at the Queens Hospital, Sidcup, to facilitate surgical access for head
and neck surgery performed by Gilles. With practice many anaesthetists became
proficient at the technique, which involved careful positioning of the head to facilitate
the passage of a tube through the nose and into the trachea without the need for
laryngoscopy, forceps to guide the tip of the tracheal tube, or deep anaesthesia.
The introduction of muscle relaxants in the 1940s, allowing oral intubation without
deep planes of anaesthesia, led to the blind nasal approach to intubation waning in
popularity. Recently, agents such as sevoflurane and propofol that allow laryngeal
depression and intubation with rapid recovery and equipment such as the intubating
fibre-optic laryngoscope, have resulted in the blind nasal intubation technique
becoming rarely used in current practice.
However, with concerns about prion transfer from lymphoid tissue leading to the
introduction of disposable equipment for tonsillectomy, there may now be a case for
re-evaluating blind nasal intubation. It is an easily learnt and safe technique, which
provides a secure airway using disposable equipment and without the need for inserting
a re-usable laryngoscope blade or forceps next to the tonsillar lymphoid tissue in the
oropharynx. Indications and complications of the technique are given in Figure 1.
Blind nasal intubation
Indications when its use can be considered

Poor mouth opening (e.g. trismus)
Surgery on the jaw, teeth or maxilla
Trauma to the jaw, teeth or maxilla
Swelling of the tongue, or soft tissues of the oral cavity
Lack of equipment (e.g. laryngoscope, in an emergency)
Complications
Trauma to the structures in the nasopharynx
Trauma to the larynx and vocal cords
Perforation of the pharynx or trachea
Misplacement of the tracheal tube
Oesophageal ventilation causing air to fill the stomach
Anaesthesia (local or general) may obstruct an already
compromised airway
Haemorrhage, causing airway obstruction
Coughing
Contraindications
Inadequate depth of anaesthesia
Bilateral blocked nostrils
Partial airway obstruction from tumour, abscess or trauma
Recent surgery to the airway
Coagulopathy
Fractured base of skull
Unprepared patient (e.g. full stomach)
1
Equipment
The first nasotracheal tubes used by Magill were cut from red rubber hose purchased
from a hardware store, trimmed to size and smoothed with emery paper. Advances
in plastic and latex technology now allow the manufacture of preformed, soft, shaped
tubes with cuffs to ensure an airtight seal (Figure 2). Universal connectors allow
attachment to standard anaesthetic circuits.
To be suitable for blind nasal intubation, the nasotracheal tube must be soft enough not
to cause trauma to the nasopharynx, but stiff enough to be pushed past the turbinates
and through the vocal cords without becoming deformed. It requires a curve to allow
it to sit directed dorsally as it passes through the nostril, but caudally as it enters the
trachea through the larynx and this can be achieved with both preformed (Figure 3)
and flexible tracheal tubes (Figure 2). Attachment to a standard anaesthetic circuit can
be achieved at the nostril, but this may lead to local pressure damage because of the
weight of the connectors or kinking of the tracheal tube. An alternative method is to use
a preformed north-facing tracheal tube of suitable length with the connector situated
over the forehead (Figure 3). The connector can then be padded to prevent pressure
damage to the underlying tissue.
d 2 Four nasotracheal tubes: a

uncuffed red rubber tube; b
uncuffed plastic tube; c blue
line (Portex, Hythe, UK) ivory
tube; d Mallinckrodt (St Louis,
Missouri) flexo-metallic tube.
3 Three RAE Mallinckrodt

(St Louis, Missouri) preformed
plastic tracheal tubes. a south-
facing cuffed oral; b north-
b facing cuffed nasal; c north-
facing uncuffed oral. Note the
different angles of the north-
facing oral and nasal tubes.
The diameter of the tracheal tube is important. A balance has to be achieved between a
tracheal tube that is large enough to allow air to enter and leave the lungs and one that
is small enough not to damage the tissues of the nasopharynx and larynx. A suitable
compromise is to use one with a diameter of 6.07.5 mm.
Anaesthesia
Blind nasal intubation can be performed under general or local anaesthesia and in a
patient who is either breathing spontaneously or who has received a muscle relaxant.
The use of antisialogogue premedication and topical vasoconstrictor nasal drops may
enhance the conditions for intubation.
Local anaesthesia can be achieved using nebulized lidocaine (lignocaine), but much
of the drug may be lost. Alternatively the airway can be anaesthetized using topical
applications of local anaesthetic in the nose (cocaine or lidocaine (lignocaine) applied
with pledgets, sprays or gels); the oropharynx and glottis (lidocaine (lignocaine) spray,
gargle or through bilateral superior laryngeal nerve blocks); and the trachea (lidocaine
(lignocaine) sprayed through a needle following cricothyroid puncture).
Spontaneous ventilation techniques allow breath sounds to be heard through the

tracheal tube as it is guided through the airway. They also confer the advantages of
a widely opened larynx during inhalation, increasing the aperture through which the
tracheal tube needs to pass to enter the trachea, and allowing confirmation of correct
placement of the tracheal tube in the trachea.
Position
Magill described the following position for blind nasal intubation; the optimum position
of the patients head for blind nasal intubation is simply that of a man sniffing the
morning air. The head is in normal relation to the cervical vertebrae except for slight
extension at the occiput-atlas junction. In this position the course of the airway from
nose to glottis is maximally open and a catheter mounted on a stylet or a suitably
curved rubber tube will follow that course naturally and enter the glottis in many cases.
Of course, in the recumbent position a pillow under the occiput is usually necessary for
this purpose.
Individual anaesthetists may develop their own variations on this position through trial
and error, but the sniffing the morning air description remains firmly entrenched in
anaesthetic teaching.
Technique
The patient is prepared for theatre, monitoring is attached and a suitable anaesthetic
technique performed. The patient is then positioned, either supine or sitting, in the
sniffing the morning air position with the anaesthetist either above the patients head
or to the side. A suitable, lubricated tracheal tube is advanced through a nostril initially
in a dorsal direction and advanced gently past the turbinates. The tracheal tube is then
rotated so its curve lies in the sagittal plane with the distal end directed caudally before
being advanced with gentle pressure through the pharynx. From here it will often pass
into the trachea, but the tip of the tracheal tube may also advance into the oesophagus,
or press against tissues anterior to the larynx, in the valecula or in the pyriform fossa.
These can often be seen as bulges in the soft tissue of the neck. If the trachea is not
entered, then the tracheal tube should be withdrawn into the pharynx, the patients
head repositioned appropriately and the tube re-advanced. Various modifications of the
technique have been described, which may increase the chances of success, including
inflation of the tracheal tube cuff when it is in the pharynx to position the tip of the tube
in the midline, and palpation of the larynx while lifting the chin during tracheal tube
advancement.
A disadvantage of the blind nasal technique is that direct visualization of the tube
passing through the vocal cords is not performed. Confirmation of tracheal tube position
is required using other methods, such as auscultation of the chest and abdomen,
capnography and the oesophageal detector device, before surgery continues. u
FURTHER READING
Fell D. The Practical Conduct of Anaesthesia. In: Aitkinhead A R,
Smith G, eds. Textbook of Anaesthesia. Edinburgh: Churchill Livingstone, 1990.
Magill I W. Lest We Forget. Anaesthesia 1975; 30: 4769.
McHale S P, Brydon C W, Wood M L, Liban J B. A Survey of Nasotracheal Intubating

Skills amongst Advanced Trauma Life Support Course Graduates. Br J Anaesth 1994;
72: 1957.

Difficult Airways
Ian Calder
Ian Calder is Consultant Anaesthetist at the National Hospital for Neurology and
Neurosurgery, Queen Square, London, and the Royal Free Hospital, London.
Classification of difficult airways can be based on technique (Figure 1) or aetiology,

though neither is entirely satisfactory. The aetiological approach (Figure 2) is helpful for
the examination candidate trying to remember the causes of airway difficulty.
Technical classification and prevalence of difficulty
Face mask 1:500

Laryngeal mask Rare
Direct laryngoscopy 1:100
Fibre-optic laryngoscopy Operator dependent
Intubation 1:2000 (failure, general surgery),
1:300 (failure, obstetrics)
Tracheostomy ?
1
Aetiological classification
Reflexes
Includes coughing, breath holding, laryngospasm, salivation and
regurgitation
Stiffness
Includes the arthritides affecting neck, jaws and glottis, fixation devices,
scleroderma
Deformity
Often allied with stiffness. Includes cervical deformities (Klippel-Feil),
radiotherapy and burn contractures, dwarfism, Pierre Robin, Treacher
Collins, and major facial deformity caused by trauma or chronic
infections
Swelling
Includes infections, tumours, trauma, acute burns, anaphylaxis,
haematoma and acromegaly
High tariff patients

Patients in whom additional problems may contribute to a decline in the
operators performance because of constraints in technique (e.g. patient
with full stomach) or added stress (VIPs, obstetric patients, children,
uncooperative patients)
2
Attempts at standardization have been made, such as that of direct laryngoscopy by

Cormack and Lehane (Grades 14: all glottis; only arytenoids; only epiglottis; no glottic
structure). Mask ventilation and intubation are more difficult to grade. Benumof has
suggested that the term difficult mask ventilation should apply when two operators
are needed (one holding the mask, the other squeezing the bag) and oral or nasal
airways are required. The American Society of Anesthesiologists (ASA) defines difficult
intubation as one taking more than three attempts or longer than 10 minutes. However,
Benumof notes that this misses cases in which difficulty is immediately obvious and
suggests that difficulty be recorded after failure of an optimal best attempt.
Prediction
Difficult airways are generally symptomless and routine airway examination does not
identify them. A logical approach is to try to identify patients unable to extend at the
cranio-cervical junction and/or with diminished jaw protrusion, which are the main
factors involved in both standard airway control and direct laryngoscopy.
Failure to predict airway difficulty seldom causes an airway disaster. The ASAs
analysis of closed legal claims (Figure 3) shows that disasters usually follow repeated
attempts to intubate, which result in loss of the airway due to glottic swelling,
laryngospasm, or both, or perforation leading to mediastinitis or cervical abscess.
These complications should be avoidable, whether difficulty has been predicted or not.
Main causes of anaesthetic airway mortality
Repeated attempts at intubation loss of airway
Perforation of pharynx or trachea infection
3
Expression of risk
Various methods of predicting airway difficulty have been studied. The results express
the performance of the tests in terms of sensitivity, specificity and positive predictive
value. These concepts are easily misunderstood and confused (Figure 4). The
likelihood ratio makes it easier to understand the significance of the sensitivity and
specificity data as applied to an individual patient. The likelihood ratio is calculated by
dividing the sensitivity by 1 specificity. The result is the number of times more likely
it is that a patient with a positive test result will be in the difficult group. The likelihood
ratio is interpreted against the prevalence of the problem.
Terms used in prediction
Sensitivity
Positivity in disease. Makes no comment on positivity in health. High
sensitivity tends to be associated with low likelihood of true result (e.g. Is
the patient human? supremely sensitive and useless)
Specificity
Negativity in health. High specificity means few false-positive results but
tends to lead to true-positive results being missed (e.g. Are the teeth wired
together? many other causes of difficulty)
Positive predictive value

The proportion of times a positive test is right; often confused with
sensitivity
Likelihood ratio
Sensitivity/1 specificity
The number of times more likely a positive test result makes a diagnosis
4
The best-known, and most studied test, the three grades (not four) of pharyngeal visibility
described by Mallampati (see Anaesthesia and Intensive Care Medicine 1:1: 31) has a
sensitivity of about 50% and a positive predictive value of about 10% when applied to
standard surgical populations. In other words, the test misses half the true positives and
the prediction is wrong nine times in ten. This is not to belittle the test, which remains a
logical approach to the problem, but demonstrates the difficulty of accurately diagnosing
a relatively rare condition, with many causes. Other tests such as the sternomental or
sternothyroid distance are even worse, and have been memorably described by Farmery
as having an accuracy approaching worthlessness. The positive predictive value is
increased if two or more tests are positive, but it should be kept in mind that a few more
true positives will be missed (decreased sensitivity) if the threshold for a positive prediction
is raised.
Available tests
Most tests have been studied in relation to difficult laryngoscopy (Figure 5). A recent study
of difficult mask ventilation identified five independent risk factors: age over 55 years; no
teeth; beard; BMI over 26; history of snoring. Unfortunately, the likelihood ratio of difficult
mask ventilation if two factors are present is only 2.6.
Airway difficulty prediction tests
Interdental distance
Lower limit of normal said to be 3.6 cm
Mallampati
Three grades, worst for observer error, probably measures mouth opening and
cranio-cervical extension. No evidence that large base of tongue is a factor,
though often quoted. In a general surgical population the likelihood ratio of the
Mallampati is about 2, which for difficult laryngoscopy with a prevalence of
about 1%, means that a positive result does not increase the risk of difficulty
much
Thyromental, thyrosternal distance

Said to have accuracy approaching worthlessness. Likelihood ratio about 1.8
Jaw protrusion A, B, C
B has poor positive predictive value, while C is a reliable but rare predictor
Wilson risk sum

Scoring system based on multiple tests. No real improvement on Mallampati
alone
5
Effect of increased prevalence of difficulty: the accuracy of the tests has been shown
to increase when they are applied to a population with an increased prevalence. For
instance, when applied to patients with cervical spine disease where the prevalence of
Grade 3 laryngoscopy was 20%, the Mallampati achieved a positive predictive value
of 78% and a likelihood ratio of 14. The tests are fairly reliable predictors of easiness,
because the prevalence is very high.
When to attempt prediction of difficulty: in the event of a disaster, there may be

criticism of aspects of the case that have little relevance to the outcome. Although the
available tests are inaccurate in predicting difficulty in a general surgical population it
is prudent to make the attempt. In populations with higher prevalence of difficulty, such
as cervical disease, temporomandibular joint disease or acromegaly, where a positive
prediction is more likely to be accurate, it is foolish not to record an attempt.
Communication
Patients found to have a difficult airway, should be told. Medic-Alert registration should be
considered. Failure to communicate might be regarded later as legally actionable.
Airway plans
It is sensible to consider the consequences of failure to secure an airway. The causes of
airway-related mortality mentioned above should be kept in mind. General Von Moltkes
dictum Few plans withstand contact with the enemy emphasizes the need for forethought
and flexibility. u
FURTHER READING
Benumof J. Airway Management, Principles and Practice. St Louis: Mosby, 1995.
Calder I, Calder J, Crockard H A. Difficult Direct Laryngoscopy in Patients with Cervical

Spine Disease. Anaesthesia 1995; 50: 75663.
Domino K B, Posner K L, Caplan R A, Cheney F W. Airway Injury During Anesthesia.
Langeron O, Masso E, Huraux C et al. Prediction of Difficult Mask Ventilation.

Sackett D L, Richardson W S, Rosenberg W, Haynes R B. Evidence Based Medicine: How

to Practice and Teach EBM. New York: Churchill Livingstone, 1997.
Williamson J A, Webb R K, Szekely S et al. Difficult Intubation: An Analysis of 2000

Incident Reports. Anaesthesia and Intensive Care 1993; 21: 60267.
Wilson M E. Predicting Difficult Intubation. Br J Anaes 1993; 71: 3334.

General Anaesthesia for
Dentistry
Patricia J Flynn
Leo Strunin
Patricia J Flynn is Senior Lecturer in Anaesthesia at Queen Marys School of Medicine

and Dentistry, University of London, and an Honorary Consultant Anaesthetist at St
Bartholomews Hospital and The London NHS Trust. Her research interests include the
investigation of drugs and techniques for anaesthesia and sedation for dental treatment.
Leo Strunin is BOC Professor of Anaesthesia at Queen Marys School of Medicine

and Dentistry, University of London, and an Honorary Consultant Anaesthetist at
St Bartholomews Hospital and The London NHS Trust. He is a Past President of
the Royal College of Anaesthetists and is currently President of the Association of
Anaesthetists of Great Britain and Ireland. The research interests of the Anaesthetics
Unit include neuroprotection, intensive care medicine and dental anaesthesia.
Although general anaesthesia is used to reduce the pain and anxiety associated
with dental treatment, most dental procedures can be managed with good local
anaesthesia, with or without conscious sedation. Since the 1960s, there has been a fall
in the use of general anaesthesia for dentistry and in the mortality associated with it.
However, eight people died as a result of dental anaesthesia between 1996 and 1999;
five of these were children. Investigations and inquiries into these deaths were critical of
the standard of care provided in areas such as preoperative assessment, peroperative
monitoring, resuscitation and transfer to a critical care facility. In response to these
concerns the General Dental Council (GDC), the Royal College of Anaesthetists
(RCA) and the Department of Health (DOH) have issued closely linked guidelines for
standards of care in dental general anaesthesia.
Who may administer general anaesthesia for dentistry?

Dental anaesthesia developed in free-standing dental surgeries and the administration
of a dental anaesthetic was considered a traditional right of a medical or dental
practitioner. Since 1998, the administration of dental general anaesthesia has been
restricted to the following categories of staff.
An individual on the Specialist Register of the General Medical Council as an
anaesthetist, who should meet the RCAs continuing education and professional
development requirements (CEPD).
A trainee working under supervision as part of an RCA- approved training
programme.
A non-consultant career grade anaesthetist (NCCG) with a National Health
Service (NHS) appointment, working under the responsibility of a named consultant
anaesthetist who must be a member of the NHS department where the NCCG is
employed. The NCCG should also meet the RCAs CEPD requirements.
Each anaesthetist must have had appropriate experience of, and training in, dental
anaesthesia.
The RCA recommends that all children should be anaesthetized by a consultant or

NCCG who has regular relevant paediatric experience, or a trainee supervised by
someone in the preceding categories.
Who should receive general anaesthesia for dentistry?

There is wide variation in the use of general anaesthesia for dental treatment. In 1995,
a DOH report concluded that a significant number of general anaesthetics were being
given on demand, rather than to meet a defined clinical need. It was also noted that
some practitioners failed to recognize that general anaesthesia is always accompanied
by some risk. Most dental procedures can be performed under local anaesthesia and it
is recommended that general anaesthesia is limited to the following groups.
Patients who are unable to cooperate because of immaturity or physical or mental
disability.
Patients in whom local anaesthesia has repeatedly proved unsuccessful or is
unlikely to be completely effective because of the extent of surgery or the presence of
infection.
Patients with a history suggestive of hypersensitivity or allergy to the contents of the
local anaesthetic ampoule.
Patients who suffer from extreme nervousness and who refuse to undergo any form
of dental treatment while conscious. However, many nervous adults and children can
undergo treatment successfully under local anaesthesia and conscious sedation and
facilities for conscious sedation of a high standard should be more widely available.
Assessment of the patient

The GDC expects a dentist who refers a patient for general anaesthesia to discuss
the risks involved and alternative methods of pain and anxiety control with the patient.
Clear justification for the use of general anaesthesia should be contained in the referral
letter together with details of the patients relevant medical and dental history. Referral
letters are inadequate in up to 50% of cases. Members of the paediatric, oral surgery
and other dental departments who refer patients for general anaesthesia must also
comply with the GDC guidance.
Dental, medical or nursing staff may be responsible for patient assessment and most
staff are capable of selecting patients with the aid of written guidelines specifying
medical, surgical and social criteria for ambulatory or in-patient general anaesthesia.
Ambulatory dental anaesthesia is usually limited to patients assessed as American
Society of Anesthesiologists (ASA) physical status class I and II unless the service is
located within the main hospital block.
For those with health issues, an appointment should be made for assessment by an
anaesthetist. In some centres the first opportunity to meet the anaesthetist occurs on
the day of surgery. However, a separate preoperative assessment allows more time
for the patient (or parent/legal guardian) and anaesthetist to decide together whether
general anaesthesia has an acceptable risk/benefit ratio and decreases the likelihood
of the treatment being cancelled on the day of surgery.
The anaesthetist and operating dentist should explain all the procedures that will be
performed including the method of pain relief. Treatment should be specifically aimed
at avoiding the need for repeated general anaesthesia. The current guidelines of the
regulatory bodies regarding informed consent should be followed.
Where should general anaesthesia for dentistry take place?

The traditional sites for dental anaesthesia have included dental surgeries, community
dental practices, dental hospitals, day care units, specialized outpatient clinics and the
main in-patient operating theatre of a general hospital. However, since 1 January 2002,
general anaesthesia for dentistry has been confined to a hospital setting with critical
care facilities.
The DOH has defined a hospital setting as an NHS hospital and its associated clinics
or day care facilities: where trained personnel are immediately available to assist the
anaesthetist with the resuscitation of a collapsed patient so that the patients airway,
breathing and circulation are supported fully without delay and where facilities and staff
are able to support and maintain a collapsed patient pending recovery or supervised
transfer to a high dependency unit (HDU) or an intensive care unit (ICU) which may be
on a separate hospital site.
In the context of dental anaesthesia a critical care facility refers to: an area or room
which has the space, equipment and appropriately trained personnel to enable
critical care and resuscitation to be efficiently and effectively undertaken and
should there be a sudden or serious collapse of the patient to provide expert
medical care and treatment with appropriate drugs and equipment immediately
and to have additional skilled support from personnel trained specifically as a team
which can manage life-threatening situations.
All personnel involved in the administration of general anaesthesia must have up to

date advanced life support skills.
Paediatric anaesthesia
Children requiring general anaesthesia should be treated within a hospital setting
which has a child-friendly environment. As far as possible, children should be treated
separately from adults, with provision for parents to accompany children during
anaesthetic induction and recovery. Teams providing dental general anaesthesia for
children must be able to provide appropriate emergency care, including being fully
conversant with suitable equipment and drug dose regimens and have additional skilled
resuscitation support available.
Giving a general anaesthetic for dental treatment

The same standards must apply to dental anaesthesia in terms of personnel, equipment
and drugs as for other forms of general anaesthesia.
Personnel
The status of the dental anaesthetist has been specified above. The operating dentist
must be appropriately trained and sufficiently experienced to undertake the planned
surgery. The anaesthetist and dentist must each have appropriately trained and
competent dedicated assistants (i.e. the presence of four people is required in the room
wherever a general anaesthetic is administered). Patients recovering from anaesthesia
must be continuously monitored and cared for by the anaesthetist or an individual
who is directly responsible to the anaesthetist and is appropriately trained in adequate
recovery facilities. Staffing levels should allow at least one recovery nurse for each
unconscious patient. Staff must be appropriately trained where dental anaesthetic
services are provided for both adults and children.
Equipment
Equipment must be suitable for the age of the patient being treated. The dental
chair, trolley or operating table must be able to tilt head down and suction must be
available with a selection of pharyngeal and endobronchial catheters. A continuous
flow anaesthetic machine must be used. The machine must have an oxygen/nitrous
oxide interlinkage to prevent delivery of a hypoxic mixture, an oxygen failure alarm, an
emergency nitrous oxide shut-off system and an in-line oxygen concentration monitor.
Maintenance should be in accordance with the manufacturers guidelines and the

documentation of each service episode should be retained. Facilities for the supply,
storage and scavenging of medical gases must meet relevant regulations.
The anaesthetist must check all equipment before use including the patient breathing
systems. Local guidelines must be followed with regard to all equipment designed for
single use only. A full selection of oral and nasopharyngeal airways, laryngeal masks,
laryngoscopes, nasal and oral tracheal tubes and breathing circuits should be available
in addition to appropriate dental equipment.
In the operating theatre, the Association of Anaesthetists of Great Britain and Ireland
(AAGBI) considers the use of a pulse oximeter, non-invasive blood pressure monitor,
electrocardiograph and a capnograph to be the minimum monitoring devices that
should be available. Paediatric pulse oximeter finger probes should be used in children
because adult probes may give misleading values.
The technique of anaesthesia may require vapour analysis and measurement of expired
volumes and airway pressure. In addition a nerve stimulator and a means to measure
the patient's temperature should be available. In recovery, pulse oximetry and non-
invasive blood pressure monitoring is recommended. There should be immediate
access to spare anaesthetic and monitoring apparatus in the event of failure.
Drugs
A full range of local and general anaesthetic, neuromuscular blocking, analgesic,
sedative and anti-emetic drugs must be available in addition to the drugs likely to be
needed in anaesthetic and medical emergencies.
Most patients undergoing dental anaesthesia are treated on an ambulatory basis and
appropriate drugs and techniques should be used. The duration of surgery may be
minutes or may extend to 1 hour or more.
In general, the age of the patient and the extent of surgery determine the choice of
induction and maintenance of anaesthesia, control of the airway and management
of pain relief. However brief the procedure, non-invasive monitoring should be used
though it may not be practicable to apply the sensors before induction in a small child.
Inhalational induction with sevoflurane is widely used in young children and it is difficult
to justify the use of halothane in view of its high arrhythmogenic potential in this area
of practice. An argument can be made that intravenous access for administration of
anaesthetic or emergency drugs is essential in all patients regardless of the length of
the procedure. It is helpful if other members of the team as well as the anaesthetist are
trained to insert intravenous cannulas.
Pre-emptive analgesia with paracetamol or non-steroidal anti-inflammatory drugs

by oral or other routes is effective and should be considered for every patient. The
administration of a local anaesthetic by infiltration or nerve block provides analgesia
and prevents surgically induced cardiac arrhythmias. For third molar extraction the
addition of dexamethasone has been shown significantly to diminish postoperative
swelling and decrease demand for analgesia.
Control of the airway may be by nasal mask, laryngeal mask or tracheal tube.
The nasal mask, always accompanied by a mouth pack, is suitable for brief dental
extractions. For more extensive surgery or in the presence of nasal obstruction a
reinforced laryngeal mask (RLM) should be used. The RLM decreases the incidence of
hypoxaemia when compared with the nasal mask. An RLM does not give the degree of
airway protection provided by a tracheal tube, but the RLM has proved to be
satisfactory in third molar extraction lasting up to 20 minutes. A mouth pack should
always be used.
For more prolonged surgery a preformed nasal tracheal tube is generally used, though
an oral tube is satisfactory for unilateral extractions in adults and preferable in small
children in view of the risk of haemorrhage from adenoidal tissue. A throat pack is
required and care must be taken to remove it at the end of the procedure.
A high incidence of hypoxaemia has been found in patients recovering from dental
anaesthesia. Pulse oximetry should always be applied and supplemental oxygen given
until the return of consciousness.
Management of the emergency

In addition to the risks associated with general anaesthesia, dental anaesthesia is
always accompanied by the potential for obstruction and contamination of the airway,
and the induction of cardiac arrhythmias associated with dental surgery.
The DOH requires that all personnel involved with the administration of general
anaesthesia must have up-to-date advanced life support skills. All staff involved in the
provision of dental anaesthesia or the supervision of patients during recovery should
practise simulated emergency scenarios as a team. It is unacceptable for reliance to
be placed on the general crash call team for the immediate provision of advanced life
support.
A range of appropriately sized equipment for tracheal intubation and administration

of positive pressure ventilation with 100% oxygen concentrations must be available,
in addition to equipment for administration of parenteral fluids and drugs. In addition,
a defibrillator that is suitable for all age ranges treated must be available. Most
automated external defibrillators are unsuitable for children below the age of 8 years
(25 kg). Emergency drugs should include pre-loaded syringes of agents specified
in current Resuscitation Council (UK) algorithms and other drugs necessary to deal
with anaesthetic and medical emergencies. Up-to-date adult and child advanced life
support protocols should be clearly displayed in addition to written guidelines on the
management of anaphylaxis and malignant hyperthermia. u
FURTHER READING
Apparatus. 2, 1997.
Association of Anaesthetists of Great Britain and Ireland. Information and Consent for
Anaesthesia, 1999.
Association of Anaesthetists of Great Britain and Ireland. Recommendations for

Standards of Monitoring during Anaesthesia and Recovery. 3, 2000.
Department of Health. General Anaesthesia for Dental Treatment in a Hospital Setting

with Critical Care Facilities. www.doh.gov.uk/dental/consciousguidance2.htm, 2001.
Resuscitation Council (UK). www.resus.org.uk
Royal College of Anaesthetists. Good Practice. A Guide for Departments of

Anaesthesia, 1998.
Royal College of Anaesthetists. Guidelines for the Use of Non-steroidal Anti-

inflammmatory Drugs in the Perioperative Period, 1998.
Royal College of Anaesthetists. Standards and Guidelines for General Anaesthesia for
Dentistry, 1999.
Royal College of Anaesthetists. Guidelines for the Provision of Anaesthetic Services,

1999.
Royal College of Anaesthetists. Guidelines on the Provision of Paediatric Anaesthetic

Services, 2001.

Ludwigs Angina
Hamish Gray
Mike Pead
Hamish Gray is Specialist Registrar at St Bartholomew's and the London School

of Anaesthesia. He qualified from Otago University, New Zealand, and trained in
anaesthesia and intensive care medicine at Christchurch Hospital, New Zealand, and
the Royal London Hospital. His interests include anaesthesia for maxillofacial and
dental surgery.
Mike Pead is Consultant Anaesthetist at St Bartholomew's Hospital and the London

NHS Trust. He qualified from St Bartholomew's Hospital, London, and was a general
practitioner before training in anaesthesia in the North Thames Region and in
immediate medical care with the Helicopter Emergency Medical Service. His interests
include management of the difficult airway and trauma care.
Ludwigs angina is a rapidly spreading bilateral submandibular cellulitis, usually, though

not always, from infection arising from the lower second or third molar teeth, and often
without abscess formation. It was first described in 1836 by Wilhelm von Ludwig who
noted that the tongue was pressed upwards and backwards with pressure on the larynx
causing difficulty in swallowing and breathing (angina means a suffocating sensation)
leading to death from respiratory arrest.
The submandibular space is a potential space lying above the hyoid bone and is made
up of the sublingual space above the mylohyoid muscle and the submaxillary (or
submylohyoid) space below. The sublingual space communicates anteriorly with the
submental space and posteriorly with the lateral pharyngeal spaces. The submaxillary
space is divided into central submental and lateral submaxillary spaces by the anterior
belly of the digastric muscle. However, because of free communication around the
posterior border of the mylohyoid, the sublingual and submaxillary spaces can be
considered as a single unit: the submandibular space. Also, loose connective tissue,
rather than true fascia, separates the two sides of the mouth allowing infection to
spread bilaterally.
The mylohyoid forms the floor of the mouth and attaches to the lingual surface of the
mandible in an obliquely downward line from posterior to anterior (Figure 1 and 2). The
root apices of the bicuspid and first molar teeth are usually superior to the line of this
muscle and therefore infections from these teeth tend primarily to affect the sublingual
space.
Mylohyoid line
Mylohyoid line (attachment

for mylohyoid muscle)
1
Paths of infection from the third molar causing

Ludwigs angina
Root apices of the second and particularly the third molar teeth lie inferior to the
mylohyoid line of muscle attachment. Infections from these teeth primarily affect the
submaxillary space producing a large indurated swelling at the angle of the mandible
as well as swelling towards the hyoid bone. The mandible, hyoid and superficial layer
of the deep cervical fascia limit tissue expansion anteriorly and therefore impaction and
swelling spread through the whole submandibular unit producing brawny oedema with
posterior and superior displacement of the tongue and airway compromise (Figure 3).
a b
a and b Ludwig's angina. There is cellulitis and gross oedema of the left submandibular
space extending to the right side and into the neck.
The authors thank Dr Mahesh Kumar for permission to use these photographs.
Clinical course
Ludwigs angina is primarily a disease of dental origin with over 90% of cases related
to dental infection (usually of third molars). Other causes include gland sialadenitis,
compound mandibular fractures, lacerations and wounds of the floor of the mouth,
and secondary infection of oral malignancies. The disease has also been reported in a
neonate.
Improved dental hygiene and antibiotic therapy have reduced the incidence
of Ludwigs angina and most physicians and dentists seldom see the disease.
Streptococci or mixed oral flora are the most commonly reported pathogens but
staphylococci, Escherichia coli, Pseudomonas and anaerobes such as Bacteroides
and Peptostreptococcus have also been isolated. There is likely to be synergism in
mixed infections because the production of metabolic products by anaerobes enhances
the virulence of the aerobes, which in turn provides a favourable environment for
anaerobes through oxygen removal.
If antibiotic treatment is not instituted early, or is unsuccessful, the disease progresses

rapidly leading to elevation and displacement of the tongue. There is firm, hard
induration of the floor of the mouth with perioral oedema. The patient presents with
pain, fever, trismus and dysphagia. The patient may experience anxiety about their
inability to swallow or maintain an airway. Unchecked, the disease may spread
posteriorly to involve secondary fascial spaces known collectively as the masticator
space causing severe trismus. Occasionally there may be spread to deep cervical
spaces and even to the mediastinum with serious life-threatening sequelae.
Ludwigs angina can produce systemic sepsis with fever (or hypothermia), tachycardia,
respiratory distress and leucocytosis.
Management
Patients who present to hospital with Ludwigs angina are seriously unwell with an
infection that may produce upper airway obstruction with alarming speed. Successful
management involves the cooperation of the medical staff including the dentist,
maxillofacial surgeon, anaesthetist, intensivist and microbiologist. Airway control is the
priority.
Airway control
Asphyxia is the most common cause of death and control of the airway is essential.
The swollen, elevated tongue pushed up against the palate with associated glottic
oedema in an already anxious and septic patient ensures that any technique is
extremely challenging. There are three options for managing the airway.
Observation may be appropriate in a high dependency environment allowing early

aggressive medical therapy an opportunity to work. However, signs of impending
respiratory obstruction (dyspnoea, stridor and cyanosis) may appear rapidly and late,
heralding a medical emergency. Because medical staff now have little exposure to this
disease a judgement to manage the patient conservatively with observation must be
considered carefully by senior staff. Generally, observation is appropriate for patients
who present in the early stages and who have no signs of airway obstruction.
Surgical airway a tracheostomy performed under local anaesthesia is associated

with immediate and long-term morbidity. Surgery also risks spreading the infection to
deep cervical or mediastinal structures.
An anaesthetic airway can be established by a gaseous induction and direct

placement of a tracheal tube or use of the fibre-optic intubating laryngoscope. The
technique chosen depends on the skills of the staff involved. Although many authorities
recommend the fibre-optic endoscope as the gold standard the literature contains
many case reports and series where gas induction has been used successfully to
secure the airway in these patients. With either technique an armoured tracheal tube
should be used as the submandibular swelling has been reported to compress an
ordinary PVC tube, rendering ventilation impossible.
Choice of airway: a review of the literature found that only 35% of patients required
oral or nasal tracheal intubation or tracheostomy for airway control. Since the 1980s,
the use of tracheostomy under local anaesthesia has become less common. All
patients with Ludwigs angina have submandibular oedema with an elevated tongue
and trismus, therefore these signs are poor differentiators of the need for definitive
airway control versus observation. Radiological investigations, particularly CT scan
and ultrasound, may help define the extent of tissue oedema or presence of loculated
infection and therefore help in any decision about airway control.
Antibiotics
The advent of surgical decompression of the submandibular space reduced mortality
from 100% in 1850 to 4060%. The introduction of antibiotics reduced that figure to
under 5%. Traditionally, high-dose penicillin was used. A broader spectrum of therapy
is now recommended to cover penicillin-resistant Gram-positive cocci and anaerobes.
A combination of clindamycin, penicillin (or ciprofloxacin) and metronidazole is usually
recommended before definitive microbiological results are received.
Surgery
Surgical drainage was once universally required but some authorities now recommend
reserving it for cases in which antibiotic therapy fails. Isolated removal of the infected
tooth and limited intra-oral drainage is unsuccessful. CT-guided needle aspiration of
the submandibular space has also been tried but as the disease is essentially a fascial
cellulitis often without localization of pus this technique is unhelpful.
Surgery usually involves bilateral incisions parallel and inferior to the mandible with
deep dissection into the submandibular triangle, through the mylohyoid muscle and into
the sublingual region. The primary goal is decompression of all fascial spaces and the
secondary goal evacuation of pus and obtaining tissue for microbiology. Any infected
teeth are also removed. The classical cut throat incision between the chin and the
hyoid bone is no longer deemed necessary. Clinical experience has demonstrated that
even if there is no pus, serious cellulitis resolves more rapidly if incised. Submandibular
incisions also allow the swelling to extend inferiorly releasing the pressure that forces the
tongue onto the palate and posterior pharynx.
Corticosteroids
The use of glucocorticoids in septic patients is controversial, but some authorities
recommend their use to reduce the submandibular swelling. One regimen includes
an initial dose of dexamethasone, 1020 mg followed by 46 mg every 6 hours for 48
hours. The role of corticosteroids in outcome has not been evaluated.
Medical support of the patient
The patient must be nursed in a high dependency environment with maintenance of
fluid balance/hydration and regular cardiovascular and respiratory monitoring.
Dental care
Continuing primary oral health care following the acute infection is important. u
FURTHER READING
Barakale M S, Jensen M J, Hemli J M, Graham A R. Ludwig's Angina: Report of a Case
and Review of Management Issues. Ann Otol Rhinol Laryngol 2001; 110: 4536.
Marple B F. Ludwig's Angina: A Review of Current Airway Management. Arch

Otolaryngol Head Neck Surg 1999; 125: 5968.
Neff S P W, Merry A F, Anderson B. Airway Management in Ludwig's Angina. Anaesth

Intens Care 1999; 27: 65961.
Patterson H L, Kelly J H, Strome M. Ludwig's Angina: An Update. Laryngoscope 1982;

92: 3707.
Sparks C J. Ludwigs Angina causing Respiratory Arrest in the Solomon Islands.

Anaesth Intens Care 1993; 21: 4602.

Sedation for Dental Procedures
Meg Skelly
David Craig
Meg Skelly is Head of the Department of Sedation and Special Care Dentistry at the
Guys, Kings and St Thomas Dental Institute, London, UK. She qualified from Guys
Hospital Dental School, London. Her interests include pain and anxiety control in
dentistry and education in this field.
David Craig is Associate Specialist in Dental Sedation at Guys Hospital, London.

He qualified from Manchester University and has held appointments in oral surgery,
anaesthetics and general dental practice.
Most patients regard dental treatment as uncomfortable and potentially painful: their
reactions range from normal apprehension, through various degrees of anxiety to
irrational fear or even phobia. The adverse physiological effects of these psychological
responses can increase the risks of treatment and should be controlled. This may be of
even greater importance in patients with medical conditions (Figure 1).
Medical conditions and sedation
Conditions for which sedation is beneficial

Angina
Controlled hypertension
Asthma
Epilepsy
Movement disorders
Conditions that may require modification of techniques

Controlled heart failure
Chronic anaemia (diagnosed and managed)
Chronic airways disease
Well-controlled diabetes
Conditions in which caution is required

Severe cardiorespiratory disease
Hepatic disease
Severe psychological illness
Drug abuse
Alcohol abuse
1
The General Dental Council (GDC) defines conscious sedation as: A technique
in which the use of a drug or drugs produces a state of depression of the central
nervous system enabling treatment to be carried out, but during which verbal contact
is maintained throughout the period of sedation. The drugs and techniques used to
provide conscious sedation should carry a margin of safety wide enough to render loss
of consciousness unlikely. The level of consciousness must be such that the patient
remains conscious, retains protective reflexes and is able to understand and respond to
verbal commands.
The GDC also requires that all clinicians using dental sedation have clinical experience
of the technique and that they are assisted by a second person who is able to monitor
the patient and assist in the event of an emergency.
The purpose of sedation is to:
enable treatment to be provided and/or accepted
reduce stress associated with traumatic or prolonged procedures
control gagging
stabilize blood pressure in patients with cardiovascular or cerebrovascular disease.
Patient assessment
A satisfactory first visit is crucial to the success of subsequent treatment under
sedation. Ideally, this meeting should take place away from the surgery environment.
Patients should be given instructions for sedation at this visit (Figure 2). Dental
treatment must be appropriate and realistic. The management options are listed in
Figure 3. The simplest technique is generally considered to be best.
Instructions for patients receiving dental sedation
For your safety, please read and follow these instructions carefully
Before sedation: on the day of treatment

Take your routine medicines at the usual times
Have only light meals and non-alcoholic drinks on the day of your
appointment
Bring a responsible adult with you who is able to escort you home
and then care for you for the rest of the day
After sedation: until the following day

Do not travel alone travel home with your escort, by car if
possible
Do not drive or ride a bicycle
Do not operate machinery
Do not drink alcohol
Do not return to work or sign legal documents
2
Management options for dental treatment
Local anaesthesia
Alone
With nitrous oxide/oxygen mix
With intravenous sedation (e.g. midazolam)
With oral sedation
General anaesthesia
3
Inhalational sedation
The use of nitrous oxide and oxygen in subanaesthetic concentrations as a method
of sedation became popular in the late 1940s. Nitrous oxide has excellent anxiolytic,
sedative and analgesic properties, with little depression of myocardial function or
ventilation (Figure 4). Induction and recovery are rapid. Administration by titration
reduces the risk of over-sedation.
Inhalational sedation
Advantages
No needles
Level of sedation easily altered
Minimal impairment of reflexes
Rapid induction and recovery
Some analgesia
Disadvantages
Sedation depends on good psychological support
Mask may limit access
Postoperative amnesia variable
Nitrous oxide pollution
Contraindications
Nasal obstruction
Poor cooperation
First trimester of pregnancy
Fear of masks
4
Equipment
Inhalational sedation (Relative Analgesia) machines are similar to traditional Boyles
anaesthetic machines, but modified to make them safe for use by an operator-
sedationist. Typical Relative Analgesia machines have independent controls for
regulating total gas flow and the mixture of oxygen and nitrous oxide. Modern machines
are incapable of delivering a gas mixture containing less than 30% oxygen and have
breathing systems with scavenging for the removal of waste gases.
Clinical procedure
The nasal mask is attached and the machine adjusted to administer 100% oxygen at
an appropriate flow rate. Verbal encouragement is important at this stage. 10% nitrous
oxide is introduced and the patient informed that they may feel light-headed, have
changes in visual or auditory sensations or tingling of hands and feet and a feeling of
suffusing warmth. This concentration is maintained for 1 minute, during which verbal
reassurance continues. The concentration of nitrous oxide is then increased by 10%
for a further 1 minute and then in increments of 5% until the patient appears and feels
sufficiently relaxed. Local analgesia is then administered. When correctly titrated,
patients are aware of operative procedures and are cooperative without being fearful.
Restlessness is often an indication that the concentration of nitrous oxide is too high. At
the end of treatment, 100% oxygen is administered.
Monitoring
The sedationist and the dental nurse must observe the patients respiration, the level of
sedation and skin colour. Electromechanical devices (e.g. pulse oximeter, ECG) are not
routinely used unless the patient has serious medical problems.
Nitrous pollution and scavenging

Long-term exposure to nitrous oxide is potentially harmful. The Health and Safety
Executive specifies a time-weighted maximum level of 100 ppm of nitrous oxide in the
working environment. This is normally achievable only using active scavenging.
Intravenous sedation
Midazolam is well suited to sedation for dentistry (Figure 5). It is impossible to
determine the correct dose of midazolam on the basis of the patients body weight or
age therefore a titration technique is essential.
Sedation with midazolam
Advantages
Rapid onset (5 minutes or less)
Good patient cooperation
Good amnesia
Disadvantages
No clinically useful analgesia
Respiratory depression
Occasional disinhibition effects
Occurrence of sexual fantasies (rare)
Postoperative supervision for a minimum of 8 hours is
required
Not reliable for sedating children
Elderly patients are easily over-sedated
Absolute contraindication
Allergy to any benzodiazepine
Caution required
Pregnancy and breastfeeding
Severe psychiatric disease
Alcohol or drug abuse
Impairment of hepatic function
Needle phobia
Doubts about the ability to provide a suitable escort
Intravenous midazolam produces a period of acute detachment for 2030 minutes

followed by a state of relaxation for a further 1 hour or so. Most patients have little or no
recollection of the operative procedure. Some respiratory depression occurs in patients
undergoing midazolam sedation. Overdosage and/or excessively rapid bolus injections
may cause profound respiratory depression. This is unpredictable, and so pulse
oximetry must always be used.
Clinical procedure
It is important to ensure that the patient is prepared for the procedure and that the
dental team is prepared for the patient. Written consent is required for both the dental
procedure and sedation. Induction should be carried out with the patient lying supine.
Pulse oximetry is mandatory for all patients and must be in place before induction.
Continuous blood pressure and/or ECG monitoring may be advisable for unfit patients.
Supplementary oxygen must be available.
The following regimen is appropriate for most fit patients aged 1665 years, though
variation in the response to sedation is common. Midazolam, 2 mg, is administered
slowly, followed by a pause of 90 seconds. Additional 1 mg increments are given every
30 seconds until a satisfactory level of sedation is achieved. Slurring of speech and/or
a slowed response to commands and a relaxed demeanour confirm that the sedation
end-point has been reached. Ptosis is an unreliable sign. Local analgesia is then
administered.
Elderly patients often require small doses of midazolam. A suggested administration

regimen for these patients is 1 mg injected slowly followed by a wait of at least 4
minutes, then additional 0.5 mg increments given every 2 minutes until sedation is
adequate. At the end of the procedure, the patient must remain under the supervision of
the sedationist or a suitably trained nurse. Patients must be discharged into the care of
an escort, who must be given written and verbal care instructions.
Reversal of midazolam sedation

Flumazenil reverses the sedative, cardiovascular and respiratory depressant effects
but not intraoperative amnesia. Elective reversal with flumazenil may occasionally
be indicated. Flumazenil has a shorter half-life than midazolam. However, clinically
significant re-sedation does not occur when midazolam is used for short clinical
procedures.
Oral and intranasal sedation

Oral sedation is useful for patients who are unable to accept venepuncture. The
sedation produced may be adequate for the dental procedure to be carried out or it may
then be possible to administer intravenous sedation. The most commonly used
drugs are temazepam and midazolam. Midazolam may also be administered
intranasally. Oral and transmucosal techniques are less predictable and should be used
by experienced sedationists
only. u
FURTHER READING
General Dental Council. Maintaining Standards. Guidance to Dentists on Professional
and Personal Conduct. General Dental Council, November 2001.
Roberts G J. Inhalation Sedation (Relative Analgesia) with Oxygen/Nitrous Oxide Gas

Mixtures. 1. Principles. Dental Update 1990; 17: 13946.
Roberts G J. Inhalation Sedation (Relative Analgesia) with Oxygen/Nitrous Oxide Gas

Mixtures. 2. Practical Techniques. Dental Update 1990; 17: 1906.
Skelly A M. Sedation in Dental Practice. Dental Update 1992; 19: 617.
Society for the Advancement of Anaesthesia in Dentistry. Standards in Conscious

Sedation for Dentistry. Report of an Independent Expert Working Party, October 2000.

Special Needs Patients and
Dental Procedures
Lisa Kritzinger
Jane M Silk
Lisa Kritzinger is Paediatric Anaesthesia Research Fellow at St Bartholomews

Hospital and the London NHS Trust. She qualified from St Bartholomews Hospital,
London, and trained in anaesthesia in Northampton and London.
Jane M Silk is Consultant Paediatric Anaesthetist at St Bartholomews Hospital

and the London NHS Trust. She qualified from St Bartholomews Hospital, London,
and completed her paediatric anaesthesia training at Great Ormond Street Hospital,
London.
Terms such as special needs, disability and handicap have different interpretations.
Definitions have been proposed by the World Health Organization in the International
Classification of Impairment, Disabilities and Handicap, and special educational needs
are defined in the 1993 Education Act. In practical terms, the special needs patient is one
who has learning and/or physical disabilities. Downs syndrome, cerebral palsy and autism
account for most cases, but rare syndromes are also encountered. Some rare diseases
have profound anaesthetic implications, such as airway and cardiac problems in patients
with Goldenhars syndrome. An anaesthetist was recently convicted of manslaughter after a
child with Goldenhars syndrome died during dental treatment.
Special needs patients often allow only limited dental examination and treatment, so
that dental care may have to be carried out under general anaesthesia. The use of
local anaesthetic alone, or with sedation, has a limited place in moderately or severely
affected patients.
The clinical setting: in contrast to efforts aimed at supporting special needs patients
in their community, general anaesthesia is being increasingly confined to the hospital
environment. Day surgery units allow patients to be treated and discharged home within
6 hours, minimizing the disruption to their lives. It is ideal to have a regular team of staff
and considerate scheduling of lists within the day surgery unit.
Preoperative assessment: the patients cooperation may be limited, making

examination difficult. The patients medical history should be sought from other sources
(e.g. hospital or GP records). The anaesthetic value of any investigations should be
determined. Preoperative assessment is best carried out by the same senior clinicians
carrying out the procedure. Good communication between members of the dental,
anaesthetic and theatre teams is important. The decision to ask patients to attend
hospital for a separate pre-anaesthetic assessment must be balanced against the
inconvenience caused to the patient and the risk of unexpected admissions to hospital
if they do not attend. Prolonged preoperative starvation should be avoided.
Consent: in England, Wales and Northern Ireland, no one can give consent to
treatment on behalf of another adult. However, doctors can treat incompetent adult
patients without consent if they need treatment, and if it is in the patients best interest.
This decision is made after consulting the patients carer, but they have no legal status
in the decision-making process.
Premedication: special needs patients often require repeated general anaesthetics

and any measure that improves the experience for them should be embraced. Many
patients do not need sedative premedication if parents or carers are involved and
simple distraction techniques are used. However, premedication is necessary for some.
The choice of drug is best tailored to the individual patient, bearing in mind that some
will not swallow pills or tolerate the use of topical anaesthetic cream. Intramuscular
ketamine, 4 mg/kg, given 10 minutes before induction is used. However, ketamine is
now a controlled drug. Therefore, injectable midazolam, 0.5 mg/kg up to a maximum of
15 mg, added to paracetamol elixir, 20 mg/kg, to mask its bitter taste and given orally
3040 minutes before its desired effect, is a useful alternative.
Peroperative anaesthetic technique: the choice is influenced by:

the difficulties of communicating with patients, their limited cooperation and the
presence of a carer
an understanding of the dental treatment plan, which may involve all four quadrants
of the mouth and last over 1 hour.
Induction of anaesthesia can be challenging and carers often express the patients
anxiety. Practices used in paediatric anaesthesia are useful for children and adults.
These include involving the carer to reassure and distract the patient, omitting formal
monitoring before induction if it increases distress and a flexible approach to the
choice of intravenous or inhalation induction (with sevoflurane followed by intravenous
cannulation when the patient is asleep).
A nasotracheal tube is the airway of choice (unless contra-indicated) together with

a throat pack, allowing good access for the dentist. Neuromuscular paralysis with a
nondepolarizing neuromuscular blocker and mechanical ventilation are often used,
given the high incidence of co-existing medical disease and the duration of treatment.
Simple analgesics combined with local anaesthesia are usually satisfactory. Diclofenac,
1 mg/kg, given as a suppository in children or in an infusion in adolescents and adults
is helpful unless contraindicated. Opioids are seldom used.
Recovery: patients generally make a good recovery to their pre-operative status, but
conventional discharge criteria must be modified for each patient, and are usually best
agreed with the patients carer. The carer will also know whether tablets or elixirs
are preferred when prescribing medicines to take home. u
FURTHER READING
Leyman J W, Mashni M. Anaesthesia for the Elderly and Special Needs Patient. Dental
Clin N Am 1999; 43: 30115.
Maestre C. The Use of General Anaesthesia for Tooth Extraction in Young

Handicapped Adults in France. Br Dent J 1996; 180: 297302.

Endocrinology
Anaesthesia
on CD-ROM
Anaesthetic Management of
the Diabetic Patient
Amanda L Porter
Alastair McCrirrick
Amanda L Porter is Specialist Registrar in Anaesthesia at Gloucestershire Royal

Hospital, Gloucester, UK. She qualified from St Marys Hospital, London, and after
starting anaesthesia in London, moved to the South West Deanery to complete her
specialist registrar training.
Alastair McCrirrick is Consultant in Anaesthesia and Intensive Care at

Gloucestershire Royal Hospital, Gloucester, UK. He qualified from Southampton
University Medical School and joined the Royal Air Force. He completed his anaesthetic
training in Bristol and the South West Region. He now specializes in intensive care
and anaesthesia for major bowel and vascular surgery. His particular interests include
anaesthesia for carotid endarterectomy.
Diabetes mellitus is the most common endocrine condition encountered in surgical

patients. 50% of diabetic patients require surgical intervention, usually for ophthalmic,
vascular or infective complications. They have increased perioperative mortality and
morbidity compared with the general population. The main aims in the anaesthetic
management of these patients are:
to reduce the period of starvation with early recourse to oral intake and a normal
glycaemic regimen
to optimize blood glucose levels throughout the perioperative period in order to
minimize metabolic disturbance and end-organ damage.
Diagnosis
Diabetes mellitus includes a number of disorders in which the universal finding is
hyperglycaemia. Recently, the World Health Organization (WHO) and the American
Diabetes Association (ADA) have jointly published new diagnostic criteria. This has led
to an increase in the number of people recognized as having diabetes mellitus. The
diagnosis may be confirmed by a random plasma glucose concentration greater than
11.1 mmol/litre or a fasting plasma glucose concentration greater than 7.0 mmol/litre
(previously 7.8 mmol/litre), providing this result can be replicated. Impaired glucose
tolerance, now renamed impaired fasting glycaemia, is confirmed by a fasting plasma
glucose concentration of 6.17.0 mmol/litre.
Classification
The WHO and ADA have also developed a new classification system identifying four
types of diabetes mellitus.
Type I is caused by autoimmune or viral destruction of susceptible cells in the islets of

Langerhans in the pancreas, which are responsible for the production of insulin. Their
destruction results in no endogenous insulin being produced. Type I usually presents in
patients under 30 years of age. Its inheritance is multifactorial. There is a strong genetic
association with increased expression of human leucocyte antigens (HLA) DR3 and
DR4 found on chromosome 6. The worldwide incidence of type I diabetes mellitus is
0.4%, but it is more common in developed countries.
Hyperglycaemia occurs as a result of reduced peripheral uptake of glucose, which is

usually insulin mediated. There is also increased proteolysis, lipolysis and subsequent
gluconeogenesis. This leads to massive protein loss and depletion of fat stores, further
increasing the plasma glucose concentration. Glucose cannot be used for energy in
these circumstances, therefore the liver produces ketoacids as an alternative energy
source. This results in acidaemia. Exogenous insulin is vital to maintain glucose and
acidbase
homeostasis.
Type II patients have reduced secretion of the active form of the insulin molecule.
They have increased amounts of inactive insulin precursors, combined with increased
peripheral insulin resistance as a result of impaired glucose transport mechanisms.
This also reduces muscle glycogen synthesis. The worldwide incidence is 6.6%. The
diagnosis is more common in patients over 40 years of age and in populations that
have changed from a traditional to a Western diet and lifestyle. Type II diabetes has a
strong familial link, with over 90% concordance between monozygotic twins.
Patients are usually overweight (unlike type I patients who are often thin) and do not
have the propensity for acidotic states because they usually have enough insulin to
prevent ketoacidosis. They may occasionally present with hyperosmolar non-ketotic
coma (HONK). Glycaemic control can be maintained with oral hypoglycaemic agents
but exogenous insulin may be used in extreme situations. These diabetic patients
are the most susceptible to end-organ disease, therefore good blood sugar control is
mandatory.
Type III patients suffer from hyperglycaemia precipitated by drugs (e.g. thiazide
diuretics, corticosteroids, -blockers) or concurrent disease. Associated diseases may
include genetic disorders (e.g. Huntingdons chorea, Downs syndrome, dystrophia
myotonica), pancreatic disease (e.g. pancreatitis, haemochromatosis) or endocrine
diseases (thyrotoxicosis, acromegaly, Cushings syndrome). Successful treatment or
removal of the cause usually results in normoglycaemia.
Type IV is also known as gestational diabetes. It usually presents during the third
trimester of pregnancy and affects about 4% of pregnancies. Detection and treatment
are vital to prevent fetal macrosomia. Oral hypoglycaemic agents are teratogenic and
subcutaneous insulin is usually needed. Insulin requirements drop suddenly post-
partum and normal glucose homeostasis is quickly restored. The mother has an
increased risk of developing type II diabetes later in life (3050% incidence within 10
years).
Long-term complications
Poor blood glucose control can result in acute metabolic disturbance and, if sustained,
can cause chronic end-organ damage. The treatment of acute diabetic emergencies is
outside the scope of this article.
There are two theories explaining how chronic hyperglycaemia may cause damage at
the molecular level.
Protein glycosylation in which irreversible covalent bonds form between excess
glucose and protein compounds, altering their function and interaction with other
compounds.
Polyol pathway in which glucose is metabolized to fructose via sorbitol. Saturation of
this pathway produces excess sorbitol, which activates aldose reductase, an enzyme
that further enhances sorbitol production. A positive feedback loop is produced.
The increased level of sorbitol causes tissue damage. Animal studies using aldose
reductase inhibitors have shown promising results in the reduction of end-organ
damage but they may be toxic to humans.
The pathological findings associated with chronic hyper-glycaemic end-organ damage

are primarily those of micro-vascular disease, particularly affecting the cerebral and
coronary vessels. The cardiovascular, neurological, renal and ophthalmic systems
are those most commonly affected. Microvascular organ damage may be the main
indication for surgery and it also complicates perioperative anaesthetic management.
Cardiovascular: patients with diabetes mellitus have accelerated formation of

atheromatous plaques as well as generalized microvascular disease. Perioperative
myocardial ischaemia and infarction are more common than in the general population.
The risk of life-threatening arrhythmias is greater because the threshold for the initiation
of ventricular fibrillation is reduced. Hypertension is common, caused by the loss
of vessel elasticity secondary to protein glycosylation. Good blood pressure control
can reduce mortality, though -blockers, thiazide diuretics and calcium antagonists
can worsen glycaemic control. Other cardiovascular complications include peripheral
vascular disease and cardiac failure.
Neurological: peripheral and autonomic neuropathies are the most common

neurological complications of diabetes mellitus. Peripheral neuropathies typically have
a symmetrical glove and stocking distribution. The extent of the neuropathy should be
documented accurately to prevent medico-legal problems. Up to 40% of type I patients
and 17% of type II patients have autonomic neuropathy. A careful history may elicit
symptoms but the condition is often asymptomatic and detectable only by screening.
Autonomic neuropathy should be suspected if the patient complains of abnormal
sweating, bladder dysfunction, diarrhoea or dizziness. Other features may include
cardiovascular instability and gastroparesis (potentially causing regurgitation and/or
aspiration). Autonomic neuropathy can be confirmed by:
a drop in postural blood pressure on standing, or absence of increase in diastolic
blood pressure after 5 minutes of hand grip
absence of sinus arrhythmia on ECG or by palpation
absence of cardiac response to the Valsalva manoeuvre.
Renal: patients with type I diabetes mellitus have the highest incidence of end-stage
renal disease and progress most rapidly from microalbuminuria to proteinuria, nephrotic
syndrome and eventually chronic renal failure. Strict glycaemic control can delay the
onset of microalbuminuria, which signals the inevitable progression to end-stage renal
disease. The extent of renal disease can be assessed by preoperative creatinine, urea
and electrolyte measurements.
Ophthalmic: blindness may be caused by cataracts or exudative or proliferative

retinopathy. Perioperative hypertension can cause vitreous haemorrhage.
Respiratory: problems include a reduction in lung volumes and a decrease in diffusing

capacity. Chest infections are common. Obese diabetic patients may demonstrate
signs and symptoms of obstructive sleep apnoea (see Anaesthesia and Intensive Care
Medicine 3:6: 196).
Stiff joint syndrome: the high incidence of difficult intubations in patients with type I
diabetes may be caused by protein glycosylation. Airway assessment may be normal
but the inability to perform prayers sign (approximation of the palmar proximal
interphalangeal joints) as well as limited atlantoaxial extension can indicate a potentially
difficult intubation.
Infection: hyperglycaemia may result in leucocyte dysfunction. This increases the

incidence of wound infection and delayed healing, particularly if the blood glucose is
above 14 mmol/litre. Peripheral vascular disease exacerbates poor wound healing.
Insulin requirements increase in the presence of infection.
Treatment
Treatment iscovered elsewhere.
The aim of perioperative management is to maintain good blood sugar control.
Hypoglycaemia can occur preoperatively following excessive starvation or late
cessation of long-acting hypoglycaemic agents. Hyperglycaemia is exacerbated by
the metabolic response to surgery. Controlling hyperglycaemia prevents immediate
metabolic disturbance and electrolyte abnormalities and reduces the incidence of long-
term end-organ damage.
Metabolic response to surgery: metabolic disruption occurs in all patients undergoing

surgery, the extent depending on the operation as well as the severity of the underlying
disease. The stress response involves the release of catecholamines, cortisol, growth
hormone, thyroid hormones and other catabolic hormones. The production and
peripheral action of insulin, an anabolic hormone, is decreased, causing an overall rise
in blood glucose levels. Metabolic disruption is exaggerated in diabetic patients and
may continue postoperatively because peripheral insulin resistance remains high.
Preoperative preparation: patients must be evaluated to assess their current and

long-term glycaemic control and the efficacy of their present treatment regimens
(Figure 1). Simple bedside tests and glycosylated haemoglobin (HbA1C) levels can
assess recent control of blood sugar. An HbA1C level less than 10%, indicates good
control over the previous 68 weeks. Acute hyperglycaemia is a contraindication to
surgery and anaesthesia because it may cause postoperative metabolic disturbance,
increased infection, microvascular damage and delay wound healing. Patients must be
metabolically stable and assessment may require blood gas analysis if recent diabetic
ketoacidosis has been a problem.
Preoperative investigations
Full blood count haemoglobin; raised white cell count

indicates infection
Urea and electrolytes renal function
Glucose current glycaemic control
HbA1C long-term glycaemic control
ECG arrhythmias, ischaemia, previous cardiac events
Urinalysis glucose ketones
1
Associated complications (cardiovascular, renal, neuropathic) must be actively sought

and investigated appropriately. It is particularly important that cardiac disease is
excluded and an ECG is mandatory. Autonomic neuropathy must be identified because
it may have major anaesthetic implications. Pre-existing renal impairment may affect
drug choices. Airway assessment is important to anticipate unexpectedly difficult
intubation. Diabetic patients should have operative priority to reduce the starvation
period.
Perioperative blood sugar management: the aim is to maintain blood sugar levels
at 610 mmol/litre. This may be achieved in several ways. Management should include
measurement of blood glucose every 2 hours and of electrolytes every 6 hours. The
regimen used depends on the type of diabetes mellitus and the extent of surgery.
Type II for minor surgery in patients with good blood sugar control, short-acting oral
hypoglycaemic agents should be omitted on the morning of surgery. Longer-acting
medication must be stopped 24 hours before surgery. Blood glucose levels should be
monitored closely throughout the perioperative period. Once oral intake has resumed,
oral hypoglycaemic medication should be restarted immediately. If the patient is
controlled by diet, monitoring blood glucose levels is usually the only requirement.
Insulin should be considered in patients with poor glycaemic control. For major surgery,
patients should be converted to an insulin regimen and treated as if they had type I
diabetes mellitus.
Type I for minor surgery, patients may follow a no insulin, no glucose regimen
provided both carbohydrate and insulin are administered early postoperatively.
Postoperative nausea and vomiting must be minimized and blood glucose monitoring is
imperative. Alternatively, an infusion of 5% dextrose may be commenced and 5075%
of the patients normal morning insulin dose given subcutaneously. Both regimens
have drawbacks including an increased risk of ketoacidosis and an enhanced stress
response. Absorption of insulin from subcutaneous tissues is inconsistent during
surgery because skin and muscle perfusion may be altered by other physiological
variables. For anything other than minor surgery, insulin and dextrose infusions
remain the management of choice. Long-acting insulin should be omitted 24 hours
preoperatively, but short-acting preparations may be continued until the morning
of surgery. The insulin/dextrose infusion should be commenced concurrently with
starvation and continued until oral intake is resumed postoperatively. There are two
main insulin/dextrose regimens. In the Alberti regime (Figure 2) insulin is added to
a 500 ml infusion bag containing 10% dextrose and potassium. It is a safe regimen
because simultaneous infusion of both insulin and dextrose is guaranteed. The
disadvantage is that if blood glucose levels are outside an acceptable range a new
infusion must be prepared with a different amount of insulin. Insulin is also adsorbed
by plastic and glass surfaces. This may be a problem with the Alberti regimen, which
has a high volume solution with a low insulin concentration. The alternative approach is
to use separate infusions of insulin and 5% dextrose containing potassium (Figure 3).
This is much more flexible because the two infusions can be controlled independently.
If a single cannula is used for both infusions a one-way valve must be incorporated
to prevent insulin entering the dextrose administration set. Ideally, separate cannulas
should be used but hypo- or hyperglycaemia may occur if either of the cannulas
occludes.
Alberti regimen (Alberti and Thomas, 1979)
500 ml 10% dextrose solution + 10 U insulin + 10 mmol KCl

Run at 100 ml/hour, check blood glucose every 2 hours
If blood glucose < 5 mmol/litre, use 5 U insulin per bag
If blood glucose 59.9, use 10 U insulin per bag
If blood glucose 1014.9, use 15 U insulin per bag
If blood glucose 15, use 20 U insulin per bag
2
Insulin sliding scale
5% dextrose + 10 mmol/litre KCl run at 125 ml/hour

0.9% NaCl + insulin at 1 U/ml
If blood glucose 4.9, give 0.5 U insulin/hour i.v.
If blood glucose 514.9, give 2 U insulin/hour i.v.
If blood glucose 1519.9, give 4 U insulin/hour i.v.
If blood glucose 20, review
3
Postoperative management: the insulin/dextrose infusion regimen should be

continued until the patient is able to resume and maintain oral intake. Intravenous
administration can be converted into subcutaneous boluses before each meal, with
regular blood glucose monitoring. During recovery, insulin requirements reduce and it is
recommended that once subcutaneous requirements are less than 20 U/day a normal
preoperative regimen may be restarted. Early patient mobilization hastens a return to
metabolic homeostasis. This requires attention to adequate analgesia. Treatment of
postoperative nausea and vomiting allows an earlier return to a normal diet.
Choice of anaesthetic: the aim is to minimize metabolic disturbance.
Regional anaesthesia has many advantages. A conscious patient permits early

detection of hypoglycaemic episodes and reduces the risk of aspiration. Postoperative
nausea and vomiting is minimized allowing the patient to return to a normal diet
sooner. Regional techniques for pelvic and limb surgery reduce the stress response to
surgery, and thus reduce a rise in blood glucose. Hypotensive episodes related to the
regional technique may be exaggerated in the presence of autonomic neuropathy and
may cause further deterioration of end-organ function. Strict asepsis is vital to avoid
infection, especially epidural abscess formation. Regional anaesthesia in patients with
peripheral neuropathy is not recommended for medico-legal reasons.
General anaesthesia can mask the signs of hypoglycaemia and therefore requires
regular blood glucose measurement. A rapid sequence induction may be required
in patients with evidence of autonomic neuropathy to prevent aspiration; difficult
intubation should always be anticipated. Hypoxia and hypercarbia may exacerbate
the stress response, hypotension may worsen end-organ damage and hypertension
increases the risk of vitreous haemorrhage. The stress response may be lessened
by the use of high doses of opiates. The resulting respiratory depression and delayed
return to consciousness may be confused with hypoglycaemia. Sympathomimetics
and diuretics antagonize insulin, while clonidine, monoamine oxidase inhibitors and
-blockers potentiate its action. It is advisable not to use fluids containing lactate
(e.g. Hartmanns solution) because metabolic acidosis may be exacerbated; lactate
is converted to glucose by gluconeogenesis, further disrupting glycaemic control.
Transfusion of packed cells may disrupt glucose homeostasis because citrate promotes
gluconeogenesis. Stiff joints require great care with preoperative positioning. Diabetic
patients are also at risk from skin trauma, ulceration and nerve injury. u
FURTHER READING
McAnulty G R. Anaesthetic Management of Patients with Diabetes Mellitus. Br J Anaes
2000; 85(1): 8090.
Scherpereel P A. Perioperative Care of the Diabetic Patient. Eur J Anaes 2001; 18:
22794.

of Phaeochromocytoma
Andrew K McIndoe
Andrew K McIndoe is Consultant Anaesthetist and Senior Clinical Lecturer in the

Sir Humphry Davy Department of Anaesthesia, Bristol Royal Infirmary. He is also the
Phaeochromocytomas are tumours of chromaffin cells. The name derives from the
observation that catecholamine storage granules in these cells turn brown when
stained with chromic acid. Although phaeochromocytomas are thought of primarily as
tumours of the adrenal medulla, they occur wherever chromaffin cells are found. 95%
occur in the abdomen, of which 85% are in the adrenal gland. The remainder tend to be
near the kidney or in the organ of Zuckerkandl. Outside the abdomen they occur in the
sympathetic chain, the heart and the posterior mediastinum.
The sympathetic nervous system

The sympathetic nervous system comprises the sympathetic chain (T1L2), a number
of peripheral plexuses and the adrenal medulla. All are supplied by preganglionic
cholinergic neurons connecting the CNS to sympathetic effectors derived from
chromaffin cells. Chromaffin cells produce noradrenaline, adrenaline and dopamine.
The sympathetic chain lies posterior to the aorta on either side of the thoracic column
and is made up from the cell bodies and ganglia of most of the chromaffin cells.
Postganglionic neurons derived from the sympathetic chain are noradrenergic and
innervate vascular smooth muscle, mediating vasoconstriction. More peripheral
chromaffin cells are located in the cervical ganglia, carotid bodies, and a number of
abdominal plexuses, but most significantly in the adrenal medulla. Typically the normal
adrenal medulla contains four to five times as much adrenaline as noradrenaline.
Catecholamine secretion is achieved by exocytosis into the blood stream, in response
to pain, stress, hypoglycaemia and hypoxia. Chromaffin cells are also present in the
remains of the organ of Zuckerkandl located near the inferior mesenteric artery, which
is a significant source of catecholamines during fetal development.
Catecholamine biochemistry
The principal catecholamines are adrenaline, noradrenaline and dopamine (Figure
1). All are derived from dietary tyrosine or synthesized from the amino acid precursor
phenylalanine. Within the chromaffin cells, tyrosine is hydroxylated to dopa (dihydrox
yphenylalanine), which is transported to the nerve terminals. Dopa is decarboxylated
to dopamine and accumulates in storage vesicles or granules in the nerve terminal.
The membranes of these vesicles contain dopamine -hydroxylase, which catalyses
the conversion of dopamine to noradrenaline. There is no further conversion in the
peripheral sympathetic nerve terminals, but in the adrenal medulla noradrenaline
is N-methylated to adrenaline in a reaction controlled by phenylethanolamine-N-
methyltransferase (PNMT) and facilitated by glucocorticoids. The adrenal medullary
catecholamines are stored in granules with ATP. Mg2+ -dependent ATPase controls
uptake into these granules and inhibits subsequent release.
Once released, the amines are rapidly eliminated. Up to 90% of the noradrenaline
released at the synapse is taken up again by the presynaptic nerve ending (uptake
1). The process is highly energy dependent and is saturable. It is blocked by cocaine,
metaraminol, tricyclic antidepressants and phenothiazines (Figure 2). Noradrenaline
is recycled into storage granules or deaminated by mitochondrial monoamine oxidase
(MAO). Although circulating catecholamines can also be destroyed by this route,
70% of adrenaline is methoxylated by catechol-O-methyl transferase (COMT) in the
liver and kidney (uptake 2) a process that is also saturable. Most of the circulating
adrenaline and noradrenaline is destroyed by COMT, therefore measurement of urinary
O-methylated derivatives (metanephrines) has traditionally been viewed as a good
index of secretion (Figure 1). A small proportion of catecholamines are conjugated with
sulphate or glucuronide in the liver, gut and red blood cells.
Catecholamine synthesis and elimination
Facilitation Inhibition
Synthesis
Tyrosine hydroxylase Metyrosine
Dopamine
Noradrenaline
Storage
Dopamine -hydroxylase Reserpine
Guanethidine
Release
Angiotensin 2 -receptor stimulation
Ephedrine Magnesium
Amphetamine Guanethidine
Bretylium
Reuptake
Noradrenaline Cocaine
Metaraminol
Tricyclic antidepressants
Phenothiazines
Monoamine oxidase (MAO)
breakdown
Progesterone Monoamine oxidase
inhibitors (MAOIs)
Oestrogen
COMT breakdown Corticosteroids
Phenoxybenzamine
2
The overall cardiovascular response to adrenoreceptor stimulation is moderated by

the baroreceptors and other reflex mechanisms (Figure 3). Thus, a sudden rise in
aortic pressure in response to an 1-agonist (e.g. phenylephrine) may result in reflex
bradycardia and subsequent redistribution of plasma volume. Specific agonists and
antagonists at the four adrenoreceptor subtypes are listed in Figure 4.
Adrenoreceptor effects
Receptor Principal effects

1 Vasoconstriction, uterine contraction, increased
sweating, decreased insulin release, decreased
glucagon release
2 Inhibition of further noradrenaline release (presynaptic

adenylate cyclase inhibition)
1 Chronotropy, inotropy, arrhythmogenicity, renin

secretion
2 Smooth muscle relaxation in the bronchi, vascular wall,

uterus, adipose tissue, lipolysis, insulin and glucagon
secretion
3
Adrenoreceptor agonists and antagonists
Agonists Antagonists
1-receptor
Phenylephrine Doxazosin
Methoxamine Phentolamine
Adrenaline Phenoxybenzamine
Noradrenaline Magnesium
Isoprenaline (weak)
2 -receptor
Clonidine Phentolamine
Adrenaline Phenoxybenzamine
Noradrenaline
Isoprenaline (weak)
1 -receptor 1- and 2-receptor antagonists

Isoprenaline Propranolol
Adrenaline Esmolol
Noradrenaline Labetalol
2 -receptor Atenolol
Isoprenaline Bisoprolol
Adrenaline Celiprolol (1 selective)
Noradrenaline (weak)
4
Predisposition
Most phaeochromocytomas (90%) occur sporadically and are benign. However, familial
predisposition occurs in multiple endocrine neoplasia type 2 (MEN 2A, 2B and 2C),
von HippelLindau disease, neurofibromatosis type 1 (von Recklinghausen disease),
and familial carotid body tumours. MEN 2A (Sipples syndrome) displays autosomal
dominant inheritance and is characterized by the association of medullary thyroid
carcinoma, phaeochromocytoma and parathyroid hyperplasia. The underlying genetic
link seems to be a mutation of the RET gene resulting in an oncogene that drives
cellular proliferation in the target endocrine organs that make up the MEN 2 triad.
These patients often have bilateral adrenal phaeochromocytomas and are more likely
to have adrenaline-secreting tumours than sporadic phaeochromocytomas. In von
HippelLindau syndrome the mutation is slightly different, resulting in the inactivation
of a tumour suppressor gene. Patients can develop bilateral kidney tumours and cysts,
phaeochromocytomas, retinal angiomas, pancreatic cysts and tumours, cerebellar or
spinal haemangioblastomas, epididymal cystadenomas, and tumours of the inner ear.
Diagnosis
History and physical examination: symptoms are variable. Hypertension is the
most common clinical sign. It may be sustained or paroxysmal. Patients also describe
episodes of anxiety, excessive sweating, palpitations (both fast and slow) and
headache. The presentation depends on the nature of the tumour. Those secreting
mainly noradrenaline present with hypertension, headaches and slow, thudding
palpitations, whereas those secreting adrenaline present with tachycardias and anxiety
attacks. Nausea and vomiting may be a result of excessive dopamine release. Intense
vasoconstriction can also give rise to pallor and goose pimples. The symptoms are not
specific, only 0.5% of those tested on clinical suspicion with hypertension prove to have
a phaeochromocytoma.
Differential diagnosis: it is difficult to distinguish the normally functioning sympathetic
nervous system from the episodic overactivity of a phaeochromocytoma because
catecholamines tend to be reabsorbed or metabolized quickly following their release.
Attempts at measurement of plasma catecholamines give only a brief snapshot of
the pharmacological state of the sympathetic system and may give rise to false-
negative results. Sensitivity may be improved by detecting the plasma metabolites
normetanephrine and metanephrine (Figure 1). The abnormal threshold for
normetanephrine is 2.5 pmol/ml and that for metanephrine is 1.4 pmol/ml. Alternatively
the 24-hour excretion of urinary catecholamines and metabolites can be measured.
The abnormal threshold is over 140 nmol/litre for adrenaline and over 800 nmol/litre for
noradrenaline.
Phaeochromocytomas are rare and biochemical screening tests give many false-
positive results despite repeat testing. Specificity can be enhanced by follow-up
of borderline abnormal patients with a clonidine suppression test. Clonidine is an
2-agonist and usually causes a decrease in physiological release of noradrenaline
from sympathetic nerve terminals. Lack of suppression is suggestive of a
phaeochromocytoma in the absence of reuptake inhibitors (tricyclic antidepressants,
cocaine, metaraminol, phenothiazines). Alternatively a glucagon stimulation test can
be used which, in the presence of a phaeochromocytoma, results in a greater than
threefold increase in plasma noradrenaline within 2 minutes of intravenous glucagon
administration.
Localization: CT localizes adrenal phaeochromocytomas with a sensitivity of 93

100%. Sensitivity is 90% for extra-adrenal tumours but is slightly higher using MRI.
Both techniques have poor specificity, but if there is doubt, nuclear imaging using 123I-
metaiodobenzylguanidine scintigraphy enhances the ability to identify and localize the
catecholamine source. Extra-adrenal tumours can also be located by selective vena
caval sampling for plasma catecholamines and metanephrines or by positron emission
tomography for selectively bound radionuclide markers.
Preoperative preparation
Surgical excision can be undertaken safely only when stability has been imposed
pharmacologically on the sympathetic system. The main clinical objectives are to
achieve stable blood pressure, heart rate and rhythm and to allow time for blood
volume to be restored to normal. The over-production of catecholamines can be
interrupted, blocked or antagonized at the point of synthesis, release or receptor action
(Figures 24). Control of blood pressure by -adrenoreceptor blockade alone may
cause hypertension secondary to 2 -blockade or may cause cardiac failure because of
the fall in contractility in the face of high afterload. The traditional approach is to institute
-adrenoreceptor blockade and then to add -adrenoreceptor blockade if necessary.
Oral phenoxybenzamine has been used for many years. It covalently binds to 1-
and 2-adrenoreceptors. It blocks catecholamine-induced vasoconstriction and
catecholamine reuptake (Figures 3 and 4) resulting in -adrenoreceptor stimulation that
manifests as a tachycardia. Therefore, use of phenoxybenzamine usually necessitates
the use of adjuvant -blockade. Preoperative control is good, but postoperatively,
patients remain sleepy and may require large amounts of intravenous fluid to maintain
blood pressure until the blockade has worn off, despite stopping phenoxybenzamine
2448 hours before surgery.
Doxazosin is a competitive selective 1-adrenoreceptor antagonist that can be given as

a single daily oral dose of up to 16 mg. Because doxazosin does not block presynaptic
2-adrenoreceptors, it does not cause a tachycardia and -blockade is necessary only
if the tumour secretes adrenaline. Doxazosin has a longer duration of action than other
competitive antagonists (e.g. prazosin) so administering the drug up to and including
the eve of surgery allows adequate perioperative cover without the complication of
significant postoperative hypotension.
Selective 1-adrenoreceptor blockade is indicated for patients who have an adrenaline-

secreting phaeochromocytoma. It is also likely to be required for those established on
phenoxybenzamine preoperatively with a tachycardia induced by 2-adrenoreceptor
mediated reuptake inhibition. Suitable options include atenolol, 100 mg/day, or
bisoprolol, 1020 mg/day.
Having achieved preoperative cardiovascular stability, the main determinant of

perioperative risk is the baseline myocardial state of the patient. Chronic exposure to
high circulating catecholamine concentrations can result in cardiomyopathy therefore a
screening echocardiogram is advisable in addition to an ECG (Figure 5).
General principles of elective phaeochromocytoma surgery
Preoperatively
Determine where the tumour is and what it secretes
Investigate myocardial function with ECG and echocardiogram
Establish 1 -adrenergic blockade to control hypertension (e.g.
doxazosin)
Consider adding 1 -adrenergic blockade to control heart rate or rhythm
(e.g. atenolol or bisoprolol)
Peroperatively
Sedative premedication
Invasive blood pressure monitoring pre-induction
Obtund pressor response to intubation at induction
Central venous pressure (CVP) monitoring (antecubital long line or
internal jugular line)
Maintain anaesthesia with a moderate degree of vasodilatation (e.g.
isoflurane)
Establish adequate surgical analgesia by T9L1 epidural or opioid
infusion
Control blood pressure surges in response to surgical manipulation with:
-receptor antagonists (e.g. phentolamine, 12 mg) magnesium
sulphate infusion (therapeutic range 24 mmol/litre)
Control tachydysrhythmias with -blockade (e.g. labetalol, 5 mg)
Wind down epidural infusion before final cross-clamp of drainage veins
of tumour
Keep up with fall in CVP with intravenous fluids when pressor effects
diminish
Postoperatively
HDU/ITU care with invasive blood pressure/CVP monitoring until
normalized
Wake up early to minimize hypotension secondary to residual
1 -blockade
Use posture and intravenous fluids to maintain blood pressure;
vasopressors tend to be ineffective
5
Peroperative management
Adrenalectomy can be performed using an open lateral retroperitoneal approach or by
laparoscopic transperitoneal surgery. Open surgery is quicker and less likely to result
in surges in catecholamine release, but is more painful postoperatively. Recovery
time from a laparoscopic procedure is shorter and patients mobilize within 24 hours
and can be discharged within 48 hours. However, they spend longer on the operating
table and more marked peaks in catecholamine release are observed during surgical
manipulation. Control of these cardiovascular perturbations is the main challenge facing
the anaesthetist because they occur regardless of depth of anaesthesia, analgesia
and efficacy of central neural blockade. Preoperative preparation with adrenoreceptor
antagonists blunts the magnitude and rate of cardiovascular change but does not
eliminate the effects of physical manipulation of the tumour. Reliable invasive monitoring
of arterial and central venous pressure is essential. Use of epidural analgesia (T9L1)
or opioid infusion (e.g. remifentanil, alfentanil) helps by eliminating noxious stimuli
from provoking catecholamine release but more direct antagonists are also required.
A general anaesthetic using one of the volatile agents has the advantage of providing
some vasodilatation, but in practice this will need to be supplemented by other agents
(Figures 24).
Magnesium sulphate has several potentially beneficial actions. It is anti-arrhythmic as

a result of myocardial calcium channel blockade, regulation of intracellular potassium
and ATP activation. It acts as a vasodilator by blocking the adrenoreceptor response to
noradrenaline and angiotensin II. It also inhibits catecholamine release from the adrenal
medulla and peripheral adrenergic nerve terminals. It is normally presented as a 50%
solution in a 10 ml ampoule (500 mg/ml = 2 mmol/ml). The effective therapeutic plasma
concentration is 24 mmol/litre. This can usually be achieved with an initial loading
dose of 4060 mg/kg intravenously followed by an infusion of 2 g/hour. Side-effects
include a prolongation of neuromuscular blockade and inhibition of platelet activity.
Phentolamine is a competitive 1- and 2-adrenoreceptor antagonist that can be given

intravenously by infusion or in 12 mg increments. It acts within one circulation time
and can be administered in direct response to observed changes in systemic blood
pressure. It is generally presented as a 10 mg/ml preparation in a 1 ml ampoule which
should be diluted to a 1:10 solution for clinical use. Side-effects include a tachycardia
secondary to presynaptic 2-blockade.
Labetalol is a combined - and -adrenoreceptor blocker. Given in incremental

doses of 5 mg it takes about 5 minutes to achieve an effect that can last for several
hours. Used intravenously it causes a 7:1 : blockade. Therefore an observed fall in
blood pressure may be accompanied by a profound fall in heart rate. It makes a useful
second-line agent to deal with adrenaline-induced tachydysrhythmias and tachycardias
secondary to use of 2-adrenoreceptor antagonists.
Sodium nitroprusside is a mixed arterial and venous dilator that reduces preload
and afterload. It acts by stimulating the formation of cyclic guanosine monophosphate
(GMP) that relaxes vascular smooth muscle. Onset time is rapid over a few seconds
and its duration is short with a plasma half-life of 34 minutes. Cyanide poisoning can
occur with infusion rates greater than 2 g/kg/minute but are unlikely in the short term
(less than 24 hours).
Towards the end of the operation one needs to anticipate the sudden exponential drop
in blood pressure that usually accompanies application of the final clamp to vessels
draining the phaeochromocytoma (Figure 6). Even with the presence of central venous
monitoring it can be difficult to predict the final volume status of the patient, because
the intermittently high levels of circulating catecholamines during the procedure tend to
cause marked changes in central venous filling pressure. This is a time to reduce the
hypotensive effect of other agents including the epidural.
Clamping of adrenal vein accompanied by fall in

blood pressure during elective laparoscopic
adrenalectomy1
6
Postoperative care should be based in a high dependency care area with facilities
to monitor and react to continuous invasive blood pressure and central venous
pressure changes. Postoperative hypotension is the most commonly encountered
problem (Figure 6), because the source of catecholamines has been removed but
the effects of adrenergic blockade remain. It can be difficult to treat because pressor
agents in standard doses are ineffective. Attention to fluid balance and posture
are the most effective interventions. Early extubation should be attempted. An
awake reticular activating system helps to maintain blood pressure by stimulating
release of noradrenaline from sympathetic nerve endings. Normal secretion of
catecholamines from the contralateral adrenal gland will have been suppressed by
the phaeochromocytoma, and adrenoreceptors will be blocked and down-regulated
for some time. Analgesic requirements depend largely on whether surgery has been
open or laparoscopic. Those who have had open surgery probably require continued
epidural analgesia, while those who have had laparoscopic surgery tend to require oral
analgesia only. Blood glucose should be monitored because hypoglycaemia may occur.
Steroid replacement therapy is not usually required unless bilateral adrenalectomies
have been performed
Emergency presentation
Phaeochromocytomas may present unexpectedly during coincidental surgery because
of their non-specific symptoms and episodic nature (Figure 7). An awareness of the
known associations should alert the anaesthetist to the possibility of an underlying
phaeochromocytoma when faced with a sudden unexplained severe hypertensive
episode, but because most cases are sporadic one needs to keep an open mind. If
the diagnosis is suspected on the table, all stimulation should be stopped immediately.
If the tumour secretes predominantly noradrenaline, systemic hypertension may be
accompanied by a baroreceptor-mediated reflex bradycardia. Peripheries will be cold
and pale as a result of vasoconstriction and the patient may have goose bumps.
Emergency presentation of a noradrenaline secreting

phaeochromocytoma during thyroidectomy1

Myocardial ischaemia may be evident on the ECG and may be complicated by

tachydysrhythmias, especially if the tumour secretes adrenaline. Severe hypertension
may be accompanied by pulmonary oedema. There is no justification for proceeding
with surgical excision in these circumstances, because mortality is unacceptably high
without preoperative adrenoreceptor blockade. Control should be attempted with the
agents described above (Figure 4) and the operation should be terminated with the
minimum of surgical stimulation as quickly as possible. Postoperative intensive care
should include cardiac troponin assay and 24-hour urinary catecholamine excretion.
The patient can then be re-booked at a later date, having planned and implemented a
multidisciplinary approach to the problem. u
FURTHER READING
Linehan W M, Walther M M. Molecular Genetic Abnormalities Associated with
Pheochromocytoma. In: Pacak K, moderator. Recent Advances in Genetics, Diagnosis,
Localization, and Treatment of Pheochromocytoma. Ann Intern Med. 2001;134: 31617.
Prys-Roberts C. Phaeochromocytoma Recent Progress in its Management. Br J


ENT/head and neck
Anaesthesia
on CD-ROM
Airway Trauma in ENT
Anil Patel
Hospital, London, UK. He qualified from University College London, and trained in
anaesthesia at Guys Hospital, London.
Airway trauma in ear, nose and throat (ENT) surgery can be broadly categorized as:
external laryngeal injury caused by blunt trauma or penetrating injuries to the neck
iatrogenic injury related to intubation trauma, prolonged intubation or tracheostomy.
External laryngeal injury

Patients requiring airway management can be divided into those presenting with
obvious respiratory distress requiring immediate intervention to establish a patent
airway and effective ventilation and those presenting with no obvious respiratory
distress who require careful evaluation and observation. Up to 25% of these patients
subsequently require airway intervention.
Immediate intervention for airway control may involve tracheostomy under local
anaesthetic for massive cervical and laryngeal trauma, orotracheal intubation or
intubation through a large open wound in the airway. Orotracheal intubation should
be performed by experienced personnel without the use of cricoid pressure, which
may result in cricotracheal separation and loss of airway patency. In this situation, the
risk of aspiration is less significant than the potential loss of the airway. Fibre-optic
intubation is difficult under these circumstances owing to airway distortion, bleeding
and the difficulties of passing a fibrescope past areas of airway damage. It is not
recommended.
Orotracheal intubation should be attempted with a selection of small tubes, with
straight and curved laryngoscopy blades available. If elevation of the vallecula with
a curved blade fails to pull a dislocated epiglottis forward, a straight laryngoscope
blade may be required to elevate the epiglottis directly. Oral intubation may cause
further laryngeal trauma by forcing debris lower down the airway and worsening
laryngotracheal disruption.
No obvious respiratory distress patients presenting with no obvious respiratory
distress require a high degree of suspicion for airway trauma. Preventable deaths
occur in up to 10% of patients with airway trauma. Symptoms suggestive of laryngeal
trauma include dyspnoea, pain, dysphagia and hoarseness. Examination may reveal
abrasions over the anterior neck, upper airway noises resulting from oedema or
foreign bodies, stridor, haemoptysis with frothy blood, subcutaneous emphysema,
loss of palpable landmarks in the thyroid or cricoid cartilage, and pneumothorax.
Careful, gentle assessment should be undertaken to avoid accidental dislodgement
of unstable cartilage fragments, which may cause airway compromise. Flexible fibre-
optic laryngoscopy identifies oedema, haematomas and vocal fold paralysis caused by
recurrent laryngeal nerve injury while CT scans identify laryngeal cartilaginous damage.
Small mucosal lacerations, small haematomas and single non-displaced fractures of
the thyroid cartilage can be managed conservatively with close observation. Treatment
includes voice rest, head elevation, humidified air to prevent crusting, antibiotics and
early steroid use to reduce oedema. Intervention by oral intubation or tracheostomy
may be required if airway deterioration occurs.
Iatrogenic airway trauma

Laryngeal trauma from tracheal intubation still occurs despite the change to high
volume, low pressure cuffs in patients of all ages. Although most changes are
superficial and heal quickly, a few patients develop glottic or subglottic stenosis and
present with airway compromise many weeks or months after a period of prolonged
intubation. Some patients sustain severe airway damage after relatively short periods
of intubation. Early, nonspecific changes in the airway include oedema and superficial
ulceration resulting in granulation tissue, which may form firm scar tissue.
Patients who complain of a sore throat and weak voice after intubation may have
arytenoid subluxation. Attempts to induce this lesion in cadavers have failed and it
has been suggested that the condition is better termed post-intubation crico-arytenoid
dysfunction. An understanding and awareness of the factors that predispose to
iatrogenic laryngeal trauma is important in reducing morbidity associated with these
injuries (Figure 1). u
Factors predisposing to intubation trauma
Tube placement
Emergency intubation by unskilled individuals
Repeated attempts at intubation
Improper use of introducers
Abnormal larynx
Tube characteristics
External diameter, shape, stiffness and material
Cuff volume and pressure
Duration of intubation
No universal agreement on safe period
Decision for tracheostomy at 514 days dependent on general condition
Longer duration with infants than with adults
General conditions
Gastro-oesophageal reflux with spillover
Impaired mucociliary clearance
Acute or chronic disease states with poor tissue perfusion and hypoxia
Infection

Anaesthesia for Endoscopic
Surgery
Anil Patel
Hospital, London, UK. He qualified from University College, London, and trained in
anaesthesia at Guys Hospital, London. His interests include the role of the laryngeal
mask airway in ENT surgery, jet ventilation and airway surgery.=
Anaesthesia for endoscopic procedures of the supraglottis, glottis and subglottis

requires close cooperation between anaesthetist and surgeon, an understanding
of each others problems and knowledge of specialist equipment. Shared airway
procedures are unique in that both anaesthetist and surgeon are working in the same
anatomical field. The anaesthetist is concerned with adequate oxygenation, removal
of carbon dioxide, maintenance of an adequate airway and the prevention of soiling
of the tracheobronchial tree, while the surgeon requires an adequate view of a clear
motionless operating field.
Patients vary from young, otherwise fit and well individuals, presenting with voice
changes secondary to benign vocal cord pathology (e.g. small nodules, polyps),
to elderly, heavy smokers with chronic obstructive pulmonary disease presenting
with voice changes, dysphagia and stridor caused by glottic carcinoma. Different
anaesthetic techniques are suitable for different patients.
Standard airway assessments to predict the ease of ventilation, visualization of the
laryngeal inlet and tracheal intubation should be performed. An assessment of airway
pathology and its impact on airway management should be made.
A history of previous endoscopic procedures and outcome should be noted. Dysphagia,

best breathing position, breathing pattern during sleep, voice changes and stridor give
an indication of the severity of disease. Patients may have no obvious stridor on initial
examination but it may become apparent as the patient lies down, changes from their
best breathing position or on minimal exertion. Inspiratory stridor is usually associated
with lesions above the glottis whereas expiratory stridor is usually seen with lesions
below the glottis.
The severity and size of lesions at the glottic level are assessed by direct or indirect
laryngoscopy, undertaken by surgeons in an outpatient setting; a photograph of the
findings is often recorded in the notes. Information about subglottic and tracheal lesions
is provided by chest radiography, CT and MRI.
The size, mobility and location of lesions should be identified before anaesthetizing the
patient.
Size of the lesion gives an indication of potential airflow obstruction. Stridor indicates
a significantly narrowed airway. In the adult, stridor implies an airway diameter of less
than
4.5 mm, but the absence of stridor does not exclude a significantly narrowed airway.
Mobility very mobile lesions (e.g. multiple large vocal cord polyps or papillomas) can
cause airway obstruction following induction of anaesthesia because their mobility and
the loss of supporting tone in the larynx can allow them to fall into the airway.
Location supraglottic lesions, if mobile, can obstruct the airway or make visualization
of the laryngeal inlet difficult. Subglottic lesions may allow a good view of the laryngeal
inlet but cause difficulty during the passage of a tracheal tube or during jet ventilation.
Foreign body aspiration is most common in children aged 14 years and most foreign
bodies enter the right main bronchus. The symptoms and signs are relative to the
size of the object, its mobility and location. Partial obstruction of the larynx or trachea
presents as stridor, dyspnoea, coughing and drooling. Bronchial foreign bodies mainly
cause coughing, wheezing, dyspnoea and reduced ventilation on the affected side.
Vocal cord pathology

Nodules are benign lesions of the vocal fold that are usually bilateral and caused by
vocal abuse.
Polyps are benign lesions of the vocal fold, common in adults. They are usually
unilateral and can be sessile or pediculated, oedematous or angiomatous. The
aetiology is multifactorial and includes vocal abuse and trauma. They often require
surgery with careful dissection or laser phonosurgery.
Cysts are benign lesions commonly seen in adults. They are caused by obstruction
of a glandular duct resulting in a mucous retention cyst. They are often seen in young
women, particularly professional voice users, and are treated with careful dissection.
Granulomas are benign lesions induced by healing granulo-matous tissue, which

develops after microtrauma. They are usually found on the posterior third of the vocal
process following trauma during intubation or extubation. Resection is required if they
are large and disturbing breathing.
Papillomas are benign lesions caused by human papilloma virus infection and can
undergo malignant transformation. In adults, hoarseness is usually the main symptom
while in children airway obstruction can occur. Following laser resection, papillomas
can recur and some patients require repeated laser phonosurgery at 312-monthly
intervals.
Malignant tumours are usually unilateral and occur mainly on the middle third of the
vocal fold. 80% are found in men aged 4065 years. Over 97% of patients are smokers
with a high alcohol intake. Treatment depends on tumour staging and involves local
resection, radiotherapy or transoral laser resection.
Other lesions are caused by haemangiomas, submucous haemorrhage, Reinkes

oedema and chronic laryngitis.
Anaesthetic techniques for endoscopy

Ideal technique: there is no ideal anaesthetic technique for all endoscopy procedures.
The technique depends on the patients general condition, the size, mobility and
location of the lesion, the use of a laser and surgical requirements.
The ideal technique would:

be simple to use
provide complete control of the airway with no risk of aspiration
control ventilation with adequate oxygenation and carbon dioxide removal
provide smooth induction and maintenance of anaesthesia
provide a clear motionless surgical field, free of secretions
not impose time restrictions on the surgeon
not be associated with the risk of airway fire or cardiovascular instability
allow safe emergence with no coughing, bucking, breath holding or laryngospasm
produce a pain-free, comfortable, alert patient with minimum hangover effects.
Some of these ideals conflict. The presence of a cuffed tracheal tube provides control
of the airway and prevents aspiration but may obscure a glottic lesion and is not laser
safe (Figure 1b). A cuffed laser tube provides some protection against laser-induced
airway fires but has a greater external diameter to internal diameter ratio and may
obscure laryngeal lesions. Jet ventilation techniques require specialist equipment and
knowledge and an understanding of their limitations.
Basic technique: following intravenous induction of anaesthesia, mask-bag ventilation

is manually confirmed before administration of muscle relaxants appropriate to the
length of surgery. Laryngoscopy is undertaken to visualize the lesion, establish
laryngoscopy grade and administer topical local anaesthetic (lidocaine (lignocaine)).
Confirmation of pathology is important because the disease may have progressed
since the last outpatient visit and the anaesthetic plan may have to be changed.
Topical local anaesthetic is essential for the supraglottis, glottis and subglottis for
cardiovascular stability, reduction of airway reflexes and smooth recovery.
Intubation techniques
Microlaryngoscopy tubes
Microlaryngoscopy tubes have a small internal and external diameter and have
been designed specifically for endoscopy procedures because the small external
diameter allows the surgeon a good view of the glottis (Figure 1c). Advantages of
microlaryngoscopy tubes include control of the airway, the presence of a cuff, which
protects against aspiration, and a motionless field for the surgeon. Disadvantages
include the inability to use a laser because of the risk of an airway fire, obscuring the
posterior commissure area where pathology may be missed, and increased airway
resistance allowing spontaneous ventilation for short periods only.
Laser tubes
Laser microsurgery of the airway allows precise surgical cutting, coagulation and
sealing with little postoperative oedema. Lasers are used for the resection of
papillomas, vascular lesions of the vocal cords, granulomas and laryngeal carcinomas.
Carbon dioxide lasers are the most commonly used in airway surgery and are targeted
towards the glottis by aiming mirrors integral to operating surgical microscopes. The
two main hazards from the use of a laser are the risk to operating theatre staff from
diverted laser radiation and the risk to the patient from a laser-induced airway fire.
An airway fire occurs only if the three components of the fire triangle are present
(Figure 2). To minimize these risks the inspired oxygen concentration should be
the lowest that maintains adequate oxygen saturations, and air should be used in
preference to nitrous oxide. The potential fuel source should have laser-resistant
properties (laser tubes) or be removed (supraglottic jet ventilation technique). The
only non-flammable laser tube is the Norton (Figure 3) which is constructed of steel.
Most laser tubes have laser-resistant properties, but ignite with sustained laser energy
strikes. Laser tubes have greater external diameter to internal diameter ratios owing to
their laser-resistant protective coverings and may obscure airway lesions.
Anaesthetists involved in cases using lasers for airway surgery should be familiar with
the causes of a laser airway fire, the limitations of laser-resistant tubes and an airway
fire drill (Figure 4).
Non-intubation techniques
Spontaneous ventilation technique
Spontaneous ventilation techniques are used in the management of foreign body
aspiration and for the dynamic assessment of the airway in patients with, for example,
tracheomalacia. The technique allows a clear view of an unobstructed glottis.
Anaesthetic management of patients with foreign body aspir-ation should aim to
provide adequate oxygenation, a smooth induction, prevention of fragmentation or distal
movement of the foreign body, sufficient depth of anaesthesia to prevent coughing,
bronchospasm and laryngospasm, and smooth recovery.
3a Metal Norton tube with
no cuff. b 5.0 mm internal
diameter Xomed Laser Shield
II. c 5.0 mm internal diameter
Portex microlaryngoscopy
tube.
Airway fire drill
Immediate action simultaneously

Put out fire flood field with saline (which must be immediately available)
Remove energy source stop laser
Remove oxidant source disconnect circuit, stop ventilation, stop gases
Remove fuel source extubate and remove burning fragments
Urgent action
Review airway ensure no burning fragments
Oxygenate 100% oxygen by bag and mask
Review damage flexible or rigid bronchoscopy
Establish airway re-intubate, laryngeal mask airway or jet ventilate
Assessment
No airway damage may proceed with surgery
Severe airway damage tracheostomy or oral intubation, ICU admission
and controlled ventilation
4
Following inhalation induction with sevoflurane or halothane in 100% oxygen,

intravenous access is established at an appropriate depth of anaesthesia, if not
already present. When a suitable depth of anaesthesia is reached, laryngoscopy is
undertaken and topical local anaesthetic (lidocaine (lignocaine)) administered above,
below and at the level of the vocal cords. 100% oxygen is administered by face mask
with spontaneous ventilation and anaesthesia continued with inhalational or intravenous
(propofol) agents. At a suitable depth of anaesthesia the surgeon undertakes rigid
laryngoscopy and bronchoscopy.
Insufflation technique
The insufflation technique requires a spontaneously breathing patient. Insufflation of
anaesthetic gases and agents can be via a number of routes, including:
a small catheter introduced into the nasopharynx and placed immediately above the
laryngeal opening
a tracheal tube cut short and placed through the nasopharynx emerging just beyond
the soft palate
a nasopharyngeal airway
the side-arm or channel of a laryngoscope.
Insufflation techniques are useful in the removal of foreign bodies, evaluation of airway
dynamics (tracheomalacia) and relatively fixed lesions (glottic, subglottic stenosis).
Movements of the vocal cords are minimal or absent despite a spontaneously breathing
technique provided an adequate level of anaesthesia is maintained. Limitations of
insufflation techniques include:
no control over ventilation
loss of protective airway reflexes and the potential for the airway soiling
theatre pollution with volatile agents requiring the presence of high-intensity suction
catheters near the mouth.
Insufflation techniques may not be suitable for soft floppy lesions, particularly in the
supraglottis or glottis, which may obstruct the airway following the onset of general
anaesthesia.
For satisfactory insufflation techniques an adequate depth of anaesthesia is vital. If

the depth of anaesthesia is too light, movement may occur, the patient may cough or
laryngospasm occur. If the depth of anaesthesia is too great the patient may become
apnoeic with cardiovascular instability. Careful observation throughout the procedure,
noting movements, respiratory rate and depth, cardiovascular stability and constant
observation for unobstructed breathing are vital, with the concentration of volatile
anaesthetic adjusted accordingly.
Intermittent apnoea techniques

Intermittent apnoea techniques have been described for the laser resection of juvenile
laryngeal papillomatosis, where the presence of a tracheal tube obstructs surgery.
Following induction of general anaesthesia and confirmation of ventilation by face
mask, muscle relaxants are administered followed by tracheal intubation. The patient is
hyperventilated with a volatile anaesthetic agent in 100% oxygen. The tracheal tube is
then removed, leaving the surgeon a clear unobstructed immobile surgical field. After
an apnoeic period of typically 23 minutes, surgery is stopped, the tracheal tube is
reinserted and the patient hyperventilated once more. The advantages of the technique
are the immobile unobstructed surgical field and the inherent safety in the use of a laser
with the potential fuel source (tracheal tube) removed. Disadvantages of the technique
include:
risk of aspiration of blood and debris with the tracheal tube removed
variable levels of anaesthesia
interruption to surgery for reintubation
potential trauma through multiple reintubation.
Jet ventilation techniques

In 1967, Sanders first described a jet ventilation technique using a 16-gauge jet placed
down the side-arm of a rigid bronchoscope and relying on air entrainment to continue
ventilation with an open bronchoscope. Sanders used intermittent jets of oxygen (rate
8/minute, 3.5 bar driving pressure) to entrain air and showed the technique maintained
supranormal oxygen pressure with no rise in the carbon dioxide pressure
Since 1967, modifications to Sanders original jet ventilation technique have been made
for endoscopic airway surgery. Supraglottic jet ventilation describes a technique in
which the jet of gas emerges in the supraglottis by attachment of a jetting needle to
the rigid suspension laryngoscope (Figure 5). Subglottic jet ventilation involves placing
a small (23 mm) catheter or specifically designed tube (Benjet, Hunsaker) through
the glottis and into the trachea. Transtracheal jet ventilation involves the placement of
specifically designed percutaneous transtracheal catheters through the cricothyroid
membrane or trachea.
5 Rigid suspension
laryngoscope with jetting
needle.
As well as modifications to the site at which the jet of gas emerges, changes to the
frequency of jet ventilation have been described. High frequency (greater than 1 Hz,
60 breaths/minute) is used with ventilatory rates typically about 100150/minute. High
frequency jet ventilation allows:
a continuous expiratory flow of air, enhancing the removal of fragments of blood and
debris from the airway
reduced peak and mean airway pressures with improved cardiovascular stability
enhanced diffusion and interregional mixing within the lungs resulting in more
efficient ventilation.
These advantages are of particular importance in patients with significant lung disease
and obesity.
A typical jet ventilation technique includes preoxygenation followed by intravenous

induction and maintenance with a target-controlled infusion of propofol, supplemented
by bolus administration or infusion of alfentanil or remifentanil. At a suitable depth of
anaesthesia, manual confirmation of mask ventilation is made before administration
of muscle relaxants. Laryngoscopy is undertaken and topical lidocaine (lignocaine)
administered. Face mask ventilation is continued with 100% oxygen until the surgeon
is ready to site the rigid (suspension) laryngoscope on to which a jetting needle has
been attached in preparation for supraglottic jet ventilation. Alternatively, a laryngeal
mask airway can be inserted after induction and used to ventilate the patient with 100%
oxygen until the surgeon is ready to site the laryngoscope. At the end of surgery, the
laryngeal mask airway is reinserted before antagonism of residual muscle relaxation
and cessation of intravenous anaesthesia, to facilitate smooth emergence.
Supraglottic jet ventilation (Figure 6a) is commonly used in endoscopy procedures

because it allows a clear unobstructed view for the surgeon with no risk of laser-
induced airway fires. In common with all jet ventilation techniques, there is a risk
of barotrauma with possible pneumomediastinum, pneumothorax, subcutaneous
emphysema and pneumopericardiun. Other problems include:
gastric distension with entrained air
malalignment of the rigid suspension laryngoscope or jetting needle resulting in poor
ventilation
blood, debris or fragments being blown into the distal trachea
vibration and movement of the vocal cords
inability to monitor end-tidal carbon dioxide concentration.
6
Subglottic jet ventilation (Figure 6b) allows delivery of a jet of gas directly into the
trachea. The technique is more efficient than supraglottic jet ventilation and results in
reduced peak airway pressures, no vocal cord motion, a good surgical field and no
time constraints for the surgeon in the placement of the rigid laryngoscope. The main
disadvantages are the potential for a laser-induced airway fire due to the presence
of a potential fuel source within the airway, and a greater risk of barotrauma than in
supraglottic jet techniques.
Ventilators incorporating alarms and automatic interruption of jet flow when preset
pause pressure limits have been reached (i.e. blockage of entrainment and exhalation
have occurred) should be used.
Transtracheal jet techniques (Figure 6c): elective transtracheal catheter placement

under local anaesthesia in individuals with significant airway pathology or under general
anaesthesia for elective laryngeal surgery has been described. Transtracheal jet
techniques carry the greatest risks of barotrauma of all jet ventilation techniques. Other
potential problems include blockage, kinking, infection, bleeding and failure to site the
catheter. The use of transtracheal jet ventilation for endoscopic surgery of the larynx
requires careful evaluation of the potential risks and benefits.
Recovery from anaesthesia

Smooth emergence and recovery from anaesthesia are essential. Some studies
show a 1020 fold increase in reintubation following laryngoscopy or panendoscopy
when compared with general surgical re-intubation rates. The recovery profile with a
laryngeal mask airway provides smooth emergence from anaesthesia and some groups
advocate the exchange of microlaryngoscopy tubes, tracheal and laser tubes for a
laryngeal mask airway for recovery. u
FURTHER READING
Abitol J. Atlas of Laser Voice Surgery. London: Chapman and Hall, 1995.
Briggs R J, Bailey P, Howard D J. The Laryngeal Mask: A New Type of Airway in

Anaesthesia for Direct Laryngoscopy. Otolaryngol Head Neck Surg 1992; 107: 6035.
Donlon J V. Anaesthetic and Airway Management of Laryngoscopy and Bronchoscopy.

In: Benumof J L, ed. Airway Management: Principles and Practice. St Louis: Mosby,
1996; 66685.
Hunsaker D H. Anesthesia for Microlaryngeal Surgery: The Case for Subglottic Jet
Ventilation. Laryngoscope 1994; 104: 130.
Sosis M B. Anesthesia for Laser Airway Surgery. In: Benumof J L, ed.

Airway Management: Principles and Practice. St Louis: Mosby, 1996; 698735.

ENT Emergencies
Richard Semenov
Richard Semenov is Consultant Anaesthetist at the Royal National Throat, Nose and
Ear Hospital, London, UK. He obtained postgraduate training at the Middlesex and
Royal Free Hospitals. His interests include anaesthesia for ENT surgery and the shared
airway.
Ear, nose and throat (ENT) emergencies can cause acute life-threatening situations;
they require a calm approach and good leadership skills. Good communication
between anaesthetist and surgeon is vital in the management of these patients. This
article concentrates on three emergency situations.
Acute epiglottitis
Acute epiglottitis is caused by Haemophilus influenzae type B. Epiglottic swelling can
cause upper airway obstruction. It is most common in children aged 25 years and
can progress rapidly from a simple upper respiratory tract infection to acute airway
embarrassment. The typical clinical picture is a drooling child, who wants to sit up,
with tachypnoea, suprasternal recession and stridor. The absence of a cough helps
to distinguish it from laryngotracheobronchitis (croup). Complete airway obstruction
may be provoked by pharyngeal examination, intravenous cannulation and excessive
excitement. In severe cases, the diagnosis is made on clinical assessment.
The child and parents should be kept calm while experienced anaesthetic, paediatric
and ENT help is sought. Anaesthesia should be induced using sevoflurane in 100%
oxygen with the patient in the sitting position until tracheal intubation is possible.
Induction is usually slow and the apparatus for difficult intubation and the facilities for
urgent tracheostomy must be available. Atropine may be given once the intravenous
cannula is sited. An oral tracheal tube one size smaller than normal should be
used and this can be changed to a nasal tube for increased comfort if intubation is
straightforward.
Halothane has been the agent of choice for inhalational induction when a patients
upper airway is partially obstructed. Recently, reports of the use of sevoflurane in the
difficult airway have been published. If the airway obstructs completely after reaching
a deep plane of anaesthesia, the redistribution of the inhalational agent from the brain
to the other body compartments is the primary determinant of time to awakening.
Halothane has a higher blood gas solubility, therefore it should redistribute to other
compartments more quickly than sevoflurane and the brain concentrations of halothane
should fall more rapidly and the patient should regain consciousness faster than with
sevoflurane. However, induction with halothane takes longer than with sevoflurane
because of its higher blood:gas solubility coefficient, which allows more time for
halothane to distribute round the body. The concentration gradient from blood, brain
and alveoli to other compartments is therefore lower than with sevoflurane. The blood:
tissue solubility coefficient is similar for the two agents. As a consequence, when the
airway obstructs, it takes longer to return to consciousness with halothane.
Acute epiglottitis is becoming rare in children, probably because of effective vaccination

against H. influenzae. The Hib vaccine was introduced in the UK in October 1992.
Hib-vaccinated children who develop epiglottitis grow penicillin-sensitive streptococci,
making penicillin the first choice treatment, rather than the cephalosporins or
chloramphenicol required for H. influenzae.
The incidence of acute epiglottitis in adults has increased because of the frequent use
of antibiotic agents in childhood with an associated failure to develop immunity against
H. influenzae. Greater awareness and recognition of the disease may also have played
a role. Cases of epiglottitis caused by unusual pathogens are being reported among
immunocompromised patients, such as drug abusers.
Obstructed airway in head and neck surgery

If asked about the management of an obstructed airway, many anaesthetic trainees
suggest an awake fibre-optic intubation. However, serious complications may be
associated with its use. There are three main sites of obstruction:
supraglottic and glottic lesions causing obstruction
mid-tracheal obstruction, often secondary to retrosternal goitres and thyroid
carcinomas
lower tracheal and bronchial obstruction, usually from large mediastinal masses (e.g.
lymphomas, thymomas, carcinomas).
Supraglottic and glottic lesions

Careful preoperative assessment is essential for the management of upper airway
obstruction. The implication of stridor is that there is a reduction of airway diameter of at
least 50%. Patients often present late owing to the slow-growing nature of the tumours.
With severe obstruction there may be difficulty in breathing that wakes the patient at
night in a panic. The presence of nocturnal symptoms suggests advanced obstruction.
A fibre-optic nasendoscopy will usually have been performed by the ENT surgeon in
the outpatient clinic. It does not involve spraying the larynx with local anaesthetic or
making contact with the vocal cords, both of which are hazardous and can precipitate
complete airway obstruction. A CT scan of the neck is helpful to assess the subglottis
and the lower extent of the tumour.
Senior ENT and anaesthetic staff should discuss the case before the patients arrival in
the anaesthetic room. If it is decided to undertake a general anaesthetic a secondary
plan should be prepared, in case problems arise, and it should be discussed with the
patient. Patients with moderate stridor, in whom intubation is considered possible,
should be managed with an inhalational induction in theatre with the ENT surgeon
gowned and ready (plan A). A tracheostomy tray and rigid ventilating bronchoscope
should be available. Safety lies in the maintenance of spontaneous ventilation, induction
takes time and should not be hurried. Difficulty often arises when the patient first loses
consciousness. The skill lies in avoiding coughing and subsequent laryngeal spasm. A
nasal airway can be helpful.
When anaesthesia is deep enough, laryngoscopy should be attempted and a rapid

decision made as to whether a tube can be passed. If a decision is made to intubate,
a maximum of two attempts should be made because persistent attempts may result
in total obstruction. Correct position should be confirmed with capnography. If it proves
impossible to intubate, the surgeon should perform a tracheostomy while the patient
maintains spontaneous respiration (plan B). A laryngeal mask airway can be useful to
maintain the airway but may prove difficult to insert with a supraglottic tumour.
Patients with severe stridor resulting from a supraglottic or glottic lesion (Figure 1)
often come to hospital for the first time as an emergency or have deteriorated following
radiotherapy. They should have no sedation and be given a helium:oxygen mixture to
improve symptoms. They should have a preliminary surgical airway performed under
local anaesthetic. This can be a tracheostomy or an emergency cricothyroidotomy
cannula can be placed through the tracheal rings below the level of the tumour to allow
subglottic jet ventilation. A formal tracheostomy may be difficult because these patients
are often hypoxic, hypercarbic and confused, therefore a short procedure to secure
adequate ventilation is often advisable.
1 Glottic stenosis causing stridor.
Mid-tracheal obstruction
With mid-tracheal obstruction the fibre-optic bronchoscope may be useful. The
exact site and extent of the obstruction should be defined before embarking on an
anaesthetic. A CT scan is essential for lesions of the trachea and bronchi. As in the
case of upper airway tumours, the formulation of plan A and plan B is critical. The
scan provides a guide to whether a 7 mm tube will pass through the narrowest site of
the compression. If this is the case, a conventional induction of anaesthesia can be
performed. If there is any doubt, evidence of malignant invasion into the trachea or
marked tracheal deviation, an awake fibre-optic intubation is the method of choice,
which requires an experienced operator.
Lower tracheal and bronchial obstruction

Patients with symptomless lower tracheal and bronchial obstruction from mediastinal
masses can develop unexpected respiratory obstruction during anaesthesia. During
spontaneous respiration there is a subatmospheric intrapleural pressure and widening
of the airways during inspiration. Administration of a muscle relaxant may alter the
support of the bronchial tree and collapse of the airway can occur with positive-
pressure ventilation. Tissue biopsy should be performed whenever possible under local
anaesthetic and if superior vena caval obstruction is present urgent radiotherapy and
chemotherapy may be necessary, even in the absence of a histological diagnosis. A
rigid bronchoscope may relieve obstruction. Cardiopulmonary bypass may have to be
considered.
The bleeding tonsil

The problems of the bleeding tonsil include:
stomach full of blood and risk of aspiration
potential difficult airway, oedematous and obscured by blood
hypovolaemia
not yet recovered from a recent anaesthetic.
Anaesthetists should be alert to the possibility of an unsuspected bleeding disorder. A

recent episode of tonsillitis makes the procedure technically more difficult and increases
the risk of postoperative haemorrhage. There is conflicting opinion as to whether non-
steroidal anti-inflammatory drugs used for postoperative pain increase the incidence of
bleeding.
Post-tonsillectomy haemorrhage is seldom a catastrophic acute arterial bleed. It is

usually a venous or capillary ooze and therefore resuscitation rather than immediate
operation is the first management step. The child may have swallowed a lot of blood
and hypovolaemia can be severe before the diagnosis is made.
After effective resuscitation, the patient presents further problems in theatre. There is a
risk of aspiration of gastric contents (mostly altered blood), and significant amounts of
the anaesthetic agents used previously may still be present. Experienced anaesthetic
assistance is required. There are two methods of intubation.
An inhalational induction in the left lateral position, with suction available, the trachea
is intubated during spontaneous ventilation. Induction may be prolonged and hindered
by continued bleeding. Few have much experience of intubating in this position.
A rapid-sequence induction and intubation has the advantages of familiarity and
rapidity. It should be attempted only if intubation was easy at the initial procedure.
Visualization of the larynx may be difficult if there is torrential haemorrhage, two
separate suction units should be ready for use.
Nasogastic aspiration should be performed before extubation. Extubation should be

performed when the patient is awake and laryngeal reflexes have returned, to minimize
the risk of aspiration of gastric contents. u

Gas, Tubes and Flows
Kwong Fah Koh
Kwong Fah Koh is Associate Professor in Anaesthesia at the National University,

Singapore. He graduated from the National University of Singapore. He trained in
anaesthesia in Singapore and did a fellowship in neuroanaesthesia at the National
Understanding fluid flows through tubes and airways requires a knowledge of fluid
mechanics. Oxygen, air and nitrous oxide are gaseous fluids and largely obey the laws
of fluid dynamics.
Gas laws
Gases are described in terms of pressure, volume and temperature. The three are
related according to the ideal gas law:
PV = nRT
where: P is the pressure (kPa), V the volume (ml), T the temperature (Kelvin), n
is Avogadros number (number of moles of a gas in a fixed volume) and R the gas
constant (8.3143 J/gm mol/K). A mole of gas contains 6.023 x 1023 molecules and
occupies 22.4 litres at standard temperature and pressure (i.e. 0C and 760 mm Hg).
The ideal gas law incorporates Boyles and Charles laws. At a constant temperature,
the volume of a given mass of gas varies inversely with its absolute pressure (Boyles
law). At a constant pressure, the volume of a given mass of gas varies directly with
its absolute temperature (Charles law). However, there are no ideal gases because
there are significant intermolecular attractions (van der Waals forces) between gas
molecules, therefore constants are added to both the pressure and volume relationship
in the ideal gas laws:
(P+a/V2).(Vb) = nRT
where a corrects for attraction between molecules and b corrects for the volume
occupied by molecules.
In clinical practice, mixtures of gases are used and their behaviour is described by
Daltons law of partial pressures. This states that in a mixture of gases, the pressure
exerted by each gas is the same as that it would exert if it alone occupied the container,
so the total pressure in a system is a sum of all the partial pressures of the different
gases.
Movement of gases
Fluids flow when there is a pressure difference. HagenPoiseuilles law states that flow
through a horizontal straight tube of uniform diameter is proportional to the pressure
gradient and the fourth power of the radius, and is inversely related to the viscosity of
the gas and the length of the tube.
Pr4
F= 8l
where: F is the flow rate through the tube (cm3 /s), P the pressure gradient, is 3.14,
r the radius of the tube (cm), the fluid viscosity (g/cm/s), and l the length of the tube
(cm).
The law assumes that flow is laminar. When flow exceeds a critical velocity, the flow
velocity profile loses its parabolic profile and becomes turbulent. This occurs when the
Reynolds number becomes larger than 4000. Reynolds number is affected directly by
flow rate through the tube and density of the gas and is inversely related to viscosity of
the gas and the radius of the tube. The higher the number, the more turbulent the flow.
Flow is laminar at Reynolds numbers less than 2000.
Flow becomes turbulent when the velocity is high, when there are sharp angles,
changes in diameter or multiple branching (Figure 1). This can be seen in the upper
airway. During normal respiration, flow in the trachea is usually a mixture of turbulent
and laminar flow. If there is an obstruction (e.g. glottic stenosis), the radius of the airway
decreases and the flow velocity increases. This accentuates turbulence and gas flow
decreases. Such patients often assume an extended neck position to minimize the
angles present and increase the upper airway diameter in an attempt to decrease the
turbulence and improve gas flow.
Laminar and turbulent flow characteristics
Laminar flow Turbulent flow

Viscosity Density
Radius 4 Radius2
P4 P12
Reynolds number < 2000 Reynolds number > 4000
Flow, viscosity and density

The viscosities of common anaesthetic gases are fairly similar but their densities differ
greatly (Figure 2). When the airway is narrowed, flow becomes turbulent and the
density of a gas assumes greater significance. The density of oxygen is quite close to
that of air, but the density of 70% nitrous oxide in oxygen is 60% higher. The density
of 80% helium in oxygen is only 30% that of air. During an airway obstruction, using
heliox (80% helium, 20% oxygen) can improve gas flow by reducing turbulence. This
improved flow can be 1.73 times greater than air or 100% oxygen. Nitrous oxide should
be avoided during induction if there is significant airway obstruction.
Density and viscosity of gases at 20C, 101.3 kPa
Viscosity Density
Air 18.2 1.196
Nitrogen 17.6 1.165
Oxygen 20.4 1.331
Nitrous oxide 14.6 1.831
Helium 19.6 0.166
Air contains 0.04% carbon dioxide with 50% relative humidity
Flow through tracheal tubes

The largest possible tracheal tube used to be regarded as the correct size (8 or 9 mm
internal diameter). However, larger tracheal tubes cause more trauma to the pharynx,
larynx and tracheal wall. Smaller tubes are easier to insert and cause less trauma.
Studies have shown that smaller tracheal tubes (6 or 7 mm internal diameter) do not
significantly increase airway resistance (Figure 3). Airway pressure is usually measured
at the proximal end of the tracheal tube. Because of this, the airway pressure measured
is higher when a small tube is used than when a larger diameter tube is used. However,
when the intratracheal pressures are measured, they are not significantly higher during
the inspiration and expiration phases. Tube sizes of 6 and 7 mm internal diameter are
acceptable for positive-pressure ventilation during routine anaesthesia.

Applied Respiratory
Physiology
3
In intubated patients, mechanical ventilators can overcome impedance to inspiratory

flow, but not the impedance to passive expiration. In weak patients, resistance to
exhalation through long narrow tubes, compounded by turbulence, can delay weaning.
Such patients benefit from a larger tracheal tube or a tracheostomy. The reduced
resistance (from using a short, large- bore tube) during expiration minimizes the work of
breathing during expiration and thus aids weaning.
Flowmeters
A flowmeter consists of a bobbin in a tapered glass tube. As the bobbin moves
upwards, the gap around it increases so that a higher flow is required to support
the bobbin. At low flows, the gap between the bobbin and the tube is small so the
flowmeter resembles a tube. The flow is laminar and thus is dependent on the viscosity
of the gas. At higher flow, the gap is wider and the flowmeter resembles an orifice that
has a turbulent character. Gas flow is thus dependent on density rather than viscosity. If
oxygen and helium are passed through identical flowmeters, the measurements of flow
will be accurate at low flows, because their viscosities are quite close. However, at high
flows, the helium will relatively under-read as flow is increased because of its lower
density.
Flow through constrictions

The Bernoulli effect describes the fall in pressure at points of constriction, where flow
velocity is higher. This effect is seen in devices using the Venturi principle, such as gas
nebulizers, some flowmeters and face masks (Ventimask). Jet ventilators force gas
through a narrow orifice. The resultant jet creates a low pressure area that causes gas
entrainment. When a jet ventilator is used, it is important that the airway is unobstructed
during inspiration (to allow entrainment) and expiration (to prevent breath stacking).
Some effects of high gas pressures

Gas density increases in direct proportion to pressure. Air at 10 atmospheres has ten
times the density of air at sea level. Thus, the work of breathing at higher atmospheric
pressure (e.g. during diving) is greater. The maximum breathing capacity is decreased
because density is increased due to increased pressure. To circumvent this problem,
helium, with a density one-seventh that of nitrogen is used with oxygen (heliox) at high
pressure.
Flowmeters are affected by pressures, because flow is affected by density at higher

rates of flow. A flowmeter would read lower at high pressures. u
FURTHER READING
Benumof J L. Airway Management: Principles and Practice. St Louis: Mosby, 1996.
Koh K F, Hare J D, Calder I. Small Tubes Revisited. Anaesthesia 1998; 53: 469.
Nunn J F. Applied Respiratory Physiology. Sevenoaks: Butterworths, 1987.

Obstructive Sleep Apnoea
John Ruddock
John Ruddock is Consultant Anaesthetist at the Royal National Throat, Nose and Ear
Hospital, part of the Royal Free Hampstead Hospital Trust, London, UK. It is a specialist
hospital for ENT and head and neck surgery. He is actively engaged in the diagnosis
and treatment of patients with sleep-related breathing disorders.
Adults who are said to have obstructive sleep apnoea (an apnoea-hypopnoea index
(AHI) of more than 15 episodes per hour of sleep) have a variety of upper airway
conditions. In this article, the term obstructive sleep apnoea (OSA) is used for the
occurrence of repeated obstructive episodes over several respiratory cycles. Sleep-
disordered breathing is a better general term.
The nature of sleep

The principal function of sleep is to restore the function of the prefrontal cortex, thereby
restoring higher centre cognitive activity. This is brought about by the delta (slow)
wave activity generated by the cerebral cortex under the influence of centres in the
thalamus. This is the EEG activity that characterizes the Rechtschaffen and Kales sleep
stages 3 and 4. The delta activity per 30-second sleep epoch in these sleep stages is
2050% in stage 3 and over 50% in stage 4. Normally 2540% (23 hours) of sleep
should occur in these stages. They occur mainly in the first two or three 90-minute
sleep cycles. Even small amounts of sleep deprivation result in measurable changes
in certain cognitive function tests. Making appropriate responses to unexpected events
is particularly impaired and while alertness can be restored by stimulants such as
caffeine, these higher centre cognitive functions cannot be restored by stimulants.
To achieve sleep stages 3 and 4 the individual needs to progress through stages
1 and 2 and it is in these lighter sleep stages that airway inadequacy may express
itself in sleep-disordered breathing. The progression to deep sleep coincides with the
establishment of regular respiration and anything that impairs this regularity, impairs the
progression to deep sleep.
Airway maintenance during sleep

The upper airway is maintained by tone in the skeletal musculature of nose,
nasopharynx, oropharynx, tongue and larynx. Efferent discharges to these muscle
fibres have tonic and phasic components. The phasic components are in synchrony
with inspiration. The effect is to brace the airway against a tendency to collapse. (The
flaring of the nostrils with intense inspiratory effort is part of this phasic activity.) During
sleep, the tonic efferent discharge falls in parallel with the reduction in tone throughout
all the skeletal musculature and is at a minimum during rapid eye movement (REM)
sleep. The upper airway becomes increasingly susceptible to forces provoking airway
narrowing, such as pressure from fat around the pharynx or the collapsing effect of
inspiration, which is accentuated when there are pathological conditions, such as nasal
obstruction, affecting the upper airway. The airway may become unable to support
adequate respiration during sleep. How the brain senses this inadequacy is not known,
but the result is the inability to progress to deep sleep.
Compensations for airway impairment during sleep

Airway impairment during sleep is compensated for by posture, respiratory drive,
pharyngeal reflexes and sleep disruption.
Posture normally individuals automatically adjust their sleeping posture to

compensate for airway narrowing. They may turn their head to the side, elevate their
head to the sniffing the morning air position, turn on their side or lie prone. The
afferent loop for this response is unknown. The airway remains patent or is occluded
for only a few respiratory cycles until the compensating adjustment in posture has been
made. During REM sleep, when the individual is sleeping on their back, the generalized
paralysis prevents compensatory changes in posture and OSA events may persist
throughout the REM period.
Pharyngeal reflexes when people with airway narrowing are given a sedative, such
as midazolam, 35 mg, and propofol, 50100 mg, their airway may become obstructed
if they are lying on their back. Just as in REM sleep, they are unable to move to
make appropriate compensatory postural changes. The obstruction persists, but is
intermittently relieved, probably because the respiratory drive increases as the carbon
dioxide level rises. Local pharyngeal reflexes respond to a negative pressure within the
lumen to increase the tone of the airway musculature and these would be stimulated
when the force of inspiration increased against the airway obstruction. The afferents
for these reflexes may also be within the thorax because airway obstruction leads to
negative intrathoracic pressure. In addition, the increased respiratory drive augments
the phasic tone of the airway musculature.
Failure to progress in sleep when progressive airway narrowing during sleep has
produced maximal levels of respiratory drive and phasic tone the final measure to
preserve adequate respiration during sleep is sleep disruption. Arousal is linked by
neural mechanisms within the brain to a certain critical level of respiratory stimulation.
The arousal causes the tone in the airway to return and so relieve the airway
obstruction. This is the situation in OSA.
Categories of sleep-disordered breathing

Upper airway resistance
Upper airway resistance is an arbitrary term for two typical responses.
Postural changes, such as head extension, may be inadequate to compensate
for airway impairment. An increase in respiratory drive may be required to overcome
the resistance and augment the phasic component of tone in the airway musculature.
There are no apnoeas, but airflow may wax and wane (hypopnoea) owing to increasing
obstruction. There may be paradoxical respiration. The respiratory drive increases until
the arousal threshold is exceeded. The arousal causes the tone in the airway to return.
The airflow is increased and the snoring is reduced.
Others have a different response, which may be induced by a lower metabolic rate
and cardiac output. In these individuals, the waning airflow seems to be the result of a
reduced respiratory drive and any snoring occurs when the airflow increases during the
arousal phase. The inference is that airway reduction impairs respiration and leads to
a rise in the partial pressure of carbon dioxide in arterial blood (PaCO2) until this has a
stimulatory effect on the respiratory centre, which incurs a delay. At a particular level of
respiratory stimulation there will be an arousal, hyperventilation and overcompensation.
The PaCO2 falls below the respiratory threshold and there is a hypopnoea or central
apnoea and the cycle is repeated.
OSA
Effective compensatory reflexes safeguard the airway during sleep and prevent
persistent obstruction. Significant OSA occurs when the ability of these reflexes is
exceeded. There is a limit to which postural change can aid the situation, the respiratory
drive can be at a maximum and the protective pharyngeal reflexes may be impaired.
Mild OSA in REM sleep, postural changes are obtunded but there are other
compensations in response to OSA. There may be a microarousal (momentarily
coming out of REM sleep) or REM sleep may be reduced. Commonly, OSA occurs in
REM sleep only when the individual is lying on their back; when they lie on their side,
they have REM sleep without apnoeas and without desaturations. These individuals
desaturate when on their back during each of their three or four REM episodes each
night, probably to 70%. Mild OSA does not have an impact on daytime somnolence.
In the presence of coronary vascular disease there are probable implications in the
postoperative management of people with mild OSA (see rebound REM below). Many
people desaturate during REM sleep without having OSA because a reduction in
respiratory effort occurs as part of the normal reduction in skeletal muscle tone that
occurs during REM sleep.
Moderate OSA obstructive apnoeas occur in sleep stages 1 and 2 if individuals

sleep on their back. There is probably an impairment in the local pharyngeal reflexes.
The theory is that pharyngeal mucosal oedema from the repeated trauma of airflow
turbulence and actual damage to nerve endings has resulted in the impairment or loss
of these protective pharyngeal reflexes. The result is that the airway is obstructed, the
carbon dioxide level rises, the oxygen level falls and the respiratory drive increases until
the individuals arouse. They suffer repeat arousals, of which they are not usually aware,
but sleep is disrupted and progression to deep sleep is impaired. Individuals with
moderate OSA who lie on their side may not have obstruction and sleep can progress,
though they may show features of upper airway resistance. They may not have severe
daytime somnolence.
Severe OSA patients either obstruct in all sleep positions or remain on their backs
throughout the night despite repeated obstructive events. They do not have any
sustained delta sleep and REM sleep is usually severely disrupted. These patients
are somnolent with severe impairment to their quality of life. Treatment is with nasal
continuous positive airway pressure (CPAP). Patients will still obstruct if they do not
use CPAP, unless during their treatment period they have lost a great deal of weight.
However, treatment eliminates somnolence and their cardiovascular system is not
subjected to the strain of repeated episodes of hypertension and tachycardia.
Cardiovascular system negative intrathoracic pressure during apnoea leads to a

fall in systemic blood pressure and heart rate. It also causes increased venous return
and stimulation of the baroceptors of the aortic arch and therefore at the end of the
apnoea when the arousal results in relief of the airway obstruction, there is a rise in
blood pressure and heart rate. This is usually coincident with the nadir in peripheral
oxygen levels. The result is severe cardiovascular instability. Cardiac dysrhythmias
(supraventricular and ventricular ectopics, atrial fibrillation and periods of complete
heart block) often occur in these patients. There is an increase in daytime blood
pressure. Essential hypertension in these patients may be refractory to medical
treatment until the OSA is treated with nasal CPAP, similarly in patients with upper
airway resistance.
Central apnoea
The central event is caused by a reduction in respiratory drive. The most common
cause is when an individual enters an episode of periodic respiration as a result
of a change in sleep stage or position and there are alternations of hypo- and
hyperventilation. They may be a normal event during sleep onset, after an arousal
or during REM sleep. Their association with upper airways resistance has been
discussed. In addition, central apnoeas may occur when there is respiratory failure
the hypoxic drive during sleep results in hypocapnia and respiratory cycling. Altitude
causes similar events. Respiratory drive and airway musculature are affected in
patients with brain lesions (e.g. after a stroke). In addition, there is the long-period
respiratory cycling of CheyneStokes breathing in which the low cardiac output of heart
failure results in a prolongation of feedback.
Mixed apnoea
Some patients have mixed apnoea (obstructive plus central apnoea). They have a
central apnoea with an initial patent airway, however, the absence of phasic drive and
the presence of surface tension effects from the mucous lining of the airway result in
airway closure. Also, pharyngeal reflexes do not operate when there is no respiration.
When respiration restarts, the opening of the airway produces a characteristic snore.
OSA
Aetiology: a number of head and neck and neuromuscular pathologies provoke
sleep-disordered breathing and may render the individual unable to compensate
effectively. The most common aetiology is a history of nasal obstruction that originates
in developmental or traumatic abnormality of the nasal airway. Over time the increased
respiratory effort required for adequate breathing results in pharyngeal wall collapse,
thickening and folding of the mucosa, elongation of the uvula, submucosal oedema and
a tendency to breath through the mouth, that restricts the post-lingual airway. In middle
age, particularly in men, fat is deposited in the neck and this further compresses the
airway. These occurrences are insidious as are their effects on sleep. An individual and
resilient sleep pattern is established.
Investigation: a simple sleep study is all that is required, provided it is interpreted with
an understanding of what may be happening to the sleep staging. A polysomnogram is
unnecessary and impractical for investigating most people. The important parameters
of the sleep study are gender, body mass index, Epworth Sleepiness Score, sleep
position, snoring events, oxygen saturation, heart rate, abdominal and chest respiratory
efforts and airflow. Monitoring leg movements is also useful. In the Epworth Sleepiness
Score the patient is asked to score their likelihood of falling asleep on a scale of 03
for eight different activities or periods of the day. The maximum score for extreme
sleepiness is 24; normal scores are less than 10.
Implications for anaesthesia: few patients have perioperative sequelae due to OSA.
Often those at risk are in or approaching the morbidly obese range and appropriate
anaesthetic safeguards (e.g. short-acting agents, awake fibre-optic intubation) are used
for that reason. However, there are reports of cases in which the anaesthetist has not
been prepared for OSA and anecdotal reports of patients, not necessarily obese, who
have died during the perioperative period in whom OSA has been implicated.
The confounding factors related to obesity are difficult venous access, difficult airway
maintenance, difficult intubation, hypoxia, thromboembolic phenomena and gastro-
oesophageal reflux. Apart from these, the focus of concern for adults with OSA is the
recovery period. The airway is maintained in these patients by the respiratory drive and
the capacity for arousal; the factors that are obtunded by general anaesthetics. The
anaesthetic technique must ensure that when the patient is required to maintain their
own airway, they will be awake with a good respiratory drive. Appropriate anaesthetic
agents to achieve this aim are desflurane and remifentanil.
Preoperative assessment: patients who are likely to have OSA have a history of
snoring, sleep apnoea and daytime somnolence. Men are more likely to have the
condition than women because of the different distribution of fat tissue in the neck.
Obese patients with severe OSA have a reduced functional residual capacity and
desaturate profoundly, regularly to 60% throughout the night. A person with OSA who
is not obese will not desaturate to this degree. The diagnosis is made from an overnight
oximeter recording on an obese patient who is sleeping; conversely the anaesthetist
can be reassured by a negative trace. Objective evidence that the patient has been to
sleep can be obtained from the heart rate record. If severe OSA is suspected, elective
surgery must be deferred. A patient with severe OSA needs to be stabilized on nasal
CPAP.
Upper airway resistance and moderate OSA are often present in patients with
a history of snoring and sleep apnoea, in those with a thick neck, large tongue or
retracted mandible. The recovery position and Guedel airway are likely to be needed
until the patient is awake. The need for effective postoperative analgesia in these
patients may warrant the use of an oximeter or care in the high dependency unit.
Low body mass index (BMI) and severe OSA most patients with significant sleep
apnoea have a BMI of 30 or more. However, severe OSA can occur in patients with a
normal BMI as a result of maldevelopment of maxilla or mandible. If the condition is
associated with neurological deficit or motor weakness, hazards for the patient following
general anaesthesia include laryngeal incompetence, which could lead to aspiration or
respiratory failure.
Mild OSA and rebound REM all patients have impaired sleep during the immediate
postoperative period. For patients with sleep-disordered breathing, this means that the
number of hypoxic events will be reduced. In particular, there is inhibition of REM sleep,
partly due to the effect of analgesic drugs such as morphine. A person who desaturates
during REM sleep may not therefore desaturate during the first few nights after surgery.
A few nights later, there may be increased amounts of REM sleep to compensate for
the period of deprivation. As a result, the patient may desaturate for long periods in the
postoperative period when they will not usually be receiving supplementary oxygen. For
most patients, desaturation during REM is probably not hazardous, but where there is
coronary insufficiency, it should be avoided by the use of nasal CPAP. The combination
of mild OSA and coronary insufficiency may be responsible for postoperative
myocardial infarction.
Anaesthesia in severe OSA: a patient with severe OSA who is having surgery to
remove nasal polyps to assist nasal CPAP therapy can probably have their airway
managed with a flexible laryngeal mask (LMA) in the hands of an experienced
anaesthetist. After securing intravenous access and giving an anticholinergic agent,
glycopyrrolate, 200 g, anaesthesia is induced with oxygen and sevoflurane, with
or without propofol, 10 mg increments. A Guedel or nasopharyngeal airway may be
needed. If airway compromise occurs, suxamethonium, 100150 mg, may be needed,
alternatively if hand ventilation is achieved without suxamethonium, a small amount of
atracurium, 25 mg. Remifentanil, 10 g increments, are given and the flexible laryngeal
mask (size 5 males; size 4 females) inserted. Anaesthesia is maintained by ventilating
with oxygen, desflurane with or without air or nitrous oxide and by using a remifentanil
infusion. If normal levels of ETCO2 (end-tidal carbon dioxide level) are not achieved for
a maximum inspiratory pressure of 20 cm H2O, the use of a tracheal tube needs to be
considered.
At the end of the operation the muscle relaxant is reversed and the patient recovered,
sitting up, with the flexible LMA and bite guard in place until they are well awake. The
LMA is removed, provided adequate levels of oxygen saturation and ETCO2 have
been achieved. Patients with nasal packs require nursing in the high dependency unit.
Postoperative CPAP intervention requires a full-face mask.
If a tracheal tube has been used for anaesthesia for surgery, then awake extubation
with the patient sitting upright is the preferred option with the use of a nasopharyngeal
airway or rigid LMA where appropriate. Postoperative analgesia with opiates may need
to be withheld and the patient warned about this. Non-opiate analgesia is preferred.
Regional anaesthetic techniques are not necessarily indicated because they impact on
the strength of respiration. u
FURTHER READING
Stradling J R. Handbook of Sleep-related Breathing Disorders. Oxford: Oxford
University Press, 1993.
Copyright 2003 J Ruddock

Percutaneous Tracheostomy
Robert Broomhead
Robert Broomhead is Specialist Registrar in Intensive Care Medicine at the

Hammersmith Hospital, London. He graduated from Leeds University and is training in
anaesthesia and intensive care medicine on the North West Thames rotation.
Prolonged ventilatory support of intensive care patients using nasal or oral tubes, is
associated with a number of problems. Tracheal tubes are uncomfortable and require
the patient to be sedated. These tubes are more liable to occlusion (kinking, biting,
secretions) and their length and contours make it difficult to pass catheters for effective
tracheobronchial suctioning of secretions. Oral tubes can be difficult to secure and
constant movement increases the chance of tracheal damage. They also prevent
adequate oral hygiene procedures. Nasal tubes are associated with infection in the
paranasal sinuses.
Placement of a tracheostomy reduces or removes these problems. It also reduces the

dead space and the resistance to, and work of, breathing. The benefits of tracheostomy
are outlined in Figure 1 and the complications listed in Figure 2. The decision to
perform a tracheostomy is based on an appraisal of the risks and benefits for each
patient (Figure 3). Tracheostomy was advocated after 1 week of continued ventilation
to avoid subglottic ulceration. Recently, the trend has been towards early placement
in patients predicted to have prolonged requirements for ventilatory support, or airway
protection.
Advantages of percutaneous tracheostomy
May be performed in the ICU (removing the hazards of transferring

critically ill patients)
Performed by intensivist/anaesthetist (does not require referral to a
surgeon and organization of theatre time)
Often quicker than open surgical technique
Fewer postoperative infections
May be reduced incidence of tracheal stenosis
Aids weaning from ventilator
May reduce patient's length of stay in ICU
1
Complications of tracheostomy
Immediate
Submucosal placement of guidewire and/or dilation
Cricoid damage
Trauma to the posterior wall of trachea
Marked fall in oxygen pressure
Cardiac dysrhythmia
Haemorrhage
Surgical emphysema
Pneumothorax
Misplacement of tracheostomy tube into pretracheal tissues
Occlusion of tracheostomy tube tip against tracheal wall or due to
cuff herniation
Perioperative death
Delayed
Infection of stoma
Tracheostomy tube blockage with secretions
Ulceration of trachea at site of the cuff
Erosion at stoma site leading to catastrophic bleeding (innominate
artery) or tracheo-oesophageal fistula
Pneumonia
Late
Granuloma formation in the trachea
Tracheomalacia
Tracheal stenosis
Failure of stoma to close once decannulated
2
Contraindications for percutaneous tracheostomy
Infection/inflammation at the proposed tracheostomy site

As a means of emergency airway access
Uncorrected bleeding diathesis
Enlarged thyroid gland
In children
Burns/trauma to anterior neck
Difficult anatomy (e.g. obesity, deformity)
Marked cardiovascular or respiratory instability
3
Consent percutaneous tracheostomy is usually undertaken on patients who are

already sedated and intubated in the ICU and from whom formal consent cannot be
obtained. If the patient is sufficiently awake the procedure should be explained to allay
anxiety. An explanation should also be given to the relatives.
Technique
All the apparatus required is checked and prepared before the procedure (Figure 4).
A tracheostomy tube is selected and checked to ensure that the cuff inflates correctly,
and that it fits over a suitable dilator/introducer. A tracheostomy tube of 8.0 mm internal
diameter is adequate for most adults and usually fits satisfactorily over a 24 FG dilator.
Percutaneous tracheostomy
These illustrations show insertion at a lower than normal site
f Blue
Rhino
dilator
a passed
Surface over
anatomy. guidewire.
b
Identification g Gentle
of the dilation, no
tracheal excessive
lumen with force
cannula. required.
h Dilation
c of stoma.
Insertion Marks
of on dilator
guidewire indicate
through depth of
cannula. insertion.
d i Introduction
Preliminary of
dilation of tracheostomy
stoma. tube.
e Dilator
guide j
passed Connection
over to
guidewire. ventilator.
Inset: laryngoscopic appearance.

Figures reproduced with the permission of Cook Critical Care Products.
An anaesthetist undertakes responsibility for the anaesthetic, and the management

of the airway, partially withdrawing the tracheal tube at the appropriate time. Most
units use a fibre-optic laryngoscope or bronchoscope via the tracheal tube during
the procedure. This allows visualization of the tracheal puncture site, and the correct
position and orientation of the guidewire placed by the operator.
Blood pressure, ECG and oxygen saturation are monitored throughout the procedure.
Monitoring end-tidal carbon dioxide is also strongly recommended. The patient is
anaesthetized, paralysed and ventilated with 100% oxygen. A positive end-expiratory
pressure (PEEP) of 510 cm H2O is generally recommended. Pressure-controlled
ventilation may be useful to maintain tidal volumes during withdrawal of the tracheal
tube.
The patient is positioned supine with head and neck extended sufficiently to allow
identification of the landmarks. This is facilitated by the placement of a pillow or
rolled towel under the shoulders. Problems may occur with the final position of the
tracheostomy tube as a result of the head and neck being extended too far. The trachea
and skin each move to a different extent during extension.
Full surgical aseptic technique is used; the operator should scrub and wear surgical
cap, mask, gown and gloves. All personnel should wear eye protection and a mask
because the patient's blood and secretions may be blown into the air around the
operative site.
The anterior neck and upper chest is cleaned and prepared using an alcoholic
chlorhexidine skin preparation solution and the operative area is draped. The cricoid
cartilage is identified below the thyroid notch. The position of the second tracheal
cartilage is estimated below this. These points may be marked. The area of skin at the
intended tracheostomy site is infiltrated with 1% lidocaine (lignocaine) containing 1:
100,000 adrenaline (epinephrine). This provides local analgesia, causes blanching of
the area and reduces oozing from skin vessels.
A short horizontal skin incision (about 1.5 cm) is made over the trachea. Some
operators advocate blunt dissection in the midline down to the trachea using curved
artery forceps. The aim is to identify the space between the first and second (or second
and third) tracheal rings, which are the recommended sites of tracheostomy stoma.
At this point, the anaesthetist pulls back the tube to avoid it being transfixed by the
needle. Withdrawal requires deflation of the cuff, therefore the ventilator settings will
have to be adjusted to maintain adequate ventilation. Withdrawal of the tube is best
performed under direct laryngoscopy, until the top of the deflated cuff is visible in the
glottic aperture. The palpating finger of the operator can also feel as the tip of the tube
passes above the site of intended puncture. Once the tube is withdrawn sufficiently it is
secured in this position for the remainder of the procedure.
The Ciaglia Percutaneous Tracheostomy Introducer Set (Cook Critical Care Products)
provides a cannula over a needle, which can be attached to a 5 ml syringe. The
anterior wall of the trachea is punctured; confirmation of which is provided by the ability
to aspirate air. The syringe may be partially filled with saline, if desired; aspirated air
can then be seen to bubble through the saline. The cannula is then advanced off the
needle in a caudal direction and a J-tipped guidewire passed through the cannula
and down the trachea. The fibre-optic laryngoscope is invaluable in confirming the
correct position and orientation of the guidewire. With the guidewire in position, the
cannula is removed and the initial puncture site is preliminarily dilated to accept a
guiding catheter, over which, either serial dilators, or the Blue Rhino tapering dilator is
passed, to enlarge the stoma progressively. Marks on the dilators indicate the limit to
which the dilator should be introduced into the trachea. Unnecessary force or incorrect
alignment of the dilator during its insertion may result in failure to follow the contour of
the guidewire. This can cause kinking of the guidewire increasing the risk of introducing
the dilator into the pre-tracheal tissue and causing damage to anatomically related
structures.
Once a suitably sized stoma has been created, a previously checked flexible
tracheostomy tube is loaded onto a dilator and guided through the stoma into the
trachea. The dilator is removed, the cuff inflated and the patient ventilated through
the new tracheostomy. Only when ventilation is assured and satisfactory via the
tracheostomy should the tracheal tube be removed.
The tracheostomy tube is secured with tape round the patients neck with the patient's
head and neck flexed to a normal position. Some operators suture the flange of the
tracheostomy tube to the skin but this is not essential, may lead to a false sense of
security and often results in skin infection at the suture site.
Alternative methods of maintaining the airway

In surgical tracheostomy the surgeon dissects the anatomy and is in control of the
airway directly, before the tracheal tube is withdrawn and the stoma is created. In
percutaneous tracheostomy, the tracheal tube is withdrawn early in the procedure and
maintained in a precarious position until the stoma is created and the tracheostomy
tube inserted. Techniques to improve the traditional partially withdrawn tracheal tube
method include:
oxygen insufflation via a catheter at the level of the carina
use of a microlaryngeal tube inserted to a level beyond the intended stoma site and
not withdrawn during tracheal puncture
tracheal tube through a laryngeal mask airway.
Aftercare
A newly created tracheostomy stoma is a surgical wound and should be treated
accordingly. High standards of aseptic technique should be maintained during wound
dressing. The stoma does not mature for 710 days. Every effort should be made to
ensure that the tracheostomy tube is secured in its correct position and is not being
pulled into unsatisfactory angles by the weight of ventilator tubing.
If displacement of the tracheostomy tube occurs within the first few days of creating
the stoma, replacing it may be impossible and the attempt may create a false passage.
It is much safer to re-intubate the patient and re-establish the tracheostomy under
controlled conditions. u
FURTHER READING
Ciaglia P, Firsching R, Syniec C. Elective Percutaneous Dilatational Tracheostomy.
Chest 1985; 87: 71519.
Freeman B D, Isabella K, Lin N, Buchman T G. A Meta-analysis of Prospective Trials

Comparing Percutaneous and Surgical Tracheostomy in Critically Ill Patients. Chest
2000; 118: 141218.
www.cookcriticalcare.com (Provides an illustrated tutorial).

Straight Laryngoscopy:
Function, Technique and
Design
John Henderson
John Henderson is Consultant Anaesthetist at the Western Infirmary, Glasgow,

UK. He trained at Glasgow Royal Infirmary, was a fellow in New York and staff
anesthesiologist in Boston. He has used awake fibre-optic intubation since 1977. He is
Guidelines Project Officer of the Difficult Airway Society.
Tracheal intubation under vision was originally performed with the straight
laryngoscope. Curved laryngoscopy with the Macintosh laryngoscope (introduced in
1943) became the standard technique because it was perceived to be less demanding
than straight laryngoscopy. There is increasing evidence that tracheal intubation can
be achieved under vision with the straight laryngoscope in most patients in whom this
is impossible with the Macintosh. Many of the complications of difficult intubation with
the Macintosh laryngoscope might be avoided if anaesthetists were skilled in straight
laryngoscopy.
Straight laryngoscopy has a good theoretical basis. All laryngoscopes are used to move
the tongue to the left and to elevate the epiglottis so that the vocal cords are revealed.
The normal relationship of the laryngeal cartilages and the hyoid bone is shown in
Figure 1a. Figure 1b shows the tip of the Macintosh laryngoscope in the vallecula, close
to the hyoepiglottic ligament. Elevation of the hyoid tensions the hyoepiglottic ligament
and thus elevates the epiglottis indirectly. Figure 1c shows the situation where no more
than the tip of the epiglottis is seen with the Macintosh laryngoscope. Some of the
bulk of the tongue remains trapped between the tip of the laryngoscope and the hyoid
bone, and the tip of the laryngoscope cannot enter the vallecula. The epiglottis cannot
be elevated and is displaced posteriorly so that it obstructs the potential line of sight of
the larynx. Figure 1d shows the position of the straight laryngoscope, introduced from
the side of the mouth, in such a patient. The tip of the laryngoscope is posterior to the
epiglottis, which is elevated directly. Theoretically, the straight laryngoscope performs
better than the Macintosh because of its ability to elevate the epiglottis directly in
difficult patients, and to improve the line of sight.
The technique of straight laryngoscopy is different from the Macintosh, and initial use
often proves difficult.
The laryngoscope is inserted and kept lateral to the incisors. The tip may pass
initially into the right pyriform fossa, so that medial movement of the tip is necessary.
Maximum mouth opening requires more deliberate
attention.
The tip of the laryngoscope is passed posterior to the epiglottis, which is elevated
directly.
Optimum depth of insertion (tip close to vocal cords) requires attention.
Vector of force applied to the laryngoscope handle is different.
Further information about the technique is available from the Further reading or, in more
detail, from the author.
The most widely used straight laryngoscope is the Miller. Passage of the tracheal tube
with the Miller laryngoscope can be difficult. The Belscope is angulated to reduce the
risk of dental damage. The Henderson laryngoscope shares with the Belscope an
atraumatic tip and a light that cannot be dimmed by secretions or soft tissues. The
cross-section of the Henderson laryngoscope is designed to facilitate passage of the
tracheal tube so that tracheal intubation is integrated with direct laryngoscopy in a
single rapid process. Optimal (paraglossal) technique with any of these laryngoscopes
has much to offer. Moderate expertise requires 50 or more initial intubations, followed
by continuing regular use. u
FURTHER READING
Henderson J J. The Use of Paraglossal Straight Blade Laryngoscopy in Difficult
Tracheal Intubation. Anaesthesia 1997; 52: 55260.
Henderson J J. Questions about the Macintosh Laryngoscope and Technique of

Laryngoscopy. Eur J Anaesthesiol 2000; 17: 25.
Henderson J J, Frerk C M. Remember the Straight Laryngoscope. Br J Anaesth 2002;
88: 1512.
Horton W A, Fahy L, Charters P. Factor Analysis in Difficult Tracheal Intubation:

Laryngoscopy-induced Airway Obstruction. Br J Anaesth 1990; 65: 8015.
Sofferman R A, Johnson D L, Spencer R F. Lost Airway during Anesthesia Induction:

Alternatives for Management. Laryngoscope 1997; 107: 147682.

Transtracheal Jet Ventilation
Ali Diba
Ali Diba is Consultant Anaesthetist at the Regional Burns/Plastics and Maxillofacial

Hospital in East Grinstead, West Sussex, UK. He qualified from Southampton
University. He is an expert in the management of the difficult airway. His interests
include critical care of burns patients and infusional anaesthesia.
Transtracheal jet ventilation (TTJV), also called needle cricothyroidotomy, is a simple,

safe and effective technique for ventilating apnoeic lungs electively or in an emergency.
No patient should suffer hypoxic injury as a result of failure to ventilate the lungs without
a competent attempt at TTJV having been made. Failure to ventilate still causes death
under anaesthesia. An incidence of about 1/10,000 is quoted for failure
to intubate associated with failed mask ventilation at anaesthesia.
Using dedicated equipment minimizes the chances of apparatus-related failure. Little

experience is necessary, however, familiarity encourages earlier use in an emergency
and allows a more confident approach to the difficult airway as a whole, especially if the
technique is available as a backup in case of failure of the first strategy for management
of the patients airway. A number of centres worldwide use TTJV electively for
peroperative ventilation.
History
In 1967, Sanders demonstrated ventilation of the lungs of anaesthetized patients using
high-pressure oxygen at bronchoscopy. Transtracheal ventilation was described in
1971 by Spoerel in India. In 1983, Layman reported TTJV, without complication, in 60
patients with gross pathology requiring oral surgery, using an intravenous catheter
inserted through the cricothyroid membrane. In 1985, Ravussin designed a dedicated
transtracheal catheter, which remains the device of choice.
Apparatus
Safety in TTJV depends on intratracheal placement of the catheter. The ability to freely
aspirate air from the catheter following insertion is paramount. Conventional plastic
intravenous cannulas tend to kink at the skin or within the trachea because of the acute
angle between skin entry and tracheal axis which may preclude this safety check and
decrease the efficiency of ventilation.
The Ravussin Jet Ventilation Catheter (VBM Medizintechnik GmbH, D-7247 Sulz a.N.
Germany) is available in 13 G for adults (Figure 1) and proportionately shorter 14 G
and 18 G versions for children and babies. It is made of Teflon, which is stiffer than
plastic and is gently curved with an angled connector, which when sitting flush on the
skin allows the catheter to point axially down the trachea without kinking. A Velcro strap
passed around the neck keeps the whole assembly firmly in place. A 15 mm diameter
ISO male connector around the Luer-Lock allows temporary low-pressure oxygen
insufflation from a conventional anaesthetic system.
1 Ravussin Jet Ventilation

Catheter for adults (13 G).
The TTJV catheter is connected to a high pressure (4 bar) oxygen source through a
Sanders injector. A variable outlet pressure version (Figure 2) is used for added safety
if the system might be used in children.
2 Variable pressure
injector.
A complete TTJV system should be available in all areas where anaesthesia is

administered or where unconscious patients may be admitted (Figure 3). It is not
feasible to assemble the equipment from disparate items when the need for TTJV is
identified in an emergency situation.
3 Difficult intubation trolley.
Low pressure gas, as delivered from the common gas outlet of an anaesthetic machine
(limited by the machine safety pressure relief valve or anaesthetic bag compliance to
320 or 80 cm H2O) and delivered through a narrow-bore transtracheal catheter will, at
best, provide temporary apnoeic oxygenation by providing gas flows of only 200 to 80
ml/s for a 14 G cannula. TTJV requires a high-pressure gas source and implies that
adequate gas exchange can be maintained.
For protracted ventilation, high frequency jet ventilators are available that allow the
driving pressure, breath rate and I:E ratio to be controlled individually. They can
measure end-expiratory intratracheal pressure through the ventilating cannula, thus
stopping subsequent breaths if gas egress from the lungs is obstructed.
Technique
The patients head is positioned as if for a tracheostomy with head and neck extension.
The trachea is most easily approached percutaneously through the cricothyroid
membrane, though lower cartilaginous interspaces are also practicable. The membrane
is best identified with the fingertip and nail and may be marked. An intradermal bleb of
local anaesthetic should be administered in the conscious patient, and this syringe and
needle can also be used as a seeker to confirm correct identification by easy passage
though the membrane and aspiration of air. Intratracheal lidocaine (lignocaine) is not
essential because the catheter tends not to irritate the airway.
A 5 ml syringe is attached to the catheter/needle assembly which is inserted in a slight

caudad direction with negative pressure maintained on the syringe plunger (Figure 4).
A slight give followed by further easy passage and aspiration of air signifies entry into
the trachea. The catheter should advance easily off the needle, which is then removed
(Figure 5). Further free aspiration of air from the catheter and a perfect end-tidal
carbon dioxide trace on gas sampled from the catheter in the breathing patient confirm
its position (Figure 6). The injector is then connected using Luer-Lock tubing and a
single test breath should be administered to test the integrity of the system. The awake
patient usually coughs at this stage, and all patients must be carefully observed for
chest deflation after each breath. If air cannot be aspirated from the catheter it must be
resited.
4 Needle insertion.
4 Needle insertion.
5 Withdrawal of cannula.
6 Checking catheter position.
In the elective situation anaesthesia can be induced, and jetting may proceed with
the following provisos. Pre-oxygenation guards against desaturation in the interval
between induction of anaesthesia and the onset of paralysis and jet ventilation.
Neuromuscular paralysis ensures there is no jetting against a forcibly closed glottis
risking barotrauma.
Appropriate craniocervical extension and/or jaw thrust allows an adequate expiratory
airway in most patients, even those with obstructing glottic lesions. An oral,
nasopharyngeal or laryngeal mask airway (LMA) may also be needed. There is no
record of a patient needing a second needle for gas escape, though this remains
an option. It is important not to ventilate while the airway contains anything that may
occlude the upper airway (e.g. the passage of a tracheal tube over a fibre-optic
endoscope).
A mannequin or dummy neck can be used to practise the technique (Figure 7).
7 Practising the technique on

a dummy neck.
Applications
TTJV, using a small diameter cannula, is preferable to tracheostomy in an emergency
because it is faster and simpler to perform and involves fewer complications.
Assuming the anterior neck can be accessed in an elective patient in the absence of
significant overlying tissue swelling or infection, TTJV may be indicated as an interim
manoeuvre (surgical access for tracheostomy is not impeded by TTJV) or as the
definitive airway management technique. The categories are not mutually exclusive.
Emergency/resuscitation: TTJV can be used in the cant ventilate, cant intubate

situation; where there is failure to intubate the trachea and established failure to
ventilate the lungs by other means (such as face mask or LMA) owing to abnormal
anatomy, trauma or disease.
Elective: TTJV alone is appropriate for airway management for suspension

microlaryngoscopy, endoscopy, tracheal surgery, or laser surgery of the airway.
If there is uncertainty about the ability to maintain airway competence following

induction of anaesthesia TTJV may be used as an alternative to awake intubation.
Siting a TTJV catheter in the awake patient secures the ability to ventilate the lungs
following induction. This does not require confidence with local anaesthetic techniques
or patient cooperation and allows safe, unhurried and comfortable airway instrument-
ation for patient and anaesthetist. In children with orofacial tumours for example, the
cannula may be sited under ketamine sedo-analgesia allowing fibre-optic intubation
under general anaesthesia with muscle relaxation. This combination constitutes a
powerful technique.
TTJV may be used as an alternative to a surgical airway if fibre-optic intubation is

inapplicable, for example because of airway soiling by blood or obstructing laryngeal
tumours with pinhole trachea. Awake tracheostomy is a difficult procedure even for
the experienced head and neck surgeon; it may be impossible in the patient needing to
sit to struggle to breathe or spit out blood. Siting a TTJV catheter is easier and permits
tracheostomy or tumour resection to be carried out under general anaesthesia. Debris
and blood tend to be blown out of the oropharynx.
Complications
The most common problem is failure to cannulate the trachea. Use of curved cannulas
and other manoeuvres aimed at getting the catheter to lie axial to the trachea tend to
make cannulation more difficult, but ultimately increase safety and success.
There are no reports of problematic haemorrhage, though TTJV is not advised if

there is involvement of the anterior neck or trachea in vascular malformations. A small
dried rivulet of blood in the trachea on endoscopy is not uncommon following catheter
insertion.
The sequence of barotrauma, pneumothorax, pneumo-mediastinum and subcutaneous

emphysema usually follows failure to ensure a clear expiratory pathway during surgical
instrumentation and is more common in children. Meticulous technique, a high index
of suspicion and prompt treatment mitigate against this complication becoming a
catastrophe.
A dry cough is often reported after TTJV. The tiny puncture site normally seals on
removal of the catheter. Pressure should be applied to the site to prevent subcutaneous
emphysema.
There are no specific recognized late complications of perioperative TTJV. u
FURTHER READING
Benumof J L. Management of the Difficult Airway. Anaesthesiology 1991; 75: 1087110.
Benumof J L, Scheller M S. The Importance of Transtracheal Jet Ventilation in the

Management of the Difficult Airway. Anaesthesiology 1989; 71: 76978.
Layman P R. Transtracheal Ventilation in Oral Surgery. Ann R Coll Surg Engl 1983; 65:
31820.
Ravussin P, Freeman J. A New Transtracheal Catheter for Ventilation and

Resuscitation. Can Anaesth Soc J 1985; 32: 604.
The Difficult Airway Society (of UK). Techniques of Difficult Airway Management.
CDROM 1998.

Ethics
Anaesthesia
on CD-ROM
Clinical Governance
Gregor Imrie
P G M Wallace
Gregor Imrie is Specialist Registrar in Anaesthesia at the Western Infirmary, Glasgow,

UK. His subspecialty is intensive care medicine.
P G M Wallace is Consultant Anaesthetist at the Western Infirmary, Glasgow, UK. He

is President of the Association of Anaesthetists of Great Britain and Ireland and past
President of the UK and Scottish Intensive Care Societies.
Britains National Health Service (NHS) was constituted in 1948 as a universal system,
funded predominantly by taxation, to provide healthcare without financial barriers to
access. At its inception it was essentially a paternalistic service where the professionals
delivering the care defined the needs of patients and set up services to meet those
needs. The expectation was that high individual professional integrity and competence
would lead to a high quality service. This system served the country well for several
decades, however, various attempts have been made by successive governments to
improve the NHS. These initiatives have been driven by rising public expectations over
the lifetime of the service. In recent years, added impetus for change has developed as
a consequence of high profile failures within the NHS (e.g. paediatric cardiac surgery in
Bristol).
Clinical governance is the centrepiece of the latest government initiative aimed at

improving the NHS. It was first described in the White Paper of 1997 The New NHS.
It builds on several previous national quality initiatives (Figure 1). While high individual
professional standards remain essential for a good quality service, clinical governance
aims to instil an overall ethos of corporate responsibility to improve quality of care in the
NHS.
History of national quality initiatives
Resource management 1980s

Medical audit 1989
Patients Charter 1993
Clinical guidelines 1993
Clinical effectiveness 1995
Clinical governance 1997
Definition
Almost anything done under the name of quality in the NHS may now come under
the clinical governance umbrella. As a result of a lack of an intuitive meaning to
the term, and partly owing to its enormous scope, it has proved difficult to give a
clear definition of clinical governance. The most widely used definition, and the one
quoted by government agencies is Clinical governance is a system through which
NHS organizations are accountable for continuously improving the quality of their
services and safeguarding high standards of care by creating an environment in which
excellence in clinical care will flourish.
Alternatively, in 1998, Sam Galbraith MP gave a statement, which touches on the role
of clinical governance in meeting the rising public and political expectations of the
NHS. Clinical governance is the vital ingredient that will enable us to achieve a health
service in which the quality of healthcare is paramount. The best definition that I have
seen of clinical governance is simply that it means corporate accountability for clinical
performance. Clinical governance will not replace professional self-regulation and
individual clinical judgement, concepts that lie at the heart of healthcare in this country.
But it will add an extra dimension that will provide the public with guarantees about
standards of care.
A more succinct definition is Clinical governance is corporate responsibility for clinical

performance.
Responsibility
Clinical governance applies to all patient services in the NHS. The statutory duty to
seek quality improvement through clinical governance rests with Trust chief executives.
The governments aim is to ensure that quality of care is as important as financial
matters at Trust board level. Trust chief executives are now expected to:
ensure a culture in which the highest standard of clinical care is the responsibility of
everyone in the organization
introduce structures and processes that allow this to happen.
These duties are considerable and delegation is required. A degree of local discretion is
allowed in how this is achieved but a common model is as follows.
Individual doctors remain responsible for their clinical decisions.
Departmental heads and clinical directors have responsibility for quality of care in
their directorate and they report on quality issues to a clinical governance
committee.
This committee assumes oversight of the clinical governance activities of the Trust.
It should ensure that the appropriate structures for clinical governance are in place
and that they work well.
The clinical governance committee reports directly to the Trust board and chief
executive.
Trusts are assessed by the national bodies described below.
Key components of clinical governance at Trust level

It is hoped that by adherence to the key tenets of clinical governance (reviewed below)
at a local level, Trusts will have well trained and motivated staff producing safe and
effective evidence-based care; and as a consequence of good communication, patients
will be well informed and involved in the decisions regarding their care.
Education, training and professional development of staff: good quality healthcare

depends on the quality of staff. Time should be set aside for staff education, training
and continuing professional development. This has important resource implications for
Trusts.
Evidence-based clinical practice: Trusts should ensure that the care they deliver
is based on the best available evidence. Systems should be in place for receiving,
distributing and implementing evidence-based guidelines as they are published.
Adherence to evidence-based practice must be audited (see below).
Clinical audit requires:

structured review by clinicians of their practice and results against agreed standards
sharing of audit results across clinical teams
modification of care as dictated by the results of audit
remonitoring to ensure quality of care has improved.
Trusts should ensure that good audit systems are in place. This requires investment in
information technology systems and extra staff to facilitate the process.
Risk management: Trusts must have established protocols to identify adverse events.
A blame-free culture in which to report adverse events should be cultivated. Structures
to allow identification of patterns, and the initiation of prompt change should be in
place. Risk management within Trusts should be pro-active and lessons painfully learnt
in other parts of the health service should be applied locally. Risk management staff
may be useful in designing systems to minimize risk. Trusts should also aim to reduce
problems and complaints by means of good communication.
Communication with patients and relatives: poor communication is regularly

highlighted as a cause of patient dissatisfaction. Trusts should provide training in
communication skills for their staff and ought to factor in the time required for good
communication when planning staffing levels. The development and provision of
information leaflets can aid staff in this activity. Trusts should encourage comments
and suggestions from patients and relatives regarding the services they provide and
institute change as necessary.
Complaints procedures: there should be accessible, well-publicized complaints

procedures available to patients and relatives. Good clinical governance requires
thorough investigation of complaints in an environment that is supportive of the staff
involved.
Tackling poor clinical performance: while only a part of clinical governance, this
is the area most associated in doctors minds with the concept. It has been widely
recognized that the pre-existing regulatory systems have, on occasion, failed to
detect and correct poor clinical performance at an early stage. Extensive new national
regulatory measures are being developed to reduce this problem. Despite these
measures it remains probable that other doctors in a department will be the first to note
a colleagues poor performance or conduct. Anaesthetic departments should aim to
be vigilant in detecting, correcting and supporting their poorly performing members.
If good structures are in place it may be possible to correct poor performance before
it has a major impact on standards of care. The Royal College and the Association of
Anaesthetists have published useful guidance for departments in this area.
Support structures for clinical governance: Trusts should have a simple clinical
governance chain of command so there is clarity about who is doing what within the
Trust. Clinical governance support staff have in the past been appointed in a rather
scattergun fashion (e.g. separate staff for clinical audit, risk management and clinical
effectiveness). Such staff should be integrated into a single clinical governance
department to increase their effectiveness.
Major national components

With the inception of clinical governance a significant regulatory and support industry
has developed. These structures are not fully established and continue to evolve. The
major organizations with associated websites are listed in Figure 2. Their present roles
are described below.
Organizations with major roles in clinical governance
General Medical Council www.gmc-uk.org

Revalidation www.revalidationuk.info
Royal College of Anaesthetists www.rcoa.ac.uk
Association of Anaesthetists of www.aagbi.org

Great Britain and Ireland
Department of Health www.doh.gov.uk

Appraisal www.appraisaluk.info
National Service Frameworks www.doh.gov.uk/nsf
Clinical Governance Support www.cgsupport.org
Team
National Clinical Assessment www.ncaa.nhs.uk

Authority
National Institute for Clinical www.nice.org.uk

Excellence
Commission for Health www.chi.nhs.uk

Improvement
National Patient Safety Authority www.npsa.org.uk
Scottish Intercollegiate www.sign.ac.uk

Guidelines Network
Health Technology Board for www.htbs.co.uk

Scotland
Clinical Standards Board for www.clinicalstandards.org

Scotland
Clinical Resource and Audit www.show.scot.nhs.uk/crag

Group
Clinical Resource Efficiency www.n-i.nhs.uk/crest

Support Team
Appraisal
Appraisal was introduced by the Department of Health with the support of the medical
profession in April 2001. On an annual basis, trained appraisers will review the activities
of the doctor being appraised; agree with him key objectives for the following year
and outline the doctors requirements of his employer to allow him to achieve these
objectives.
The main objective of appraisal is to encourage continuing professional development

but it also incorporates elements of performance review. The appraisal is based around
the main tenets of the General Medical Council document Good Medical Practice.
All consultants in England should have undergone appraisal by April 2002. This
deadline was not met, but following the completion of consultant appraisal it is planned
to introduce appraisal for all other grades of NHS doctor.
General Medical Council (GMC) and revalidation

The GMC was set up in 1858 and its regulatory role in maintaining standards in the
medical profession is long established. More recently, disquiet has been expressed by
the profession, government and the public that the GMC could be more effective. In
response, the GMC has examined its structures and proposes to develop an additional
regulatory system for doctors. The GMC plans that all doctors will have to demonstrate,
on a regular basis, that they remain fit to continue in medical practice a process it has
termed revalidation.
Revalidation involves an assessment against a standard fit-ness to practise and will

result in the renewal or withdrawal of a doctors licence to practise medicine after each
revalidation process. Revalidation will take place every 5 years. The full details of
revalidation are yet to be decided. As appraisal and revalidation will be based largely
on the same sources of information, appraisal summaries are likely to be used in the
revalidation process.
Government and the GMC expect the legislation to make revalidation mandatory to be
passed in December 2002. If pilot schemes are successful revalidation will commence
2 years after this date.
The medical Royal Colleges

The individual Royal Colleges have long guided and supervised consultants and
trainees in achieving and maintaining high standards activities that now come under
the clinical governance umbrella.
The Royal College of Anaesthetists, often in conjunction with the Association of

Anaesthetists of Great Britain and Ireland, has been active in this regard. Major
examples of their clinical governance activities include:
assessment of trainees core competencies as they progress through training
the good practice guide for departments of anaesthesia
publication of guidelines for anaesthetic practice
an obligatory continuing educational and professional development programme for
consultants
publication of patient information materials (e.g. on pain relief in labour)
support for critical incident reporting.
The new clinical governance ethos should put more weight behind College initiatives.
In theory, as a result of clinical governance, managers will be more willing to fund the
quality of care and safety measures that the College advocates (e.g. the removal of
anaesthetic machines that can deliver a hypoxic mixture).
National Clinical Assessment Authority (NCAA)

The NCAA was established in April 2001 as a support service for employers of doctors
whose performance is giving cause for concern. Its budget for 20022003 is 10.1
million.
The NCAA will consider referrals from employers (or self-referrals by doctors) on the
full range of potential performance difficulties (i.e. clinical, behavioural and health
matters). When a referral is received, the NCAA will:
offer support and advice aiming for a local solution
if this fails it will move to a formal assessment of the doctors performance
after assessment, a plan of action is recommended which might involve, for
example, re-education or a change in working environment
while it would hope to facilitate local resolution of problems, appropriate referral will
be made if its assessment reveals matters that require investigation by the GMC or
CHI.
Formal assessment of doctors began only in April 2002 and the role of the NCAA is not
yet fully established. However, it does appear to have the advantage of being a half-
way house where problems can be identified and tackled at an early stage before a
major breakdown in quality of service occurs or before suspension and referral to the
GMC become mandatory.
National Institute for Clinical Excellence (NICE)

NICE was set up in April 1999. Its budget in the tax year 20012002 was 10.6 million.
It is the main national facilitator for clinical governance issues. The functions of NICE
are to:
issue guidance on the full range of health technologies including drugs, medical
devices and surgical techniques
produce guidelines on the management and care of specific conditions
oversee the four confidential inquiries (Confidential Inquiry into Maternal Deaths,
Confidential Inquiry into Stillbirths and Deaths in Infancy, National Confidential
Inquiry into Perioperative Deaths, Confidential Inquiry into Homicide by People with
Mental Illness)
advise on audit methodology and in particular to advocate audit of how well the
advice it gives is adhered to.
The guidance produced by NICE is based on cost and clinical effectiveness. Adherence
to its advice should contribute to an improvement in standards of care nationally and
reduce regional variations in care.
National Service Frameworks (NSF)

The Department of Health instituted a rolling programme of NSF in 1998 as part of the
clinical governance initiative. NSF set national standards to be attained in a particular
area. There are, for example, NSF for coronary heart disease and for the elderly.
They are broad in scope and of strategic importance. Usually only one new framework
is published a year. They aim to drive improvement in standards of care across the
country. NSF can impact on anaesthetic services by setting objectives that departments
need to plan for and accommodate, for example the Older People NSF states that
patients with fractured hips should have repair carried out by experienced staff within
24 hours of admission.
Commission for Health Improvement (CHI)

The CHI was established in November 1999 as the principal regulator of the clinical
governance initiative in England and Wales. Its budget in the year 20012002 was
24.5 million. Its main roles are to:
assess every NHS organization on a 4 yearly basis by means of a detailed clinical
governance review, the results of which are published
monitor the implementation of the national guidelines produced by NICE and NSFs
investigate system failures within the NHS at local, regional and national level.
One of CHIs strengths is that its reports achieve national prominence, particularly
when they include adverse findings. They are a strong impetus to improvement
when services are found wanting. CHIs recommendations have to be enforced by
Health Authorities and the National Assembly of Wales.
Clinical Governance Support Team (CGST)

The CGST was established in September 1999 to support the implementation of clinical
governance across the NHS in England. To date it has educated 400 teams from NHS
organizations on clinical governance issues under its Clinical Governance Development
Programme. Among other activities, it publishes on its website the details of successful
local clinical governance schemes, and operates a Trust board level development
programme.
National Patient Safety Authority (NPSA)

The NPSA was established in July 2001 to provide national leadership on patient
safety and adverse event reporting. Its budget for 20022003 is 15 million. It will
establish and operate a mandatory national system for reporting adverse events and
near misses. This information will be collated and distributed to allow the early initiation
of preventative measures throughout the NHS. It is hoped by these means to prevent
recurrence of tragedies such as the intrathecal injection of vincristine (at least 13
patients are known to have died or been paralysed since 1985).
Organizational variations in the UK

Appraisal, under the auspices of the Department of Health, applies to doctors in
England. Similar appraisal systems are being instituted in the rest of the UK.
The GMC and the Royal College of Anaesthetists operate throughout the UK.
NICE, CHI and the NPSA operate in England and Wales. NSFs apply to England.
The CGST and NCAA apply to England only, but it is probable the Welsh Assembly
will accept their roles.
In Scotland, though there is not an exact duplication of systems, similar roles to CHI
and NICE are performed by the Clinical Standards Board for Scotland, aided by the
Scottish Intercollegiate Guidelines Network, the Health Technology Board for Scotland,
and the Clinical Resource and Audit Group. In 2003, these bodies, with the exception of
the Scottish Intercollegiate Guidelines Network, together with the Scottish Health
Advisory Service and the Nursing Midwifery Practice Development Unit will
amalgamate to form NHS Quality Improvement Scotland.
In Northern Ireland, the Clinical Resource Efficiency Support Team has published
guidelines and audited services since 1988. An extensive review of health service
provision is nearing completion which may lead to the introduction of further clinical
governance measures. u
FURTHER READING
Bristol Royal Infirmary Inquiry. Learning from Bristol: the Report of the Public Enquiry
into Childrens Heart Surgery at the Bristol Royal Infirmary 19841995. London:
Stationery Office, 2001.
General Medical Council. Good Medical Practice. London: GMC, 2001.
Goodman N W. Sacred Cows Clinical Governance. Br Med J 1998; 317: 17257.
Halligan A, Donaldson L. Implementing Clinical Governance: Turning Vision into

Reality. Br Med J 2001; 322: 141317.
Klein R. Whats Happening to Britains National Health Service. New Engl J Med 2001;
345: 3058.
Walshe K. The Rise of Regulation in the NHS. Br Med J 2002; 324: 96770.

Consent: Ethical Considerations
Nick Pace
Nick Pace is Consultant Anaesthetist at Western Infirmary, Glasgow. He qualified

from Glasgow University and trained at the Glasgow Western and Royal Infirmaries,
University Hospital of South Wales and Parkland Memorial Hospital, Dallas, Texas. His
interests include airway management and anaesthesia for renal and adrenal diseases.
He is currently completing a PhD in medical law.
The relationship between doctor and patient is not uniform. Ethical codes of conduct
and laws of consent, confidentiality and negligence vary according to the role played by
the doctor and the objective of the contact between patient and doctor.
In the therapeutic model the relationship is therapeutic and the doctors main
objective is the well-being of the patient and improvement in that patients health.
In the research model the relationship changes and the doctors aim is the
accumulation of medical knowledge. The benefits are designed to aid future patients,
though there is potential for the research subject to obtain benefit.
In the relationship between an occupational health doctor and a patient, the doctors
duty is to his employer and not necessarily to the patient.
Rapid developments in medicine have been accompanied by a tendency for patients

to ask for greater involvement and control over what happens to them. Physicians and
other healthcare professionals do not have a right to do anything to patients without
their consent because the right to consent to or to refuse treatment is grounded in the
ethical principle of respect for autonomy. A feature of our society is the emphasis on
the value and dignity of the individual. Principles of inherent natural rights dictate that
a competent person should decide what happens to his or her body. All medical codes
of ethics now hold that physicians must obtain the informed consent of patients and
subjects before undertaking procedures.
Informed consent
The concept of informed consent needs clarification. Various commentators have
reduced the concept to shared decision-making between doctor and patient, so that
informed consent and mutual decision-making are identical ideas. The British Medical
Association, for example, states that the relationship between doctor and patient is
based on the concept of partnership and collaborative effort. Decisions should be
made through frank discussion, in which the doctors clinical expertise and the patients
individual needs and preferences are shared, resulting in the selection of the best
treatment option. Patients are therefore actively involved in deciding what is to be done
to them.
For the patients consent to be a valid authorization for the professional to proceed,
it must be based on understanding and must be voluntary. Because of the unequal
distribution of knowledge between professionals and patients the principle of respect
for autonomy entails that professionals have a prima facie obligation to disclose
information, to ensure understanding and voluntariness, and to foster adequate
decision-making. Thus, the information component can be said to consist of adequate
disclosure followed by the understanding and comprehension of what is disclosed. The
consent component, in turn, refers to a voluntary decision-making process which is
followed by authorization. Therefore, informed consent can be analysed in terms of the
elements in Figure 1.
The elements of informed consent
Threshold element
Competence
Information elements
Disclosure of Information
Understanding of information
Consent elements
Voluntariness
Authorization
1
Competence
Competence is a precondition of being able to give consent. It is closely tied to
autonomy. Law, medicine and to some extent philosophy presume a context in which
the characteristics of the competent person are also the properties possessed by the
autonomous person. Although autonomy and competence are different in meaning
(autonomy meaning self-governance and competence meaning the ability to perform a
task), the criteria of the autonomous person and of the competent person are strikingly
similar. Thus an autonomous person is necessarily a competent person. A person
is thus generally competent to authorize or refuse to authorize an intervention if and
perhaps only if that person is autonomous.
Disclosure
There is a requirement for doctors to inform the patient about the material risks of a
planned procedure or intervention. However, the patient is not compelled to accept or
refuse the treatment that is offered. The patient should be allowed to choose the type
and scope of treatment and to base this choice on adequate information about success
rates and risks. It is impossible for a health professional to give all available information
to the patient. It is not the doctors role to provide a list of alternatives from which the
patient selects options, according to their need and desires. Ideally, the doctor should
inform the patient about any risks in the treatment that may be particularly important
to that patient, as well as explaining the risks and benefits of alternatives and of
non-treatment. Without an adequate transfer of information from doctor to patient
there is insufficient information for decision-making. However, the professionals
own perspective, opinions and recommendations are often essential for the patients
deliberation, as well as for mutual understanding.
Professionals are generally obliged to disclose a core set of information. This
includes:
those facts or descriptions that patients or subjects usually consider material in
deciding whether to refuse or consent to the proposed intervention or research
information the professional believes to be material
the professionals recommendation
the purpose of seeking consent and the nature of consent as an act of authorization.
Despite these general recommendations, controversy surrounds the issue of what

should be disclosed about a procedures risks and negative consequences, as well as
about the nature and purpose of the procedure, its benefits and alternative procedures.
Should a health professional discuss all the alternatives, including those considered
too risky? For example, consider an operation in which a Tenckhoff catheter is inserted
into the abdomen to allow peritoneal dialysis in a patient with renal failure. Several
anaesthetic techniques may be used to allow this operation to proceed including
general anaesthesia, infiltration of local anaesthetic by the surgeon, or an epidural or
spinal anaesthetic administered by the anaesthetist. If the general anaesthetic option
is taken, should one insert a laryngeal mask airway (LMA) or intubate the patient? If
an LMA is inserted, should one use muscle relaxants? Time does not allow a detailed
discussion of all the available options with the patient. Thus, the usual attitude is
to discuss none of the options, possibly infringing the requirement for information
disclosure and thus infringing the patients autonomy. However, a recent personal audit
has shown that patients require very little information from their anaesthetist. Indeed,
the most common preoperative question concerned the duration of the anaesthetic.
Despite this, it is clear that the more serious the risk or harm done to the person the
greater the degree of information required. The legal standards that govern disclosure
of information are discussed on page 426.
Understanding
Informed consent implies a duty to disclose information; however, it may be better to
use the term comprehend because the information disclosed may not be understood.
Increasingly, the ethical focus is changing from the doctors obligation to disclose
information to the quality of a patients or subjects understanding and consent.
Understanding, therefore, is a more important element than disclosure and arguably

the most important element in the process of obtaining informed consent. The key
to effective communication, understanding and decision-making is participation by
patients in an exchange of information. Ordinarily, a professional has only limited
insight into the distinct values, fears, hopes and information needs of others. Asking
questions, eliciting the concerns and interests of the patient, and establishing a climate
that encourages the patient to ask questions may be more important to the persons
understanding than a mass of disclosed information.
Clinical experience and empirical testing indicate that patients exhibit wide variations in
their understanding of information about diagnoses, procedures, risks and prognoses.
For example, in one study up to 44% of postoperative patients who signed consent
forms were unaware of the exact nature of the procedure they had undergone. This also
highlights the dubious usual practice of allowing the most inexperienced member of the
surgical team to explain the operation to the patient and get consent.
Although some patients are calm, attentive and eager for dialogue, others are nervous
or distracted in ways that impair or block understanding. Many conditions, other than
lack of sufficient information, can limit their understanding, such as illness, irrationality
and immaturity.
It has been argued that patients cannot comprehend enough information or appreciate
its relevance sufficiently to make informed decisions about medical care. Ingelfinger
stated that the chances are remote that the subject really understands what he has
consented to.
There may be many reasons for this. Doctors and patients may use the same word
but it may have different meanings to them. Fasting, for example, may mean to the
patient do not take any food, thereby allowing them to drink as much liquid as they
like. Enabling a patient to comprehend and appreciate risks and benefits can be a
formidable task. It can be difficult for patients to appreciate the projected expectations
of, for example, pain in labour or following surgery.
Patients presenting at antenatal clinics often state they wish to have a completely
natural childbirth. This is clearly documented in the case notes, with the staff forbidden
to use painkillers or epidural injections. However, once the contractions (and pain) set
in, all that was previously stated is quickly forgotten and pain relief demanded. In this
situation, can the previous refusal (illustrating respect for autonomy) be overridden?
Let us assume for a moment that severe pain can make ones choices irrational and
hence make one incompetent (a debatable point). It could be claimed that, because of
the pain, the patient is no longer able to make a rational decision and, from a respect
for autonomy, the healthcare staff should not administer painkillers. In such a situation,
clearly, the principles of beneficence (do good) and non-maleficence (do not cause
harm) would overcome any principle for respect for autonomy, leading to painkillers or
an epidural being administered, to the obvious comfort of the patient. The point is that it
may be difficult for patients to appreciate the nature and degree of pain in advance and
thus they cannot fully understand what they are refusing.
Similar arguments can be applied to the appreciation of risks. The general public has
a poor understanding of the probabilities of something occurring. Indeed, preferences
can be affected simply by framing outcome in terms of probability of survival instead
of probability of death, described as a cognitive illusion. If a misconception occurs
regarding a particular risk which is material to decision-making, it implies that adequate
understanding was not attainable and thus an autonomous authorization was not
given. Even the amount of information that can be meaningfully processed is limited.
Information overload may be as likely to lead to uninformed decisions as failure to
disclose. This is the reason research ethics committees request research information
sheets to be as short as possible and written in laymans terms.
Thus, the requirement of an ideal standard of full disclosure and full understanding
cannot be attained. However, because actions are never fully informed, voluntary or
autonomous, it does not follow that these actions are never adequately informed, free,
or autonomous. It is clear that understanding does not need to be full or complete,
because a substantial grasp of central facts and other descriptions is often
sufficient.
It is also interesting to note what Beauchamp and Childress claim would be ethically
acceptable if a patient has an unreasonable belief. For example, a patient may refuse
a life-saving operation because of an irrational belief that he or she will die under
anaesthesia, based on the fact that a relative died in similar circumstances. There may
be overwhelming medical evidence that such a belief is unjustified. 'The position does
not imply that we should never coerce patients or subjects to change their beliefs or to
process information differently. If a patients or subjects autonomy is limited by his or
her ignorance, as in the case of a false belief a patient has difficulty in surrendering, it
may be legitimate and even obligatory to promote autonomy by attempting to impose
the information on a patient who finds it unwelcome. And if this proves impossible, the
principles of beneficence and non-maleficence may still justify overriding the patients
non-autonomous choices.'
Voluntariness
Voluntariness is the condition of a patient being independent of manipulative and
coercive influences exerted by others in order to control that person. There are degrees
of influence and three primary categories have been described: coercion, manipulation,
and persuasion. Coercion occurs when one person intentionally uses a credible and
severe threat of harm or force to control another. This entirely compromises autonomy.
At the other end of the spectrum lie weak forms of influence such as rational
persuasion. Here a person is convinced to agree to something through the merit
of reasons advanced by another person. Such situations are probably common in
the doctorpatient relationship. Manipulation means getting people to do what the
manipulator wants by means other than coercion or persuasion. For the purposes of
decision-making in healthcare, the most important form of manipulation is informational
manipulation, a deliberate act of managing information that successfully influences
a person by non-persuasively altering the persons understanding of a situation and
thereby motivating the person to do what the agent of influence intends. Some forms of
informational manipulation are incompatible with informed consent. For example, this
could occur if clinicians withhold information not because of non-maleficence but to
manipulate patients into agreeing to their recommendations.
It is easy to inflate the threat of control by influence beyond its proper significance. Most
decisions in life are made in the context of competing influences, such as wants, needs,
familial interests, legal obligations and persuasive arguments. Although significant,
these influences may not be controlling to any substantial degree.
From a clinician's point of view, although there is an obligation to abstain from

controlling influences, there can be occasions when doctors are blameworthy if they
do not attempt to persuade resistant patients to pursue treatments that are medically
essential. This reasoned argument may be vital to ensuring understanding and should
never be considered an unjustified form of influence.
The future
The issue of informed consent within medical practice is coming to the fore as the
balance of power in the doctorpatient relationship moves relentlessly towards patients.
Doctors will have to learn to inhabit the complicated world in which
philosophers feel comfortable. The question whether contemporary medicine and
research should always be held to the standard of autonomous decision-making is
not easy to answer. Respect for patient autonomy is generally regarded as one of the
central ethical principles in medical practice. Many would claim a moral imperative of
respecting human autonomy in almost all circumstances, and that failing to respect
the autonomy of competent people is to inflict harm on them that is just as morally
unacceptable as direct physical or mental harm. However, making respect for autonomy
a trump moral principle, rather than one principle in a system of principles, places an
inappropriately high premium on autonomy. It is not the only principle and should not
be overvalued when it conflicts with other values. In certain situations it may take on a
secondary importance and other moral principles may outweigh it. However, it is clear
that such situations are limited. u
FURTHER READING
Beauchamp T L, Childress J F. Principles of Biomedical Ethics. 4th ed. Oxford: Oxford
Doyal L. Informed Consent A Response to Recent Correspondence. BMJ 1998; 316:

10001.
Ingelfinger F J. Informed (but Uneducated) Consent. New Engl J Med 1972; 287: 465
6.
McNeil B J, Pauker S G, Sox H C, Tversky A. On the Elicitation of Preferences for

Alternative Therapies. N Eng J Med 1982; 306: 125962.
Smith R. Informed Consent: Edging Forwards (and Backwards). BMJ 1998; 316: 949
51.

Consent and Malpractice
Litigation
Nick Pace
Nick Pace is Consultant Anaesthetist at Western Infirmary, Glasgow. He qualified

from Glasgow Univeristy and trained at the Glasgow Western and Royal Infirmaries,
He is currently completing a PhD in medical law.
Malpractice litigation has numerous functions. It provides an incentive to practitioners to

maintain a high standard of care, though the law is mainly concerned with guaranteeing
that a minimal level of competence is achieved. It allows injured parties to bring a
malpractice action as a way of gaining retribution against health professionals, who they
believe, need to be punished for harming them. It may also lead to compensation. One
of the most important reasons that leads to a legal action being brought is a quest for
an explanation of what went wrong.
To win a negligence case the plaintiff (i.e. the patient) is required to prove three things:
that a duty of care existed and the professionals sued were responsible for the
victims care at the time of the mishap
that the professionals failed to reach the accepted standard of practice required by
law
that the injuries they suffered were caused by the failure to practise properly.
If successful, the patient is entitled to damages.
Duty of care
Establishing a duty of care is not usually a problem when patients are in hospital.
The anaesthetist is clearly responsible and has a duty of care to the patient being
anaesthetized. However, there are limits to duty of care. For example, in the UK,
professionals who pass a road traffic accident have no legal obligation to stop and
assist anybody who has been injured, though they may have a professional obligation
to do so.
Accepted standard of practice

In most cases of medical negligence the key question is whether the professional
failed to reach the standard of care required of them by law. That standard was first
established in Scotland in the case of Hunter v. Hanley (1955) and 2 years later in
England in the case of Bolam v. Friern HMC (1957). In the Hunter case a hypodermic
needle broke during an injection and the plaintiff alleged failure to use a suitable
needle. The Bolam case concerned the failure of use of muscle relaxants to control the
violent convulsions and spasms during ECT. In both cases it was held that a doctor was
not guilty of negligence if he acted in accordance with a practice accepted as proper
by a responsible body of medical men skilled in that particular art. In other words,
doctors are judged against the standards of their peers. Therefore, if experts from
the defendants profession are prepared to accept that the actions were proper, the
negligence claim will fail. The experts merely have to regard the defendants actions as
being within the range of acceptable practice. This means a minimal level of acceptable
practice, not what the expert would have liked to happen.
This implies that medical experts establish the standard of care and not the courts,
with determination of the legal duty being left to the judgement of doctors. However,
there are suggestions that the law is slowly moving away from this view. In the case
of Sidaway v. Bethlem Royal Hospital Governors (1985; discussed later) the court
reserved the right to decide that even standard practice may be negligent. Similarly,
the recent court of appeal case of Bolitho v. Hackney HA (1993) indicated that judges
are becoming less reluctant to set standards for doctors. Here Farquaharson noted the
possibility of an accepted medical practice being held to be negligent because it put the
patient unnecessarily at risk.
Current interpretation seems to be that the fundamental principle is that medical

negligence is to be judged against the standards of the medical profession through
the evidence of medical experts. This expertise is to be overridden when the medical
experts hold views that the judges believe no reasonable doctor could hold.
The rule of acceptable practice applies to other areas of practice. For example, when
professionals attempt to do something that they are not qualified to do, the failure to
refer the patient to someone properly skilled may be negligence (Wilsher v. Essex
AHA, 1996). The development of hospital policies may also have a significant impact
on the way in which the standard of care is defined. It is easier to prove that health
professionals have been negligent if they have failed to follow policies or protocols.
Such protocols are usually designed to clarify acceptable practice and guard against
risks by incorporating suitable safeguards. However, a departure from such a guideline
or policy does not automatically mean that the person is negligent. It suggests that
unless the circumstances indicate that there were good reasons for departing from the
usual practice the professional will be found liable. Failing to provide such a justification
indicates negligence.
In certain cases, the fact that a particular accident happened is held to be so obviously
negligent that it requires the defendants to rebut the presumption that they were in
breach of their duty. This maxim, res ipsa loquitur (the mishap is said to speak for
itself), can be of particular significance in cases were the treatment is complex or
the plaintiff is unconscious and is thus of particular importance to anaesthetists. In
Saunders v. Leeds Western Health Authority (1985), a 4-year-old child suffered a
cardiac arrest during an operation to correct a congenitally dislocated hip and became
quadriplegic, mentally retarded and blind. At the trial, evidence was given that the heart
of a fit child does not arrest under anaesthesia if proper care is taken. The plaintiff
did not need to show what act or omission had caused the arrest. The defendants
explanation of a paradoxical air embolism was rejected and the court found in favour of
the plaintiff. The defendants had been negligent.
Cause of the injuries

The third step in proving a negligence claim is showing that the failure to provide a
satisfactory standard of care was the cause of the victims injuries. Unless this can be
proved, the claim will fail, even if the defendants were clearly at fault. Where the injury
is caused by the care a health professional gives, such as severing a nerve during the
course of an operation, it is easy to show that the professionals actions caused the
injury. However, it is more difficult in cases in which the patient claims their underlying
complaint should have been cured or alleviated but was not. Often it cannot be proved
that the patients injuries were not a result of natural causes, such as the underlying
medical problems or an unavoidable accident.
Criminal charges
In most circumstances, malpractice is the concern only of the civil law. However, in
extreme cases there may also be criminal implications. For example, if a mistake
causes the death of a patient, the health professional could be prosecuted for
manslaughter. For this to occur, there must have been gross negligence not merely
negligence. A recent determination has been that of the anaesthetist Dr Adomako in the
House of Lords. He failed to notice that for over 4 minutes a tracheal tube had become
disconnected during an operation under general anaesthetic. An alarm sounded but
the connection of the tube was not checked until the patient had suffered a cardiac
arrest. One expert prosecution witness stated that a competent anaesthetist should
have spotted the problem within 15 seconds. The defendant accepted that he had been
negligent, but denied that he was grossly negligent so as to be guilty of involuntary
manslaughter. The House of Lords held that the question of whether the degree of
culpability was such that the anaesthetist should be liable to criminal sanctions was a
matter for the jury. It also approved tests from earlier cases that adopted a suggestion
that gross negligence describes cases where the defendant has shown such disregard
for the life and safety of others as to deserve punishment. This focuses attention on
the recklessness of the professionals behaviour, that is, the failure to concentrate
on the patients interests. Thus, where health professionals have shown an obvious
indifference to the risks to the patient, they may be charged with manslaughter.
Consent
A more contentious area regarding malpractice litigation arises when dealing with
issues of consent. The consent of the patient legalizes medical examination and
treatment. Significant case law has arisen owing to doctors failing to communicate
adequately with their patients, either because there had been no proper consultation
before treatment or because the medical practitioner failed to disclose the risks inherent
in the proposed treatment.
If an individual wants to buy a car, the vendor is not obliged to point out defects in the
car. If specifically questioned, the vendor commits fraud if he answers dishonestly,
but he is not obliged to volunteer information that may be detrimental to the sale. On
the other hand, the relationship between patient and doctor is one known in law as a
fiduciary relationship. Any person such as a physician, attorney, priest or other who
enters into a relationship of trust and confidence with another has a positive obligation
to disclose all relevant facts. The essence of a professional relationship is that the
professional knows more about his subject than the person who seeks his help,
therefore an affirmative duty of disclosure has always existed.
Patients need to be given a clear explanation of any treatment proposed, including

any risks and alternatives, before they decide whether they agree to the treatment.
Although consent, expressed or implied, must be given in most cases before treatment
is lawful, this does not mean that consent needs to be fully informed. Indeed, the author
does not believe that fully informed consent can ever be achieved. Lord Donaldson
has pointed out that consent plays two quite different functions in the doctorpatient
relationship. One, which he called the legal function, is to provide a legal justification for
care. Without such consent health professionals would commit a crime (battery) and a
tort (trespass to the person) when they touch their patient. The other function, termed
clinical by Lord Donaldson, is to secure the patients trust and cooperation. This aspect
of consent may involve more extensive counselling on the implications, risks and side-
effects of treatment than the laws of trespass and battery require.
Battery
A battery is an intentional or reckless unlawful application of force to another person
and is a crime as well as a tort at common law. Theoretically many procedures a doctor
performs might be batteries (e.g. injections, surgery, manipulations) if done without the
consent of the patient. The touching of a person in this manner without consent violates
an individuals right of self-determination and constitutes an act of trespass to the
person.
The main importance of battery lies in its role in emphasizing that patients are entitled
to refuse the care provided by health professionals. They have a right to refuse
treatment. In the words of Justice Cardozo from 1914: 'Every human being of adult
years and sound mind has a right to determine what shall be done with his own body;
and a surgeon who performs an operation without the patients consent commits an
assault.'
The common law has long recognized the principle that every person has the right to
have his bodily integrity protected against invasion by others. The seriousness with
which the law views any invasion of physical integrity is based on the strong moral
conviction that everyone has the right to self-determination with regard to his body.
The distinction between an action based on battery and one for negligence is important.
Battery, which is a non-consensual touching, is itself a legal wrong, whether or not
any specific damages can be shown to result. Thus, a patient may bring a successful
action for battery even when the procedure that was carried out without consent was
clearly for his or her benefit. By contrast, in negligence, in addition to showing that the
professional fell below the required standard the patient must prove that some damage
resulted. This means a patient will lose their case if the procedure benefited them or
where the carelessness of the professional did not cause the damage.
Lawyers acting on behalf of patients have argued that, if the patients consent for an
operation or a mode of treatment was given on the basis of inadequate information,
either of the risks of the treatment or of the extent of the treatment, the case should
be heard in battery and thus have a right to compensation under the laws of battery.
However, the UK courts have been intolerant of attempts to try these cases under the
laws of battery. Any such attempt has been seen as a device to side-step difficulties
in sustaining an action for negligence based on failures to communicate proper
information, and the courts have been consistent in holding that actions for battery
should play a limited role in healthcare law. Although this position has been criticized,
it is unlikely to be altered in the foreseeable future. As a result, battery can normally
be successfully alleged only when there was no consent to the procedure. This usually
occurs when there has been a blatant error by healthcare staff, such as when the
wrong leg is amputated, or when no consent was obtained. Liability in such cases is
virtually always admitted and usually settled out of court. In the case of Allan v. New
Mount Sinai Hospital (1980) the patient told the anaesthetist not to use the left arm for
injections. Unfortunately, the anaesthetist forgot this, and the injection into the left arm
leaked out causing tissue damage. The patient successfully sued under an action for
battery.
Disclosing information
On the other hand, it is clear that if professionals fail to counsel patients in a way
recognized by their peers as appropriate they may be negligent. Thus, patients
who allege that they have been given insufficient information must argue that the
professionals have been negligent in carrying out their duty to advise them about the
decision. This means that this important aspect of consent is governed by the same
principles that apply to ordinary malpractice cases. Furthermore, the extent and quality
of information that should be provided depends on whether the standard is based on
the patients expectations, that is a patient standard, or on a professional standard.
The professional standard test is the standard of disclosure that the profession would
be expected to tell the patient, that is, in accordance with the Bolam test or Hunter v.
Hanley. If a responsible body of medical opinion would not have disclosed what was not
disclosed by the defendant the doctor would not be found guilty of negligence. Thus,
even a significant minority of doctors in agreement will leave the plaintiff in difficulties.
Lord Scarman has attacked this reasoning. Although he would permit the medical
experts to establish the standard of care in relation to diagnosis and treatment, he
found it unacceptable in relation to informed consent. He has commented that the
laws standard is, in effect, set by the medical profession. If a doctor can show that his
advice or his treatment reached a standard of care that was accepted as adequate
by a respectable and responsible body of medical opinion he cannot be made liable
in damages if anything goes wrong. It is a totally medical preposition erected into a
working rule of law.
The patient-centred standard, on the other hand, can be subdivided into two,
the particular patient standard and the prudent patient standard, corresponding to
subjective or objective standards.
The particular patient (subjective) test defines what the plaintiff would have done
if notified of all relevant facts. This test suffers from the use of hindsight and since the
relevant facts exist only in the mind of the individual an accusation is hard to refute.
However, it is a desirable standard in so far as it embodies personal factors, including
many that are non-medical, which might affect a particular persons decision.
The prudent patient test requires the plaintiff to establish that a reasonable person
would not have undergone a recommended procedure after having been advised of
all significant risks. This suffers from the impossibility of defining a reasonable person
for each case. However, it appears fair to both sides in that a reasonable doctor and a
reasonable patient are meeting on comparable terms.
Other views: if the Bolam test is assumed to be representative of the current law,
the doctor would have to warn of all risks that a responsible body of medical opinion
considers the patient should be warned of, as opposed to every possible risk. The
British Medical Association (BMA) claims that how much or how little is considered
adequate varies with each patient. 'It must also be a matter of clinical judgement and
the standards set by other doctors. From an ethical viewpoint, the criteria should be
as much information as the patient needs or desires. It is interesting to note that in the
Bolam case, the law set the level at the standard adopted by the medical profession
and a doctor who gives as much detail as a recognized body of medical opinion
considers appropriate would be unlikely to be held liable in law.'
It is interesting to note that the BMA considers it unlikely doctors would be held liable in
law. The reason for this is that Bolam has been softened by various statements made
in cases such as Sidaway v. Bethlem Royal Hospital Governors (1985). In this case the
plaintiff suffered from persistent pain in her arms. Preoperatively the surgeon decided
that an operation to relieve pressure on the fourth cervical nerve root was required.
During the course of the operation the patients spinal cord was damaged and she
suffered severe disability. She sued the hospital and the surgeon, not for negligence in
performing the operation, but for failing to warn her of the risk of damage to the spinal
cord. Evidence was presented at the trial that this risk was less than 1%. Medical
witnesses stated that, in keeping with a practice common to other neurosurgeons, they
would also not mention the risk of paralysis or death in order not to frighten the patient.
The trial judge therefore dismissed the claim.
The Court of Appeal affirmed the trial judges view that the law in relation to failures in
diagnosis and treatment also applied to failures in the realm of advice. Lord Donaldson,
the Master of the Rolls, reviewed the leading transatlantic cases giving rise to the
prudent patient test in the doctrine of informed consent, but declined to incorporate
those principles: 'what information should be disclosed and how and when it should
be disclosed is very much a matter for medical judgement, to be exercised in the
context of the doctors relationship with a particular patient in particular circumstances.
It is for this reason that I would reject the American formulation of the duty by reference
to a prudent patient test'.'
However, the adoption of the medical standard implicit in Bolam was not seen by him
as abdicating responsibility to the medical profession. The practice held by the body
of responsible practitioners had to be one that was rightly and properly held, and the
court would not: 'stand idly by if the profession by an excess of paternalism denies their
patients real choice.' In the same case, Lord Justice Browne-Wilkinson formulated a
proposition that a doctor was under a duty to disclose to the patient information relevant
to the decision the patient would have to take.
It is therefore clear that the courts and medical literature in the UK have suggested that
disclosure is the key item and chief condition in the act of giving an informed consent.
This allows medical authority and physician responsibility to take preference over
patient autonomy. This is not in keeping with the meaning of informed consent which
is better analysed in terms of autonomous authorization. Furthermore, good practice is
not necessarily interchangeable with the legal minimum. However, it is very clear that
the UK, when considering standards of information disclosure, differs significantly from
other jurisdictions, such as Australia, Canada and the USA. Indeed, the position is at
odds with that in most other common law countries and is notably isolated within the
European Community. u
FURTHER READING
BMA. Medical Ethics Today: Its Practice and Philosophy. London: BMA, 1993.
Mason J K, McCall Smith R A. Law and Medical Ethics. 4th ed. Oxford: Butterworths,
1994.
Montgomery J. Health Care Law. Oxford: Oxford University Press, 1997.
Nelson-Jones R, Burton F. Medical Negligence Case Law. London: Fourmat Publishing,

1990.
Scarman L. Law and Medical Practice. In: Byrne P, ed. Medicine in Contemporary
Society. London: King Edwards Hospital Fund for London, 1987, 134.

Ethics of Research
W Graeme Hilditch
Nick Pace
W Graeme Hilditch is Specialist Registrar working as a Clinical Lecturer in

Anaesthesia at the University of Glasgow, UK. He qualified from Glasgow University
and trained in anaesthesia in the West of Scotland. His research interests include
preoperative assessment and information technology.
Nick Pace is Consultant Anaesthetist at the Western Infirmary, Glasgow. He qualified

He is a member of the British Transplant Societys Ethics Committee, and is currently
completing a PhD in medical law.
Research is vital in improving the health and healthcare of the population; patients have
the right to expect the best available prophylactic, diagnostic and therapeutic methods.
At present, research involving human participants is not governed by
legislation, but doctors involved in research have an ethical duty to show respect for
individual rights and follow good research practice.
Patients want to receive the best possible treatment based on evidence derived from
previous clinical trials. It could therefore be argued that there is an obligation on
current patients to participate in the procurement of this evidence for future patients.
However, the interests of the research subject are paramount. Even if research may
lead to advances in medical knowledge, the outcome may not justify the risk to the
participants. Respect for human life and individual autonomy of the research participant
is the primary aim of the ethical review of research.
Ethical approval
All human research should follow ethical principles and be approved by an ethics
committee. Ethical review of medical research has had a protracted development since
World War II following the inhumane procedures carried out by Nazi doctors in the
name of medical research. At the Nuremberg trials, 23 doctors were convicted and the
exposure of their deeds led to adoption of the first internationally recognized code of
medical ethics, the Nuremberg Code. The rights of research subjects were highlighted
in the code, in particular the right of an individual to withdraw from a study at any time.
The formation of ethical review by committee followed the World Medical Association
Declaration of Helsinki in 1964, the publication of Pappworths The Human Guinea Pig
in the UK and Beechers Experimentation in Man in the USA. They all added weight to
the discussion of the ethics of clinical trials, creating a framework for the principles for
biomedical research. The Royal College of Physicians issued reports in 1967 and 1973,
making various recommendations for the setting up and structure of ethical review
committees. In 1975, the Department of Health and Social Security produced guidance,
though the resulting system was varied in quality.
In 1991, a revised set of guidelines was issued by the Department of Health

reconstituting all Research Ethics Committees (REC) to a standardized structure.
Every health district required a local REC and detailed guidance on their composition
and function was given. These RECs are convened to provide independent advice to
participants, researchers, employers and care organizations on the extent to which
proposals for research studies comply with recognized ethical standards. The purpose
in reviewing study proposals is to protect the dignity, rights and safety of research
participants. In addition, RECs have an obligation to society and researchers to
encourage research that will improve healthcare and health.
The International Conference on Harmonization of Technical Requirements for the

Registration of Pharmaceuticals for Human Use (ICH Guidelines) was established in
1990 as a joint regulatory project to improve the efficiency of the process for developing
and registering new medical products in Europe, Japan and the USA. The guidelines
describe internationally accepted principles and practices for the conduct of individual
clinical trials and overall development strategies for new medical products.
Aim of research
Research is often categorized as therapeutic or non-therapeutic, though this is
increasingly challenged. In therapeutic research, the subject may benefit from being
involved in the research project. In non-therapeutic research there is no clinical benefit
to the subject. The distinction is useful when discussing ethical issues and is one of a
number of factors that RECs consider.
The aim of research is the generation of knowledge, not the improvement of the
health of the research subject, though it may lead to this. Research must be capable
of identifying and confirming improvements in clinical management, however small,
or improving medical knowledge. Research is justified only if there is a reasonable
likelihood that the populations in which the research is carried out stand to benefit
from the results of the research. Duplicate or redundant research is unethical because
it involves finite risk to the participant with no beneficial outcome. The REC must
reassure itself that the research project will lead to a meaningful result. Pre-recruitment
statistical analysis must show, for example, that sufficient numbers of participants will
be recruited to allow valid results to be produced.
The risks involved with research apply to the participant during the research period.
The benefits accrue to future patients if the therapy or diagnostic test being researched
is then implemented. This unequal distribution of risk (to the subject) and benefit (to
future patients) requires the protection of the research participant who may receive no
benefit from the research. The REC must be satisfied that the risks to participants are
minimized. However, significant risks may be acceptable under certain circumstances.
For example, patients who are critically ill may participate in research involving novel
treatment despite known or suspected serious side-effects.
In non-therapeutic research it is essential that all risks should be mentioned and all
foreseeable risks kept as low as possible. Potential benefits must greatly outweigh the
risks of participation. Although it may be possible to define risk, whether the balance
between risk to the individual and the benefit to others is acceptable is difficult to
determine. Often the balance is subjective and some suggest the research subject
could make the decision. However, this is unethical for several reasons. The REC has
more experience and access to advice and knowledge than research subjects and is
better able to assess the degree of risk. Also, research subjects may feel they owe a
duty to the researchers looking after them and thus subtle coercion may come into play
(see later). The REC can come to a collective judgement using individual expertise
rather than individual judgement. Furthermore, the cumulative experience of the REC
allows identification of serious risks. It is essential to ensure that involvement in the
research project is not contrary to the subjects interests.
Consent
Ethical review of research not only considers what risks are acceptable but also
ensures that the participants autonomy is respected. Proper mechanisms for
consent must be in place. The principles governing consent are provision of sufficient
information to allow choice and freedom to decide without influence from the
researcher.
Each participant must be adequately informed of the aims, methods, anticipated

benefits, and the potential risks of the study. The participant must be informed of the
right to abstain from participation in the study or to withdraw participation at any time
without reprisal. Once the researcher has ensured that this information has been
understood the participants freely given informed consent must be obtained. This
presents a problem in some areas of research, namely, day surgery, emergency
medicine and ICU.
Day surgery: the time available for consent is restricted and there is inadequate
opportunity for the patient to process the information, reflect on the risks and benefits,
and discuss the proposals with relatives. Efforts should be made to discuss
the research with the patient before the day of surgery, allowing formal written consent
to be obtained on their arrival for surgery. This may increase the workload for the
researcher but failure to do this is deemed by some RECs to be unethical.
Emergency medicine: obtaining consent in emergency medicine and ICU is further

compromised because patients are unable to comprehend the information provided
owing to their clinical condition. Treatment that is part of a research project may be
permitted if the risks of the treatment being studied are not thought to be greater than
standard treatment. This causes an ethical dilemma. The benefit to future patients
must be balanced against the risks to the research participant and the protection of
autonomy. There are no rules governing this balance and individual RECs must assess
each study individually. However, it is generally accepted that it is ethical to involve
adults who lack capacity, such as in the ICU, in therapeutic research. The situation
for non-therapeutic projects is less clear and potentially illegal in England and Wales,
though probably not in Scotland through a recent law giving relatives the right to
consent on behalf of their incompetent relative. Paradoxically, it is increasingly regarded
as ethical throughout the UK, provided certain safeguards are applied. RECs have a
major part to play in such decisions and researchers are strongly urged to seek their
views.
Recruitment
During recruitment, principles of consent, provision of information and freedom to
decide, can be compromised because of the vulnerability of participants. During illness,
comprehension and decision-making can be difficult. The research subject can be
influenced by a desire to show gratitude and obligation to the doctor, which may make
them susceptible to pressure from the researcher, however unintentional. This sense
of gratitude can also prohibit a patients voluntary withdrawal from the research. A
suggestion to the patient that they will benefit by participating in research may be an
inducement to participate. During recruitment, patients must be protected from pressure
to participate and reassured if they decide to refuse participation. Any issues that
arise during the research must be addressed and the imbalance of power between
researcher and participant minimized.
Despite these problems, it is ethical to recruit from vulnerable groups. The vulnerability
of different groups must be anticipated, recognized and taken into consideration by the
researcher during recruitment. Participants must be correctly identified and exclusion
criteria established. Efforts must be made to ensure that the research could not be
carried out on a less vulnerable group. This is a general moral requirement for all
research and precludes individuals who are less mature, frail, severely ill or confused
from participating in research unless there are special circumstances.
Ethical errors
All research must be based on a properly developed protocol that has been approved
by an REC (Figure 1). The aims, design, and methodology of the study must be
justifiable, verifiable, scientifically valid and ethical.
Basic components of a Research Ethical Committee proforma
Purpose of the study

Background of the work
Information to be obtained
Proposed benefits
Details of the procedure

Explain how the study will be executed
Duration of research
Treatment allocation
Procedures undertaken
Recruitment
Age range of participants
Principal inclusion and exclusion criteria
Minimum number of subjects and justification for these numbers, with
power calculations where appropriate
How patients will be approached
Trial products
Description of all drugs used, stating their known pharmacology,
side-effects and toxicity
If a new drug is to be used, a copy of the Clinical Trials Certificate or
Clinical Trials Exemption Certification from the Committee on Safety
of Medicines must be included
List approved and new indications
Patient information
Purpose of study, nature of procedure, discomfort and possible risks
in terms that the subject can understand
Consent
A standardized form should be used
Finances
All sources of support for the work should be stated including details
of all payments to be made to investigators, patients and healthy
volunteers
1
The aims of the study determine the benefit, and therefore, must be clear, focused and
reflected in the study design. The temptation to obtain as many answers as possible
from the same number of participants can lead to serious methodological problems.
The normal level of statistical significance is that there be no more than one chance in
twenty that a given result is due to random variation. Clearly, the more outcomes that
are measured the greater the chance that the researchers will identify a false-positive
observation. Poor methodology is unethical because it subjects participants to risk for
possibly invalid results.
Control groups
Research is susceptible to bias. The outcome measured can be influenced by
participant characteristics that are independent of the process being tested. The
variability of different individual patients must be overcome by using controls. These
are research participants who are closely matched to those in whom the new treatment
is being investigated. Thus, variables such as age, weight and diet are similar in both
groups; the only difference is the therapy and therefore any difference between the
groups can be assumed to be due to the therapy.
An ethical dilemma presents if the control group also requires treatment. This is
overcome by giving this group the best current therapy and comparing its benefits, risks
and effectiveness to the new treatment. This does not exclude the use of placebo or
no treatment in studies where no proven method exists. No trial design should prevent
a patient who needs active treatment from receiving it, though the trial therapy may be
less effective than the standard treatment.
To eliminate bias, the allocation of controls and study patients must be done in a
manner that reduces the introduction of un-recognized but influential factors. The
researcher should not choose the controls but use a valid method of randomization.
Blind procedures
Researchers and subjects must be prevented from introducing their own expectations
and hopes, which could influence outcome. The effects of a placebo are well
documented. Similarly, researchers may be influenced during the measurement of
the effect if they know which treatment has been given. Therefore, it is important
that neither the researcher nor the subject knows to which group subjects have been
allocated. Blinding of patients and researchers is crucial if bias is to be minimized
and the results of a trial accepted. It is essential that randomization, the nature of the
process and reasons for it are mentioned to the research subjects before their consent
(contrary to the Zelen design). In a double-blind trial neither the researcher nor the
subject knows whether the subject is receiving treatment or is in the control group.
The ethical problem with randomization and blinding is that the standard treatment is
no longer prescribed by the doctor to the patient, but is chosen by a random decision
process. The normal doctorpatient relationship is thereby compromised. This problem
can be intensified if the clinician is blinded and unaware of the treatment the patient
is receiving. If the patient subsequently becomes worse than expected during a trial,
it is the responsibility of the researcher to provide a quick and effective means for
withdrawal from the study and identification of the treatment received.
Sample size
Essential to the planning of a randomized trial is estimation of the required sample size.
The investigator should ensure that there is sufficient power to detect, as statistically
significant, a treatment effect. If a trial with negative results has insufficient power,
a clinically important effect may be ignored or taken to mean that the treatment
under study made no difference. Such a trial may be scientifically useless, and
deemed unethical because patients may be put at risk with no apparent benefit.
Likewise, studies that are too large are unethical because they involve supernumerary
participants and incur unnecessary costs.
Placebos
Care should be taken in the use of placebos. Section 29 of the revised declaration of
Helsinki states that the benefits, risks, burdens and effectiveness of a new method
should be tested against those of the best current prophylactic, diagnostic and
therapeutic methods. This does not exclude the use of placebo, or no treatment, where
no proven prophylactic, diagnostic or therapeutic method exists.
This is highly contentious and seems to rule out some vital uses of placebo-controlled
trials in areas where proven treatment already exists. However, failure to use placebos
may occasionally reduce the reliability of trial conclusions and increase the
proportion of wrong decisions. Placebo-controlled trials are generally more reliable,
providing their own check of internal validity and more conclusive proof of efficacy.
Using placebos does not mean that the subject receives no treatment, because other
medications are permitted in both groups. Rescue medication is also prescribed for
specific circumstances.
Epidemiological research
Epidemiological research and disease registers involve collecting and analysing data
from large numbers of patients, often without identifying individuals or their clinical
involvement. The main aim is the investigation of the incidence and prevalence of
diseases, often determining environmental and social factors. This is vital to protect
and enhance public health. However, the investigators are bound by the principles of
respect for the patients autonomy. Records made for one purpose (e.g. anaesthetic
charts) should not usually be disclosed for another purpose without the patients
consent.
The Data Protection Act 1998 requires researchers to make sure that patients are clear
how their personal health information may be used and to give them an opportunity to
opt out. The Act does not require the use of formal consent forms or signatures from
patients before information is shared. However, the Act does require reasonable steps
to be taken. A summary of the main principles of the Act is given in Figure 2.
Data Protection Act and Caldicott Guardians
Data Protection Act 1998

This brings into UK law European Directive 95/46/EC on the
processing of personal data. It came into effect on 1 March 2000
and, in comparison with the 1984 Act, it is concerned with both
records on paper and records held on computers. The act is based
on eight principles
1 Personal data shall be processed fairly and lawfully

2 Personal data shall be obtained only for one or more specified
and lawful purposes, and shall not be further processed in any
manner incompatible with that purpose or those purposes
3 Personal data shall be adequate, relevant and not excessive
in relation to the purpose or purposes for which they are
processed
4 Personal data shall be accurate and, where necessary, kept up
to date
5 Personal data processed for any purpose or purposes shall
not be kept for longer than is necessary for that purpose or
those purposes
6 Personal data shall be processed in accordance with the rights
of data subjects under this Act
7 Appropriate technical and organizational measures shall be
taken against unauthorized or unlawful processing of personal
data and against accidental loss or destruction of, or damage
to, personal data
8 Personal data shall not be transferred to a country or territory
outside the European Economic Area unless that country or
territory ensures an adequate level of protection for the rights
and freedoms of data subjects in relation to the processing of
personal data
Caldicott Guardians
In 1997, the Caldicott Committee reported on its review of
information that identifies NHS patients.
Following the recommendations, a new system of data protection

officers, Caldicott Guardians, was established.
Each Health Authority, Trust and Primary Care Group required a

guardian to agree and review internal protocols for the protection
and use of identifiable information obtained from patients
2
Systems of information collection should be constructed to balance public need and

the rights of privacy of the individual. Consent should be obtained where practical,
with anonymization of data if possible. However, data that have been encoded are
regarded by the Data Protection Act as personal if the key for decoding remains in
existence. Thus, coded data fall within the Data Protection Act and the researchers
ethical responsibility, even if the key is not readily available to the researcher. If full
anonymization is impossible, the use of pseudonymous data (creating codes and
restricting access to them) should be considered, though this can still be interpreted as
personal data.
The issues of consent and anonymization are complex, and uncertainties about the
interactions between researchers, data protection officers, RECs and the new Caldicott
Guardians are not yet clarified. u
FURTHER READING
Central Office for Research Ethics Committees. www.corec.org.uk
Evans D, Evans M. A Decent Proposal: Ethical Review of Clinical Research.1st ed.

Chichester: Wiley, 1996.
General Medical Council. Research: The Role and Responsibilities of Doctors. London:
General Medical Council, 2002.
Strobl J, Cave E, Walley T. Data Protection Legislation: Interpretation and Barriers to

Research. Br Med J 2000; 321: 8902.
World Medical Association. Declaration of Helsinki. 2000. www.wma.net

Jehovahs Witnesses
Manfred Staber
Nick Pace
Manfred Staber is Specialist Registrar at the Western Infirmary, Glasgow, UK. He

qualified from the Technical University in Munich, Germany. He trained in anaesthesia
and intensive care in Germany, Australia and the UK. His research interests include
trauma and critical care.

The Jehovahs Witness Christian movement was founded in the north-eastern USA
about 120 years ago. There are more than 5.9 million Jehovahs Witnesses in over
230 countries. The headquarters of the church organization, the Watchtower Bible and
Tract Society, is based in Brooklyn, New York. In general, Jehovahs Witnesses are
obliged to refuse blood transfusions or other blood-based products. This is based on
the prohibition of the consumption of blood as outlined in the Bible (Genesis 9:34,
Leviticus 17: 1112 and Acts 15: 2829). Accepting banned blood products is a serious
offence and may lead to excommunication and enforced shunning. This leads to social
isolation because friends and family are instructed to avoid the offenders company.
Changes in policy
Vaccinations for Jehovahs Witnesses were banned from 1929 to 1952, as were organ
transplants from 1967 to 1980. The policy of refusal of blood dates back to 1945 and
was enforced in 1961 with the threat of judicial sanctions and excommunication.
In June 2000, the Watchtower Society announced a change in procedure for offenders
and in the blood policy. If through personal choice members accept blood transfusion
they automatically disassociate themselves from the religion. If they repent, spiritual
support is offered with the possibility of redemption. In other words, members resign
from the religion rather than being expelled by a judicial committee.
The more important change from the medical communitys view is the expansion in
what are acceptable blood products. The ban on primary components (defined as red
and white blood cells, platelets and plasma) and whole blood is still upheld. However,
it now appears that the Society permits the use of all fractions of so-called primary
components, the so-called secondary components. At what point a primary blood
product becomes a secondary product is open to debate and becomes an individual
decision. It appears that nearly all components can be transfused as long as they are
given piecemeal or processed (e.g. albumin, all clotting factors, immunoglobulins). Red
cells stripped of their outer membrane may be transfused in the form of haemoglobin
transfusions. Haemoglobin-based blood substitutes have entered phase 3 clinical trails
and may become an acceptable treatment. Bone marrow transplants and the use of
peripheral stem cells for autografting are often considered as transplants rather than
infusions of primary blood products.
The current blood policy is confusing and complex and not every Jehovahs Witness is
aware of the official position of the Watchtower Society. Therefore, in most major cities,
Jehovahs Witness Hospital Liaison Committees have been set up to resolve these
medical issues. An anonymous group within the Jehovahs Witnesses is trying to reform
the blood policy of the Watchtower Society. Until this happens, more premature and
avoidable deaths will occur.
Informed consent
As with any other competent adult, Jehovahs Witnesses are entitled to accept or refuse
treatment or even only certain aspects of it (e.g. the administration of blood products).
Many Jehovahs Witnesses leave copies of detailed healthcare advance directives (a
living will concerning all kinds of personal matters) with their general practitioner, family
and friends. In addition, Jehovahs Witnesses may carry a signed advanced directive
declining blood in all circumstances and releasing the treating doctor from liability for
the consequences. Doctors who knowingly give the patient blood despite the presence
of an advanced refusal are likely to be held guilty of assault.
Each Jehovahs Witness must decide individually if he or she can accept the blood-
derived products mentioned above. Doctors should discuss acceptable treatment, and
the medical consequences of not receiving blood products, with the patient.
Blood transfusion
Jehovahs Witnesses believe that blood removed from the body should be disposed
of. They object to techniques involving intra-operative blood collection, storage and
haemodilution. However, provided the extracorporeal circulation is uninterrupted, many
Jehovahs Witnesses agree to autotransfusion as a continuous blood salvage with
reinfusion (e.g. during cardiac bypass). Isovolaemic haemodilution may be performed
provided a closed continuous loop is maintained. Even epidural blood patches may be
accepted provided the injecting syringe remains connected to the circulation. A long
extension line from the venous cannula to the syringe and injection via a three-way tap
into the epidural space maintains continuity. The use of pre-donation, storage and re-
transfusion of blood is unacceptable.
Emergency situations
If a patient is incapable of giving consent (e.g. following trauma) and his or her views
as a Jehovahs Witness are unknown, life-saving transfusions should not be delayed.
This intervention is not subject to the religions sanction or judicial process because the
individual has not conscientiously accepted blood. If time permits, the patients relatives
or general practitioner can be contacted to establish the patients views, though they
do not have a legal right to refuse transfusions in England and Wales. However, the law
in Scotland may be changing shortly, giving relatives legal authority to make treatment
decisions. Evidence must be provided, for example in the form of an advance directive,
that the patient would not accept blood even if that resulted in death. An advance
directive is legally binding, but concerns have been raised because it is often unclear
if, at the time of signing, the person was adequately informed of the risk and benefits of
blood transfusion and the obligation to comply with church rules may have influenced
their decision.
Child of Jehovahs Witness

In the UK, children under the legal age of consent, but capable of understanding the
issues, can refuse transfusion without the consent of the parents or legal guardian,
though the legal standing of such a refusal is unclear. If blood transfusions are required
for an elective procedure and the parents refuse to consent, it may be necessary to
apply to a court to make the child a ward of court. At this stage, a second opinion
should testify that the childs life or long-term wellbeing is in danger unless it receives
blood products during the proposed procedure. A court decision may become
necessary to clarify who can give lawful consent, for example, if the child opposes the
parental decision or if the parents are divorced and have different views.
In an emergency with the immediate requirement for blood transfusions, there is

insufficient time to wait for a court order and blood should be transfused irrespective of
the parents wishes. A second medical opinion, confirming the necessity of immediate
requirement for blood should be documented. The courts are highly likely to uphold the
decision of the doctors.
Managing Jehovahs Witnesses

Anaesthetists and refusal to treat: in the elective situation individual anaesthetists
may decide not to get involved in the care of a Jehovahs Witness, but in an emergency
they are obliged to provide appropriate care and to respect the wishes of the patient if
known.
Preoperative management: a preoperative consultation should be done early,

before the planned procedure, to discuss and document acceptable treatment. Private
consultations may be necessary because peer pressure is exerted on members to
refuse transfusions. If a Jehovahs Witness accepts blood transfusions it is essential
to maintain medical confidentiality. It is important to avoid transfusions during visiting
hours and to keep fluid and prescription charts away from the patients bedside. Access
to medical notes should be restricted to the treating medical team. These precautions
allow patients to remain silent about the medical treatment if they wish and avoid
sanctions or disassociation from the church. Agreed procedures should be signed
by the patient and kept in the medical records. Failure to respect the patients wishes
is unlawful and ethically unacceptable and may lead to criminal or civil proceedings.
Preoperative anaemia is an important determinant of operative outcome, particularly in
patients with underlying ischaemic heart disease. Anaemia should be investigated and
treated. The use of iron tablets combined with erythropoietin is effective.
Intra-operative management: surgery under regional anaesthesia can be associated

with major blood loss, especially in obstetrics. Confronted with major haemorrhage
and the need for urgent transfusion, Jehovahs Witnesses may accept life-saving blood
products. This change of consent has to be accepted and life-saving transfusion given,
even if the patient had sedation and may not strictly meet the legal standards to give
informed consent. Any change in the pre-existing consent should be documented and
witnessed in the notes.
Managing anaemia and blood loss: haemoglobin levels of 810 g/dl are safe,
even in the presence of cardiorespiratory disease. Critical levels of oxygen delivery
in fit, healthy and resting adults are reached at about 5 g/dl. For elective procedures,
a course of vitamin K, iron, folic acid and erythropoietin can be given. Strategies to
reduce intra-operative and postoperative haemorrhage include cell savers and the
use of antifibrinolytic drugs (e.g. tranexamic acid, aprotinin). Desmopressin (DDAVP)
a synthetic analogue of antidiuretic hormone (ADH) may be used to control bleeding
associated with acquired disorders of haemo-stasis, including chronic renal failure and
liver diseases and some platelet disorders. In addition, elective ventilation, paralysis
and sedation minimize oxygen consumption. Hyperbaric treatment, perfluorochemicals
and active cooling have been described, though the latter may impair homeostasis.
Recently, Sn-meso-porphyrin, a potent inhibitor of haeme oxygenase, has been used
as therapy for severe hyperbilirubinaemia in Jehovahs Witness newborns as an
alternative to exchange transfusions. u
FURTHER READING
Association of Anaesthetists of Great Britain and Ireland. Management of Anaesthetists
for Jehovahs Witnesses. London: Association of Anaesthetists of Great Britain and
Ireland, 1999.
Osamu Muramoto. Bioethical Aspects of the Recent Changes in the Policy of Refusal of
Blood by Jehovahs Witnesses. Br Med J 2001; 322: 379.
Scottish Intercollegiate Guidelines Network (SIGN). Perioperative Blood Transfusion for

Elective Surgery. SIGN Publication no. 54. Edinburgh: SIGN, 2001.
(http://www.sign.ac.uk)
The Associated Jehovahs Witnesses for Reform on Blood (AJWRB):

http://www.ajwrb.org

Transplantation Ethics
John Crawford
Lisa Manchanda
Nick Pace
John Crawford is Consultant Anaesthetist at the Western Infirmary and Gartnavel

General Hospital, Glasgow. He qualified from Glasgow University Medical School, with
postgraduate training in Scotland and Singapore, and has an honours degree in sports
physiology. His interests include the history of organ transplantation, and the ethics of
non-heart-beating organ donation.
Lisa Manchanda is Specialist Registrar in the West of Scotland School of Anaesthesia.

She qualified from Glasgow University Medical School. Her interests include pain
management and the ethical aspects of anaesthesia.

University Hospital of South Wales and Parkland Memorial Hospital, Dallas, Texas.
There have been ethical dilemmas about transplantation since the first successful
human kidney transplant in 1954. That transplantation proceeded in the belief that the
psychological benefit of live donation outweighed the unknown outcome. Advances
in transplant biology and technology have produced new ethical issues. These vary
between individuals, countries and cultures, but many arise owing to the scarcity of
suitable donor organs.
Allogenic (same species but different genetic constitution) solid organ transplantation
is now an established treatment for end-stage organ failure (kidney, heart, lung, liver,
pancreas), and a successful transplant results in improved duration and quality of life
for the recipient. Unmet demand means patients die waiting for heart, lung and liver
transplants because there are no alternative treatments. The success of long-term
renal replacement therapy creates growing waiting lists for renal transplantation.
Most societies, and the main religions, accept that organ donation and transplantation
is justified by the good it brings.
Transplant organ supply
Brainstem death
Brainstem death (BSD) is a product of modern intensive care. The concept is now well
established in most societies. Acceptance took place in several stages and was central
to the development of transplantation. In the UK, BSD heart-beating donors have been
the main donors since the mid-1970s. Maintaining ventilation and circulatory support on
these dead patients allows time for discussion with relatives, screening of donor, and
a controlled approach to organ retrieval, allowing the use of the kidneys, heart, lungs,
liver and pancreas with short warm ischaemic times.
BSD criteria provide an important demarcation between medical care for the patient
(including the determination of death) and the separate involvement of transplant teams.
Despite this, there is often discomfort at performing a lethal operation on a body with
signs of life even though they are secondary to techno-logical interventions.
Some cultures hold beliefs about death that make it difficult to equate brain death
with death. Organ harvesting from BSD donors was not permitted in Japan until 1997
because of the belief that death was not complete until funeral rituals were concluded.
This was combined with a loss of trust in the medical community when the initial heart
harvest led to a murder charge. Japanese citizens may now elect to permit their death
(for the purposes of organ donation) to be elicited using BSD criteria.
Anencephalic donors
It has been suggested that brain death could be extended to anencephalic infants who
could become organ donors byplacing them in a special category of death. This might
be justified by prolonging life for the recipients, however, anencephalic infants have
a functioning brainstem and are not brain dead. Moreover, transplanted organs from
anencephalic infants have not worked well. Altering the definition of death in specific
cases may also present risks to other patients (e.g. those in a persistent vegetative
state).
Elective ventilation
In 1988, the Royal Devon and Exeter Hospital developed an elective ventilation
protocol. Dying patients in deep irreversible coma were transferred to the ICU to allow
artificial ventilation to be instituted immediately after respiratory arrest. This support
continued until brainstem death ensued. The purpose was to increase the donor
pool and optimize the condition of organs in preparation for transplantation. Strong
arguments have since been made that it was wrong to prolong life and alter the mode
of dying only for the benefit of others. The practice also risked patients entering a
vegetative state. This practice was abandoned and the Department of Health forbids
it. Treating patients for the purposes of organ donation rather than for their benefit
risks charges of assault under the Criminal Offences Against the Person Act 1861.
Calls for permissive legislation in this area, with patient consent given through an
advance directive, must also be balanced against possible damage to the existing BSD
programme from loss of public trust.
Non-heart-beating donors
Non-heart-beating donors are being increasingly considered as an important source
of organs because demand is unmet by BSD donors. Non-heart-beating donors are
declared dead after the irreversible cessation of circulation and respiratory function.
Irreversible brain damage

Patients with profound irreversible brain damage (not BSD) for whom continued
support is considered futile by relatives and doctors often have life-sustaining treatment
removed and die soon afterwards. In such cases it is possible to harvest organs in
controlled conditions (with short warm ischaemic times) shortly after circulatory arrest,
with the consent of the patient or relatives. Contentious issues include pre mortem
placement of femoral catheters and pre mortem administration of drugs (e.g. heparin,
phentolamine) to optimize retrieved organ function that cannot benefit the patient and
may cause harm.
Patients dying in hospital

Other patients dying in hospital may also be potential donors but in a less controlled
manner (e.g. death following resuscitation). Delay caused by lack of prior consent
has sometimes led to measures such as post mortem in situ cooling of the body via
percutaneous catheters until relatives are contacted and consent to harvest obtained. Is
it justifiable to perform these extraordinary procedures without consent in order only to
benefit others? Some argue there is an obligation to help others and such actions offer
the family this chance. The limited time in which consent and harvest must be carried
out risks misunderstandings. When has irreversible cessation of circulation occurred?
Is prolonged resuscitation necessary first, or always ethical itself? Should there be a
minimum period between the declaration of death and harvesting? The traditional loose
definitions and timings of cardiac death are challenged in the context of non-heart-
beating donors. The conflicting interest of reducing warm ischaemic damage must
not influence good medical care (appropriate resuscitation, care and respect for the
dying) and it is clear that there must be transparent separation between the medical
and transplant teams. Likewise the transplant community should avoid any changes in
definitions of death. It has been suggested that such a programme should only follow
education of, and general acceptance by, the community in which it is to operate. Donor
and family wishes and values must be taken into account at all times.
Poor graft survival from so-called marginal donors is also a concern, and the recipients
must be made aware of differences in outcome from different sources. Recent evidence
suggests that kidneys retrieved with warm ischaemic times of about 30 minutes (with
no percutaneous cooling), have delayed initial function but similar long-term survival to
those obtained from heart-beating cadavers.
Executed prisoners
In some countries, organs are retrieved from prisoners after execution. This is
condemned by many, as is the involvement of physicians. Others argue that it is
immoral not to use such organs if they exist, given the benefit they can provide.
Living donors
Before BSD criteria were accepted, living donors provided many kidneys for transplant.
Living donation (kidney, liver lobe and lung lobe) has increased as cadaveric organs
remain scarce. In Norway and the USA, about 50% of kidney transplants involve
living donors compared with 27% in the UK (2001). The benefits to the recipient
include reduced waiting time, scheduled procedure, healthy donor organ, reduced
cold ischaemic time and longer graft survival. The main benefits to the donor are
psychological.
The risks of morbidity and mortality to the donor vary depending on the organ (or partial
organ) donated. The magnitude of these risks should alter the way in which decisions
are made. Adult-to-adult transplantation of the right liver lobe has a donor mortality of
about 1%, while kidney donation has a mortality of 0.03%. The risk to the donor may
contradict the obligation to cause no harm. The donor must be aware of all risks and
alternatives, and allowed an informed decision free from coercion. The doctrine of free
consent allows this non-therapeutic surgery provided the consequences are not against
the public interest. What role does the transplant community have in deciding if the
risks are unacceptable to a particular donor? It is also worth considering the benefits
that individuals and institutions gain from running such programmes and the distinction
between allowing a person to risk harm and actively encouraging it.
Living emotionally related donors are not related by blood but by a close relationship
such as friendship or marriage. The reward of seeing the recipient in better health
is thought to justify their altruistic and risky donations. Most countries permit such
donations.
Living unrelated donors: in the USA there have been recent cases of unrewarded
altruistic kidney donation from live donors to unknown recipients. They are also
known as undirected donors. Concerns include difficulties in accepting that a true
understanding of risk has been made; and what should be done if conditions are
attached.
Consent for cadaveric organ donation

Opt in: in the UK, individuals are asked to register their intention to be an altruistic
donor to society on the NHS donor register. The number of donors from this pool has
diminished owing to improved road safety and a shortage of neurosurgical facilities.
Over the last 10 years, the 20% reduction in the number of cadaveric organ donors has
been matched by a 3% increase per year in patients listed for transplantation. The UK
cadaveric kidney transplant rate of 24/1 million population is about half that required
to service the waiting list. Spain achieves about 48 cadaveric kidney transplants per
1 million population. The current opt-in system may fail the utilitarian principle of
maximizing benefits for society because about half of potential donors fail to become
donors.
Opt-out presumed consent: an alternative strategy of presumed consent assumes

an individual wants to donate unless they have opted out by previously registering
an objection. An individuals silence is equated with assent whereas there may be
a lack of understanding or ambivalence. Opt-out laws, with registers that can be
accessed quickly, have advantages in permitting early cooling of potential non-heart-
beating donors. Presumed consent laws are accompanied by an obligation to ensure
widespread understanding in society and ease of opting out.
Consent from relatives: many countries using opt-in or opt- out systems still
seek consent from relatives. Allowing relatives to veto wishes made by a potential
donor offends the principle of self-determination. Donor rates may not be increased
in opt- out countries taking this softer approach. Countries taking less account of
relatives wishes may demonstrate higher rates but this may not be transferable to other
countries without risking loss of trust.
Required request: failure to ask the relatives of suitable donors because of discomfort
or antipathy may be a common reason for losing organs, resulting in policies of
required request. Disconnecting a ventilator from a BSD individual without making
inquiries into the possibility of their organs being used for transplantation is thereby
identified as unethical. The individuals and familys right to donate may be denied, and
the potential benefit to society lost if relatives are not approached. In the USA, financial
penalties have been used to enforce this approach.
Conditional donation occurs when agreement to donation is made dependent on who

may receive the organs. A recent UK case involved relatives stipulating the skin colour
of the recipient; the conditions were accepted and transplantation proceeded. Review
by the Department of Health ruled that organs should not be allocated on the basis of
race and that such practice would breach the Race Relations Act 1976. Organs should
be accepted when freely given, as a gift, to society. Society has not extended to the
donor or their family the right to decide who receives it.
Rewards for donation
Commercialization of organ transplantation is illegal in most countries, however,
trade in organs occurs. This may seem unethical and distasteful to those in developed
countries, especially those not exposed to a market healthcare system. It may
be socially accepted in some countries without a cadaver transplant programme.
An individual may argue it is his or her right to sell their organs and undergo non-
therapeutic surgery while knowing and understanding the risks. To prevent such
transactions may be paternalistic and attack autonomy. The financial pressures to
sell may be as important as other moral pressures such as donating an organ within
the family. Altruistic donation may be unable to meet demands and the alternative for
the recipients may be death. However, the facts suggest that hospitals and doctors
undertaking this provide poor quality grafts and poor continuing care, and thus
exploit donor and recipient. Such rewarded donation may inhibit the development
of sustainable transplant programmes. It is also clear that organ tourists visit poorer
countries for transplantation.
Compensation: the boundary between sale and other rewards such as compensation
may be blurred. Living donors in the USA are entitled to receive compensation for loss
of earnings and expenses. In the USA, the introduction of ethical incentives (Figure 1)
to increase living and cadaveric donation has been suggested. There have also been
arguments for regulated reward systems to benefit donors and increase organ quality.
However, this undermines the principle that one should not sell one's body, and would
promote organs as products for sale. Some argue that non-commercialism of the body
is paramount and commercialization can never be justified even if it increases the
number of organs for transplant. Others point out that payments are often made for
blood and gametes.
Proposed ethical incentives
Medals of honour for bereaved families

Reimbursement of funeral expenses
Allowing regulated organ exchanges
Donors receive highest priority if organ failure develops
Donor insurance in case of morbidity/mortality
Should ICUs be given bonuses or other incentives, in an effort to encourage requests

to relatives for organ donation? Does this differ from penalizing them for failing to make
a required request?
Access to transplantation
The corollary of demanding that cadaveric organs be unconditionally donated to society
is that a just system must exist to distribute this scarce resource.
Access: in the UK, geographical differences in the referral rates for liver transplant
may reflect true differences in referral practice and thus inequitable access. Likewise,
not all patients may have the same access to living donor programmes. In some health
systems, funding for lung transplant is dependent on health insurance. Thus the lung
is effectively donated to the part of society that can afford insurance. Without equity of
access it could be argued that the best allocation schemes are unjust.
Allocation: UK Transplant controls organ allocation in the UK. Other countries have
similar organizations. They aim to maximize overall benefit while meeting individual
need in a fair and unbiased way (efficacy, utility, equity, urgency). The exact system
differs with organ but includes blood group, and scoring systems for tissue matching,
age, urgency of transplantation and location.
To what extent should prognosis after transplantation be taken into consideration?

Should continuing alcohol, or other drug misuse be a contraindication for organ
transplantation or alter position on a waiting list? Should young recipients have priority?
What should be done about differences in outcome that are race dependent? Equity
would stress that these factors not be taken into account, but what about using scarce
organs for new indications with unknown efficacy? The balancing of utility with justice is
a duty for all of society and not just for the transplantation community. It is essential that
the criteria for organ allocation are transparent and debated by the public.
Legislation and the Regulation of Transplantation

In the UK, the Human Tissue Act 1961 and the Human Organ Transplants Act 1989
govern organ donation and transplantation.
The Human Tissue Act 1961 allows the person in lawful possession of a body to
authorize the removal, from the body, of any part that the person wished to be used
for therapeutic, education or research purposes. If no such wish was made then
the person lawfully in possession may still authorize such removal, after having
made reasonable enquiries that there is no reason to believe that the deceased had
expressed an objection or that the surviving spouse or any relative objects.
The Human Organ Transplants (HOT) Act 1989 permits anyone suitable to
donate all or part of a vital organ to a close blood relative. It was enacted to regulate
transplantation of living donor organs after a scandal involving the purchase of kidneys
from Turkish living donors. The Unrelated Live Transplant Regulatory Authority
(ULTRA) was set up under this Act to approve all transplant operations involving a living
donor who is not a close blood relative of the recipient. The purpose is to ensure that
no payment is involved, other than expenses, and that full understanding and consent
is obtained without coercion. The process includes the donor being interviewed by
an independent assessor. The HOT Act does not apply to transplants of regenerative
tissues.
Other legal issues

Domino transplants require ULTRA approval. This refers to organs becoming
available from a recipient during a transplant procedure which could be used for
someone else (e.g. a healthy heart, during a heartlung transplant). The necessity for
ULTRA approval in domino transplants has been questioned because the opportunity
for organ trafficking is effectively non-existent. However, this would require an
amendment of the HOT Act.
Paired exchange involves one donor/recipient pair donating to, and receiving from,
another donor/recipient pair to resolve tissue incompatibilities, which would prevent
transplant within a pair. A variation is an incompatible living donor donating to the
general recipient pool in exchange for their relative going to the top of the cadaveric
waiting list. In the UK, these swaps are forbidden because they involve elements of
coercion (e.g. I will donate only if X receives) while the HOT Act supports only altruistic
donation.
Xenotransplantation is transplantation between different species. It offers the

possibility of unlimited organ supply. Failed attempts have been made with great
controversy, and remain experimental. Immunological problems remain the main
barrier to efficacy. The collective risk of trans-species infection is currently considered
greater than the potential benefits to individuals and has led to a moratorium on further
xenogeneic organ transplants by the UK Xenotransplantation Interim Regulatory
Authority (UKXIRA). There is a wide diversity of opinion on the issue of animal rights
and welfare. One opinion is that animals are not people and have no value in their
own right and human needs should be given precedence because of our special moral
status. A counter-argument is that we are animals ourselves, part of nature, not set
apart from it and that animals have their own rights as sentient beings. u
FURTHER READING
British Transplant Society www.bts.org.uk
Cecka J M. Donors without a Heartbeat. New Engl J Med 2002; 347: 2813.
Delmonico F L, Arnold R, Scheper-Hughes N et al. Ethical Incentives Not Payment

for Organ Donation. New Engl J Med 2002; 346: 20025.
Stiller C R, Abbott C. Ethical Issues in Transplantation. In: Sharpe M, Celb A, eds.

Anesthesia and Transplantation. USA: Butterworth-Heinemann, 1998, 45363.
UK Transplant www.uktransplant.org.uk

History
Anaesthesia
on CD-ROM
Chloroform la reine
Neil Adams
Neil Adams is Consultant Anaesthetist at the West Suffolk Hospitals Trust, Bury St
Edmunds, UK. He qualified from Oxford University and St Thomas Hospital, London,
and trained in anaesthesia in Nottingham, Canada and Cambridge. His historical
interests include the social aspects and reaction to the introduction of anaesthesia.
On Thursday 7 April 1853, John Snow administered chloroform to Queen Victoria

during the birth of Prince Leopold, hence the expression, chloroform la reine. The
three casebooks of John Snow survive in the library of the Royal College of Physicians
in London and document his activities as an anaesthetist from 1848 to 1858. The late
Dr Richard Ellis transcribed these books as a supplement to Medical History. The use
of chloroform by Queen Victoria is described in Snows own words. Ellis notes the
particular care Snow took with this entry and the possible slip of the pen (marked with
an asterisk) where the word after should have appeared.
Administered chloroform to the Queen in her confinement. Slight pains had been
experienced since Sunday. Dr Locock was sent for about nine oclock this morning,
stronger pains having commenced, and he found the os uteri had commenced to dilate
a very little. I received a note from Sir James Clark a little after ten asking me to go to
the Palace. I remained in an apartment near that of the Queen, along with
Sir J Clark, Dr Ferguson and (for the most part of the time) Dr Locock till a little
a(*) twelve. At a twenty minutes past twelve by a clock in the Queens apartment I
commenced to give a little chloroform with each pain, by pouring about 15 minims by
measure on a folded handkerchief. The first stage of labour was nearly over when the
chloroform was commenced. Her Majesty expressed great relief from the application,
the pains being very trifling during the uterine contractions, and whilst between the
periods of contracting there was complete ease. The effect of the chloroform was not at
any time carried to the extent of quite removing consciousness. Dr Locock thought that
the chloroform prolonged the intervals between pains, and retarded labour somewhat.
The infant was born at 13 minutes past one by the clock in the room (which was 3
minutes before the right time); consequently the chloroform was inhaled for 53 minutes.
The placenta was expelled in a very few minutes, and the Queen was cheerful and well,
expressing herself much gratified with the effect of the chloroform.
With regard to the historical context of this case, it is possible that two myths have
passed down through history. Firstly, was the doctrine of a campaign opposing the
use of chloroform in midwifery and surgery by the Church. This idea arose after the
publication in 1848 by Sir James Young Simpson of The Answer to the Religious
Objections Advanced Against the Employment of Ansthetic Agents in Midwifery
and Surgery. Secondly, was the idea that the use of chloroform by Queen Victoria
provided an impetus to the general acceptance of the use of anaesthesia in midwifery.
For example, Cartwright states that it was the acceptance of the Queen herself that
changed the minds of the opponents, while Longford's biography of Queen Victoria
states It was fitting that the battle royal should be won forDr Simpson by the Queen
herself.
Queen Victoria photographed by Charles Clifford.

National Portrait Gallery.
In examining the use of chloroform by Queen Victoria, Connor and Connor throw
considerable doubt on the claim of public acceptance following the Queens usage,
noting that the event was largely ignored by the lay newspapers, and that Snows own
obstetric practice did not increase proportionately after April 1853. Turning to religious
objection, again much doubt exists because no single piece of evidence has yet been
found in contemporary religious writings confirming such opposition.
Snows services were to be required at the Palace, once again, on Tuesday 14 April
1857 to administer chloroform to Queen Victoria in her ninth confinement for the birth of
Princess Beatrice. u
FURTHER READING
Ellis R H, ed. The Case Books of Dr John Snow. Medical History 1994; Supplement 14.

Curare, and Griffith and
Johnsons use in 1942
Neil Adams
Neil Adams is Consultant Anaesthetist at the West Suffolk Hospitals Trust, Bury St
Edmunds, UK. He qualified from Oxford University and St Thomas Hospital, London,
and trained in anaesthesia in Nottingham, Canada and Cambridge. His historical
interests include the social aspects and reaction to the introduction of anaesthesia.
Curare appears in European writing as early as 1516, when Peter Martyr dAnghera
described the arrow poison of the South American Indians. In 1595, Hakluyt also
describes it in his work on Sir Walter Raleighs voyage to South America.
The explorer Waterton brought a curare extract back from the Amazon and in 1814
demonstrated, with the help of Sir Benjamin Brodie and Mr Sewell of the London
Veterinary College, that its paralysing effects were transient. They injected a curare
extract into a she-ass and kept it alive by ventilation of the lungs with a bellows inserted
into the animals windpipe through a tracheotomy.
The attempted use of curare in clinical practice goes back at least as far as 1858, when
Sayres and Burrall attempted, unsuccessfully, to use the drug locally to treat tetanus.
Beigel described the clinical effects in man in 1868, using calabash curarine. In 1935,
Harold King, working with Sir Henry Dale, isolated the pure curare alkaloid from a
specimen in the British Museum, but it took until 1943, for Wintersteiner and Dutcher,
working in the laboratories of Squibb, to demonstrate that the curare alkaloids could
be extracted from the plant Chondrodendron tormentosum. Squibb then went on to
produce the first commercial preparation of curare under the trade name Intocostrin.
Squibb were able to manufacture the drug in a known strength by the rabbit head
drop test being calculated from the smallest amount that would cause a rabbits head to
drop without affecting respiration. The first clinical use was in Omaha, Nebraska, where
McIntyre and Bennett were assessing the effect of intravenous Metrazol to produce
convulsions in the treatment of schizophrenic patients. The violence of the convulsions
caused 50% of the patients to suffer spinal compression fractures, but a small dose of
Intocostrin significantly reduced the fracture rate.
Samples of Intocostrin were sent to Professor Rovenstine at Columbia Medical School,

where his assistant E M Papper spent the night resuscitating the two patients who
received the drug. This led Rovenstine to believe that Intocostrin was not safe for
clinical use. Cullen, in Iowa, used the drug on dogs, but bronchospasm ensued and he
came to the same conclusion as Rovenstine.
Harold Griffith, Professor in Montreal, was approached by Squibbs medical

representative, Lewis Wright. He reviewed the work of McIntyre and Bennett, including
a film they had made. Noting that the psychiatric patients had not died, he reasoned
that the worst possibility was to ventilate a paralysed patient, a technique with which he
had gained confidence under the training of Ralph Waters in Madison, Wisconsin (with
whom, interestingly, Rovenstine and Cullen had also worked). Griffith agreed to try the
drug.
Harold Randall Griffith 18941985.

Osler Library of the History of Medicine,
Montral, Qubec, Canada.
On 23 January 1942, Griffith and his assistant Enid Johnson, used Intocostrin on a
20-year-old man undergoing appendicectomy. The result is reported as dramatic, the
abdominal muscles were completely relaxed, and the surgeon was able to remove the
appendix with ease. The anaesthetic record survives, intact, in the Sir William Osler
Library in Montreal.
Remarks: Intocostrin, Squibb (Curare) 3.5 cc given intravenously in 112 minutes as

operation started no appreciable effect on pulse or respiration. After 5 minutes
another 1.5 cc of Intocostrin given. Apparently complete relaxation of abdominal
muscles resulted and continued for 20 minutes, during which time cyclopropane was
lightened. At the end of this period muscle tone returned, probably from wearing off
of curare effect. Cyclopropane was then increased in concentration and anaesthesia
continued in the usual way. There was no demonstrable change in pulse, blood
pressure or respiration
.
Shortly afterwards, Griffith and Johnson submitted a series of 25 cases of the use
of curare to the journal Anesthesiology and so began a new chapter in the history of
anaesthesia. u
FURTHER READING
Bodman R, Gillies D. Harold Griffith, The Evolution of Modern Anaesthesia. Toronto
and Oxford: Hannah Institute and Dundurn Press, 1992.

Punch Drunk
Neil Adams
Neil Adams is Consultant Anaesthetist and Clinical Director, Surgical Services, at

the West Suffolk Hospital, Bury St Edmunds, UK. He qualified from Oxford University
and St Thomas' Hospital, London, and trained in anaesthesia in Nottingham, Canada
and Cambridge. His historical interests include the social aspects and reaction to the
introduction of anaesthesia.
Following the introduction of inhalational anaesthesia in 1846, it did not take long for
the humorous possibilities to be explored. The cartoon shown here and nine articles
appeared in Punch during 1847 and 1848.
Given that society in 1846 was very different from that of today, with child labour,
slavery in America, and literacy rates of about 20% in some socioeconomic groups, it is
interesting to see that a humorous perspective was already well developed.
WONDERFUL EFFECTS OF ETHER IN A CASE OF

SCOLDING WIFE
Patient This is really quite delightful a most

beautiful dream
Animal rights
Clearly concerned for the welfare of animals in 1847, Punch reports that the inhalation
of ether had been resorted to professionally by various pork butchers with great
success. The chief difficulty they experienced had consisted of the opposition of the
patient; but when the natural obstinacy of the pig had been overcome, and he had been
persuaded to inhale the ether, he had been killed with comfort to himself, and without
disturbance to the neighbourhood. Other uses reported include the opening of oysters,
and the skinning of eels.
Punch noted that in France, bees had been etherized so as to be able to take their
honey while they were in a state of inaction, without the necessity of destroying their
lives. The article extrapolates to find a method of etherization that would render John
Bull insensible to the operation of income tax!
Stages of anaesthesia
An article of 1847 suggests that the first description of the stages of anaesthesia may
not be from Snow or Guedel, but from a fictional character, Cimabue Potts, a historical
painter.
Potts writes: Sir I have imbibed ether, and shall continue to do so till I have
painted a work destined for immortality, which I confidently expect to do next week. I
subjoin what I remember of my feelings during the ethereal state.
First stage: Imagined myself in Rome, in company with Rafaelle, Mr. Etty (RA), and
the editor of Art-Union, the latter in chains, and trampled upon by us in succession (you
are aware that I have been the butt of his malignant criticism for years).
Second stage: Felt immortal, and was congratulated by the daily and weekly
papers.
Third stage: Produced an historical picture, 25 feet by 15, representing the
discovery of the dead body of Harold after the Battle of Hastings; received the premium
of 700 from the Fine Arts Commissioners, and was dragged home by the populace in
my own carriage!
Last stage: Recovered and found myself, with the bladder empty, in the Goose and
Gridiron.
Politics
The absence of items in Hansard suggests that Parliament was indifferent to the
introduction of anaesthesia. The Times, reporting from an article in Punch points out
political possibilities.
However desirable this invention may be in a surgical point of view, we have every
hope that it will soon be applied to the more delicate operations of politics. How useful
would it have been during the last session, when the Conservative body had to undergo
the painful process of the cutting off of so many members! Had the new process been
known, the political amputations might have taken place without any pain. Considering
the frequent severings that Sir Robert Peel has been obliged to undergo, and the
numerous occasions upon which he will again most probably feel it necessary to submit
to amputations, the new process must be most welcome. As the plan is calculated
to prevent pain in all cases of removal, we should recommend its being tried on the
next occasion of a removal from office by Her Majestys Ministers. This has always
been a most distressing operation, from the suffering it has inflicted on the parties
concerned; and all the friends of humanity must be delighted at the prospect there is of
its becoming an entirely painless proceeding. u

The Royal Humane Society
Resuscitation Guidelines
1774
Neil Adams
Neil Adams is a Consultant Anaesthetist and Clinical Director, Surgical Services, at the
West Suffolk Hospital, Bury St Edmunds. He qualified from Oxford University and St
Thomas Hospital, and trained in anaesthesia in Nottingham, Canada and Cambridge.
His historical interests include the social aspects and reaction to the introduction of
anaesthesia.
It is impossible to define when the techniques of resuscitation began. They may have
ancient origins, for example, there is archaeological evidence of trephining removing
a piece of bone from the skull. Another example is found in the Bible, the Second Book
of Kings, Chapter 4, verses 34 and 35, in which the Prophet Elijah is described as
bringing back the dead child of the Shunamite woman by warming and mouth-to-mouth
resuscitation. In this long history, the work of the Royal Humane Society is fascinating.
In the 18th century, drowning was one of the main causes of death following the
development of the canal system as a means of transport. In the UK, the Royal
Humane Society had its origins in a meeting held on 18 April 1774 at the Chapter
Coffee House, St Pauls Churchyard, London, between Dr William Hawes and Dr
Thomas Coggan. Each invited 16 of their friends to help found the Society. Initially
The Society for recovery of persons apparently drowned, this became The Humane
Society in 1776 and Royal in 1787.
The remarkable instructions of the Society as to how revival of the apparently dead
may be achieved are printed below. Figure 1 shows the apparatus of the Society; this
example is kept in the Museum of the Association of Anaesthetists.
1 The apparatus used by the

Royal Humane Society.
The Association of
Anaesthetists of Great Britain
and Ireland.
Cautions
1 Lose no time
2 Avoid all rough useage
3 Never hold the body up by the feet
4 Nor role the body on casks
5 Nor rub the body with salt or spirits
6 Nor inject tobacco smoke or infusion of tobacco
Restorative means
Send quickly for medical assistance: but do not delay the following measures.
i Convey the body carefully, with the head and shoulders supported in a raised
position, to the nearest house.
ii Strip the body, and rub it dry, then wrap it in hot blankets and place in a warm bed in
a warm chamber.
iii Wipe and cleanse the mouth and nostrils.
iv In order to restore the natural warmth of the body:

1 Move a covered warming pan over the bed.
2 Put bladders or bottles of hot water, or heated bricks to the pit of the stomach,
the armpits, between the thighs, and to the soles of the feet.
3 Foment the body with hot flannels, but if possible,
4 Immerse the body in a warm bath, as hot as the hands can bear without pain,
as this is preferable to the other means for restoring warmth.
v In order to restore breathing, introduce the pipe of a common bellows (where the
apparatus of the Society is not available) into one nostril, at the same time drawing
downwards and pushing gently backwards the upper part of the windpipe, to allow more
admission of air; blow the bellows gently, in order to inflate the lungs, till the breast be
a little raised and make a moderate pressure with the hand upon the chest. Repeat the
process till life appears.
vi Inject into the stomach, by means of an elastic tube, half a pint of warm brandy and
water, or wine and water.
vii Apply sal volatIle or hartshorn to the nostrils.
If apparently dead from noxious vapours etc.
1 Remove the body into a cool fresh air.
2 Dash cold water on the neck and face and brush frequently.
3 If the body be cold, apply warmth as recommended.
4 Use the measures recommended for inflating the lungs.
5 Let electricity (particularly in accidents from lightening) be early employed by a

medical assistant.
Some of these themes would be familiar to those engaged in resuscitation in the

21st century, demonstrating a repeated historical cycle of methods discovered, then
forgotten, then re-discovered. u

Informatics
Anaesthesia
on CD-ROM
Anaesthetic Records
Tim Peachey
Tim Peachey is Consultant Anaesthetist at the Royal Free Hospital, London, UK.
He qualified from Kings College Hospital, London. His clinical interests include liver
transplant and cardiac anaesthesia. His research interests include computerized
record-keeping systems.
For almost as long as anaesthetics have been given, a comprehensive system

of recording their conduct and effect has been emerging. When John Snow was
practising anaesthesia in the 1850s he kept comprehensive notes on the conduct of
his anaesthetics in a notebook. Although less systematized than modern anaesthetic
records this approach had the advantage that all the records were in a central location
and were available for review. Contrast this with todays method of filing anaesthetic
records among a plethora of other documents in a case file. All anaesthetists are aware
of the limitations of the modern approach, the usefulness of each record, for tracing the
anaesthetic history is dependent on the availability of the case file and a record having
been filed. Even in Snows time, the anaesthetic records contained histories of previous
anaesthetic episodes. In the search for a good record-keeping solution, the merits of
manual and computer-based systems should be considered.
Purposes of the anaesthetic record

Anaesthetics are probably documented to a greater degree than any other aspect
of medical practice. Manual systems of data recording, document the effects of
anaesthesia and surgery on the patient at a time resolution typically 12-fold greater
than that of manual data recording systems in critical care units. The purpose of such
detailed record keeping is multiple. Several authors have tried to define the optimum
content of the anaesthetic record, but its format has remained a matter of local
preference and has not been standardized. Various functions have been agreed by a
number of authors.
Facilitating clinical care during anaesthesia in designing, or compiling an

anaesthetic record, the facilitation of clinical care should be the primary consideration.
Although records from two centres are seldom the same, most have similar features.
All are based on a time-based chart of physiological observations, drug and fluid
administration, events and notes. All should contain information about the patient and
their preoperative status together with an operative procedure description (proposed
and actual). Most records contain elements of a preoperative checklist and all contain
some description of the anaesthetic methodology or technique. As the chart is created
during anaesthesia, patterns of response may emerge and trends may be noted. An
ideal record should contain all the information required for another anaesthetist to
continue the conduct of anaesthesia safely, though this goal is seldom achieved in
practice. It follows that the recording of adverse events is as important, if not more
important, than recording a series of normal values. However, adverse events are less
likely to be recorded than normal occurrences. Other features may be included, which
are specifically designed to improve care or avoid an adverse outcome, for example a
tick box labelled Throat pack removed.
Augmenting the handover processes the handover of any anaesthetized or

recovering patient from one person to another is a potentially hazardous process break.
There are protocols for the handover of patients in post-anaesthesia care areas or
recovery rooms and recent guidance has been issued in the UK. The presence of an
anaesthetic record does not diminish the obligations of anaesthetists in this regard; a
well-kept record should answer most questions that arise during the care of the patient.
Advising the providers of future care implicit in the safe conduct of anaesthesia is
the ability to predict difficulties in management or the likelihood of adverse outcomes.
One of the most valuable pieces of information sought from patients in preoperative
assessment is their anaesthetic history, particularly any previous problems. A previous
anaesthetic record greatly assists in planning another episode of care. A section of the
record that documents warnings to future care providers has been advocated. Also, the
certain knowledge that a patient is straightforward to intubate is of much greater value
than the patients own recollection of there having been no problems with a previous
anaesthetic.
Informing statistical processes collective sets of anaesthetic records may be used

to assess the quality of care offered by a group of anaesthetists as well as providing
activity data that may be useful in service planning. Anaesthetics are administered
in huge numbers, with a low risk of a negative outcome. The serious adverse effects
of anaesthesia are now so rare that their prediction and assessment of probability is
difficult. Variations in outcome are subject to a large number of variables, the individual
effects of which may be quite subtle. For example, the number of variables that affect
the rate of postoperative nausea and the uncertainty that any one approach to the
problem will be effective may make the analysis of anaesthetics in large numbers
desirable.
Reviewing clinical care anaesthetic records are the only method by which the
quality of anaesthetic care can be evaluated after the passage of time from the episode.
Memory of events deteriorates, therefore accurate documentary evidence is essential if
retrospective reviews of care are to be possible. Many of these reviews are for clinical
audit and clinical governance but some records will be used for complaint investigation
and even litigation. Poorly kept and incomplete records may be eliminated from group
audits, but such records will reflect poorly on the standard of care delivered when
subject to legal scrutiny.
Optimum content
The anaesthetic record set suggested by the Royal College of Anaesthetists is
shown in Figure 1. Recommendations from the Australia and New Zealand College of
Anaesthetists are similar, but slightly broader in scope, less detailed and emphasize
the recording of problems and their management. Documentation of the name of the
supervisor and the level of supervision, when trainees are administering anaesthesia, is
advocated.
The list in Figure 1 is not an exhaustive account of everything that could be included,
but offers sound guidance. The inclusion of information regarding the checking of
anaesthetic equipment is controversial. An anaesthetic record that contains the
question Anaesthetic machine checked Yes / No is most unlikely to be answered in
the negative. Nor can it be inferred from looking at a given record that the equipment
was checked immediately before the anaesthetic in question. The documentation of
critical incidents (especially those where no harm results) in the anaesthetic record has
not been widely adopted, nor, in the author's opinion, is it likely to be in the near future.
In the UK, printed anaesthetic records vary considerably from the suggested record set.
Suggested anaesthetic record set 1
Pre-operative information
Patient identity
Name/ID no./gender
Date of birth
Assessment and risk factors
Date of assessment
Assessor, where assessed
Weight (kg) (height (m) optional)
Basic vital signs (blood pressure, heart rate)
Medication (including contraceptive drugs)
Allergies
Addiction (alcohol, tobacco, drugs)
Previous general anaesthesia, family history
Potential airway problems
Prostheses, teeth, crowns
Investigations
Cardiorespiratory fitness
Other problems
ASA grade comment
Urgency
Scheduled listed on a routine list
Urgent resuscitated, not on a routine list
Emergency not fully resuscitated
Peroperative information
Checks
Nil by mouth
Consent
Premedication, type and effect
Place and time
Place
Date, start and end times
Personnel
All anaesthetists named
Qualified assistant present
Duty consultant informed
Operating surgeon
Operation planned/performed
Apparatus
Check performed, anaesthetic room, theatre
Vital signs recording/charting
Monitors used and vital signs (specify)
Drugs and fluids
Dose, concentrations, volume
Cannulation
Injection site(s), time and route
Warmer used
Blood loss, urine output
Airway and breathing system
Route, system used
Ventilation: type and mode
Airway type, size, cuff, shape
Special procedures, humidifier, filter
Throat pack
Difficulty
Consent
Block performed
Entry site
Needle used, aid to location
Catheter yes/no
Patient position and attachments
Thrombosis prophylaxis
Temperature control
Limb positions
Postoperative instructions
Drugs, fluids and doses
Analgesic techniques
Special airway instructions, including oxygen
Monitoring
Untoward events
Abnormalities
Critical incidents
Preoperative, peroperative, postoperative
Context, cause, effect
Hazard flags
Warnings for future care
1
Reproduced with permission from the Royal College of Anaesthetists Newsletter
1997; 36
Manual records
About 10% of an anaesthetists time is spent making records during anaesthesia. This
might be regarded as time that could have been spent being more vigilant, considering
options for the patient, or planning ahead, but the act of record keeping probably
ensures that the anaesthetist has mentally registered the values of the parameters he is
recording. Attention to the chart may make the detection of trends more likely. However,
when critical events occur, the first task that is lowered in priority is record keeping.
The value of an anaesthetic record after a critical event may be seriously compromised
by inaccuracies in time and recorded values. One study (using simulation) found that
over 20% of values recorded during critical incidents were in error by at least 25%
and some by 100%. The variability between recorded values and actual values has
been known for some years, as has the tendency for real data to be smoothed before
they are recorded, so that extreme values and sudden changes are attenuated. It
is perhaps not surprising that we feel the desire to make things look good but every
anaesthetist knows that most patients have some measurable physiological disturbance
during the course of an anaesthetic. The lack of objective evidence for this is a
failure of documentation rather than reflection of reality. If records are misfiled, lost or
inaccessible the value of keeping them is largely negated.
Computerized records
Computerized anaesthetic records have been in use for over 20 years and commercial
systems have been available for at least 10 years, but they have yet to gain widespread
acceptance. The medical profession is now embracing electronic patient records but
anaesthesia has been passing up the opportunity for at least 10 years. This may be
due to the perception among hospital managers that anaesthesia is expensive enough
as it is and that computerized record-keeping systems do not save money. (Failure to
save money has been a feature of most medical informatics projects and is a poor test
of benefit.) The profession has also been slow to accept the benefits of such systems
and associates some risk with their adoption. Computerized recording systems offer
a number of benefits. They are more accurate than manual data recording systems
and offer more detailed data collection for no additional effort. Some systems can now
offer documentation of an anaesthetic, even for the shortest of cases, in less time than
it takes to write it down. However, there is a perception that the accurate recording of
data and the possible recording of monitoring artefacts, may make the defence of the
conduct of anaesthesia more difficult. In a sense this is illogical because physiological
variability and monitoring artefacts are normal occurrences during anaesthetic practice,
not faults of individual anaesthetics or anaesthetists. However, because anaesthetists
do not generally record them, this is difficult to prove. Perhaps the most persuasive
argument in favour of computerized systems is that all records are kept by the
anaesthetic department in a central store and can be recovered instantly for reference,
collective statistical analysis, comparison, quality control, transmission to other
interested parties or for defence.
Legal aspects
The law does not prescribe any particular format or content for an anaesthetic record.
In fact, there is no statutory requirement for a record to be kept. Common law, however,
provides that the standard of care offered to a patient has to be higher than that which
could not be condoned by a reasonable body of ones peers (the Bolam principle).
Therefore, as most anaesthetists keep records, it must be regarded as required in
common law to do so. Powers has stated: As a matter of evidence, medical records
do not prove themselves any more than a newspaper article is proof of the facts to
which it relates. It would seem reasonable though, to assume that a record compiled
electronically by automatic collection of data from a vital signs monitor would gain
higher standing as evidence of fact than a manual set of notes that are known to suffer
from inaccuracies in transcription. While the possibility of tampering with computerized
data exists, in reality it is highly unlikely. If an anaesthetic is properly conducted and
accurately recorded, it is difficult to see how the anaesthetists legal position could be
damaged by this, almost incontrovertible, evidence. The strength of such evidence is
related to the likelihood that a set of data fit with each other and with the story they are
asked to support. Figure 2 shows data taken from a real case record. The fall in end-
tidal carbon dioxide associated with a period of hypotension, and the subsequent after-
drop in temperature fit well with sudden massive blood loss and fluid resuscitation. u
FURTHER READING
Byrne A J, Sellen A J, Jones J G. Errors on Anaesthetic Record Charts as a Measure
of Anaesthetic Performance during Simulated Critical Incidents. Br J Anaesthesia 1998;
80: 5862.
Ellis R H, ed. The Case Books of John Snow. London: Wellcome Institute for the History
of Medicine, 1994.
Mushin W L, Rendell-Baker L, Faning E. The Cardiff Anaesthetic Record System. Br J

Anaesthesia 1954; 26: 298312.
Powers M. Record-keeping in Anaesthesia: What the Law Requires. Br J Anaesthesia

1994; 73: 224.
Smith A. New College Guidelines for Anaesthetic Records How do Current Forms
Measure up? R Coll Anaesthetists Newsl 1997; 36: 35

Clinical Service and Audit
Ranjit Verma
Ranjit Verma is Consultant Anaesthetist at the Derby City General Hospital. He

qualified from the University of Manchester and is the Honorary Secretary and
Chairman Elect of the Society for Computing and Technology in Anaesthesia (SCATA)
and a council member of the Association of Anaesthetists of Great Britain and Ireland
(AAGBI).
The purpose of audit is to provide an efficient, safe and reliable healthcare service that
offers the best quality patient care achievable under the circumstances. By looking
critically at the processes, mechanisms and quality of healthcare delivery, areas of
deficiency can be identified and improvements made or remedial action taken. To
facilitate this, various organizations have been formed and many processes created.
National Health Service (NHS) Trusts are now required to implement these processes
and can be severely penalized if they fail to comply with them.
Patient expectations have also changed following a series of highly publicized events
including problems at the Bristol surgical cardiac unit, which resulted in two surgeons
being struck off the medical register in 1998 and Dr Harold Shipmans conviction for
murder in January 2000. Therefore, it is imperative that a culture of self-examination,
accountability and openness is established and becomes part of normal clinical
practice.
Kings Fund Organizational Audit

Kings Fund is an independent charitable organization that was founded in 1897. Its
aims are to support health, mainly through improving the quality of health and social
care services. It supports research, addressing issues relating to funding of the NHS
and the inequalities of access to healthcare, and promotes development work in service
provision, such as implementing clinical effectiveness, better services to carers and
education in NHS management.
In 1989, it launched a project called the Kings Fund Quality Programme, which looked
at the quality of healthcare delivery in NHS hospitals based on specified standards.
In 1990, this became the Kings Fund Organizational Audit and most organizations
delivering healthcare, both NHS and private, subscribed to its standards. In 1998, the
Kings Fund Organizational Audit was relaunched as the Health Quality Service.
Health Quality Service

The Health Quality Service is an independent charitable organization and is the
successor to the Kings Fund Organizational Audit. It gained accreditation from the
UK Accreditation Services as an ISO9002 certified body in 1999. This means that it
can award ISO9002 certification to health organizations that fulfil its criteria. It has
developed accreditation criteria for acute hospitals, community, mental health, learning
difficulties, palliative care and hospices. Its programme for accreditation is voluntary
and several NHS Trusts and many private hospitals subscribe to its quality standards.
Audit Commission
The Audit Commission was first established in 1983 to regulate auditors of local
authorities in England and Wales. In 1990, its role was extended to include the NHS. Its
remit now covers over 13,000 bodies who, between them spend nearly 100 billion of
public money annually. The Audit Commission is an independent body which appoints
auditors to assess and monitor the way the money is spent and to determine if the
various bodies get value for money. Its most recent project involving clinical services
is the Acute Hospital Portfolio. This is a collection of audits available for auditors to
undertake at acute hospitals. They focus on key service areas or resources within the
Trusts. Each year the Commission plans to select up to four topics from the portfolio to
survey across all the Trusts in England. The topics are clinical and non-clinical.
National Institute for Clinical Excellence (NICE)

NICE was established as a Special Health Authority of the NHS in 1999. Its purpose
is to provide authoritative, robust and reliable guidance on current best practice to
patients and their carers and to health professionals and the general public. Projects
are undertaken at national level and evaluated by a panel of experts, which includes
NHS professionals and members of the lay public, including clinical professionals,
patient and carer representative groups, NHS managers, members from industry
and research bodies and from the Royal Colleges and professional societies and
associations. NICE produces three types of guidance.
Technology appraisals are independent reviews of the clinical usefulness and cost-
effectiveness of specific technologies such as the use of a drug, equipment, diagnostic
technique, surgical procedure or health promotion activity. Technology appraisal can
take up to 1214 months to produce.
Clinical guidance is produced for healthcare professionals and patients to help them
make the right decisions about healthcare in specific clinical circumstances. These
guidances are intended to be used in conjunction with current knowledge to help make
the right decision for a given scenario. Clinical guidance can take about 2 years to
produce.
Interventional procedures relate to the efficiency or effectiveness of new procedures,

for example the use of a new surgical technique and its implications in the wider
context.
Commission for Health Improvement (CHI)

CHI was launched by the Government in April 2000 aimed at improving the quality
of patient care in the NHS. One of its most significant aspirations is to abolish the
inequality of standards that exists throughout the NHS. CHI aims to achieve this by
undertaking clinical governance reviews, by visiting every NHS Trust and Health
Authority including Primary Care Groups, Local Health Groups and General Practices
in England and Wales on a rolling programme every 4 years. It investigates any serious
failures and checks that the NHS is following national guidelines. It makes its findings
public. A typical review takes 17 weeks and has clear objectives and deadlines, which
include consultation, data collection and analysis.
Commission for Healthcare Audit and Inspection (CHAI)

CHAI is the next step in the Governments plans to monitor quality of healthcare
delivery in the NHS and is planned to be implemented by 2004. It will have appropriate
legislation from Parliament and its purpose is to inspect every part of the NHS and
private healthcare. It will monitor and review the quality of healthcare delivery and
assess how well the NHS is using its funds. It will report to Parliament. It will take over
all of CHIs current functions and the National Care Standards Commissions (NCSC)
responsibilities for inspecting the private health sector. The Audit Commissions value-
for-money studies relating to healthcare, as well as some of its other functions, will also
come under CHAIs umbrella, and it will be responsible for a star rating system for NHS
hospitals and for instigating special measures in those organizations that fail.
The NHS Litigation Authority (NHSLA)

The NHS Litigation Authority is a Special Health Authority that handles claims and
indemnifies NHS bodies in respect of both clinical negligence and non-clinical risks.
Clinical negligence claims are handled through the Existing Liabilities Schemes for
pre-1995 claims, and the Clinical Negligence Scheme for Trusts for incidents after April
1995.
The incidence of claims against clinical negligence continues to rise. In 1999/2000, the
NHS spent 386 million in settling negligence claims and it is estimated that the net
value of claims outstanding against the NHS alleging clinical negligence is about 2.6
billion. There is also an estimated liability of a further 1.3 billion for negligent episodes
that are likely to have occurred, but for which claims have not yet been received. On
average, claims take over 5 years to resolve and there were 23,000 claims outstanding
in 2002.
Clinical governance
Clinical governance strives to improve and assure a high standard of clinical practice.
It was first described by the Government in 1998 as a new system in NHS Trusts and
primary care to ensure that clinical standards are met, and that processes are in place
to ensure continuous improvement, backed by a new statutory duty for quality in NHS
Trusts. The responsibility for clinical governance rests with the chief executive of each
Trust, but it is usually implemented jointly by consensus between senior management
and clinicians. The process is open to public scrutiny and every clinician is required
to take part. It is a multifaceted process and involves participation in several activities
such as clinical audit, education and training, research and development and risk
management.
Evidence-based medicine
Evidence-based medicine is a process of systematically reviewing, appraising and
using clinical research findings to aid the delivery of optimum clinical care to patients.
It is seen as increasingly important in assuring clinical effectiveness in terms of
treatments and of cost-effectiveness. Evidence is gathered from existing sources
such as research and scientific reviews, and is subjected to a critical appraisal. Critical
appraisal is a method of assessing and interpreting the evidence by systematically
considering the validity, results and relevance to the problem being considered.
Following the appraisal process, evidence-based guidelines are produced and
disseminated for implementation.
Clinical effectiveness
Clinical effectiveness is the extent to which specific clinical interventions do what they
are intended to do (i.e. maintain and improve health and maximize health gain from
available resources). It consists of obtaining evidence (e.g. from journals, national
guidelines or other sources), implementing changes based on the evidence, and
assessing the effect of the changes.
Risk management
No activity is without risks. In healthcare delivery there can be risks to the patients,
to the practitioners and to the organization providing the healthcare service. Risk
management is a process that tries to keep these risks to a minimum. If things go
wrong, the process attempts to find out why and ensures that it does not happen again.
A risk management strategy should ensure a safe working environment. Training should
be appropriate for the tasks being undertaken and untoward or critical incidents should
be easily identified and reported. There should be an effective claims management
mechanism in place.
Clinical audit
The NHS Executive defines clinical audit as the systematic critical analysis of the
quality of healthcare, including the procedures used for diagnosis, treatment and
care, the use of resources and the resulting outcome and quality of life for patients. It
embraces the work of all healthcare professionals.
Clinical audit can be retrospective, prospective or related to significant events. It is a

cyclical process in which standards are agreed and data collected. Analysis of the data
shows if the standards are being met. If not, changes are planned and implemented
and data collected for a second time and analysed to see if any improvements have
resulted from these changes (Figure 1). It is important to realize that data are collected
and analysed on two occasions. The first data collection is to establish the current
position and the second is to see if any improvements have been made. The audit
process should allow sufficient time for the changes to take effect and it may be
necessary to repeat the audit cycle several times before the benefit is seen.
The audit cycle
Select or re-select topic
Evaluate effects Define criteria

of change Set standards
Implement Plan
changes methodology
Collect and
analyse data
1
Clinical audit is likely to be successful if it is done voluntarily rather than being imposed.
The topic selected should be relevant and potentially beneficial to the patient or to the
organization and amenable to improvement. The whole process should be trans-parent.
The criteria being measured should be meaningful and clearly defined. The standard
against which the criteria are measured should be realistic and based on what is right
for the local circumstances. Careful planning of how the audit will be done is critical
and the methodology should be kept as simple as possible. Only data that are relevant
to the topic should be collected (collection of superfluous data is time-consuming
and wasteful). Data collected for clinical audit, unlike clinical research, is not usually
subjected to rigorous statistical techniques, simple percentages are usually sufficient.
If the first run shows that the stipulated standards have been met, it is important to
consider if this is because the performance is genuinely satisfactory or whether the
standards were set too low. If the analysis shows that standards are not being met,
changes need to be agreed and implemented and the process repeated to see if the
changes have achieved an improvement.
PDSA (Plan, Do, Study, Act) cycle

The PDSA cycle (Figure 2) is a tool for bringing about change in an organization by
breaking it down into small manageable elements. It consists of looking at small areas
to see if improvement can be made to benefit the whole. Large numbers of individuals
involved in small, simple PDSA cycles are more productive in terms of seeing the
process through and instigating minor changes that make a significant difference to the
whole.
Plan a small area of perceived benefit is identified by any individual working in a

given environment. A change in working practice is planned with clear objectives in
mind. It is important to be aware of who might be affected by this change.
Do the plan is executed over a short period of time. Careful documentation and
unexpected observations are recorded. Analysis of the results as they are collected
may be started.
Study the analysis is completed and results compared with predictions.
Act if the original precept is justified, the proposed changes are incorporated as a
matter of policy and disseminated throughout the organization. If there is no significant
gain, the cycle may be repeated or the idea for that particular change dropped.
The PDSA cycle
Plan
Act Do
Study
Informatics
The Government has committed itself to an expenditure of 1 billion over a 7-year
period to modernize the NHS inform-ation technology (IT) infrastructure. The
programme, which was started in 1998, focuses on five main areas:
NHS Direct
NHS Net
National Booked Admissions Project
National Electronic Library for Health (NeLH)
Electronic Health Record.
All Trusts have been building up their IT infrastructures to enable them to exploit these
developments. As these technologies come on stream it should make audit of clinical
services easier, simplifying data collection, analysis and report generation. The use
of e-mail to facilitate communications in the NHS is already well established. Medline
and Embase offer excellent electronic access to peer journals while the Cochrane
Collaboration, through their network of collaborative review groups, provide objective
reviews of various topics to enable healthcare professionals to improve clinical
management of patients. u
FURTHER READING
Department of Health. The New NHS: Modern, Dependable. London: Stationery Office,
1998.
http://audit-commission.gov.uk
http://www.chi.nhs.uk
http://www.cochrane.org
http://www.embase.com
http://www.hqs.org.uk
http://www.kingsfund.org.uk
http://www.nao.gov.uk
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi
http://www.nice.org.uk

Communication: Health
Records
Roger M Tackley
Roger M Tackley is Consultant Anaesthetist at Torbay Hospital, Torquay. He is

devoting increasing amounts of time to developing electronic patient record systems
for the South West region. He has been involved in the NHS Clinical Terms Project,
Headings Project and Maternity Data Care Project, and is currently the Chairman of the
Society for Computing and Technology in Anaesthesia.
Treating and caring for patients usually involves a team of clinicians who work
different shifts and may work in different locations. Unless there are good methods of
communication, clinical care will be delayed or compromised. The limitations of holding
health records on paper are becoming more obvious as the throughput of patients
increases, staff work shorter shifts with more handovers, patients demand access to
their records and new rules for confidentiality are introduced. In response to this, the
NHS published Information for Health in 1998, which outlined its plans to computerize
hospitals and the benefits that would follow to patients, staff and public. A key target
is that all acute hospitals will have an Electronic Patient Record by 2005. This was
supported by another White Paper in July 2002 entitled Delivering 21st century IT
support for the NHS.
Health records
The importance of clinical records is often underestimated. According to the Audit
Commission report Setting the Record Straight in 1995, clinicians spend at least 25%
of their time recording, reading or manipulating information. Health records are kept for
several reasons.
Record care given to monitor progress and reaction to different treatments. It also
records what has been explained to the patient.
Communication information is shared among the clinical team and, increasingly, with
the patient.
Source of data for aggregate analysis information for audit and clinical governance
is often extracted manually from notes.
Archive notes are kept as an historical record.
Legal record notes are often used to support or refute complaints and medico-legal
actions.
Standards for clinical record keeping: guidelines for record keeping have been
developed by The General Medical Council (GMC) (Figure 1), the Clinical Negligence
Scheme for Trusts (CNST), Royal College of Anaesthetists Good Practice Guide
(Figure 2), CASPE Accreditation and Development of Health Records and many other
clinical bodies. It is the clinicians responsibility to keep good records because so
much depends on them. The NHS Litigation Authority uses the standards developed
by the CNST to accredit hospitals into different categories of medico-legal risk. This
affects the insurance premium each Trust has to pay. It is clear from the standards (see
NHSLA web site) that there is less risk, for instance, when different clinical disciplines
all use the same health record.
GMC Good Medical Practice 2001 (extract)
In providing care you must:

keep clear, accurate, and contemporaneous patient records
which report the relevant clinical findings, the decisions made,
the information given to patients and any drugs or other
treatment prescribed'
'keep colleagues well informed when sharing the care of
patients'
RCA Good Practice Guide 1998 (abbreviated)
'The record must be such that if another doctor were required to

take over the case this record would give him/her systematic and
ready access to all the information required'
Points to include
Basic data: names of surgeon(s) and anaesthetist(s), date,
proposed operation
Patient identification: name, age, gender, hospital number
Preoperative assessment: relevant history, physical
examination, drugs, allergies
Intravenous drugs administered
Relevant equipment monitoring
Patient monitoring used: recommendations of the Association of
Anaesthetists
Physiological variable recorded: not less frequently than every
15 minutes
Fluid balance: evidence of venous cannulation and record of
fluids
Postoperative pain relief: clear and appropriate postoperative
analgesic orders
Other postoperative instructions
Critical incidents and complications must be accurately
documented
Handover from one anaesthetist to another should be noted
Archiving NHS records: in the UK, there are statutory requirements for how long
health records must be kept. In the case of hospital records some examples are:
8 years, in general, unless specified below
children up to 25th birthday
donor records 11 years post-transplantation
maternity 25 years
mentally disordered 20 years after last treatment
patients in clinical trials 15 years after end of treatment
litigation 10 years
audit documents 2 years
theatre registers local decision in consultation with health professionals.
Electronic patient records (EPR)

The NHS defines EPR as 'A record containing the patient's personal details
(demographics), their diagnosis or condition, and details about the treatment/
assessments undertaken by a clin-ician. Typically it covers the episodic care provided
mainly by one institution.' In practice, there are separate EPRs for a patient in a number
of Trusts, GP surgeries and specialist clinical systems (e.g. anaesthetic record keeping
systems). The NHS has defined six levels for EPR; each builds on the previous level:
clinical administrative data
integrated clinical diagnosis and treatment support
clinical activity support
clinical knowledge and decision support
specialty specific support
advanced multimedia and telematics.
Telemedicine allows clinicians in remote areas to access expert advice from specialists.
Other multimedia applications allow the storage of video or sound clips in the patients
notes. Well-designed EPR screens allow a user-defined composite view of patient
information. Figure 3 shows a problem list, an in box of current messages and a
timeline summary of clinical results. The screen is interactive so the clinician can click
on any item and find more details, and if security allows, edit or add further orders.
3 Example of electronic patient record screen.
Electronic health record (EHR)

The NHS defines EHR as the concept of a longitudinal record of patients health and
healthcare cradle to grave. It combines the information about patient contacts with
primary healthcare as well as subsets of information associated with the episodic
elements of care held in EPRs. EHRs will probably follow the introduction of EPRs; pilot
sites are expected to be running by 2005.
The use of an EHR is epitomized in the following scenario. There is an emergency

admission of a confused, semiconscious patient with abdominal pain following a road
traffic accident. Using the details found in his wallet, it is realized that he is not on the
hospital patient administration system, and so the EPR software is used to access the
National Strategic Tracing Service (NSTS) to obtain his NHS number. Doctors treating
this patient will then have access to the EHR and using the patients NHS number can
look up his:
current medication (e.g. insulin)
current diagnoses (e.g. diabetes, porphyria, angina)
previous contacts shows current GP and last admission to hospital.
It is then possible to contact the last hospital for details of any previous anaesthetic and
possibly obtain an electronic reply. Even without it, the anaesthetist is forewarned about
many aspects that improve the patients care.
Clinical language
If information is to be shared, clarity is essential. To share information, clinicians must
use the same language. For instance, there are many ways of recording a prolonged
suxamethonium effect:
suxamethonium apnoea
sux apnoea
scoline apnoea
prolonged succinylcholine block
dual block.
All of which can be further confused by spelling mistakes. This problem is exacerbated
by the use of computers, which are very good at legible recording and rapid display, but
can interpret only what they have been programmed to recognize. Therefore a search
for all the scoline apnoeas will not automatically find the sux apnoeas. To improve
communication between disciplines and to allow computerization of health records a
comprehensive, but flexible, set of terms must be used.
Statistical classifications
For many years, the NHS has been compiling statistics based on diagnoses and
operations recorded during a hospital admission. For accuracy, there are strict rules
about which codes must be used for which concepts. The International Classification of
Diseases (ICD, now in version 10) and the Office of Population Censuses and Surveys
(OPCS) classification of operations and procedures (version 4) have been used for
many years to code diagnoses and operations which are then sent to the Department
of Health hospital episode statistics (HES) department for aggregation.
One disadvantage of these classifications is that the terms used are often unsuitable
for clinical use; for example, Epidural anaesthetic using sacral approach, Biopsy of
cerebellum NEC. Despite this, many electronic systems incorporate these terms and
expect clinicians to use them. Another disadvantage is that OPCS4 (about 7000 terms)
does not include procedures for nursing or physiotherapy, and is revised so seldom
that newer techniques have to be included as OS (otherwise specified). ICD10 (about
11,000 terms) includes very few symptoms and signs so that it is impossible to record a
full clerking or nursing assessment.
Clinical terminologies
In the UK, over half of GPs use computerized record systems. They need to be able to
record symptoms and signs, treatments and operations. In the 1980s, a GP called Dr
Read developed a coding system that covered most of what a GP needed to record.
This was bought by the Department of Health in 1990 and expanded to include what
hospital clinicians needed. The resulting clinical terms (CTV3) were comprehensive
(nearly 300,000), but at the time too complex for most system suppliers to take on.
In 1999, the NHS formed an alliance with the College of American Pathologists
to merge CTV3 with SNOMEDRT (Systematized NOmenclature for MEDicine
Reference Terminology), a terminology in use in the USA. The NHS expect that this
new terminology (SNOMEDCT) will be in use in clinical systems by mid-2003. Being
an international terminology there are many advantages to clinical system suppliers
in using it. SNOMEDCT has 325,000 concepts and over 800,000 terms including
synonyms and so it has to be used in a computerized environment.
SNOMEDCT maps to other coding systems (e.g. ICD10 and OPCS4) which means that
even if clinical information is recorded only in SNOMEDCT, it can be semi-automatically
mapped to other classifications, saving many hours of coding work. Figure 4 shows the
progression from recording notes in free text, which is unreliable to analyse, to using
SNOMEDCT which allows recording of clinical detail in a reproducible format, and
then classifications (e.g. OPCS4) which can be used to generate Healthcare Resource
Groups for management purposes.
Aggregation of clinical terminology
Team working
Communication with other members of the clinical team may be by sharing the health
record, by correspondence or by conversations (face to face or by telephone). The
members of the clinical team may be based on one site but more often are not. Each
discipline tends to use their own structures for recording patient assessments; for
example, doctors use history and examination headings and nurses use activities
of daily living. In order to share information effectively, there must be a structured
handover. This may be face to face, but often staff are too busy to do this for all
patients. It is recommended that clear summaries of the patients problems and
progress are kept so that any clinician can quickly understand the relevant issues.
Laurence Weed has written many papers on the benefits of Problem Oriented
Medical Records. Out of this has come the concept of a shared problem list which
is much easier to maintain in an electronic patient record, and is accessible to all
authorized staff, at any time and simultaneously if necessary.
Structured notes and discharge summaries

Many studies have shown that doctors prefer to use semi-structured notes for clerking,
discharge summaries and anaesthesia. They speed the entry of information, reduce
omissions and make it easier to find important facts. GPs prefer to receive discharge
summaries set out with sections for: reason for admission, diagnoses, investigation
results, operations performed and drugs on discharge. As yet there are no standard
headings but the National Headings project (see NHSIA website) has proposed a
set that has worked well in many pilot sites and should be used as guidance when
designing any structured clinical notes. u
FURTHER READING
Audit Commission. Setting the Record Straight, 1995.
Burns F. Information for Health. NHS Executive, 1998.
Coiera E. Guide to Medical Informatics, the Internet and Telemedicine. London:

Chapman & Hall Medical, 1997.
NHS Information Authority www.nhsia.nhs.uk. This has links to the Headings Project,
Clinical Terminology and SNOMEDCT, Electronic Records Development.
NHS Litigation Authority. CNST Standards. www.nhsla.com
Royal College of Anaesthetists. Good Practice Guide. www.rcoa.ac.uk.
Weed L L. Medical Records that Guide and Teach. New Eng J Med 1968; 278: 593
600.

Confidentiality and Security of
Information
David Jones
David Jones is Consultant Anaesthetist at the Royal Gwent Hospital, Newport, Wales.
He qualified from Manchester University and trained in anaesthesia in Birmingham and
Cardiff. He gained an MSc in medical informatics at the University of Wales, Cardiff. His
interests include day-case anaesthesia, diving medicine and informatics.
Keeping patient information confidential is not a new issue (it is one of the professional
responsibilities placed on doctors by the GMC), but because of the rapid rise in
electronic processing it has acquired greater emphasis. In addition, there has been
increasing dependence on information technology in healthcare and a greater need
for information to be made more widely available. To address the consequent security
implications, the UK government has produced new guidelines and there have been
changes to the law. While much of the provision of security may lie at a corporate level,
individual health workers have obligations dictated by these guidelines and laws.
Information security is about preserving confidentiality, integrity and availability of

information (Figure 1). Security can never be perfect and there is an element of
mutual incompatibility with this triad. Making information more easily available, even
for authorized access, can compromise confidentiality and the more the information
is made available by accessing, updating and transmitting, the more likely its integrity
may suffer. Failure of these three principles can cause problems. Service disruption can
occur if vital data are unavailable; there can be loss of privacy; patient harm can result
if vital information is incorrect or unavailable, and financial loss can be incurred with
the replacement of lost equipment and information. There are also the wider issues of
falling foul of the law and loss of public confidence.
Information security
Confidentiality a for your eyes only principle, access is confined to

those who have authority
Integrity relates to the preservation of information in the form that it

was recorded
Availability involves ensuring that information can be provided to the

right person when required
1
Department of Health directives

In the UK, a number of government documents relate to information technology.
The most relevant are the Department of Healths prescription for the future use of
information technology Information for Health and the more technical Building the
Information Core. They describe computer systems using lifelong electronic records,
and are available round the clock to health workers in all disciplines across the
whole NHS. The security implications of this are recognized in the documents. It is
acknowledged that patients must be made aware of the intention to share information
and their objections respected and that all systems should have access controls to
preserve confidentiality and adhere to legislation.
Growing confidentiality problems led to the government convening a committee chaired

by Dame Fiona Caldicott with the purpose of reviewing the confidentiality issues of
patient-identifiable information. This Caldicott Committee identified principles of good
practice that NHS Trusts are obliged to adopt for all information flows. Each Trust
is required to appoint a Caldicott Guardian, a board-level healthcare professional,
whose role is to supervise the production and execution of local policies ensuring
confidentiality. Every use of patient-identifiable information must be justified and where
possible excluded in information flows. Trusts are responsible for ensuring that only
those with authorization and a need to know should have access and even then only
to those items that they need to see. Trusts must regularly review their practice and
institute appropriate security, ensuring that all uses of information are legal and that
those with access are aware of their responsibilities and legal obligations.
Legislation
The 1998 Data Protection Act came into force in the UK on 1 March 2000, replacing
the 1984 version and incorporating the 1990 Access to Health Records Act. It defines
data processing as collecting, using, modifying, storing and disclosing information. It
uses the terms data controller to describe those responsible for processing information
and data subject as the person whose information is recorded. It is designed to protect
individuals by preventing misuse of their personal information and defines situations in
which those who process personal information should register their use. It applies to
living persons; the 1990 Access to Health Records governs access to records of the
dead.
The Act uses the word data where the word information might be preferable. In
precise terms data is a pure collection of values or terms without meaning and as such
has no confidentiality issue. Information is data with meaning. I have used the word
data where it is used in reference to the Act. The Act has eight principles.
Data shall be obtained and processed fairly and legitimately the criteria given for
fairness are that the common law duty of confidence is complied with and that the data
subject was not misled into providing information. The data subject should be aware of
how the information will be used and who will use it. To be legitimate, either consent
must be given or there must be a valid reason as described by the Act. Two schedules
define valid use (schedules 2 and 3). Schedule 3 describes the use of sensitive
information such as health records, defined by the Act as information relating to the
physical or mental health or condition of an individual which have been made by or on
behalf of a health professional in connection with the care of that individual.
Data shall be obtained only for specified and lawful purposes the information
cannot be used for a purpose other than that specified without consent of the data
subject.
Data shall be adequate, relevant and not excessive pro-cessed information must
be sufficient to perform the specified task but no more than the minimum required data
items must be used.
Data shall be accurate and where appropriate up to date it is a duty of the

controller to take reasonable steps to ensure information remains accurate.
Data shall be kept for no longer than necessary they should be retained only for
the duration of the specified purpose.
Data shall be processed according to a data subjects rights subjects have a

right to see what is recorded about them (subject access), though the Act provides
an exception if awareness could be considered harmful to their physical or mental
health. For a small fee (10; though documents such as radiographs can cost up to
50) they are entitled to a description of the information, its purpose, who may use it,
a copy in a form they can understand (but not the original) and how it was obtained.
Where processing contravenes the Act a subject has the right to prevent processing
and demand rectification. There is a right to control use of data where it is used for
automated decision making, for instance, where patients may be placed on a waiting
list. In such circumstances they have a right to demand a manual analysis. The
Information Commissioner, formerly known as the Data Protection Registrar (currently
Elizabeth France), can be asked to make an assessment if there is a dispute and,
where appropriate, take action against the data controller.
Data shall be protected by appropriate security the Act does not define
appropriate. There is considerable scope for interpretation of what is reasonable.
Data shall not be transferred without adequate protection this principle governs
international transfer. Personal data must not be transmitted unless that country or
territory ensures an adequate level of protection of the rights and freedoms of data
subjects in relation to the processing of their personal data.
Consent
The Data Protection Act does not require consent for using personal information
in healthcare. The important criterion is that the data controller can show that the
specified purpose could not readily be achieved without its use. In any other instance,
anonymized information should be used or explicit informed consent obtained from
the data subject. The Commissioner interprets healthcare quite broadly to include
preventative medicine, medical diagnosis, medical research, the provision of care
and treatment, and the management of healthcare services. If patient information is
disclosed to others, the data controller has a duty to ensure that those to whom the
information is disclosed have the same justification. Because of the proposed wider
use of health records in the NHS and potential disclosures the safest option would be
to obtain explicit consent to that wider use. While Trusts generally produce leaflets
for patients on the use of health records, obtaining explicit informed consent does not
seem the norm.
The Act defines other valid processing purposes which could apply to doctors: for
the performance of a contract; where required by statute (e.g. infectious disease
notification); and circumstances that are considered to be for the greater public good.
The latter is open to interpretation. There are many potential consequences of the Act
that have yet to be tested in Court. For their own protection, health service employees
who record and use patient information should ensure they do so within local guidelines
based on Caldicott recommendations, which are governed by the law. These guidelines
will develop as the NHS implements technological strategies.
The Computer Misuse Act 1990 protects information systems from the acts of
individuals. It makes it an offence to access a computer system without authority and
an offence to cause modification to that system.
Other laws relate to information security, but the two described above are the most
relevant.
Security measures
Security breaches fall into three categories:
denial of access
unauthorized disclosure
unauthorized destruction or modification of data.
Appropriate countermeasures to deal with these issues require resources, and their
cost has to be considered relative to the cost of the assets to be protected and the risk
of harm.
Theft prevention is a major security problem in any large organization and loss of
equipment is a common cause of denial of access. Controlling physical access to
secure areas by ensuring locks are used is essential. There is a need for a cultural
change in the NHS where open access to areas that should be secure has been the
norm.
Information security covers all communication, even what is spoken, therefore general
office security must cover information given over the telephone or sent by fax, in both
cases the recipient may not be the intended person. Media containing confidential
information should be locked away and sensitive documents shredded when no longer
needed.
Network security
Access to hospital systems is generally made over a network and the logging in
process attempts to restrict access to those authorized. Each user has a user name
provided by the system administrator. This identifies the user to the system for the
purpose of determining to which parts of the network and to which processes the user
has valid access. This can also offer accountability because an automated system log
records the actions of individual users. User names are not secret and a password is
also used to authenticate an individual. The password is provided by the system initially,
but should be changed to the users choice as soon as possible. User names and
passwords should not be shared; each user must have their own.
There are some simple basic rules for the choice and use of passwords. Passwords
should be memorable and not a random sequence of characters; they should be kept
secret and not written down. Personal details such as family member names are too
easily guessed. Ideally they should be eight characters or more in length and contain
at least one non-alphabetic character. Passwords should be changed from time to time
and always changed if compromised. Some of these rules, particularly those relating to
length, characters used and the frequency of changes may be enforced by the system.
Different processes, accessible via the same network, may require additional user
identification and passwords, though sometimes a single log in provides access to all.
The former is more secure, but the latter is more convenient. Users are required to log
out of systems when finished and this should be done when leaving the computer to
avoid unauthorized access. Monitors should face away from public areas and have a
facility for screen blanking or a screen-saver to protect information from prying eyes.
E-mail communications can be read on any of the servers on the electronic route from
sender to receiver and therefore are not very secure. Patient-identifiable information
should be encrypted in e-mails. The NHS began rollout of encryption tools in March
2002.
Privacy enhancing technologies (PETs)
Access control and encryption are examples of PETs. The term has also been
associated with features designed to protect identities that substitute identifiers
such as names, addresses and registration numbers with pseudonyms. If it is never
necessary to know the identity of the individuals to whom personal data relates, then
all personal identifiers should be removed. However, this can lead to problems if future
cross-references are needed. Pseudonymization is the process by which pseudonyms
replace the true personal identifiers. The latter are not discarded but retained in
a secure part of the computer system allowing the original data to be retrieved if
appropriate. Normally, only the pseudonyms are visible which allows administrative
tasks to be performed on the data by those who have no need to identify an individual
patient. It could allow researchers to make more extensive use of medical records
without confidentiality becoming an issue.
Logbooks and private practice

The greatest problem for individual doctors is managing the security of patient
information that they have sole control of, such as their personal logbooks and private
practice accounts. A complete logbook database is often carried around, in many cases
on a portable computing device, which is easy to lose. The easiest and safest way to
achieve confidentiality is to remove all patient identifiers, although this precludes cross-
referencing to other information or authentication of individual records later.
Maintaining a copy of the database is essential; it is surprising how often no backup of

essential documents exists. Backup floppy disks or CDs should be verified as a true
copy and kept secure. Electronic logbooks have an advantage over paper logbooks
because they can be protected by a password and encryption. Therefore, even if others
obtain access to the device, the information can be kept secure.
There is no guaranteed way to avoid viruses, but the worst of their effects, destruction
of information, can be resolved by having backups. The risks can be reduced by using
anti-virus software, which must be used regularly and kept up to date.
Research
In the UK, patient information processed for the purposes of medical research has
some exemptions from the Data Protection Act, provided it is not processed to support
measures or decisions relating to an individual patient or in such a way that they may
suffer damage or distress. These exemptions are that personal data may be kept
indefinitely and data may be processed further, provided this is for research purposes.
In addition, subject access is not obligatory provided an individual patient will not be
identified in the results of the research.
Doctors who independently use databases containing patient-identifiable information

must notify the Information Commissioner of that use. This can be done on-line (http:
//www.dpr.gov.uk/notify/4b.html) or by telephone (01625 545740) at a cost of 35
per annum. The doctor has an obligation to ensure that patients know what is recorded,
who will use it and for what purpose. The duty of confidence requires that reasonable
steps are taken to keep information secure. u
FURTHER INFORMATION
Confidentiality General Medical Council, 178 Great Portland Street, London W1W
5JE. 2000.
http://www.gmc-uk.org/standards/secret.htm dpa
Information for Health NHS Information Authority, Aqueous 2, Rocky Lane, Aston,
Birmingham B6 5RQ
http://www.nhsia.nhs.uk/def/pages/info4health/contents.asp
Building the Information Core Implementing the NHS Plan. NHS Information
Authority
http://www.nhsia.nhs.uk/def/pages/info_core/contents.asp
NHS Information Authority provides a help desk on security issues and an Information
Security Manual 01392 251289
Caldicott Report Department of Health 1997

http://www.doh.gov.uk/confiden/crep.htm
Caldicott Guardians Manual The NHS Information Policy Unit, NHS Executive,
Quarry House, Quarry Hill, Leeds LS2 7UE. 1998.
http://www.doh.gov.uk/ipu
Data Protection Act 1998 The Stationery Office Ltd, PO Box 276, London SW8 5DT
http://www.hmso.gov.uk/acts/acts1998/19980029.htm
The Information Commissioner

http://www.dataprotection.gov.uk
BS 7799 Standard for Information Security Management British Standards

Institute, 389 Chiswick High Road, London W4 4AL. 2002.
http://emea.bsi-global.com/InformationSecurity/Standards/index.xalter

Databases
John Fairfield
John Fairfield is Consultant Anaesthetist at the Leeds Teaching Hospital NHS Trust.
He specializes in anaesthesia for spinal surgery, orthopaedics and trauma. He is
adviser to the Trust on clinical informatics and has lectured widely on the subject. He is
Clinical Governance Reviewer for the Commission for Health Improvement.
A database is any collection of data or information, that is specially organized for rapid
search and retrieval by a computer (Figure 1). Databases are built to facilitate the
storage, retrieval, modification, and deletion of data in conjunction with various data-
processing operations.
Database
One or more large structured sets of persistent data, usually associated

with software to update and query the data. A simple database might be
a single file containing many records, each of which contains the same
set of fields where each field is a certain fixed width.
A database is one component of a database management system.
Source: The Free On-line Dictionary of Computing, 19932003 Denis

Howe (http://wombat.doc.ic.ac.uk/)
A database consists of a table or set of tables. The information in the tables may be
broken down into records, each of which consists of one or more fields. Fields are the
basic units of data storage, and each field typically contains information pertaining to
one aspect or attribute of the object described by the database. Using keywords and
sorting commands, users can rapidly search, rearrange, group and select the fields in
many records to retrieve or create reports on particular aggregates of data.
Databases are designed to manage and manipulate structured information. For

example, the telephone book contains several items of information (name, address,
telephone number) about each telephone subscriber in a particular area. Each
subscribers information takes the same form. In terms of a database, the telephone
book is a table, which contains a record for each subscriber. Each subscriber record
contains three fields: name, address, and telephone number. The records are sorted
alphabetically by the name field, which is called the key field.
Figure 2 shows a small section of a table from a medical database used to store a list
of patients and their doctor; the table, a field, record and data item are marked. It can
be seen that a table is basically a collection of data with a name. The name is usually
equivalent to some object (e.g. patient, resource, procedure). One of the main features
of a database table that differentiates it from a spreadsheet is that each record must
be unique. The specific field (or in some cases combinations of fields) that guarantees
that uniqueness is known as the primary key (Figure 3). It is inevitable therefore that the
primary key must be unique.
Field Table

273 12/03/1956 Mr Smith Peterson
Record
922 01/06/1953 Dr Jones Smith
237 04/09/1987 Dr Hall Hughes
148 19/11/1976 Mr Smith Prentice
852 21/04/1945 Dr Jones Williamson
Data item
2

273 12/03/1956 Mr Smith Peterson
922 01/06/1953 Dr Jones Smith
237 04/09/1987 Dr Hall Hughes
148 19/11/1976 Mr Smith Prentice
852 21/04/1945 Dr Jones Williamson

Secondary key One-to-one link
Mr Smith 123
Dr Jones 456
Primary key
Dr Hall 789
If it is necessary to store more information in the database, it is possible to increase

the number of fields in the table. In the medical database, for example, the telephone
number that each patient needs to call to contact their doctor could be added as an
extra field (Figure 3). The use of a database using only a single table to contain all the
data is known as a flat file database. Although adding extra fields is simple, it can lead
to problems. The most important of which is data duplication, for example each doctor
and their telephone number occurs in the table many times. Therefore, there is an
increased need for storage space that can become significant in large tables and cause
slowing of the system. Also, if a doctor changes their telephone number, all the entries
in the table must be changed. A more efficient solution is to add a new table containing
the names of the doctors and their telephone numbers, then to link the new table to the
original one as shown in Figure 3. Each table has its own primary key, and the primary
key of the subsidiary table is linked to a secondary key in the master table.
Databases with linked tables, some of which are related to other tables, are known
as relational databases. The process of moving data into separate related tables is
known as normalization. In real-life databases the number of tables often increases
dramatically. One of the most important aspects of database design is deciding which
fields should go into which table. Normalization and object modelling facilitate this
process.
The object that the table as a whole represents (i.e. what its name stands for such
as doctor) plays some part in determining the fields, however, the fields must be
subjected to a formal process known as normalization to ensure whether they should
be included in the table or would be better included in a different one. If the tables are
designed from an object model they are often already normalized.
Object modelling
The purpose of modelling is to provide a description of a system of some type. It
is a method for distilling the associations between things, and requires a good
understanding of the real-world system that the database is attempting to represent.
The model requires only enough detail to describe the processes and the information
to be represented and it is always context specific. In database modelling terms, a
hospital patient is a different entity from the doctor, the finance manager and the
hospital chaplain.
Normalization ensures that a database can work. Anyone can come up with all sorts
of tables and sets of fields within each of them, but this is ineffective if the data are not
structured in the correct way. A relational database is designed to work with normalized
data and if presented with non-normalized (i.e. unstructured) data it will fail to work
correctly.
Normalization has its origins in mathematical set theory. It was first developed by Edger
Codd in the late 1960s, it is a process that consists of several clearly defined stages
and requires an understanding of functional dependency. Data are said to be in first,
second, third, etc. form indicating how structured they are. Data in first normal form
are said to be less normalized than those in second normal form which, in turn, is less
normalized than those in third normal form. Data can be in one of these normal forms
or be made to conform to one of them by applying a number of strategies, which usually
involves splitting a table up into several smaller ones.
It may sound as if something as technical as normalization should be left firmly in

the hands of experts (often referred to as knowledge domain experts) however, it
is important that data normalization is undertaken by someone who understands
database design as well as the data and their relationships in the real world.
Normalization applied by data processing staff is often done badly, because it
depends on a detailed understanding of the data used by the organization and such
an understanding is seldom held by these staff. Rather, the data are best understood
by managers and users who work with the data on a day-to-day basis. To them,
normalization represents common sense.
The definitions of the forms of normalization are beyond the scope of this article
but are well explained at the web site of DataModel.Org (http://www.datamodel.org/
DataModelReference.html) and in several of the books listed in the Further Reading.
As a result of normalization, the number of tables is often increased dramatically.

This process of increasing the number of tables, but not the number of fields, should
not be seen as increasing the complexity of the database, but the opposite. After
normalization, tables are simplified in terms of conceptual clarity (the tables often relate
more closely to real-world objects) and database operations (updating, deleting and
searching).
Resources
The following websites contain a wealth of information and links to many

other resources.
British Computer Society

http://www.bcs.org.uk
British Healthcare Internet Association

http://www.bhia.org
Datamodel.org (Data modelling made easy!)

http://www.datamodel.org/DataModelReference.html
Relational Database Management Systems

http://cbbrowne.com/info/rdbms.html
What you need to know about databases

http://databases.about.com/mbody.htm
Database management systems

If a database is a collection of data in its component tables then the computer program
that organizes and manipulates the database is a Database Management System
(DBMS). Many computer programs called databases are in reality DBMSs, for example
Access ( Microsoft Corporation), FileMaker Pro ( FileMaker, Inc.) and Paradox ( Corel
Corporation) are designed to work on desktop computers while Oracle ( Oracle
Corporation) and SQLServer ( Microsoft Corporation) are designed to work in a
networked environment.
A DBMS:
contains metadata (the structure of the data)
allows actions to be performed on the data (e.g. adding, editing, deleting, sorting)
supports queries
produces reports based on queries.
Queries and reports

Queries are the main way users retrieve database information. Typically, the user
provides a string of characters and the computer searches the database for a
corresponding sequence and provides the source materials in which those characters
appear. A user can request, for example, all records in which the contents of the field
for a patients last name is the word Smith. More complex queries can be constructed,
for example to list all patients who failed to attend Dr Smiths outpatient clinic in the last
6 months.
Most DBMSs use a standard system called Structured Query Language (SQL) to query
their tables, although most provide a graphical interface to generate the SQL itself.
SQL resembles many programming languages, and is a structured form of English.
For example, the SQL to find which of Dr Smiths patients did not attend would look
something like:
Select * from patients

where surgeon = Smith
and clinic date >( now()-183)
and DNA = True
The result of the query is placed into a new answer table.
Having performed a query to select the data required, DBMSs have the ability to format
the data in the answer table, together with many other complex elements such as other
text and graphics, to produce a report that is easier to use than the raw data. In the
example given above it could be used to produce letters to send to the patients who
failed to attend giving them a new clinic appointment. u
Computers let you make more mistakes faster than any other
invention in human history, with the possible exception of
handguns and tequila
Mitch Radcliffe
FURTHER READING
Carter J. The Relational Database. London: Chapman & Hall, 1995.
Date C J. An Introduction to Database Systems. 6th ed. Addison-Wesley, 1995.
Friedman A L, Cornford D S. Computer Systems Development: History, Organisation

and Implementation. Chichester: Wiley, 1989.

Knowledge Management
Chris Barham
Chris Barham is Consultant Anaesthetist at the Queen Victoria Hospital, East

Grinstead, West Sussex. He is Chairman of the Society for Computing and Technology
in Anaesthesia. He trained at King's College Hospital, London. His interests are
information technology, difficult airway problems and anaesthesia for maxillofacial and
plastic surgery.
A little learning may be a dangrous thing, but our problem today is a seemingly
limitless supply of information.
Data: an item of data (a datum) consists of a label and a value. Thus, pulse = 80,
systolic blood pressure = 120 are data. They convey facts, but tell you little unless you
know their context.
Information: if the above data are known to be from an adult, ASA 1 patient this
provides information. Clearly the information would be different if the data were from a
neonate.
Knowledge can be defined as the information one has acquired through learning
or experience. This implies conscious awareness and is the result of processing
information and assimilating it with other information from the environment. For
example, the doctor may decide to treat hypertension based on information on the
patient, the likely pathology, the pharmacology of antihypertensive drugs and many
other factors. All these integrate to produce knowledge (Figure 1).
Decision-making process
Guidelines
Data
Other
information Protocols
Data Context Information Integration Knowledge
Experience
Data Evidence base
Knowledge may be explicit (e.g. guidelines, protocols, evidence base) or tacit (e.g.
experience, intuition). The former may be written down, but the latter is more difficult to
record because it is in the head. In time, it may be codified, and so become explicit, for
example, the development of algorithms to manage difficult airway problems.
This process of making tacit knowledge explicit is used in decision support. This may
be any method that takes input information about a clinical situation and then produces
inferences that can assist practitioners in their decision making. For example, a
prescribing system might present advice based on information about the patient and the
drugs. It may alert one to potential hazards or interactions, and suggest alternatives. It
may tell you things you already know, but it will not overlook or forget things, as we are
prone to do.
Wisdom is required for knowledge to be useful practically. This is the ability to make
sensible judgements and decisions based on ones knowledge, experience, prudence
and common sense.
Knowledge acquisition: the two main sources are the spoken word and books, but
some others are shown in Figure 2. The textbook is accessible but expensive and
quickly becomes out of date. This journal combines the accessibility of a textbook with
currency of information.
Sources of knowledge acquisition
Books
Lectures
Multimedia
Ask a colleague (Phone a friend)
Survey (Ask the audience)
Guidelines
Journals
Internet
2
Problem-based learning: using a problem-based approach to learning influences

the recall and application of knowledge. The method is based on using a problem (real
or simulated) and access to the knowledge required for its solution. Context is also
important if the environment is real, knowledge retrieval is better. Thus, learning in the
operating theatre is better than using a simulator, but that is better than the classroom.
Learning is most effective when we have access to answers to questions at the point of
patient care. A useful strategy is to develop a personal mission statement for learning,
based on what we need to know and what we are happy to look up.
Information for patients: patients are expressing an increasing desire for information.
The implicit trust placed in the medical profession has been dented in recent years,
and concerns have led patients to search for their own information. They seek it from a
variety of sources, including family and friends, chemists, NHS Direct, the Internet and
medical consultations. The Royal College and Association of Anaesthetists has recently
developed a series of information sources on anaesthesia for patients (www.youranaes
thetic.info).
Information technology: the Internet is a source of knowledge, and the worldwide

web has become the most accessible source of information for many. Email has also
revolutionized information exchange, but it is important to be aware of the security and
confidentiality implications. Email discussion lists can be a useful means of rapidly
seeking the views of a number of colleagues.
Most hospitals now have an intranet, which is a mini-Internet accessible only within
the organization. It can provide access to locally developed information, for example
policies and guidelines. The NHS is committed to giving desktop access to all
clinicians, but this has yet to be achieved. To the anaesthetist, the desktop means the
anaesthetic machine as well as the office. u
FURTHER READING
Wyatt J C. Clinical Questions and Information Needs. J R Soc Med 2000; 93: 16871.
(This is the first of a series of 10 articles on Knowledge for the Clinician published in the
succeeding issues of the journal.)

Secondary Uses of Clinical
Information
John Fairfield
John Fairfield is Consultant Anaesthetist at the Leeds Teaching Hospital, NHS Trust.
He specializes in anaesthesia for spinal surgery, orthopaedics and trauma. He is
adviser to the Trust on clinical informatics and has lectured widely on the subject. He is
Clinical Governance Reviewer for the Commission for Health Improvement.
Information about patients is collected in huge quantities in the health service. Although
some of this information is general (e.g. patient demographics) most is clinical, relating
to the patient's medical condition. This information is stored in a host of systems, some
paper based and some electronic. Much of the information is duplicated.
The primary use of this information is to aid the management of the healthcare of
the patient to whom it relates; to achieve a diagnosis and then to plan and provide
treatment for the patient. Uses for the data that are not concerned with the day-to-day
management of an individual patients illness are termed secondary uses of clinical
information. In general, these are the use of personal information for the benefit of the
community (in its widest sense) rather than the individual. They include:
planning services at local, regional and national levels
record keeping for legal reasons
teaching (including logbooks)
performance management
adverse incident and risk management
complaints and litigation
research
audit
clinical governance, including benchmarking of performance of individuals, teams,
hospitals and regions.
Data aggregation
Many, though not all, of the secondary uses of clinical inform-ation use data that have
been aggregated (data that relate to many patients or have been taken from many
sources). For example, when estimating the number of deaths following myocardial
infarction (MI), the data may be taken from many patients, in many hospitals, following
MI from a number of different aetiologies. This aggregation can be used to define
prognosis, to measure performance, and for research. However, data aggregation is
prone to many problems.
Case-mix in order for the results of the aggregation to be accurate it is important

that all the cases are similar. For example, the mortality following MI complicated by left
ventricular failure is different from uncomplicated MI, and it is relatively easy to separate
these two groups. It is harder to understand the difference in mortality following MI in
patients treated by two cardiologists, unless one knows that one of the cardiologists has
a special interest in diabetic patients.
Data collection using the example of MI, it might seem simplest to use data from
death certification, but this is prone to error. Following MI, many patients die from heart
failure, if only patients whose primary cause of death is recorded as MI are included in
the data, then those suffering MI followed by heart failure will be missed. If heart failure
as the primary cause of death is used, then many patients who suffered heart failure
without MI will be included. The diagnosis at the time of admission could be used,
but many patients have the diagnosis of chest pain made on admission, only to have
MI confirmed later. The number of patients whose diagnosis is obscure on admission
varies between hospitals, invalidating comparison between them.
Using different terms for the same clinical entity the potential for confusion is
clear if one doctor in a hospital records all MIs as myocardial infarction but another
uses coronary thrombosis. It would be difficult to store the full English or Latin name
of every diagnosis and operation. For example, myocardial infarction could be spelt
incorrectly, other words having the same meaning could be substituted, or the doctors
handwriting could be difficult to read. Even if there was unlimited capacity to retain
and search text, it would be impossible to take account of all the possible descriptive
variables that clinicians might use.
Coding
The problem of multiple clinical terms, and that of recording the correct primary
diagnosis, is addressed by using sets of alphanumeric codes. In the UK, the diagnosis
is coded using the International Classification of Diseases, 10th revision (ICD10). The
code for myocardial infarction is I21.9. These codes use less space, are easier to
search and are specific for each disease or diagnosis. ICD also allows certain codes to
be paired to convey more information. Operations and procedures are coded using the
Office of Population Censuses and Surveys Tabular List of the Classification of Surgical
Operations and Procedures; normally referred to as OPCS4. In OPCS4, percutaneous
transluminal balloon angioplasty of the aorta is neatly reduced to L26.1.
Hospital Episode Statistics

Each NHS hospital is required to return data about each patient treated to the
Department of Health. This data set forms the basis of the Hospital Episode Statistics
(HES) system, which is a powerful database containing personal, medical and
administrative details of all patients admitted to, and treated in, NHS hospitals in
England. This information has a host of uses including:
policy development
illustrating variations in health status and health delivery through time and across
geographical areas
production of comparative statistics to assist in performance management
medical research HES contains information of use to clinicians and others who are
developing new treatments, investigating causal factors and monitoring trends.
Some technical terms
Benchmarking
The process of measuring the results of a service at a known point and position
and then evaluating that point-position on a comparative basis with other similar
services on an appropriate and repeatable basis
Case-mix
The mix of people, patients, treatments or services. It is used to understand the
needs, provision and resource uses associated with healthcare
Core Data Sets (CDS)

The core information that health professionals need to exchange and share about
the treatment of a patient with a specific condition (e.g. the national cancer data
sets)
Cochrane Library
An electronic publication designed to supply high quality evidence to inform
people providing and receiving care, and those responsible for research, teaching
and funding and administration at all levels. It is an international endeavour that
prepares, maintains and promotes the accessibility of systematic reviews of the
effects of healthcare interventions
Electronic Health Record (EHR)

The concept of a longitudinal record of a patients health and healthcare from
birth to death. It combines both the information about patient contacts with primary
care as well as subsets of information associated with the episodic elements of
care held in EPRs
Electronic Patient Record (EPR)

Contains a patients personal details (e.g. name, date of birth), their diagnosis
or condition, and the details about the treatment/ assessments undertaken by a
clinician. Typically covers episodic care provided mainly by an institution
Health Benefit Groups (HBG)

A method of linking health needs with service delivery and the expected health
benefit to assist in health needs assessment and planning service delivery
Healthcare Resource Groups (HRG)

A way of grouping the treatment of patients to allow analysis of the
appropriateness, efficiency and effectiveness of care. It is based on clinically
meaningful hospital inpatient episodes and the level of resources
Informatics
Covers all aspects of information management, information systems and
information technology for professional practice
Information management (IM)

The way in which data and information are collected, stored, processed and used
Information technology (IT)

The equipment and the mechanics of information systems
Performance Assessment Framework (PAF)

A group of 6 areas (health improvement, fair access, effective delivery of
appropriate healthcare, efficiency, patient and carer experience, outcomes of
healthcare) by which the performance of all NHS Trusts is measured
Tables summarizing the data are published annually by the Department of Health
and are available from the NHS Executive web site. The records are collected from
all hospital providers in England (Scotland and Wales have their own systems)
and are amalgamated annually. There are 40 items of information (fields) (Figure
1), including some of the patients personal details (e.g. age, gender, place of
residence), information about their admission to hospital (e.g. elective or emergency)
and11 fields provide clinical data (e.g. diagnoses and details of any operations).
Some data fields in the Hospital Episode Statistics
Dates
When admitted
When operated on
When discharged
Cause of accident
E-codes (ICD10)
Hospital Episode Statistics numeric codes
Method of admission
Method of discharge
Surgical procedures
OPCS4 codes
Provider and area codes
Hospital Unit or Trust
Health Authority
Area of residence
Periods in days
Duration of episode
Waiting time
Diagnosis
ICD10 codes
1
Diagnostic analysis
When using systems such as HES to provide answers to questions such as: How
many in-patients were diagnosed as suffering from MI during 2001? it is necessary,
for the sake of consistency, to use common standards when deciding which episodes
to count. Also, it is important to qualify answers with an explanation of how the figures
were produced. In some cases it may be impossible to give an answer because, in HES
for example, information is divided into consultant episodes, it does not deal directly in
patients or stays in hospital. Each record has space for seven separate diagnoses,
which can present another problem. Unless the questioner specifically demands
something different, it is standard to look only at the primary diagnosis field of those
episodes that finished during the year. Counting finished episodes includes some
patients who were admitted the previous year, but this is counterbalanced by those who
remain in hospital until the following year. It is important to understand, for example,
that if a patients primary diagnosis was heart failure, but they also suffered a MI, the MI
will be missed if only the primary diagnosis field is searched.
NHS Performance Assessment Framework

One of the uses of HES data is to generate the information used to produce indicators
of the quality and effectiveness of NHS Trusts. This is known to the NHS as the NHS
Performance Assessment Framework (PAF) and to the media as league tables. It
enables Hospital Trusts to assess and compare their performance against a range of
measures. It has four areas:
clinical effectiveness and outcomes
efficiency
patient/carer experience
capacity and capability.
Of most relevance to HES data are the measures relating to clinical effectiveness and
outcomes (Figure 2). Bearing in mind the problems associated with using aggregated
data, with coding some diagnoses and procedures, and with the variable quality of
the information systems in parts of the NHS, it is easy to see how the performance for
individual Trusts is easily misrepresented. u
NHS Performance Assessment Framework for acute Trusts, clinical

components
i Percentage of patients discharged to usual place of residence within

56 days of emergency admission to hospital with a stroke, aged 50 and
over (age and gender standardized)
ii Percentage of patients discharged to usual place of residence within

28 days of emergency admission to hospital with a hip fracture, aged
65 and over (age and gender standardized)
iii Emergency readmissions to hospital within 28 days of discharge

(all ages), as a percentage of live discharges (age and gender
standardized)
iv Emergency readmissions to hospital within 28 days of discharge

following treatment for a fractured hip, as a percentage of live hip
fracture discharges (age and gender standardized)
v Emergency readmissions to hospital within 28 days of discharge

following a stroke, as a percentage of live stroke discharges (age and
gender standardized)
vi Deaths within 30 days of surgery for non-elective admissions to

hospital, per 100,000 patients (age and gender standardized, includes
deaths in hospital and after discharge)
vii Deaths within 30 days of a coronary artery bypass graft, per 100,000
patients (age and gender standardized, includes deaths in hospital and
after discharge)
viii Deaths within 30 days of emergency admission to hospital with a hip

fracture, of patients aged 65 and over, per 100,000 patients (age and
gender standardized, includes deaths in hospital and after discharge)
ix Deaths within 30 days of coronary artery bypass graft, per 100,000

patients (age and gender standardized, includes deaths in hospital and
after discharge)
2
Resources
British Computer Society http://www.bcs.org.uk
British Healthcare Internet Association http://www.bhia.org
Centre for Evidence Based Medicine http://cebm.jr2.ox.ac.uk/
Cochrane Library http://www.update-software.com/cochrane
Education Training and Development http://www.nhsia.nhs.uk

Programme (NHS)
Health Centre Index http://www.healthcentre.org.uk/
Medical Information Group (MIG) http://www.hull.ac.uk/mig
National Electronic Library for Health http://www.nelh.nhs.uk/
National Health Service Executive http://www.doh.gov.uk/nhs.htm
NHS Performance Indicators http://www.doh.gov.uk/nhsperformanceindicators
FURTHER READING
Checkland P. Systems Thinking, Systems Practice. Chichester: Wiley, 1993.
Hopkins A. Measuring the Quality of Medical Care. London: Royal College of

Physicians, 1990.
Mackenzie I F, Nelder R, Radford G. Needs Assessment at a Practice Level; Using

Routine Data in a Meaningful Way. J Public Health Med 1997; 19(3): 25561.
NHS Executive. Clinical Indicators for the NHS (199495). A Consultation Document.
NHS, 1997.
NHS Executive. Information for Health An Information Strategy for the Modern NHS
19982005. NHS, 1998.

Telemedicine
Sophie M Jones
Sophie M Jones is Research Registrar in Plastic Surgery at Salisbury District Hospital,

Wiltshire, UK. She qualified from Oxford University and UMDS before completing her
surgical training in Norwich. She was involved in the development of a telemedicine
system at the Queen Victoria Hospital, East Grinstead, and carried out research in this
field.
Telemedicine is the assessment and review of patient information (history, examination

or investigations) by a health professional who is separated temporally and/or spatially
from the patient. It is the practice of medicine from a distance; from the Greek tele
meaning far.
Telemedicine is not new; it has been practised since the invention of the telephone.
However, the development of technology, specifically the Internet, has increased the
means whereby information can be acquired and transmitted over large distances.
Virtually any information relevant to patient treatment can now be shared with
colleagues over large distances in a short time. Telemedicine diminishes inequalities in
service provision, improves access to healthcare and reduces costs.
Components of telemedicine
Telemedicine requires communication between two or more sites. The fundamental
components of a telemedicine system are means of information capture, transport and
display.
Information capture: in the medical consultation it is essential to ensure privacy and

security of data using technology that is accurate, reliable and simple to use. Generally,
the patients informed consent is necessary, particularly if identifiable information (e.g. a
recognizable photograph) is to be transferred. There are no standards for photographic
technique and referring practitioners receive little or no training in clinical photography.
However, modern digital cameras are easy to use and attention to detail can result in
excellent images (Figure 1).
Digital images taken by staff and transmitted for expert opinion.
Information transmission: telemedicine can be practised almost anywhere, given

the right equipment. Satellite systems enable access from the most remote locations.
Most systems use telephone networks, digital networks (e.g. Integrated Services
Digital Network (ISDN), Local Area Networks (LANs), Global System for Mobile
communications (GSM), mobile phones, asynchronous transfer mode (ATM)) or the
Internet. Fast, sophisticated and automated telemedicine using intuitive interfaces
and powerful information management systems is possible using these methods of
transmission and current technology. However, simple telemedicine systems can be just
as effective.
Most systems use some form of encryption or exclusive LANs to transmit data securely.
In the UK, the NHSnet is an exclusive intranet which allows communication across
the National Health Service (NHS) while providing maximum security of its contents.
However, no system is completely safe against intruders.
Information display: software used to display the information should be accurate,

reliable and simple to use. Images can be displayed in a variety of formats; the most
common are BMP and JPEG files. JPEG files are smaller than most others, containing
about 300 kB. This is important because the number of pixels used for each image
influences its quality and size and therefore the download time of each file. Having
conveyed the information to an expert, the referring doctor can receive an opinion
in real-time or store-and-forward. In real-time telemedicine at least two individuals
communicate synchronously using a video-conference or a telephone call (e.g.
telepsychiatry). Store-and-forward telemedicine (Figure 2) refers to the transfer of
pre-recorded information that can be assessed in a time-independent fashion (e.g.
teledermatology, teleradiology).
2 Using a store-and-forward
telemedicine system.
History
Telemedicine has been in existence through radio and telephones since their invention.
One of the earliest examples of modern telemedicine was the monitoring of astronauts
physiological functions (blood pressure, respiratory rate, ECG and temperature) by the
US National Aeronautics and Space Administration (NASA) in the late 1960s. Also in
the USA, in 1967, doctors were invited to bring radiographs to Logan Airport in Boston
where they were scanned by a black-and-white camera and transmitted to a video
monitor in the radiology department of Massachusetts General Hospital. Physicians
could then discuss the case by telephone.
The first real-time interactive link was also set up in 1967 between the Nebraska
Psychiatric Institute in Omaha and the Norfolk State Hospital (112 miles apart). The
first use of satellite communications took place in 1976 when the Communications
Technology Satellite Hermes was launched by NASA as part of a joint project with
Canadas Department of Communications to serve remote areas of Canada; it was
used in several telemedical studies. Telemedicine continues to play an important role in
Canadian Healthcare (NORTH Network, Ontario).
Cost
Implementation of telemedicine systems has been resisted partly because of the cost
of purchasing the hardware. However, with the advancement of technology, costs have
fallen. Setting up a telemedicine system is now cheaper and running costs are relatively
low, especially for store-and-forward systems.
Education
Telemedicine enables fast and easy access to medical information and guidance.
Initially, the quality of health information on the Internet was poor, but the quality and
quantity has increased over the last few years and much of it is available to health
consumers as well as clinicians. The Internet allows clinicians to keep up to date with
the latest medical advances, consult online textbooks and share clinical problems.
Increasing numbers of hospital departments and universities arrange interactive
tutorials and case discussions via videoconference. Patients can access information
online about their disease, its management, research trials and support groups.
Legal challenges
The medico-legal implications of telemedicine have been debated extensively. Most
legal and ethical issues are similar to those in general medicine (e.g. security of data,
confidentiality, risk). The specific implications of telemedicine will be revealed by
litigation as they arise. The Health Guidance Note on Telemedicine published by NHS
Estates states that the medico-legal issues are not fully resolved.
Research
The Telemedicine Information Exchange (TIE) (http://tie.telemed.org) is a US-based
database of current research in telemedicine throughout the world. In the UK, the
Telemedicine Information Service (TIS) (www.tis.bl.uk) monitors current research and is
a good source of information.
Implementation
Implementation of telemedicine into routine health services has been impeded by lack
of scientific evidence about its clinical and cost effectiveness. The British government
stated that, without such evidence, telemedicine will not be introduced widely. The
Information Technology departments in UK hospitals are also ill-equipped to cope with
the exponential advancements in medical technology. The integration of telemedicine
into mainstream conventional healthcare is one of the greatest challenges facing the
NHS over the coming years. If met, it will change our way of thinking about the delivery
of primary and secondary care in the next millennium.
Telemedicine holds the promise of improving access to healthcare, especially in areas

where there are geographical barriers. It is evolving into a valuable, but underused,
resource for the delivery of healthcare to patients at a distance, particularly where
patient transport is impractical, expensive, complicated, and/or urgent. Progress in
its use has been slow, it is only in the last few years that telemedicine has moved
from development and evaluation of prototype systems to use in clinical practice.
Today, over 250,000 telemedicine consultations are generated annually in military and
civilian health delivery systems. Thus, slowly but surely, telemedicine is advancing and
changing the practice of medicine. u
FURTHER READING
Arunachalam S. Informatics in Clinical Practice in Developing Countries: Still Early
Days. BMJ 1999; 319: 1297.
Brahams D. The Medico-legal Implications of Teleconsulting in the UK. J Telemed

Telecare 1995; 1: 196201.
Pap S A, Lach E, Upton J. Telemedicine in Plastic Surgery: E-Consult the Attending

Surgeon. Plast Recon Surg 2002; 110(2): 4526.
Stanberry B. The Legal and Ethical Aspects of Telemedicine. London: Royal Society of
Medicine Press, 1999.
Whitten P S, Mair F S, Haycox A et al. Systematic Review of Cost Effectiveness Studies

of Telemedicine Interventions. BMJ 2002; 324: 14347.

Working Clinical Systems
Anthony P Madden
Anthony P Madden is Consultant Anaesthetist in the North Bristol NHS Trust. He

qualified from Oxford University and St Bartholomews Hospital, London. He trained at
St Bartholomews, Great Ormond Street and St Thomas Hospitals, London. He has a
special interest in electronic patient records.
Computerization of healthcare is unavoidable. All clinicians, including anaesthetists,

need to understand what computers can do for them, and what may be involved in the
procurement and implementation of such systems.
In the UK, the NHS has a clear vision and strategy for the implementation of clinical
computer systems, which is set out in documents such as Information for Health, the
NHS Plan, Delivering the NHS Plan, the Wanless Report, and the National Specification
for Integrated Care Records Service.
The problem for clinicians worldwide has been that until recently most of the effort
that has gone into computerization of healthcare has been aimed at supporting
departmental functions (e.g. pathology, radiology, pharmacy) or at supporting the
political need for information about the performance of publicly funded healthcare
systems, including the need for clinical governance.
Why computerize?
There are four main reasons for introducing computers into clinical practice.
Paper-based clinical data recording cannot effectively support new models of care.
Often the information contained in paper records is not available to clinicians when
they need it.
Paper is an inefficient way of providing the information needed for clinical
governance.
Paper processes cannot support clinical decision-making in the way that computers
can.
The way healthcare is provided is constantly evolving. The introduction of ambulatory

centres or diagnostic and treatment centres, remote from the main hospital, and the
requirement that patients should not have to travel long distances for a consultation,
means that clinicians have to travel and may see the same patient in different places
on different occasions during a single episode of care. In this system, there is
considerable risk of paper records going astray and not being available when needed.
Computerization can solve this problem, as well as the associated processes of
booking the patient into outpatient clinic and operating theatre slots, ordering tests,
scheduling transport, booking a bed, transmitting test results, keeping their GP
informed and ensuring the patient is not lost to follow-up (Figure 1).
Some reasons for implementing electronic patient records (EPRs)
making the fundamental and lasting changes that will have a major
impact on patient safety is much more difficult than simply installing
new technologiesWe must re-examine all that we do and redesign our
many and complex systems to make them less prone to human error
Editorial, BMJ, 18 March 2000
If we managed travel like we manage healthcare then travel agents

would book flights on the basis of the flight schedules they could
remember
Lawrence L Weed
Paper clinical notes are poorly legible, ill-structured, bulky and untidy
Audit Commission, 1995
1
Anyone who has spent time trawling through a pile of paper clinical records trying to
extract data for clinical audit will know that this is an inefficient way to gather data for
clinical governance and for central government returns. Paper cannot advise, guide,
or support clinical decision making in an active way. There is no guarantee that the
relevant paper document will be available when needed, for example, a hospital
protocol for the management of insulin-dependent diabetics undergoing surgery.
Computerization can help.
Classification of modern EPR systems

There is no accepted single classification of electronic patient record (EPR) systems.
Systems have a variety of origins and most are undergoing constant development. User
interfaces are being changed, and in some cases the underlying databases and data
structures are evolving. All this makes classification difficult. No single EPR system
can do everything, so a useful primary classification for the core functions of a modern
system is into:
integrated
interfaced best of breed solution.
Even this is slightly false because it begs the question of what functions are core and
what are not. An integrated EPR will need interfaces to secondary or feeder systems
(e.g. pathology, radiology) and these interfaces are typically managed by an integration
engine that translates the output of one system (e.g. pathology) into a form that is
understood by the EPR or vice versa. HL7 is an international standard for transmitting
such structured messages, but some manufacturers have enhanced the standard so
that a degree of translation is required.
A secondary classification is:

designed from scratch using modern technology
based on fundamentally old technology with a user front end that has been updated
over the years
developed from a patient administration system or a departmental system (e.g.
pharmacy).
All modern EPR systems are patient-centric. This means that when a user logs on to
the system the first thing they do is identify the patient or patients in whom they are
interested. This contrasts with older systems, in which a user typically logs in to the
functional area of interest (e.g. patient administration, radiology, pathology) and then
identifies the patient. A system that is not patient-centric cannot provide the integration
of appointment scheduling, bed management and clinical functions demanded of a
modern system.
In terms of technical architecture, modern systems are either based on a client-

server model (where the EPR software resides on the users PC) or a thin client
model (where all the processing is performed on a central server). The clients in
this environment typically use a web browser for the user interface. This may run on
a relatively lowly specified PC, or on a personal desktop assistant (PDA), tablet or
laptop device. Screen size can be a problem with PDAs because it is impossible to
display all the required information on a screen with a diagonal of 810 cm. Thin client
environments are theoretically easier to maintain because enthusiastic users cannot
interfere with the EPR software and thin client devices can be cheaper to buy than a
conventional well-specified PC. The network bandwidth may also be less demanding.
However, client-server architecture can be set up to run in a thin client mode using
special software. This may be useful for running these applications in places that are
remote from the main hospital, such as primary care health centres or community
hospitals.
Core EPR functions

The main EPR functions are:
patient administration
scheduling and tracking
clinical documentation
order communications, including laboratory and radiology requests and results,
pharmacy and electronic prescribing
clinical decision support
analysis.
Jargon buster
ADT Admissions, discharges and transfers, see PAS

AIMS Anaesthetic Information Management System
Arden syntax A programming language for medical logic modules/sophisticated
clinical decision support
DICOM A communication standard for handling digital images, mostly relevant to
diagnostic imaging (e.g. radiographs)
EHR Electronic Health Record, a term introduced in IfH and now superseded
by ICRS. The concept of a cradle-to-grave record of health and
healthcare maintained in the primary care arena
EPR Electronic Patient Record. Superseded by ICRS but still in common use.
The electronic equivalent of the hospital notes folder but with added
functions
GUI Graphical User Interface (e.g. Microsoft Windows)
HL7 Health Level 7. A standards group in the USA. Often used in the context
of structured messages used to send clinical information between
computer systems (e.g. EPR and RIS)
HTML Hypertext Markup Language. The language of the World Wide Web.
A small subset of SGML
ICRS Integrated Care Records Service. A new term encompassing the
concepts of both EPR and EHR
IfH Information for Health. The UK Governments Information Strategy for
the NHS for the period 19982005. Updated in Building the Information
Core
LIMS Laboratory Information Management System. Computer system used to
manage laboratory processes and outputs
LIS Local Implementation Strategy for IfH
Order Comms Order communications. The electronic equivalent of requesting a
radiograph or blood test or almost anything else that may be required for
a patient (e.g. a theatre slot, dietetic advice)
PACS Picture Archiving and Communication System. Uses DICOM standard.
Electronic store for digital images, mostly diagnostic
PAS Patient Administration System. Deals with appointments, waiting lists,
admissions, discharges, transfers and provides information for
Government returns regarding hospital activity
PDA Personal Desktop Assistant. A handheld computer designed to be used
in conjunction with a desktop PC (e.g. Palm or Pocket PC devices)
RIS Radiology Information System. Computer system used to manage
radiology processes and outputs
SGML Standard Generalized Markup Language, a page markup language that
was initially developed in the late 1960s by the US Graphic
Communications Association to permit the electronic transfer of page
formatting and layout instructions from publishers to printers. Adopted as
an international standard in 1986
UML Universal Modelling Language. A technique for modelling processes that
is universally applicable and facilitates the subsequent computerization
of those processes
URL Universal Resource Locator. An internet address (e.g. www.doh.gov.uk/
ipu). Also used to identify resources such as PCs or printers on a local
area network
XML Extensible Markup Language. A subset of SGML. More flexible than
HTML. Can be used to transmit structured messages (e.g. pathology
results)
Most modern EPRs have weak areas and none that the author is aware of does
everything really well, despite the claims of the software companies. Most have a
comprehensive set of patient administration system (PAS) functions, and nearly all
have good order communications functionality, though electronic prescribing can be a
weakness, largely because the software has not yet been fully developed and tested
in clinical use. The ability to document clinical findings and record clinical observations
varies from system to system. Active decision support is an area that all companies
recognize as something that must be supported, though most require work to be done
during implementation to tailor the decision support module to local needs. Analysis is
best performed on an off-line copy of the database, because running reports on the
active copy can result in unacceptably slow response times for clinical users.
Some EPRs have scheduling and tracking functions integrated into their core, thus
permitting a close link to order communications, PAS and care pathways. This
close linkage is not easy if patient scheduling and tracking functions are provided
by a separate system that has to be interfaced to the EPR. Laboratory information
management system (LIMS) and radiology information system (RIS) functions are also
sometimes available as part of the core, though it is more common for these to be
provided separately and interfaced to the EPR (Figure 2). PACS is always separate.
Modernization
Most clinicians can think of ways to improve the service they provide. The jargon
term for this is business process re-engineering, and when it involves the re-design
of clinical processes it needs a formal process to ensure that patients are not put at
greater risk.
Technical structure of a typical electronic patient
record (EPR)
User interface: patient views
Core EPR functions
Active clinical database

EPR
Data repository Analysis and reporting
HL7
Structured messages
Interface engine
Structured
messages:
HL7 or other
formats
Laboratory Radiology Other Primary
Information Information systems care
Management System
System
Picture Archiving and

Communication System
2
Process re-engineering is an essential component of implementing an EPR, and the

stages comprise:
analysis of the existing process
design of the new computerized process
configuring the EPR to deliver the new process
testing the software and running clinical scenarios in vitro before going live
piloting the new clinical processes in a limited clinical area (e.g. a single ward or
department) with careful supervision and collecting audit data if applicable
formally reviewing the outcome of the pilot and making changes if necessary
rolling out the new process and the EPR to other clinical areas.
All this requires input from clinicians if it is to work well.
Anaesthetic considerations
Information for Health specified six levels of increasing sophistication of EPRs. NHS
hospitals have some flexibility in choosing which functions in which of the six levels they
implement and when. However, there are target dates for the implementation of some
functions (e.g. electronic prescribing).
The data recording and reviewing requirements of anaesthesia are similar to those
of many other specialties. Preoperative assessment and investigation, intraoperative
recording of physiological data and drug and fluid administration, along with details of
anaesthetic technique, and postoperative data recording are not fundamentally different
from the processes that are undertaken by clinicians in many other specialties. EPRs
should be able to handle these requirements, though special anaesthetic screens may
need to be designed when the EPR is being configured following the analysis phase
and before piloting the system in a clinical environment.
Automatic downloading of physiological data from anaesthetic monitors has been

technically possible for many years. Difficulties encountered in linking all the different
devices in use in a typical anaesthetic department to an AIMS, and the fact anaesthesia
is now so safe (making the economic justification weak) may explain why these systems
are not more widely available.
It is likely that the small number of AIMS manufacturers will be squeezed as

equipment manufacturers provide devices with outputs that comply with international
communication standards and protocols, and EPRs are provided with the ability
to incorporate the data streams from critical care monitors using plug and play
technology. u
FURTHER READING
Information for Health: http://www.doh.gov.uk/ipu
The NHS Plan: http://www.doh.gov.uk/nhsplan
Delivering the NHS Plan: http://www.doh.gov.uk/deliveringthenhsplan
The Wanless Report: http://www.hm-treasury.gov.uk/Consultations_and_

Legislation/wanless/consult_wanless_final.cfm?
Building the Information Core: www.doh.gov.uk/ipu
National Specification for Integrated Care Records Service:

http://www.doh.gov.uk/ipu/whatnew/specs_12d.htm
Note: any Internet search engine will provide URLs for further reading on topics referred
to in this article. Particularly recommended is www.google.com

Intensive care
Anaesthesia
on CD-ROM
AcidBase and Blood Gas
Analysis
Peter J McQuillan
Peter J McQuillan is Consultant in Intensive Care at the Queen Alexandra Hospital,

Portsmouth, UK. He qualified from Newcastle and trained in intensive care and
anaesthesia in Newcastle, Dunedin (New Zealand), Oxford, Portsmouth, Southampton
and Perth and Melbourne (Australia). His interests include quality of acute care.
Acidbase homeostasis is important because protein structure and function, ionic

dissociation and all chemical reactions are pH dependent. Whereas plasma sodium is
controlled within a few mmol/litre, [H +] is controlled within a few nmol/litre. Acid load
comes from both respiratory sources (i.e. carbon dioxide via carbonic acid) amounting
to 1520,000 mmol H +/day, and metabolic sources (i.e. metabolism of sulphates,
phosphates, nitrates, lactate and ketoacids; 4080 mmol/day). Acute changes in acid
base state are minimized by buffering systems (which minimize the change in [H +]) and
other compensatory mechanisms, before excretion of acids or alkalis.
Definitions
pH = log[H +]=log 1
H+
(p stands for power from German Potenz)
pH is the negative logarithm (i.e. the logarithm of the reciprocal) of the hydrogen ion
concentration. In a logarithmic scale, a unit change in pH represents a 10-fold change
in H+ concentration.
Normal ranges: pH = 7.347.43 (i.e. 7.40); H+ = 4637 nmol/litre (i.e. 40
nmol/litre)
Figure 1 gives the rule of thumb for interconversion of pH and [H +]
Acidaemia/alkalaemia occur when pH or H + are outside the normal range.
Acidosis/alkalosis are the processes tending to produce an acidaemia/alkalaemia.
An acidosis or alkalosis may exist in the absence of an acidaemia/alkalaemia if:
the primary process is not sufficiently severe to change pH beyond the normal limits
compensation may have occurred to bring pH back within the normal range
mixed processes alter pH in different directions.
A rule of thumb for easy translation between pH and H+
[H+] nmol/litre [H+] nmol/litre pH If pH =7.ab and H+ = cd, then ab+cd 83

pH 7.23 => H+ = 83 23 = 60
10-7 100 7.00 H+ = 25 => pH = 7.(8325) = 7.58
10-7.2 63 7.20 The error is small and inconsequential for clinical purposes
10-7.3 50 7.30 between pH 7.1 and 7.6.
10-7.4 40 7.40
10-7.5 32 7.50
10-7.6 25 7.60
10-7.8 16 7.80
Henderson and Hasselbalch equation
This equation describes the relationship between concentrations of dissociated and

undissociated acid or base, dissociation constant and pH. The carbonic acid system is
of fundamental importance. The reaction of carbon dioxide with water forms carbonic
acid, which dissociates to form bicarbonate and hydrogen ions:
CO2 + H2O H2CO3 H+ + HCO3 1
Henderson noted that according to the law of mass action:
[H+][HCO ]=k 3
where k is a constant
[H2CO3]
=> 24. 40 (mm Hg) = 180. 5.3(kPa) = 40 nmol/litre

24 24
This simple formula allows the validity of blood gas results to be checked easily.
Hasselbalch took the logarithm of the reciprocal to produce the classical
HendersonHasselbalch equation:
=pKa +log HCO3 or HCO3

0.03 x PaCO2 (mm Hg) 0.23 x PaCO2 (kPa)
The pKa value at 37oC is 6.1. Thus pH depends on the ratio of bicarbonate to
carbonic acid or the ratio of bicarbonate to dissolved carbon dioxide. Changes in pH
or H+ occur through a change in this ratio. Compensatory mechanisms exist to return
this ratio towards 20.
Alterations to pH
Metabolic processes change HCO3 , which alters the numerator and hence the pH.
Metabolic acidosis
pH = 6.1 + log HCO3
0.23 x PaCO2
The primary change is a fall in bicarbonate (acidosis, metabolic). Compensation
produces a fall in PaCO2 to return the ratio (and pH) towards normal.
Respiratory compensation occurs quickly in spontaneously breathing patients.
Ventilated patients may have ventilation limits imposed, thereby precluding
adequate compensation. A patient with diabetic ketoacidosis may develop
a PaCO2 of 1.7 kPa to compensate: intubation and ventilation requires
the use of a high minute volume to maintain the compensated state.
Metabolic alkalosis
pH = 6.1 + log HCO3
0.23 x PaCO2
The primary change is a rise in bicarbonate (alkalosis, metabolic). Compensation
produces a (small) rise in PaCO2 to return ratio (and pH) towards normal. This
hypoventilatory ability is very limited in humans.
Respiratory processes change PaCO2, which alters the denominator and hence
the pH.
Respiratory acidosis
pH = 6.1 + log HCO3
0.23 x PaCO2
The primary change is a rise in PaCO2 (acidosis, respiratory). Compensation produces
a rise in bicarbonate to return the ratio (and pH) towards normal.
An acute rise in PaCO2 moves Equation 1 to the right prod-ucing an increase in
HCO3 (as H+ is buffered by haemoglobin) as a change in equilibrium of the reaction,
rather than a compensation. Chronically, renal retention of HCO3 is a compensatory
process taking hours to days. The expected level of HCO3 can be calculated using
the formula in Figure 2 giving an indication of the acuteness of the process. If the
HCO3 is other than the predicted value (for acute or chronic change), another process
must be involved.
Respiratory alkalosis
pH = 6.1 + log HCO3
0.23 x PaCO2
The primary change is a fall in PaCO2 (alkalosis, respiratory). Compensation produces
a fall in bicarbonate to return the ratio (and pH) towards normal.
Compensatory mechanisms move the pH back towards normal but seldom
completely normalize it.
Use of the Flenley diagram (Figure 3) allows us to see the acidbase status of the
patient, giving an indication of the process(es) involved.
Expected changes following primary acidbase abnormalities
kPa Standard base HCO3 (mmol) [H+] / PCO2 pH

excess (SBE) (mmol)
Respiratory acidosis: acute SBE = 0 PCO2 HCO3 = 0.75 PCO2 [H+] = 5.5 PCO2 0.06 PCO2
Respiratory acidosis: chronic SBE = 3 *PCO2 HCO3= 3 PCO2 [H+] = 2.3 PCO2 0.023 PCO2
Respiratory alkalosis: acute SBE = 0 PCO2 HCO3 = 1.5 PCO2 [H+] = 5.5 PCO2 0.06 PCO2
Respiratory alkalosis: chronic SBE = 3 *PCO2 HCO3 = 4 PCO2 [H+] = 2.3 PCO2 0.023 PCO2
kPa PCO2 (kPa) PCO2 (kPa) PCO2 (kPa) pH

Metabolic acidosis PCO2 = 0.13 SBE PCO2 = (0.17 * HCO3) + 1 PCO2 = 0.1H+ + 9.3 7.( HCO3 + 15)
Metabolic alkalosis PCO2 = 0.08 SBE PCO2 = (0.1 * HCO3) + 2.8 PCO2 = 0.2H+ + 13 7.( HCO3 + 15)
Metabolic acidosis and acidaemia

Blood contains anions (negatively charged) and cations (positively charged) and
electrical neutrality dictates that:
(Cl + HCO3 + albumin + phosphate + sulphate + lactate + ketones) = (Na++ K++

Ca2++ Mg2+)
If we measure only Na+, Cl and HCO3 and UC+= unmeasured cations and UA =
unmeasured anions, the above equation becomes:
Na+ + UC+ = Cl + HCO3 + UA
The anion gap (AG) = Na+ (Cl + HCO3 )

= UA UC+ = < 12 mmol/litre
Another version of the formula uses Na+ and K+ with a normal value of 15 mmol/litre.
Hypoalbuminaemia reduces the AG and can be corrected using the formula AGc = AG
0.25 (normal actual albumin).
A metabolic acidosis involves a primary fall in HCO3 . Assuming there is no change
in cations, the fall in HCO3 must be balanced by either an increase in UA or Cl.
High anion gap metabolic acidosis: an increase in UA implies a gain of acid.

Na+ [Cl + HCO3 ] implies an increase in AG. HCO3 falls and Cl is unchanged,
UA is increased.
The causes include:

lactic acidosis
ketoacidosis (diabetes, alcohol, starvation)
renal failure
salicylates, ethanol, methanol, ethylene glycol.
Normal anion gap metabolic acidosis: normal AG plus increased Cl implies a loss
of HCO3 .
Na+ - [Cl + HCO3 ] means a normal AG with no change in unmeasured anions.
The causes include:
gain of acid (ammonium chloride ingestion; lysine, arginine HCl in TPN)
reduction in renal H + elimination (renal tubular acidosis (type 1, distal or type 4,
hypoaldosteronism))
an increase in HCO3 loss which may be gastrointestinal (diarrhoea,
ileostomy, ureteroenterostomy) or renal (carbonic anhydrase inhibitors: acetazolamide,
renal tubular acidosis (type 2, proximal) or renal tubular damage).
Metabolic alkalosis
Generation of a metabolic alkalosis is associated with a net gain of HCO3 via:
loss of acid via gastrointestinal or renal routes
administration of HCO3 or its precursors (e.g. citrate in blood, lactate or acetate in
haemofiltration fluid)
loss of fluid with disproportionately more Cl than HCO3 :
sometimes called a contraction alkalosis, a decrease in extracellular volume with little
HCO3 loss leads to an increase in [HCO3 ] and hence a metabolic alkalosis.
Maintenance of metabolic alkalosis requires impairment of renal HCO3 excretion
because the kidney normally excretes HCO3 easily. This may occur in
hypovolaemia
potassium depletion
mineralocorticoid excess
hypercapnia.
Metabolic alkalosis may be:
saline (Cl) responsive (urinary Cl < 10 mmol/litre) due to vomiting, chloride
diarrhoea, diuretics or alkali ingestion
saline (Cl) unresponsive (urinary Cl > 10 mmol/litre) due to mineralocorticoid
excess, potassium depletion or renal Cl wasting (Bartters syndrome)
Interpreting blood gases
Only PaO2, PaCO2 and [H+] or pH are measured in blood gas analysers. PaCO2 defines
the magnitude of the respiratory component but there is debate about the usefulness
of the derived variables that describe the metabolic component (bicarbonate, standard
bicarbonate, base excess and standard base excess (SBE)). This is in part because
changes in PaCO2 alter bicarbonate. The following system may be useful in assessing
acidbase status.
Is the pH normal, acidaemic or alkalaemic?
pH or [H +] in normal range suggests one of the following:
no acidbase disorder exists
two or more disorders tending to offset pH or [H +] in opposite directions
partial compensation has occurred.
Does the PaCO2 change in the direction that would explain the pH change?
if it does then there is (at least) a respiratory abnormality.
if not, there must be a metabolic abnormality driving the pH change.
Does HCO3 change in the direction that explains the pH change?
if it does there is a metabolic abnormality.
if not and it changes in the same direction as the change in PaCO2 then it may
represent a compensatory change.
After identifying the primary or major abnormality (PaCO2 for respiratory or HCO3
for metabolic), what value would you expect for the other component if this were
the only acidbase abnormality present (Figure 2)? If the value is different from the
predicted value there must be another abnormality (i.e. a mixed picture). Alternatively,
if an acute respiratory abnormality exists, are the actual and predicted pH or [H +] the
same? If not, another metabolic abnormality exists.
In a metabolic acidosis, the anion gap helps to identify the cause. If the deviation
in the HCO3 from normal is different from the change in the anion gap from normal,
another abnormality may exist.
Stewart physicochemical approach of acidbase balance

Stewart suggested changes in [H+] occur from dissociation of water into H + and
OH rather than additions of acid or alkali. This dissociation potentially produces an
inexhaustible source of H + and is bound by the laws of physical chemistry, in particular
the principles of electroneutrality and of the conservation of matter. Three independent
fundamental determinants of [H +] are the strong ion difference (SID), PaCO2 and the
total weak acid concentration (ATOT). Stewart pointed out that the correlation of HCO3
with metabolic changes in [H +] is not evidence of causation, any more than the ECG
changes in myocardial infarction represent the cause.
A strong ion is one that is (nearly) completely dissociated. SID is the net charge
balance of all strong ions in solution, i.e. (Na+ + K+ + Ca2+ + Mg2+) (Cl + lactate-) =
4042 nmol/litre = apparent SID (SIDa). This is similar to the old buffer base concept.
Neither H +, nor HCO3 are strong ions. Weak acids, A (albumin and phosphate)
contribute the remaining charge to satisfy electroneutrality. A rise in SID causes less
water dissociation and an alkalosis and a fall in SID produces greater dissociation and
an acidosis (Figure 4).
SID

H2O H+ + OH
SID .
FURTHER READING
Grogono A W. Acid-base Balance: Classical Disturbances. www.tmc.edu/departments/
anesthesiology/acidbase.
Kellum J A. Determinants of Blood pH in Health and Disease. Crit Care 2000; 4(1):
614.
Schlichtig R, Grogono A W, Severinghaus M D. Human PaCO2 and Standard Base

Excess Compensation for Acid-Base Imbalance. Crit Care Med 1998; 26: 11739.

Acute Liver Failure
Kevin E J Gunning
Kevin E J Gunning is Director of the John Farman Intensive Care Unit, Addenbrookes
Hospital, Cambridge, UK. He qualified from St Bartholomews Hospital, London, and
after obtaining his FRCS, trained in anaesthesia in London. His current interests include
audit and training in intensive care.
Acute liver failure (ALF) is an uncommon condition characterized by jaundice,

coagulopathy and encephalopathy in a patient with previously normal liver function. In
the USA, there are 2000 cases a year and in the UK there are 400. The main aims of
treatment are the control of cerebral oedema and supportive management of multiple
organ failure until hepatic regeneration occurs. Sepsis and cerebral oedema are the
main causes of death.
Aetiology in the UK, paracetamol (acetaminophen) overdose is the most common

cause (70%) of ALF, but worldwide it is viral hepatitis (Figure 1).
Pathology there is centrilobular necrosis of hepatocytes with activation of

macrophages and liberation of cytokines, specifically tumour necrosis factor and
interleukins 1 and 6.
Causes of acute liver failure
Infection (hepatitis A, B, C, E, non-A non-B, cytomegalovirus, herpes

simplex virus, EpsteinBarr virus, varicella)
Drugs (paracetamol (acetaminophen), isoniazid, monoamine oxidase
inhibitors (MAOIs), non-steroidal anti-inflammatory drugs (NSAIDs),
halothane, Ecstasy, gold, phenytoin)
Metabolic (Wilsons disease, Reyes syndrome)
Cardiovascular (BuddChiari syndrome, ischaemic hepatitis)
Miscellaneous (acute fatty liver of pregnancy, lymphoma, amanita
phalloides, herbal medicines)
1
Clinical presentation
ALF usually presents with malaise, nausea and jaundice. The interval between the
onset of jaundice and the onset of enceph-alopathy depends on the aetiology and is
used to classify ALF:
hyperacute liver failure (7 days between onset of jaundice and encephalopathy)
acute liver failure (828 days)
subacute liver failure (512 weeks).
This classification has implications for the prognosis and incidence of cerebral
oedema, which is more common in hyperacute failure. As liver failure progresses,
encephalopathy becomes the characteristic feature. The grading of encephalopathy
is described in Figure 2. The mechanism of encephalopathy is not fully understood.
Ammonia, false neurotransmitters and endogenous benzodiazepine ligands that
enhance the effect of the inhibitory transmitter -aminobutyric acid have been proposed
as causes.
Grades of encephalopathy
Grade I: altered mood, impaired concentration and psychomotor

function, rousable
Grade II: drowsy, inappropriate behaviour, able to talk
Grade III: very drowsy, disorientated, agitated, aggressive
Grade IV: coma, may respond to painful stimuli
2
Diagnosis and investigations

There is no specific diagnostic test for ALF, however specific tests to identify the cause
may include:
viral serology for the hepatitis viruses
plasma caeruloplasmin and 24-hour urinary copper to diagnose Wilsons disease
hepatic ultrasound to demonstrate hepatic vascular occlusion in BuddChiari
syndrome.
There will be elevation of:

serum bilirubin (a level over 300 mol/litre implies severe disease)
plasma aspartate aminotransferase (AST) and alanine amino-transferase (ALT)
reflecting hepatocellular damage
prothrombin time (PT) (used as an indicator of the severity of the disease).
Other common abnormalities are hypoglycaemia, hyponatraemia,
hypomagnesaemia, respiratory alkalosis and metabolic acidosis.
Management
Paracetamol (acetaminophen) overdose results in the accumulation of the hepatotoxic
metabolite N-acetyl-p-benzoquinonimine which is normally inactivated by conjugation
with glutathione. N-acetylcysteine should be given as soon as possible after the
overdose according to the standard treatment nomogram, to re-plenish hepatic stores
of glutathione. The management of patients who meet the clinical indicators of poor
prognosis (Figure 3) should be discussed with a regional liver centre and they should
be transferred urgently for transplant assessment. Elective intubation and ventilation
should be considered before transfer for patients with Grade II encephalopathy and it
is mandatory for patients with Grade III or IV encephalopathy. The patient should be
transferred with full monitoring by experienced personnel.
Kings College Hospital criteria for liver transplant-ation in acute liver

failure
Paracetamol (acetaminophen) overdose

H + > 50 nmol/litre
Or all of the following:
Prothrombin time > 100 seconds
Creatinine > 300 mol/litre
Grade IIIIV encephalopathy
Non-paracetamol (acetaminophen)
Or three of the following:
Age < 10 years or > 40 years
Bilirubin > 300 mol/litre
Time from jaundice to encephalopathy > 2 days
Non-A, non-B hepatitis, halothane or drug-induced acute liver failure
3
The basis of intensive care management is to provide support for failing organs while
allowing time for hepatic regeneration.
Omeprazole or ranitidine are given as prophylaxis against gastrointestinal bleeding.
Early enteral nutrition is recommended but there is no need to restrict protein or
calories.
Hypoglycaemia is common and an infusion of 10% glucose should be administered
to keep the blood glucose level above 3.5 mmol/litre.
Agitated or aggressive patients may need ventilation to enable care to be given.
Those with grade III or IV encephalopathy should be electively ventilated, because of

the risk of cerebral oedema.
High levels of positive end-expiratory pressure (PEEP) should be avoided because
they may increase hepatic venous pressure and intracranial pressure (ICP).
Pulmonary complications such as acute respiratory distress syndrome, aspiration or
pneumonia occur in 50% of cases.
Cardiac output is high (> 5.0 litre/minute) in 70% of cases, with a reduced systemic
vascular resistance. Relative hypotension is therefore common and should be treated
by volume loading with colloids. A pulmonary artery catheter or PiCCO should be
inserted to guide therapy. Vasopressors (e.g. noradrenaline (nor-epinephrine)) may be
needed to maintain mean arterial pressure, despite adequate volume replacement.
N-acetylcysteine may be beneficial in the management of ALF even if paracetamol
(acetaminophen) is not the cause. The evidence is conflicting, but it has been shown to
increase cardiac output and oxygen delivery and is given as a loading dose of
300 mg/kg followed by an infusion of 150 mg/kg/hour.
Coagulopathy is a major feature of ALF, because the liver synthesizes all the
coagulation factors apart from factor VIII. Sepsis, reduced protein C and antithrombin III
levels contribute to low- grade disseminated intravascular coagulation (DIC). The PT is
a good measure of the severity of the disease and should not be corrected unless the
patient is actively bleeding. Thrombocytopenia should be corrected if the platelet count
falls below 50 x 109 /litre.
Infection
Infection is common as a result of neutrophil and Kpffer cell dysfunction and sepsis is
the cause of death in 11% of cases. Bacterial infections with Gram-positive organisms
are seen in the first week and fungal infections after 2 weeks. The usual signs of
infection (e.g. pyrexia, leucocytosis) may be absent and infection surveillance must be
rigorous. Prophylactic fluconazole, 100 mg/day, should be started.
Cerebral oedema
Cerebral oedema develops in 80% of patients with Grade IV encephalopathy and is
the cause of death in about 3050% of patients with ALF. There is now evidence to
suggest that it is the result of the high level of ammonia, which leads to an increase in
the synthesis of intracellular cerebral glutamine. This increases osmotic pressure in
astrocytes, resulting in cerebral oedema. The patient should be nursed with a 20o head-
up tilt to improve cerebral perfusion pressure; there should be minimal intervention to
prevent surges in ICP. Hyperventilation should be avoided and the PaCO2 should be
maintained at 4.75.2 kPa. Systolic hypertension and sluggish pupillary responses are
the most reliable clinical signs of raised ICP, which should be treated with an
intravenous bolus of mannitol 20%, 0.5 g/kg, which takes 2060 minutes to act. The
boluses may be repeated provided that the serum osmolality is less than 320 mOsmol/
litre.
Some centres measure ICP using extradural, subdural or parenchymal monitors.

However, the benefits must be balanced against the risk of haemorrhage, which occurs
in about 15%. Coagulation should be corrected before the insertion of the monitor.
Cerebral perfusion pressure should be maintained above 60 mm Hg. Thiopental
(thiopentone) as a 50 mg bolus or an infusion of 50 mg/hour can be used to treat
intractable intracranial hypertension, but may cause a fall in systemic blood pressure
and a reduction in cerebral perfusion pressure. Moderate hypothermia (3233oC)
reduced ICP in one study.
Renal failure
Renal failure occurs in 70% of patients after paracetamol (acet-aminophen) overdose
due to its nephrotoxic effect. Sepsis and hypovolaemia also contribute to renal
failure. Haemodiafiltration may be necessary to maintain fluid balance and to correct
hyponatraemia, hyperkalaemia and acidosis. A lactate-free replacement fluid should be
used, because the failing liver can not clear lactate.
There has been considerable research into the development of an artificial liver. Trials
of systems using extracorporeal perfusion of blood through columns of hepatocytes, or
dialysis against an albumin-coated membrane have been undertaken, but most studies
are small and experimental.
Prognosis
Overall survival with medical treatment is 1040%. The prognosis depends on the
aetiology and is best after paracetamol (acetaminophen) overdose and hepatitis A,
and worst for non-A, non-B hepatitis and idiosyncratic drug reactions. The time to the
onset of encephalopathy also affects prognosis, hyperacute failure has a 35% survival
and subacute failure has a 15% survival. The outcome from transplantation for ALF is
improving and is now 6575%. u
FURTHER READING
Carraceni P, Van Thiel D H. Acute Liver Failure. Lancet 1995; 345: 1639.
Gimson A. Fulminant and Late Onset Hepatic Failure. Br J Anaesth 1996; 77: 908.
Lee W M. Acute Liver Failure. N Eng J Med 1993; 329: 186272.
Singer M, Suter P M. Acute Hepatic Failure. In: Webb A R, Shapiro M J, eds. Oxford
Textbook of Critical Care. Oxford: Oxford University Press, 1999.

Acute Lung Injury and the
Acute Respiratory Distress
Syndrome
Matthew E J Callister
Timothy W Evans
Matthew E J Callister is Wellcome Research Fellow at the Unit of Critical Care,

National Heart and Lung Institute, London, UK.
Timothy W Evans is Professor of Intensive Care Medicine at Imperial College School

of Medicine and Clinical Director of Intensive Care Medicine at the Royal Brompton and
Harefield NHS Trust, London.
Acute lung injury (ALI) and its extreme manifestation, the acute respiratory distress
syndrome (ARDS), complicate a wide variety of medical and surgical conditions.
Mortality remains high (4070%) and survivors often require extensive periods of
intensive care, representing a considerable clinical and fiscal burden.
ALI and ARDS are defined by refractory hypoxaemia associated with lung
inflammation and increased pulmonary vascular permeability. The commonly accepted
radiological and physiological criteria were first established at an AmericanEuropean
Consensus Conference in 1993 (Figure 1). ALI and ARDS were defined as
separate, yet related, states on a pathophysiological continuum of pulmonary damage.
Standardization of the criteria required to diagnose these conditions greatly facilitated
the design of clinical trials allowing comparison between patient groups in various
studies. However, these definitions take no account of the prognostic significance
of the precipitating condition, and fail to specify the ventilatory strategy to be used
when the presence and severity of hypoxemia are established. It is also increasingly
recognized that individual interpretation of chest radiographs can vary widely, even
among experienced clinicians. The Consensus Conference therefore met again in
October 2000 to address these concerns in revised criteria.
Definitions of acute lung injury (ALI) and acute respiratory distress

syndrome (ARDS)
Appropriate clinical setting with one or more recognized risk factors
New, bilateral, diffuse, patchy or homogeneous pulmonary infiltrates on

chest radiograph
No clinical evidence of heart failure, fluid overload, or chronic lung disease

(pulmonary artery occlusion pressure
< 18 mm Hg)
PaO2:FiO2 ratio of < 40 kPa (< 300 mm Hg) for ALI or < 26.6 kPa (< 200 mm
Hg) for ARDS
Incidence and aetiology

Historically, the incidence of ARDS is estimated as 1.575 cases per 100,000
population. However, the only study to use the 1993 consensus criteria to define ALI
and ARDS using a prospective cohort study identified 17.9 and 13.5 cases of ALI
and ARDS, respectively, per 100,000 population. Many serious medical and surgical
conditions may precipitate ALI/ARDS, not all of which involve the lung (Figure 2).
Prognosis depends in part on the nature of the precipitating insult. Thus, trauma-
induced lung injury is associated with a more favourable outcome than that precipitated
by sepsis. The presence of multiple risk factors further increases the likelihood of
developing ARDS, as do co-morbid factors such as chronic alcohol abuse. A recent
study has suggested that a history of diabetes reduces the risk of developing ARDS
in patients with septic shock.
Causes of acute lung injury and acute respiratory distress syndrome
Pulmonary causes Non-pulmonary causes

Pneumonia Sepsis
Aspiration of gastric contents Severe trauma
Inhalational injury Cardiopulmonary bypass
Hypoxia/reperfusion injury Massive transfusion
Fat emboli Drug overdose
Pulmonary contusion Acute pancreatitis
Near-drowning
Pathophysiology
ALI and ARDS are characterized by intense inflammatory reactions in the alveolar
space. Cytokines and chemokines are released by native fibroblasts, epithelial cells and
alveolar macrophages, triggering endothelial cell activation and neutrophil recruitment.
Activated neutrophils secrete cytokines and chemokines to further upregulate the pro-
inflammatory stimulus, and release highly reactive oxygen species and destructive
enzymes (e.g. myeloperoxidase) which interfere with cellular function. Increased
pulmonary capillary permeability due to endothelial damage leads to leakage of
a protein-rich exudate from the pulmonary vasculature into the interstitium and
alveoli. Together with atelectasis of lung units, and an impaired hypoxic pulmonary
vasoconstrictor response, impaired oxygenation refractory to increases in inspired
oxygen concentration (FiO2) results. Dysregulation of pulmonary vascular tone due to
endothelial dysfunction may also lead to pulmonary hypertension and subsequent right
heart failure, the development of which is associated with a poor prognosis.
Investigations
Initial investigations should be aimed at defining the degree of lung injury (i.e. FiO2,
arterial blood gases) and elucidating the precipitating cause. Excluding cardiogenic
pulmonary oedema is vital to the diagnosis of ARDS/ALI. Traditionally a pulmonary
artery occlusion pressure of below 18 mm Hg has been used to define pulmonary
oedema that is non-cardiogenic in nature. However, there is now an increasing
realization that the pulmonary capillary wedge pressure may be a poor surrogate for
fluid status, and the new consensus guidelines will no longer recommend this as
the sole criterion to distinguish between cardiogenic and non-cardiogenic pulmonary
oedema. Instead it is suggested that a variety of investigative measures are used,
which may include echocardiography, measurement of extravascular lung water using
thermodilution techniques (e.g. pulse contour cardiac output) and measurement of
pulmonary artery occlusion pressure. Subsequent investigations detect complications
and guide therapy.
Chest radiography is easy to perform and may help in the detection of barotrauma
or superadded infection. However, CT of the thorax is more sensitive for detecting
pneumothoraces, pleural collections or pulmonary infiltrates, and is increasingly
used as a routine investigation in ALI and ARDS. CT has also contributed to the
understanding of the pathophysiology of ARDS by demonstrating patchy involvement of
lung parenchyma rather than the homogeneous appearance seen on chest radiographs
(Figure 3). Attempts have been made to use CT to predict responsiveness to
interventions, one study correlating a response to inhaled nitric oxide with CT evidence
of alveolar recruitment following increased positive end-expiratory pressure (PEEP).
Patient 1 Patient 1
a b
Patient22
Patient Patient 2
cc d
Chest radiographs and CT scans for two patients with established acute respiratory distress syndrome. The
radiographs show characteristic ground-glass shadowing bilaterally. Both CT scans demonstrate areas of
interstitial ground-glass shadowing (w) with dense opacification (x) in the dependent regions. Patient 2 has
extensive barotrauma and a pneumothorax (y) and an intercostal drain (z) are seen on the CT.
3
Fibre-optic bronchoscopy is often used to obtain microbiological samples to rule

out pulmonary infection. Analysis of bronchoalveolar lavage fluid can also provide
information concerning neutrophil infiltration and cytokine levels, which may have
implications for prognosis.
Management
Treatment of the precipitating condition and the complications of ventilation (e.g.

barotrauma, nosocomial infection) are essential in managing ALI and ARDS.
General supportive measures

Nutrition: adequate nutrition introduced early in the clinical course is now regarded as
crucial to the management of patients with ARDS. Whenever possible, nutrition should
be administered via the enteral route, and the use of prokinetic drugs, avoidance of
agents that impair gastric emptying (e.g. dopamine) and the use of post-pyloric feeding
tubes can help to achieve this. Recent research has suggested that feeds rich in certain
fatty acids and antioxidants may be of benefit in ARDS, presumably via changes in
the host immune response. Eicosapentaenoic acid (EPA) modulates production of
pro-inflammatory eicosanoids, and -linoleic acid (GLA) may suppress production
of leukotrienes while being metabolized to prostaglandin E1. A recent randomized
controlled trial of feeds supplemented with EPA/GLA in patients with ARDS has shown
improvements in oxygenation, and shorter periods of ventilation and ICU stay. Further
investigation in this area is required.
Fluid management: pulmonary oedema in ALI/ARDS is caused by increased

pulmonary vascular permeability in the face of normal pulmonary capillary pressures.
Several studies have shown an association between a persistent positive fluid balance
and poor outcome in ARDS, but it is not clear whether this represents administration
of unnecessary fluid or greater haemodynamic instability in a group with a pre-existing
poor prognosis. One clinical trial has shown that patients managed using the more
restrictive of the two had shorter periods of ventilation and reduced ICU stays.
Ventilation and gas exchange
Protective ventilatory strategies: most patients with ARDS require mechanical
ventilatory support to achieve adequate gas exchange. One study indicated that
satisfactory oxygenation can be achieved in a proportion of patients by using positive
pressure ventilation applied via a face mask, however, most patients require tracheal
intubation.
The traditional strategies of ventilation used in these patients may have contributed
to the propagation of lung injury. Experiments in animals showed that ventilation
using large tidal volumes caused disruption of the pulmonary epithelium and
endothelium, lung inflammation and impaired oxygenation. Excessive stretching of the
lung parenchyma together with cyclical opening and closing of damaged lung units is
thought to generate pro-inflammatory mediators, which exacerbate pulmonary damage,
and if disseminated into the systemic circulation also contribute to the development of
distant organ failure to which many patients succumb. As a result, ventilatory strategies
now aim to limit the shear forces applied to the lung parenchyma, and reduce the
cyclical recruitment and derecruitment of alveolar units. Thus, tidal volumes are set
at lower levels than have traditionally been thought necessary. This reduces carbon
dioxide clearance, often resulting in a respiratory acidosis. A large multi-centre trial
in the USA has shown a convincing reduction in mortality (from 40% to 31%, p =
0.007) associated with this approach (using tidal volumes of 6 ml/kg) compared with
conventional (12 ml/kg) ventilation.
High levels of PEEP can also be used to ensure recruitment and retention of
damaged lung units. PEEP can also be transiently increased in a step-wise manner
to high levels (e.g. 3540 cm H2O) before step-wise reduction to a maintenance level
above the lower inflection point of the pressurevolume curve. CT images during
such manoeuvres have demonstrated recruitment of atelectatic regions especially in
dorsal areas of the lung, which remain inflated after the PEEP is reduced, with an
associated improvement in gas exchange. A large multi-centre trial in North America
is currently investigating the effect of different levels of PEEP and transient recruitment
manoeuvres on outcome following ARDS.
Prone positioning: mechanical ventilation in the prone position is often used in the
management of patients with ARDS. About 60% of patients respond with significant
improvements in gas exchange, which may persist after the patient is returned to the
supine position. Response cannot be predicted, therefore a trial period is often used
to identify patients who are likely to benefit. There have been no controlled studies to
establish whether this technique is associated with an improved outcome, although a
large (over 300 patients) Italian study is soon to report.
Extracorporeal gas exchange is performed using veno-arterial bypass and can be

used in the absence of conventional forms of ventilation as the sole mechanism of
gas exchange, or coupled to mechanical ventilation (in which case its principal function
is to enhance carbon dioxide clearance). Neither of the two randomized trials of
extracorporeal gas exchange carried out to date revealed a survival advantage. An
increased understanding of the most appropriate way to ventilate patients with severe
ARDS is likely to lead to this technique being used less often.
Novel ventilatory techniques

High-frequency ventilation (HFV) is a mode of mechanical ventilation that
employs rapid respiratory rates (more than four times those used in conventional
techniques). Tidal volumes are reduced, and are often smaller than the anatomical
deadspace. The two modes of HFV most widely used are high-frequency jet ventilation
(HFJV) and high-frequency oscillator ventilation (HFOV). HFJV involves the intermittent
delivery of high-pressure gas jets into the tracheal tube. However, optimal gas warming
and humidification are difficult to achieve, leading to problems with airway secretions
and debris, which coupled with a reliance on passive expiration can lead to air trapping.
HFOV involves the delivery of a continuous distending pressure to the tracheal tube,
which is then modified by the movement of a vibrating loudspeaker. Humidification
and warming of the fresh gas flow are easier to achieve, and an active expiratory
phase leads to less gas trapping. The only randomized controlled trial of HFJV in
patients with severe acute respiratory failure did not show a significant improvement in
gas exchange or a survival benefit. However, recent evidence suggesting that low tidal
volumes reduce ventilator-associated lung injury, and that high levels of continuous airway
pressure (PEEP) improve recruitment and retention of lung units, has renewed interest in
HFV (especially HFOV) as an appropriate mode of ventilation in ARDS.
Liquid ventilation involves filling the lungs with biologically inert fluids called
perfluorocarbons through which oxygen and carbon dioxide readily diffuse. Ventilation
occurs either through a specialized ventilator, or if the lungs are only partially filled
(partial liquid ventilation) by using a conventional ventilator. The results of a phase II
study of partial liquid ventilation in patients with ARDS are awaited.
Pharmacological therapies
Vasoactive agents: nitric oxide is an endogenous vasodilator, which can be given by
inhalation at concentrations up to 20 parts per million. It has been shown to improve
oxygenation in ALI and ARDS through effects on ventilationperfusion matching, and
to decrease pulmonary vascular resistance. Only a proportion of patients with ARDS
benefit from nitric oxide and randomized controlled trials in patients with ALI and
ARDS have failed to show an improvement in mortality or a reduction in the duration
of mechanical ventilation. Improvements in oxygenation are transient, disappearing after
24 hours of therapy.
Prostacyclin (PGI2) is another endogenous vasodilator that may have beneficial
effects in ARDS. Like nitric oxide it is thought to redistribute pulmonary blood flow to
ventilated lung units, thus improving ventilationperfusion matching. A sequential trial of
nitric oxide and PGI2 in patients with ARDS showed the two treatments to have identical
effects on oxygenation and shunt flow, but as PGI2 is easier to monitor and deliver than
nitric oxide, it is often used in its place.
Surfactant supplementation has proved effective in neonatal respiratory distress

syndrome, and surfactant deficiency and dysfunction has been demonstrated in
adult patients with ARDS. A number of randomized controlled trials have failed to
demonstrate an effect on either mortality or length of ventilation or ICU stay. More
recently, a smaller trial has shown a survival benefit following use of bovine surfactant,
but further large-scale trials are necessary.
Antioxidants: oxidative stress is thought to be central to the pathogenesis of ARDS.

Alveolar macrophages and recruited activated neutrophils release highly reactive
oxygen species, which cause injury through interactions with proteins, lipids and
DNA. It is thought that excessive production overwhelms the endogenous antioxidant
systems that normally regulate the redox state within the lung. Attempts have therefore
been made to introduce antioxidants to redress this balance, in particular using
N-acetylcysteine, but none has shown a survival benefit nor a reproducible effect on
pulmonary physiology.
Anti-inflammatory agents: ketoconazole is an imidazole used primarily for its

antifungal effects, but which also has immune modulating functions that may be of
benefit in preventing the development of ARDS. Although a large multi-centre trial
showed that ketoconazole had no effect on mortality or duration of ventilation in patients
with established ALI or ARDS, two smaller studies in critically ill surgical patients
demonstrated a significant reduction in the incidence of ARDS.
Corticosteroids have been used to treat ARDS since the 1960s. However, several
multicentre trials in the 1980s failed to show a beneficial role for corticosteroids,
either in the prevention of ARDS in at-risk groups or in the treatment of established
ARDS. Recent meta-analyses have concluded that corticosteroids do not improve, and
may worsen, mortality in patients with sepsis (a high-risk group for ARDS). However,
despite this evidence, there has been a recent resurgence in enthusiasm for the use
of corticosteroids in the late (fibroproliferative) phase of ARDS. The only controlled
data to support such therapy randomized patients on day 7 of ARDS to receive
methylprednisolone or placebo for 32 days. Despite the small numbers of patients
studied (24), there was an impressive reduction in ICU and hospital mortality (p =
0.002 and p = 0.03, respectively) associated with corticosteroid use. However, care
must be taken to exclude continuing infection before the introduction of corticosteroids
in this setting.
Prognosis and future developments
Few interventions in ALI and ARDS have been demonstrated to improve outcome. This
may be, in part, because only about 5% of patients die as a result of respiratory failure,
and thus therapies that improve oxygenation or other ventilatory parameters are unlikely
to impact significantly on mortality. The heterogeneity of patients entered into trials as a
result of the broad definitions of ALI/ARDS may preclude the demonstration of outcome
benefit. New definitions of ALI/ARDS and an increasing focus on aetiological subgroups
of patients are needed.
Despite this, an improvement in the outcome of ARDS in single centres has been
reported in recent years, one study reporting a reduction in mortality from 66% to
34% over the years 1990 to 1997. Large-scale clinical trials (coordinated by the ARDS
network in North America) are investigating the use of late steroids, the optimal settings
of PEEP, and the effects of recruitment manoeuvres in ARDS. There is also increasing
interest in genetic polymorphisms that may predict susceptibility to develop these
conditions and thus allow early identification of high-risk patients.
FURTHER READING
McIntyre R C, Pulido E J, Bensard D D, Shames B D, Abraham E. Thirty Years of
Clinical Trials in Acute Respiratory Distress Syndrome. Crit Care Med 2000; 28: 3314
31.
Ware L B, Matthay M A. Medical Progress: The Acute Respiratory Distress Syndrome.
New Engl J Med 2000; 342: 133449.
Wyncoll D L A, Evans T W. Acute Respiratory Distress Syndrome. Lancet 1999; 354:
497501.

Acute Pancreatitis
Tony Pickworth
Tony Pickworth is Consultant in Anaesthesia and Intensive Care Medicine at the Great
Western Hospital, Swindon, UK. He qualified from Emmanuel College, Cambridge, and
Merton College, Oxford, and trained in anaesthesia in Stoke-on-Trent and East Anglia.
He is an examiner in physiology for the MRCS (London). His particular interests are
ventilation strategies and sedation for intensive care.
Aetiology and pathogenesis

Acute pancreatitis is an acute inflammatory process of the pancreas with variable
involvement of other regional tissues or remote organ systems.
Gallstones and high alcohol intake are associated with about 80% of cases. 10% of
cases are idiopathic. Other causes include:
hypertriglyceridaemia
hypercalcaemia
trauma
endoscopic retrograde cholangiopancreatography (ERCP)
drugs (e.g. sodium valproate, tetracycline, thiazides, furosemide (frusemide)).
The incidence of acute pancreatitis appears to be rising. Figures as high as 200/

1,000,000 population have been quoted; a ten-fold increase since 1970. High alcohol
intake accounts for much of this rise. The disease is most common in women aged
5060 years.
The cellular mechanisms involved in the development of acute pancreatitis are unclear,
however, a key step appears to be intra-acinar activation of trypsinogen. This causes
activation of other enzyme systems including lipase, phospholipase A2, elastase,
chymotrypsin and the kallikrein-kinin system, resulting in fat and tissue necrosis,
coagulation, vascular damage, haemorrhage, oedema formation and inflammation.
Diagnosis and assessment of severity

The clinical presentation is of rapid onset of upper abdominal or back pain, vomiting,
fever and tachycardia. Occasionally Grey Turner (bruising in the loin) and Cullen (bluish
discoloration near the umbilicus) signs may be present. In about 80% of cases the
course is mild and resolves spontaneously.
Diagnosis is most commonly made using serum amylase estimation, though there
are limitations to its specificity and sensitivity. The serum lipase level is more accurate
and a better marker for alcoholic pancreatitis. However, the laboratory measurement of
lipase was, until recently, more complicated and it is not available in many centres.
Assessment of severity the most common scoring systems are those of Ranson
and Glasgow (or Imrie). The criteria for the Glasgow system are:
patient aged over 55 years
white blood cell count over 15 x 109 /litre
serum glucose over 10 mmol/litre
serum urea over 16 mmol/litre
partial pressure of oxygen in arterial blood (PaO2) less than 60 mm Hg (8.6 kPa)
serum calcium less than 2 mmol/litre
serum albumin less than 32 g/litre
serum lactate dehydrogenase over 600 units/litre
serum aspartate transaminase over 100 units/litre.
Three positive criteria within 48 hours indicate severe disease. The disadvantage of
the above systems is that data collection is not complete until 48 hours after patient
admission. Evidence suggests that APACHE II (Acute Physiology and Chronic Health
Evaluation) scoring at 24 hours is at least as accurate.
Biochemically, C-reactive protein (CRP) is a useful test to assess severity, but only 72
hours after disease onset. An earlier marker is urinary trypsinogen activation peptide
(TAP) which is valuable at 24 hours. It has an 86% sensitivity for identifying patients
who will develop severe disease.
Imaging may be necessary to diagnose the disease or its cause. Ultrasound is useful
in suspected pancreatitis only for diagnosing gallstones. Contrast CT scanning is the
imaging procedure of choice to diagnose and monitor acute pancreatitis.
Management
General care: the basis of management is:
bed rest
analgesia
intravenous fluids
withholding of oral intake
support of failing organ systems
identification of severe cases
identification of complications.
In episodes with complications, or those predicted to be severe, the patient should

be managed in a critical care area. Physiological supportive care is required because
systemic inflammatory response syndrome (SIRS) or multiple organ failure may result.
Specific therapies include:

aprotinin
glucagon
somatostatin
octreotide
gabexate mesilate (an antiprotease agent)
fresh frozen plasma
lexipafant (an inhibitor of platelet activating factor)
peritoneal lavage.
None of these have any impact on the mortality rate, though there is weak evidence
that lexipafant, commenced within 48 hours of disease onset, can reduce complications
and organ failure.
Nutrition: in severe or prolonged cases total parenteral nutrition is commonplace. Total

parenteral nutrition seldom causes release of pancreatic enzymes, except when there is
a high lipid load. Enteral nutrition promotes pancreatic enzyme production unless feed
is delivered into the jejunum or below. Elemental feeds seem to stimulate the pancreas
even if delivered directly to the jejunum, whereas standard feeds do not.
ERCP and sphincterotomy may be necessary in the case of gallstone pancreatitis even
in the acute phase of the illness. It is recommended if there is evidence of obstructive
jaundice, or for severe pancreatitis with gallstones that does not settle within 72 hours.
Complications: the main complications of pancreatitis are:

infection and/or abscess formation
pancreatic necrosis
multiple organ failure
hypocalcaemia
pseudocyst formation
chronic pancreatitis.
The mortality from infected severe pancreatitis is over 50%. There is evidence to
support the use of prophylactic antibiotics in severe pancreatitis. Where there is proven
infection, but a specific organism is unknown, treatment with imipenem, 500 mg
8 hourly, is suitable, because of its spectrum and pen-etration into pancreatic tissue.
CT scanning is used to recognize abscess or pseudocyst formation or necrosis (Figure

1). Even if a CT scan is not required for diagnostic purposes, it should be performed
310 days after the start of a severe attack. If signs of necrosis are seen, a fine needle
aspirate of the pancreatic fluid is indicated to identify whether the tissue is infected or
not. Sterile necrosis should be managed conservatively but, if there is infection, open
necrosectomy is indicated. Repeat CT scanning is recommended every 12 weeks.
a Normal pancreas (CT with contrast);

b Inflamed pancreas with pseudocyst;
c Extensive pancreatic necrosis with gas
trapping (emphysematous pancreatitis).
1
Acute respiratory distress syndrome and multiple organ failure are common sequelae
of severe pancreatitis and require supportive care. Specifically, hypocalcaemia may
result, owing to hypoalbuminaemia, abnormal parathyroid activity, or form-ation of
intraperitoneal soaps with released free fatty acids. Other metabolic complications
include hyperlipidaemia and hyperglycaemia.
Prognosis and further management

80% of cases are mild attacks that settle in a few days with conservative management.
Mortality in such cases is less than 2%. In severe cases, mortality is about 10% overall;
20% where there is necrosis and over 50% with infected necrosis. Data from the
Intensive Care National Audit and Research Council case-mix programme indicate a
hospital mortality of 44% for patients with pancreatitis admitted to ICU.
Although the spectrum of severity is similar with different aetiology, there may be a
difference in outcome. If pancreatitis is associated with alcohol there is often evidence
of chronic fibrosis and inflammation, but with acute biliary pancreatitis the gland usually
returns to histological normality. Gallstone pancreatitis is likely to recur if the stones are
not treated, and it is recommended that cholecystectomy and clearance of the common
bile duct is performed within 4 weeks of the attack. u
FURTHER READING
Baron T H, Morgan D E. Current Concepts: Acute Necrotizing Pancreatitis. New Engl J
Med 1999; 340(18): 141217.
Dervenis C, Johnson C D, Bassi C et al. Diagnosis, Objective Assessment of Severity

and Management of Acute Pancreatitis. (Santorini Consensus Conference). Int J
Pancreatol 1999; 25(3): 195210.
United Kingdom Guidelines for the Management of Acute Pancreatitis. Gut 1997; 42
(suppl): 113.

Acute Renal Failure and Renal
Replacement Therapy in the
ICU
Sara Blakeley
Gary Smith
Sara Blakeley is Specialist Registrar in Portsmouth, UK. She qualified from

Southampton University and is training in intensive care medicine and nephrology. Her
particular interest is critical care nephrology.
Gary Smith is Consultant in Intensive Care Medicine at Portsmouth Hospital NHS Trust
and Honorary Senior Lecturer in Critical Care in the School of Postgraduate Medicine
at the University of Portsmouth. After qualifying from the University of Southampton,
he trained in anaesthesia and medicine in the South of England and at Yale University,
USA. His main interests are multiprofessional education, cardiopulmonary resuscitation
and pre-hospital trauma care.
Acute renal failure (ARF) is a sudden and sustained fall in the glomerular filtration rate
(GFR) associated with a loss of excretory function and the accumulation of metabolic
waste products and water. It leads to rising serum urea and creatinine, usually with
a fall in urine output. Definitions such as a doubling of the serum creatinine or daily
urine volumes of less than 400 ml have been used as diagnostic markers for ARF. The
absence of a universally accepted definition for ARF makes determining its incidence
difficult, but up to 10% of all patients admitted to the ICU receive some form of renal
replacement therapy.
Patients with hospital-acquired ARF are more likely than those with community-
acquired ARF to be admitted to ICU. In critically ill patients, renal failure is often a
component of multiple organ failure, and its aetiology is likely to be multifactorial.
Different incidence rates between ICUs are a reflection of their case-mix as well as
different attitudes to renal replacement therapy. Renal failure in patients on the ICU
is unlikely to resolve with conservative management; up to 70% of patients with ARF
require renal replacement therapy. In many cases this is started within 24 hours of
admission to the ICU.
The main causes of ARF (Figure 1) can be categorized as pre-renal, intrinsic or

obstructive.
Mortality in ICU, ARF alone has a mortality of 2030% but this rises if another organ
failure exists. When associated with ARF, failure of two organs leads to death in about
50% of patients, rising to over 90% if ARF accompanies three or more organ failures.
Outcome following discharge from the ICU, about 70% of those who have developed
ARF recover renal function completely. 510% of patients with previously normal renal
function remain on long-term renal replacement therapy. The figure is much higher
(about 30%) if there is a background of pre-existing renal impairment.
Causes of acute renal failure on the ICU
Pre-renal (renal hypoperfusion)

Intravascular volume depletion (e.g. dehydration, blood loss,
redistribution of fluid between body compartments)
Severe hypotension (e.g. sepsis, drugs)
Reduced cardiac output (e.g. pump failure post myocardial infarction,
myocardial ischaemia)
Intrinsic renal failure

Acute tubular necrosis (ATN)
Ischaemic (the extreme end of pre-renal failure, also seen with pancreatitis,
burns, sepsis)
Exogenous toxins (e.g. radiocontrast, nephrotoxic drugs usually occurs on
a background of volume depletion, sepsis or pre-existing renal impairment)
Endogenous toxins (e.g. rhabdomyolysis, massive haemolysis, tumour lysis
syndrome)
Hepatorenal syndrome
Acute glomerulonephritis/interstitial nephritis
(with multi-system involvement)
Increased intra-abdominal pressure
Vascular (e.g. malignant hypertension, atheroembolic conditions)
Obstructive renal failure

Unusual to be main cause of acute renal failure on the ICU
Renal replacement therapies

In an ICU, renal replacement therapies can be categorized as continuous or
intermittent. In the UK, continuous therapies predominate (Figure 2). There are few
randomized controlled trials comparing intermittent with continuous therapies, but
continuous renal replacement therapy (CRRT) is associated with reduced mortality.
CRRT usually involves the removal and return of blood through a single cannula placed
in a large vein (veno-venous therapy); arteriovenous therapies are seldom used. CRRT
causes less haemodynamic instability, because fluid removal is slower and there is time
for fluid to re-equilibrate between body compartments.
Continuous renal replacement therapies used on ICUs
Mode of therapy Principal method of solute clearance

Continuous veno-venous Convection
haemofiltration (CVVH)
Continuous veno-venous Convection and diffusion

haemodiafiltration (CVVHDF)
Continuous veno-venous Diffusion

haemodialysis (CVVHD)
Slow continuous ultra- Fluid removal by ultrafiltration

filtration (SCUF)
High flux dialysis (HFD) Convection and diffusion

2
Principles of CRRT
In CRRT, solutes are removed from blood by diffusion or convection. Different
processes remove different sized molecules (Figure 3).
Diffusion is the movement of solutes down a concentration gradient across a

semipermeable membrane. This is the main physical process occurring during
haemodialysis. Solutes (e.g. urea, creatinine) cross the dialysis membrane from the
blood to the dialysis fluid compartment. Fluid in the dialysis compartment moves in
a counter-current direction, thereby maintaining a concentration gradient. It is also
possible for solutes (e.g. bi-carbonate) to move in the opposite direction (e.g. from
dialysate to blood).
Convection if a pressure gradient is set up across the dialysis filter, water is pushed
across the membrane and carries dissolved solutes with it; this is known as the solvent
drag. The movement of fluid across the membrane as a result of this transmembrane
pressure is ultrafiltration, and the fluid produced is ultra-filtrate. The process by which
solutes move across the membrane is convection.
Size of molecules cleared by continuous renal replacement therapies (CRRT)
Type of molecule Size Example Mode of removal
Small < 500 Da Urea, creatinine, amino acids Convection, diffusion
Middle 5005000 Da Vitamin B12, inulin, vancomycin Convection better than diffusion
Low molecular 500050,000 Da 2 microglobulin, cytokines, Convection or absorption

weight proteins complement (on to filter)
Large proteins > 50,000 Da Albumin Only minimal removal by

standard CRRT
Da = Daltons
Types of CRRT
Continuous veno-venous haemofiltration (CVVH) (Figures 4a and 5) is the most
commonly used CRRT on an ICU, and is generally a continuous process. Solutes are
not cleared rapidly, but over a continuous period are cleared efficiently. The process
can be run for 24 hours a day, every day, but in practice it is often run for 2472 hours
at a time. Down time occurs to change the filter (either electively or because the filter
has clotted) or for procedures to take place. It is stopped when there is evidence of a
return of renal function.
Vein Blood flow (Qb) Vein

100300 ml/min
Ultrafiltrate (Qf) Replacement

1040 ml/min fluid
(post-dilution)
Pump
Filter

100300 ml/min
Replacement Ultrafiltrate (Qf)

fluid 815 ml/min
(pre-dilution)
Pump
Dialysis fluid (Qd)

1033 ml/min

50200 ml/min
Ultrafiltrate (Qf)
210 ml/min
Pump
Filter
4
a
b
c
d 5 The Prisma (Hospal) continuous renal replacement

e therapy machine. a Information screen; b four pumps
(dialysate, blood, replacement fluid, effluent); c filter;
d effluent bag; e replacement fluid.
Blood is usually pumped through the dialysis circuit at the highest achievable flow rate
(100200 ml/minute); this depends on the quality of vascular access and the patients
haemodynamic state. A specialized, sterile fluid (replacement fluid) replaces the
large volume of ultrafiltrate removed. There is no consensus on how long or how fast
haemofiltration should be undertaken, but an ultrafiltration rate of at least 35 ml/kg/hour
has been associated with improved survival compared with 20 ml/kg/hour. In practice
about 2 litres of ultrafiltrate are removed each hour. Either all or part of the ultrafiltrate is
replaced depending on the desired overall fluid balance.
Continuous veno-venous haemodiafiltration (CVVHD) (Figure 4b) is similar to

CVVH but combines diffusion and convection. Blood and dialysate fluid are circulated
in a counter-current fashion. As with CVVH, a transmembrane pressure is applied,
producing large volumes of ultrafiltrate. Replacement fluid is reinfused at a rate
dependent on the volume of fluid to be removed.
Haemodialysis almost exclusively uses diffusion to remove solutes from plasma but
can be combined with ultrafiltration to remove fluid. As with CVVHD, blood and dialysis
fluid are circulated in a counter-current fashion, but no replacement fluid is reinfused.
This treatment is generally performed intermittently for patients with end-stage renal
failure needing chronic dialysis. It can be performed continuously on the ICU, but its
use is not widespread.
Ultrafiltration can be applied alone as a slow and continuous therapy, termed slow
continuous ultrafiltration (SCUF) (Figure 4c). Ultrafiltrate is formed at a rate of less than
300 ml/hour and replacement fluid is not infused. It can be useful when there is volume
overload, but no solute accumulation (e.g. congestive cardiac failure).
Continuous high flux dialysis uses a highly permeable dialysis membrane with blood
and dialysate circulating in a counter-current fashion. The production of ultrafiltrate is
controlled by pressure, and is reinfused by backfiltration in the blood system, therefore
a separate replacement fluid is not needed. This process is seldom used on the ICU.
Indications for starting renal replacement therapy

It is better to start renal replacement therapy early rather than wait for complications
of ARF to develop (Figure 6). Fluid balance is a major stimulus for starting CRRT in
critically ill patients because large volumes of daily intravenous fluids are required to
maintain intravascular volume, and for drug delivery and nutrition.
Indications for starting renal replacement therapy
Indication Comments
Anuria or oliguria Urine volumes < 200 ml/12 hours
Hyperkalaemia Serum potassium persistently > 6.5 mmol/litre
Severe acidaemia pH < 7.1
Serum urea > 30 mmol/litre Values are not absolute, only a guide
or creatinine > 300 mol/litre
Refractory fluid overload Especially if compromising lung function
Uraemic complications Encephalopathy, pericarditis, neuropathy or

myopathy
Temperature control Hyper- or hypothermia
Drug overdose See Figure 7
Sepsis
6
Convection removes low molecular weight proteins of 500050,000 Da. Many of the
septic mediators (e.g. cytokines, complement) lie within this group. These mediators are
absorbed onto the filter membrane and so removed. Interest surrounds the use of high
volume haemofiltration to remove these inflammatory mediators to improve outcome
from severe sepsis. High volume filtration is defined as ultrafiltration of over 2 litres/
hour, and there is evidence that filtrate volumes up to 6 litres/hour are associated with a
significantly lower mortality in septic patients.
Vascular access
Most renal replacement therapy is veno-venous in nature, therefore vascular access
is usually via a double-lumen vascular catheter placed in a central vein. Blood is
withdrawn from the proximal lumen (arterial side) and returned through the distal
lumen (venous side).
The site of insertion is determined clinically, because critically ill patients often have
other central venous catheters in place. The subclavian route is usually avoided in
patients who may need an arteriovenous fistula for long-term haemodialysis, because
the incidence of subclavian vein stenosis following cannulation is high.
Blood flow through the catheter should be good. Poor access should not be treated by
reducing blood flow rates, because this leads to ineffective solute clearance.
Dialysis filters
As blood comes into contact with the filter (membrane) surface, complement and
leucocytes can become activated, triggering the coagulation cascade and inflammatory
pathways. The degree of activation is variable with some filters having more membrane
biocompatibility than others (more biocompatibility means less activation). It is
suggested that biocompatible membranes are associated with an improved outcome
from ARF, but the evidence is not robust.
Filter membranes are either cellulose-based or synthetic. Cellulose-based filters

(e.g. cuprophane, cellulose acetate) are very thin and strongly hydrophilic. They are
generally low flux membranes and are poor at removing middle molecules. Synthetic
filters (e.g. polysulfone, polyamide, polyacrylonitrile) are high flux membranes and are
generally more biocompatible than cellulose membranes. The flux of a membrane
refers to its hydraulic permeability and how much convective transport can take place
across it. Most filters used for CRRT are synthetic, high flux membranes with a surface
area of 0.61.2 m2.
Replacement fluid
A sterile replacement fluid replaces the ultrafiltrate removed by haemofiltration and
haemodiafiltration. The fluid is infused either before the filter (pre-dilution) or into blood
leaving the filter (post-dilution). Pre-dilution lowers the haematocrit of blood passing
through the filter thus reducing anticoagulation requirements, but leads to a 10%
reduction in solute clearance.
The main buffers in replacement fluid are lactate or bicarbonate. Many critically ill
patients already have a lactic acidosis or are unable to handle lactate appropriately. In
these patients, a paradoxical worsening of the acidbase balance may be seen with a
lactate buffer.
The concentration of sodium, potassium and glucose in the replacement fluid can be
varied depending on the clinical need. However, the fluid does not contain phosphate or
amino acids and these may have to be supplemented.
Anticoagulation during renal replacement therapy

During CRRT, blood is continually in contact with the circuit tubing and the filter, with
consequent stimulation of the coagulation cascade. Recurrent clotting of the circuit
renders treatment inadequate and is a drain on nursing and financial resources.
Often, CRRT can be performed in critically ill patients without the use of anticoagulants
because they often have deranged clotting, thrombocytopenia or both. Anticoagulation-
free CRRT is made easier with good venous access, good blood flow rates and pre-
dilution.
If anticoagulation is required, unfractionated heparin at doses that do not alter the

activated partial thromboplastin time (e.g. 510 IU/kg/hour) can be used. Full systemic
heparinization is seldom needed. Other options include low-molecular-weight heparin,
recombinant hirudin, regional heparinization and the use of prostacyclin. The latter
inhibits platelet aggregation but has no effect on coagulation parameters. Its side-
effects include vasodilatation, but this is seldom a contraindication, even in patients with
an unstable cardiovascular system.
Pharmacokinetics on CRRT
The high flux haemofilter membranes used in CRRT are per-meable to most non-
protein-bound drugs (Figure 7). While receiving CRRT, the doses of drugs should be
given on the assumption that the GFR is 1050 ml/minute. When a patient with ARF is
not receiving renal replacement therapy, the GFR should be assumed to be less than
10 ml/minute. With pre-dilution, the concentration of the drug entering the membrane
is reduced by dilution. During CRRT, the highest drug clearances occur with drugs that
are not protein-bound or when post-dilution is used. u
Pharmacokinetics
Drugs removed on haemodialysis

Salicylates
Methanol
Barbiturates
Lithium
Aminoglycosides
Cephalosporins
Drugs not removed on haemodialysis

Digoxin
Tricyclic antidepressants
Phenytoin
Benzodiazepines
-blockers
Oral hypoglycaemic agents
7
FURTHER READING
Bellomo R, Baldwin I, Ronco C, Golper T. Atlas of Hemofiltration. Philadelphia: W B
Saunders, 2002.
Levy J, Morgan J, Brown E. Oxford Handbook of Dialysis. Oxford: Oxford University

Press, 2001.
Ronco C, Bellomo R, Homel P et al. Effects of Different Doses in Continuous

Veno-venous Haemofiltration on Outcomes of Acute Renal Failure: A Prospective
Randomized Trial. Lancet 2000; 356: 2630.
www.adqi.net/Acute Dialysis Quality Initiative

Antibiotic Prescribing in
the ICU
Richard Brindle
Richard Brindle is Consultant Microbiologist and Infection Control Doctor at

Portsmouth Hospitals, Portsmouth, UK. He qualified from Southampton University
and trained in general medicine and microbiology in Coventry, the London School
of Hygiene and Tropical Medicine, and Oxford. His interests are in hospital-acquired
infections and tropical diseases.
Choosing an appropriate antibiotic

Patients in the ICU displaying signs of sepsis belong to one of the following categories:
infected with a known organism from an identified site
infected with a known organism from an unidentified site
infected, but no causal agent has been identified
uninfected.
Occasionally the clinical signs of an infection suggest the causal organism and the
appropriate antibiotic. However, the choice of antibiotic is often guided by the results
of microbiological investigation. Ideally, specimens for culture should be taken before
antibiotics are given. Appropriate specimens include:
blood cultures (preferably from different sites)
urine
respiratory secretions (non-bronchoscopic lavage samples are preferred)
wound swabs or aspirates from skin lesions
drain, fistula or other fluids or pus
other relevant specimens.
Cultures should be repeated every few days, even if the patient is improving or stable.
This allows empirical therapy to be rationalized and provides information about patterns
of resistance.
If the organism is known, a decision can be made about the most suitable antibiotic,
the most appropriate dose and dosing schedule, the ideal duration of therapy and the
need for adjunctive therapy. If the source of infection is unknown, the site can often be
suggested on the basis of an organism isolated from blood (Figure 1).
Correlation between organism and site of infection
Isolate from blood Likely sites Action

Staphylococcus aureus Infected intravenous line site Remove source, if possible, and give
Deep sepsis (abscesses) at least 14 days therapy
Endocarditis All S. aureus infections need treating
Staphylococcus epidermidis Contaminant Remove source

(coagulase-negative Colonized lines (venous and Treating colonized tunnelled
Staphylococcus) arterial) lines may be successful
Infected prosthesis
Enterococcus spp. Colonized lines Remove source

Intra-abdominal sepsis Drain collection
Endocarditis Treat, if source cannot be removed
Coliforms Urinary tract Treat

Gall bladder Drain any collections
Intra-abdominal sepsis Remove lines
Lines
Chest
Anaerobes Intra-abdominal sepsis Drain collection

Necrotizing cutaneous infections Debridement
Treat
Pseudomonas aeruginosa Colonized lines Remove source if possible (line or

urinary catheter)
Urinary tract Treat
Chest
Yeasts Colonized lines Remove source

Intra-abdominal sepsis Drain collection and give at least 14
Urinary tract days therapy
Antibiotic combinations
Combinations of antibiotics are recommended when:
the cause of the infection is unknown
multiple bacteria are involved
resistance develops easily on monotherapy
the outcome is known to be improved with combinations of antibiotics.
The most common ICU situation in which combination therapy is appropriate is in

the treatment of ventilator-associated pneumonia (VAP). This is characterized by
the onset of an inflammatory response, radiographic changes, purulent secretions
and hypoxaemia after a patient has received positive-pressure ventilation for a few
days. The organisms causing VAP are varied and depend on the patients previous
pulmonary history and previous use of antibiotics. Late onset VAP is generally caused
by Pseudomonas aeruginosa or Staphylococcus aureus. Most UK hospitals have
high levels of methicillin-resistant S. aureus (MRSA), therefore a high proportion of S.
aureus VAP is caused by MRSA. Consequently, when empirical therapy for VAP begins
it should include an agent directed against both Ps. aeruginosa and MRSA.
While the development of vancomycin resistance by MRSA with monotherapy is rare,

the development of resistance to anti-pseudomonal antibiotics while taking anti-
pseudomonal monotherapy is common. One way of reducing resistance developing in
Ps. aeruginosa is to use two anti-pseudomonal antibiotics, of different classes.
Combinations of antibiotics are also of value when resistance is high or unpredictable

and they ensure that at least one anti-biotic will be effective. Antibiotic combinations
can also be more effective than monotherapy, for example an aminoglycoside and
acylureidopenicillin (azlocillin or piperacillin) in the treatment of Ps. aeruginosa infections.
However, the risk of toxicity increases with the number of antibiotics used and, if adequate
levels of both antibiotics are not maintained, resistance to one agent can develop. This is
commonly seen with rifampicin and S. aureus infections.
Broad-spectrum and narrow-spectrum antibiotics

Most antibiotics used as empirical therapy in the ICU have a broad antibacterial
spectrum which is useful if the cause of sepsis is uncertain. However, broad-spectrum
agents are generally more expensive, have significant effects on the patients normal
flora and are more likely to lead to Clostridium difficile-associated diarrhoea, fungal
overgrowth and colonization with resistant organisms. Therefore, it is sensible to
change to a narrow-spectrum agent as soon as possible, though whether this reverses
the effect of an initial broad-spectrum agent is uncertain. Figure 2 illustrates the
spectrum of activity of commonly prescribed antibiotics.
Pseudomonas aeruginosa Staphylococcus aureus Streptococcus .
Gentamicin
Imipenem
Ceftazidime
Cefotaxime
Cefuroxime
Amoxicillin (Amoxycillin)
Co-amoxiclav
Cloxacillin
Piptazo (piperacillin with Penicillin
tazobactam)
Aztreonam
Ciprofloxacin
Vancomycin
Metronidazole
Clindamycin
Erythromycin
Only vancomycin or teicoplanin are suitable for empirical treatment of Staphylococcus epidermidis (coagulase-negative Staphylococcus) and
methicillin-resistant Staphylococcus aureus (MRSA). Bacteria such as meningococci, Haemophilus, Listeria, enterococci and the atypicals
do not fit neatly into the scheme.
Selective decontamination of the digestive tract

There is strong evidence that by reducing the bacterial load on a patient on admission
to the ICU, infection can be reduced. This can be accomplished using broad-spectrum
antibiotics and antifungals and seems to be particularly effective following trauma.
The regimen should include antibiotics active against resistant enterobacteria, Ps.
aeruginosa and MRSA. However, there is a reluctance to use the limited armoury
of antibiotics as prophylactic agents, despite the lack of evidence that selective
decontamination has increased superinfection with resistant organisms.
Early and late infections

The acquisition by patients of ICU flora is a function of their length of stay in the ICU
and, more importantly, their previous antibiotic treatment. Many patients admitted to
ICU will have received antibiotics and most ICU patients receive antibiotics at some
stage during their stay, and will also have been in hospital for some time before
admission to the ICU. For example, respiratory specimens from a patient admitted
directly to the ICU with a community acquired pneumonia may contain Streptococcus
pneumoniae. Treatment with a narrow-spectrum antibiotic is characterized by initial
clinical improvement, however, if assisted ventilation continues beyond a few days, this
flora is commonly replaced by ICU flora and the development of VAP.
Sites of infection
Line-associated sepsis and bacteraemia is common in the ICU. Blood or
intraluminal cultures identify the organism. Catheters impregnated with antibiotics or
antiseptic reduce the infection rate, but are more expensive than standard ones. If the
catheter entry site is infected, or cultures from the line are positive, the line should be
removed. S. aureus or yeast blood infection associated with a line require therapy and
are absolute indications for line removal. Bacteraemia associated with other organisms
generally resolves following line removal.
VAP therapy may need to be continued for as long as the patient is mechanically
ventilated. Empirical therapy is discussed above.
Intra-abdominal sepsis infection seldom resolves without drainage and corrective

surgery. Antibiotics such as co-amoxiclav or the combination of cefuroxime and
metronidazole are generally adequate in community-acquired infections with early
surgery. If the patient has been in hospital and taking antibiotics for more than a few
days, a broader spectrum antibiotic (e.g. piptazo, imipenem) is recommended.
Urinary tract though a high proportion of ICU patients are catheterized, and the
bladder urine may become colonized, the urinary tract is seldom the source of clinical
infection, if catheter patency is maintained. Candiduria is relatively common but may be
a reflection of colonization or a sign of candidaemia.
Diarrhoea
The widespread use of broad-spectrum antibiotics is a significant cause of diarrhoea.
C. difficile-associated diarrhoea and colitis need early recognition and treatment,
because infection may require colectomy. The current endemic strains of C. difficile
are resistant to most antibiotics and this allows their preferential survival. Withdrawal
of antibiotics may allow resolution but, if diarrhoea persists, it should be treated with
metronidazole (oral or nasogastric is preferred). If the diarrhoea does not resolve, or
has developed while taking metronidazole, oral vancomycin should be administered.
Dose
It is important to use appropriate doses because too little antibiotic may not have a
therapeutic effect and allows resistant organisms to persist; too much antibiotic may
cause toxicity. Dose needs to be individualized and knowledge of the mode of excretion
is vital. In general, the highest dose that is safe to use should be administered.
Duration
The duration of antibiotic therapy depends on the organism isolated, its source and
the clinical response. Studies of relapse and complications suggest a minimum of 2
weeks therapy for S. aureus and Candida spp. blood infections, but there are few data
on minimum duration of therapy for other ICU-acquired infections. The duration of
therapy for VAP depends on the clinical and laboratory response. Antibiotics should be
reviewed after 5 days therapy. Some patients, particularly with MRSA pneumonia, may
require repeated courses. If there is a poor clinical response, the antibiotics should be
stopped for 12 hours and cultures taken; a new empirical treatment can then be
commenced. u
FURTHER READING
Armstrong D, Cohen J, eds. Infectious Diseases. London: Mosby, 1999.
Mandell G L, Bennett J E, Dolin R, eds. Mandell, Douglas, and Bennett's Principles and
Practice of Infectious Diseases. Edinburgh: Churchill Livingstone, 2000.

Assessment and Stabilization
of the Critically Ill Patient
Outside the ICU
Gary Smith
Gary Smith is Consultant in Intensive Care Medicine at Portsmouth Hospitals NHS

Trust, and Honorary Senior Lecturer in Critical Care in the School of Postgraduate
Medicine, University of Portsmouth, UK. He qualified from Southampton University
Medical School and trained in anaesthesia and medicine in the South of England and
Yale University, USA. His interests include the organization of intensive care services,
outcome prediction and the training of doctors, nurses and paramedics.
ICU medical staff are often required to assess and stabilize patients referred for ICU
admission. They may also be asked to assess patients for the following reasons:
difficult venous access
analgesic techniques
fluid balance
tracheostomy care
inter-hospital transfer
intra-hospital transfer to a high dependency unit or the operating theatre
as a member of the cardiac arrest or medical emergency team.
The assessment and stabilization of all such patients follows similar lines, but this
contribution focuses on the patient who is referred and accepted for ICU admission.
Referral process
ICU referrals are traditionally made by doctors; however, they are increasingly
being made by nurses and physiotherapists acting on guidelines (e.g. physiological
abnormalities) previously agreed with ICUs. The ICU staff require a range of referral
details (Figure 1). If the patient has a potentially life-threatening illness, the caller should
be given simple instructions regarding therapy to be undertaken before the ICU team
arrives. Before leaving to assess the patient, the ICU doctor should share the collated
data with the senior ICU nurse and check whether an ICU bed is available.
Information required during referral to the ICU

Patients name
Patients gender
Patients age
Current location of patient
Date of referral
Time of referral
Name, grade and contact details of person making the referral
Whether the referral has been discussed with the consultant responsible for
the patients care
Whether the referral has been discussed with the patient or the patients
relatives, and their wishes
The patients diagnosis and prognosis
Relevant past medical history
Relevant social history, including quality of life
Patients current condition, especially vital signs, urine output
Patients current therapy, especially fractional inspired oxygen concentration,
fluid therapy, drugs
Patients current monitoring
Presence of intravenous lines and central venous access
Presence of a nasogastric tube, wound drains or thoracocentesis tubes
Results of recent laboratory investigations
Patients resuscitation status
Any agreed limitation of therapy
ICU retrieval team

In some ICUs, a dedicated retrieval nurse attends the patient with the ICU doctor,
in order to provide expert assistance. He/she can also support the patient during
stabilization and transfer, and provide an initial contact for the patients family. The ICU
team usually takes the necessary stabilization drugs and equipment to the patients
bedside, possibly attached to the patients stretcher.
Assessment and stabilization

Traditional history-taking and examination is often inappropriate when attending
critically ill patients, where life-saving measures must often precede diagnosis. Initially,
assessment and stabilization occur together, focusing on the rapid detection and
simultaneous treatment of potentially life-threatening emergencies. Simple questions to
the patient can establish whether the patient has a patent airway, is breathing and
perfusing his/her brain. Patients who can speak only in short sentences, or with one or
two words at a time, are usually in extreme respiratory distress and at risk of sudden
respiratory arrest. As stabilization proceeds, important aspects of the patients medical
history can be obtained from ward staff, the patients case notes and charts (e.g.
temperature, pulse, respiration, blood pressure, neurological observation chart, fluid
balance, drug prescription chart) or the patients family. Co-morbid conditions may have
a significant impact on the response to critical illness.
Throughout the period of assessment and stabilization, the ICU team should
observe good hygiene and infection control measures. In order that patients are
examined properly, full exposure may be necessary. This should be done in a way that
respects the dignity of the patient and prevents heat loss.
Airway
Assessment of airway patency involves the steps given in Figure 2. If the airway
is obstructed, immediate clearance is mandatory before assessing breathing. Simple
adjuncts (e.g. oropharyngeal or nasopharyngeal airway) suffice initially, but tracheal
intubation under general anaesthesia is usually required in the critically ill. Anaesthetic
agents invariably reduce cardiac output and vascular resistance, therefore a 200500
ml fluid bolus should be given before induction. Occasionally, vasoactive drug infusions
(e.g. adrenaline (epinephrine), noradrenaline (norepinephrine), dobutamine) are also
required. In extremely rare circumstances, a surgical airway is required. In all patients, a
chest radiograph should be undertaken as soon as possible to confirm correct tracheal
or tracheostomy tube placement.
Assessing airway patency
Look for
Foreign bodies, secretions or blood within the mouth
Obstruction of the pharynx by the tongue
Use of the accessory muscles of respiration
Chest expansion
Paradoxical breathing
Listen for
Abnormal upper airway sounds (e.g. stridor, gurgling, snoring); if obstruction is
complete, breath sounds will be absent
Feel for
Expired air
Breathing
Breathing is assessed as described in Figure 3. Unilateral chest movement suggests
underlying unilateral disease (e.g. pneumothorax, pneumonia, effusion). A high (>
20), or rapidly rising, respiratory rate usually indicates severe illness or impending
deterioration. Small pupils may reflect excessive opiate administration.
Respiratory interventions are often based on clinical signs rather than arterial blood
gas analysis. All critically ill patients must receive oxygen via a face mask with a
reservoir bag or bagvalvemask manual resuscitator, sufficient to maintain a minimum
peripheral saturation of haemoglobin by oxygen of 90% (arterial oxygen tension = 8
kPa). Inadequate minute volume requires assisted ventilation, possibly with intubation.
Positive end-expiratory pressure may be required. Pneumothoraces or large pleural
fluid collection should be treated using tube thoracocentesis. Wheezing should be
treated with inhaled bronchodilators. If the patient is in pain, initiation of an appropriate
analgesic regimen may improve ventilation.
Assessing breathing
Look for or observe

Cyanosis
Chest deformity
Respiratory rate, pattern and depth
Equality of chest expansion
Fractional inspired oxygen concentration
Peripheral saturation of haemoglobin by oxygen
Jugular venous pressure
Abdominal distension
Listen for
Wheeze, crackles, bronchial breathing
Bilateral breath sounds
Feel for or palpate

The position of the trachea
Chest wall (for surgical emphysema or crepitus)
Depth and equality of movement on each side of the chest
Percuss
To elicit dullness or hyper-resonance
Circulation
Lung or pleural pathologies (e.g. tension pneumothorax) that can compromise the
circulation, should have been treated during the respiratory system assessment. Figure
4 describes how to assess circulation. In shock, the blood pressure may be normal,
because compensatory mechanisms increase peripheral resistance as cardiac output
falls. A low diastolic blood pressure suggests vasodilatation (as in sepsis). A narrowed
pulse pressure suggests vasoconstriction (cardiogenic shock or hypovolaemia). A
thready pulse suggests poor cardiac output; a bounding pulse may indicate sepsis. The
presence of a carotid or radial pulse implies systolic blood pressures are greater than
70 and 90 mm Hg, respectively.
The nature of cardiovascular resuscitation is determined by the cause, but
should be directed at replacing fluid, controlling haemorrhage and restoring tissue
perfusion. Massive or continuing haemorrhage and cardiac tamponade (diagnosed by
hypotension, raised jugular venous pressure, muffled heart sounds, cardiomegaly on
chest radiography, or electromechanical dissociation) are life-threatening conditions
and must be treated urgently. Massive or continuing haemorrhage requires
transfusion and may require urgent resuscitative surgery. Cardiac tamponade requires
pericardiocentesis or pericardiotomy. All critically ill patients require at least one large
(16 G) cannula, preferably two, placed in large veins.
Hypovolaemia contributes to circulatory dysfunction in almost all medical and
surgical emergencies. Fluid challenges of warmed crystalloid should be given over
510 minutes to all patients, as follows:
10 ml/kg in normotensive patients
20 ml/kg in hypotensive patients
5 ml/kg in patients with known cardiac failure, in whom closer monitoring should be
initiated (listen for crepitations after each bolus, consider a line).
The goal of therapy is to improve tissue perfusion. Although blood flow is more
important than blood pressure, a minimum mean blood pressure of 70 mm Hg should
be sought (higher in hypertensive patients). If perfusion does not respond to fluids
alone (i.e. central venous pressure rises after fluid boluses without evidence of
improved cardiac output), vasoactive drugs such as dobutamine, > 5 g/kg/minute,
adrenaline (epinephrine),> 0.05 g/kg/minute, or noradrenaline (norepinephrine), > 0.05
g/kg/minute, should be commenced.
Reassessment of circulatory status is essential. If there is no improvement, the
fluid challenge can be repeated. In a few patients, fluid administration leads to cardiac
failure. If this occurs, fluid administration should be stopped and vasoactive drugs (see
above) commenced.
Disability
Rapid assessment of a patients neurological status involves:
examining the pupils (size, equality, reaction to light)
the AVPU system (A, alert; V, responds to vocal stimuli;P, responds to painful
stimuli; U, unresponsive).
Common causes of unconsciousness include profound hypoxaemia, hypercapnia,
cerebral hypoperfusion, hypoglycaemia or recent administration of sedatives,
analgesics or anaesthetic drugs. Reversible causes should be treated immediately.
Spontaneously breathing, unconscious patients are at risk of airway obstruction and
aspiration of secretions, vomit or blood. Consequently, unconscious patients are better
nursed in the lateral recovery position until intubated.
Assessing circulation
Look for or observe

Conscious level
Capillary refill (normally < 2 seconds)
Colour and temperature of digits (cyanosed, pale, cold and clammy in shock)
Venous filling (including jugular venous pressure)
Urine output
Nasogastric, stoma or drain output
Evidence of concealed or overt haemorrhage
Listen for
Heart sounds
Blood pressure (systolic, mean, diastolic); note patients normal values
Feel for or palpate

Presence, rate, quality, regularity and equality of peripheral and central pulses
End of the initial assessment and stabilization period

At the end of the initial assessment, the patient should be showing signs of
improvement. The following minimum monitoring devices should already be attached or
inserted:
pulse oximeter
capnograph (if intubated)
ECG
blood pressure measurement (usually invasive).
Other devices that may be used include: urinary catheter, central venous catheter,
nasogastric tube, and pulmonary artery catheter. Before moving the patient from the
ward, the patients oxygen saturation in arterial blood, heart rate, blood pressure,
central venous pressure, end-tidal carbon dioxide tension, ventilator settings and
performance should be noted. Actions taken during stabilization should be documented
in the patients notes. All invasive devices should be firmly secured to the patient. The
patient should be sedated to an appropriate level for transfer; muscle relaxation may be
required. Finally, the ICU should be notified of the impending arrival of the patient.

Brainstem Death
Suzie J Tanser
Gary B Smith
Suzie J Tanser is Specialist Registrar in Anaesthesia, Royal Navy Southampton

General Hospital. She qualified from St Bartholomews Hospital, London, then joined
the Royal Navy. She trained in anaesthesia and intensive care in Plymouth, Exeter,
Portsmouth, Southampton and London and completed advanced training in intensive
care in 2001.
Gary B Smith is Consultant in Intensive Care Medicine at Portsmouth Hospital NHS

Trust and Honorary Senior Lecturer in Critical Care in the School of Postgraduate
Medicine at the University of Portsmouth. After qualifying from the University of
Southampton, he trained in anaesthesia and medicine in the South of England
and at Yale University, USA. His main interests are multiprofessional education,
cardiopulmonary resuscitation and pre-hospital trauma care.
Death has traditionally been diagnosed using the triad of Bichat the failure of the
body as an integrated system, associated with the irreversible loss of circulation,
respiration and innervation. However, the development of techniques to maintain
respiration and circulation artificially, and the fact that dead patients may look alive,
have a heart beat and feel warm, has led to conceptual and practical problems with the
diagnosis of death.
The brainstem comprises the midbrain, pons and medulla oblongata. It contains the
respiratory and cardiovascular centres and integrated sensory and motor functions. It
is necessary for spontaneous respiration, consciousness and cortical activation. Death
of the brainstem is equivalent to death of the individual, even if heart, lung and spinal
cord function persist. Eventually all organs fail and asystole occurs. There has never
been a documented recovery following properly conducted brain death testing that
indicated brainstem death. It is agreed that permanent functional death of the brainstem
constitutes brain death and, once this has occurred, further artificial support is fruitless
and should be withdrawn. It is good medical practice to recognize when brain death
has occurred and to act accordingly, sparing the relatives from futile hope and freeing
valuable intensive care resources.
Incidence and aetiology

Up to 1015% of deaths in UK ICUs are brainstem deaths. In adults, the most common
primary diagnoses are trauma and intracranial haemorrhage; in children, they are
trauma and the anoxic encephalopathies (e.g. drowning). Other causes include
intracranial malignancy, intracranial abscesses, hydrocephalus and meningitis. Cardiac
arrest may lead to brainstem death, but more often, leads to a persistent vegetative
state.
Diagnosis of brainstem death

The UK code for the diagnosis of brainstem death was defined by the Conference of
Medical Royal Colleges in 1976 and has been updated subsequently. The three stages
of diagnosis are preconditions, exclusions and clinical testing.
Preconditions
The patient is in an unresponsive coma.
The patients condition is due to irreversible brain damage of known aetiology.
Exclusions
All the following reversible causes must be excluded:
drugs (e.g. narcotics, hypnotic, tranquillizers, muscle relaxants)
primary hypothermia (core temperature must be above 35oC)
circulatory (including recent circulatory arrest)
metabolic (e.g. hyponatraemia, hypoglycaemia)
endocrine (e.g. hypothyroid state).
Clinical tests
Clinical tests are performed by at least two doctors (one a consultant, the other
at least 5 years post registration) who are unconnected with the family and, if organ
donation is an option, the transplant team.
These tests are repeated twice by both doctors either indep-endently or together.
The time interval is not specified.
The tests involve reflexes involving the brainstem (Figure 1) and an apnoea test.
There should be no pupillary response to light, no corneal reflex, no vestibulo-ocular
reflex, no motor response to central stimulation, no gag and cough reflex and no
spontaneous breathing.
None No blinking on No eye movement No grimacing None

corneal touch on caloric testing on painful stimuli
Pupillary response to light the pupils do not respond directly or consensually to

sharp changes in light intensity. This tests cranial nerves II (afferent) and III (efferent).
Corneal reflex there is no response to direct stimulation of the cornea. This tests
cranial nerves V (afferent) and VII (efferent). Care should be taken to avoid damage to
the cornea. Gentle pressure using a cotton bud is the preferred method.
Vestibulo-ocular reflex there are no eye movements following slow injection of 20

ml of ice-cold water over 1 minute into each external auditory meatus in turn. A normal
response is deviation towards the stimulus. Before this a visual inspection of each
tympanic membrane must be made to ensure clear access. Local injury or disease
does not invalidate the diagnosis. This tests cranial nerves VIII (afferent) and III, IV and
VI (efferent).
Motor response to central stimulation

No motor response within the cranial nerve distribution to sustained painful stimuli to
limbs or the supraorbital notch. This tests cranial nerves V (afferent) and VII (efferent).
Spinal reflexes may occur after stimulation of the trunk or extremities. Occasionally
these can be dramatic, such as back arching or extensor posturing (Lazarus sign).
These movements may be upsetting but since they originate below brainstem level,
they do not rule out the diagnosis of brainstem death.
No reaction should be seen following painful stimulation in the cranial nerve
distribution.
Gag and cough reflex there is no contraction of the soft palate when stimulated or
response to bronchial stimulation. This tests cranial nerves IX and X.
Spontaneous breathing this tests the ability of the patients brainstem to initiate
spontaneous respiration. Before testing, the following should occur:
preoxygenation of the patient with 100% oxygen for 10 minutes
the partial pressure of carbon dioxide in arterial blood (PaCO2) should be allowed to
rise to 5 kPa (40 mm Hg) or above.
To test the function of the respiratory centre:

the patient is disconnected from the ventilator
oxygen at 610 litres/minute is insufflated into the trachea using a catheter (to
maintain adequate oxygenation)
the PaCO2 is allowed to rise to over 6.65 kPa (50 mm Hg) this requires arterial
blood gas analysis
the lack of spontaneous respiratory effort is confirmed.
Following apnoea testing, the patient is reconnected to the ventilator if:

only one set of brainstem function tests has been completed
two sets of tests have been completed, which show lack of brainstem function and the
patient is to become an organ donor.
Time of death
The legal time of death is the time of completion of the first set of brainstem tests.
Death is certified after completion of the second set of tests, regardless of when active
support is withdrawn.
Neonates and young children clinical brainstem tests alone cannot be applied to
children with a conceptual age of less than 52 weeks or less than 2 months post-term
delivery. Ancillary testing such as cortical electrical activity (EEG), sensory evoked
potentials (SEP), evaluation of brain blood flow (cerebral angiography, radionuclide
scanning or Doppler ultrasonography) or MRI has been suggested, but no tests are
foolproof. Therefore, no single method should be relied on and any clinical or ancillary
test used should be repeated two or three times over a period of up to 24 hours.
Respiratory disease apnoea testing may be invalid in patients with chronic

pulmonary disease and carbon dioxide retention. For such patients, their usual PaCO2
levels should be taken as baseline and the PaCO2 allowed to rise during apnoea testing
to at least 2 kPa above baseline or until a respiratory acidaemia can be demonstrated.
Oxygen supplementation should be reduced accordingly.
Inability to apply clinical criteria in some cases, such as severe facial trauma,
profound metabolic or endocrine disturbances, it may be impossible to apply all the
preconditions, exclusions or clinical tests. Under these circumstances, all possible tests
should be completed and supplemented with the additional tests described below.
Great care should be taken under these circumstances when declaring death because
the additional tests have not been legally validated in the UK.
Additional tests
Cerebral angiography a selective four-vessel angiography is done with contrast
media injected into both the anterior and posterior circulation. A minimum mean arterial
pressure of 80 mm Hg is required for this test. In brain death, no intracranial perfusion
other than occasional filling of the superior sagittal sinus is seen.
Radionuclide scanning a radioactive-labelled substance that readily crosses the

bloodbrain barrier can be used to image parenchymal uptake activity. In brain death
there is lack of uptake into parenchymal tissues.
Transcranial Doppler ultrasonography the intracranial arteries can be insonated

using a 2 MHz pulsed Doppler instrument. Absent diastolic flow has been reported in
brain death. However, interpretation of these tests can be difficult.
Neurophysiological tests the electroencephalogram (EEG) can be a useful

confirmatory tool especially in young children. It should not be used in isolation,
because it does not adequately assess brainstem function. Auditory and sensory
evoked potentials have also been used.
Social and religious issues

The concept of brainstem death is difficult for many relatives and has been made
more so by media reporting of so-called medical errors. It should be emphasized that
brainstem death is irrefutably death and the act of switching off the ventilator is not
killing the patient but merely ceasing to ventilate a corpse.
Allowing relatives to witness the brainstem tests may help them to understand that
death has occurred. However, witnessing the spinal reflexes tests may cause distress
and it is important to explain the process continually throughout the testing.
Some religious groups (e.g. Orthodox Jews) do not believe in the concept of brainstem
death and may refuse to allow withdrawal of ventilatory support, which they consider
to be tantamount to murder. Published data indicate that asystole results within days
of brainstem death. Therefore, to respect religious or cultural sensitivities, it may be
appropriate to wait for asystole to occur before certifying death. u

Cannulation of Central Veins
for Resuscitation and
Monitoring in the ICU
Carl Waldmann
Carl Waldmann is Consultant Anaesthetist and ICU Director of the Royal Berkshire
Hospital, UK. He qualified in medicine from Cambridge University and the London
Hospital and trained in anaesthesia in the RAF. His main interests are the setting up of
ICU follow-up programmes, and head injury management in a district general hospital.
Central venous catheters (CVCs) are integral to current medical practice, but
complications are associated with their insertion. Placement of CVCs used to be
the preserve of surgeons using general anaesthesia but the success rate was only
about 75% and the vein was compromised for future use. The introduction of the
percutaneous method led to uncontrolled use of CVCs by a variety of inadequately
trained staff with serious, potentially avoidable, complications that were sometimes
fatal. Recent advances in CVC manufacture, better training in insertion techniques,
the use of ultrasound, the development of hospital nutrition teams, and the increasing
involvement of interventional radiologists in the ICU should all ensure that CVC
placement becomes safer. Interventional radiologists should be more involved in
the management of ICU patients because they are familiar with ultrasound and
fluoroscopic techniques, have extensive experience with advanced catheter and
guidewire techniques, and are adept at retrieving catheters or parts of catheters
inadvertently lost within the vascular system.
Figure 1 lists the indications for using CVCs. Originally CVCs were of fine bore,
but newer, wide-bore, high-flow, central venous pressure lines and pulmonary artery
catheter introducers permit rapid volume replacement. Multilumen catheters allow
concurrent CVP monitoring and multiple drug infusion.
Indications for central venous catheterization

Replacement of circulating volume
Haemodynamic monitoring
Monitoring of jugular bulb venous oxygen and mixed venous oxygen
saturation
Administration of vasopressors
Repeated or frequent blood sampling
Parenteral nutrition
Chemotherapy
Insertion of pacing wires or pulmonary artery catheters
Endoluminal intervention (e.g. endocardial biopsy)
Haemofiltration
Insertion
In general, internal jugular, subclavian and femoral veins can be cannulated using
standard anatomical landmarks (Figure 2).
The technique most often used was described by Seldinger in 1953. A small needle
is inserted through the vein wall, a wire guide is advanced through the needle into the
vein and the needle replaced by a dilator over the guide. A small incision is made close
to the wire and the dilator replaced by the catheter. After cannulation of the internal
jugular vein and subclavian vessels a chest radiograph should be taken to confirm
correct CVC positioning and to ensure there is no pneumothorax.
Access sites of choice f

g a Clavicle
2 1
b 1st rib
1 High internal jugular a 3 c Suprasternal notch
4
2 External jugular
c d Sternal angle
i
5 e Right atrium
3 Low internal jugular b f External jugular vein
4 Supraclavicular k
d h g Internal jugular vein
5 Infraclavicular h Subclavian vein
j
i Left innominate vein
j Superior vena cava
k Suggested catheter tip positioning zone
e
Femoral vein
The most common use of the femoral vein in an ICU is for placement of a double-lumen
haemofiltration line. Traditional teaching suggests that the femoral vein lies medial to its
artery. However, ultrasound studies have demonstrated that the artery and vein do not
always lie side by side; the degree of overlap between vessels varies between patients
and sides. It is recommended that the femoral vein should be accessed just below the
inguinal ligament and that ultrasound-guided placement should be used in patients with
difficult anatomy, coagulopathy or peripheral vascular disease.
The femoral approach is usually used only when central access is unfeasible by
other routes, and usually only as a short-term expedient. The route is impractical for
mobile patients. Other concerns are thromboembolism and groin sterility.
Subclavian vein
The subclavian vein is the most comfortable cannulation site for patients, and is
the best for long-term parenteral nutrition, pacing wires and Hickman lines. However,
there are significant concerns because of the proximity of the subclavian vein to the
subclavian artery (pressure cannot be exerted here if the artery is punctured), lung
(risk of pneumothorax) and, on the left, the thoracic duct. Successful placement may be
impossible unless the patient is placed head-down, which they may not tolerate.
Various approaches have been described. The author prefers infraclavicular
puncture with a small needle introduced 2 cm inferior to the junction of the middle and
medial thirds of the clavicle (see Figure 2). The needle is advanced medially in the
direction of the suprasternal notch in a horizontal plane.
Internal jugular vein

Cannulation of the internal jugular vein may be difficult in obese patients or those
with goitre or neck rigidity. This route, especially the high approach, is favoured for
cannulation in the ICU because the insertion site is distant from the lung apex and
haemorrhage from an inadvertent puncture of the carotid artery is easily controlled.
However, damage to the brachial plexus, phrenic nerve and sympathetic chain are
possible.
There are several well-described approaches to the internal jugular vein (see Figure
2). Success is increased by positioning the patient head-down with a pillow under the
shoulders. The needle is inserted laterally to the palpated carotid artery, under the
clavicular head of the sternomastoid at the apex of the posterior triangle. It is directed
caudally and anteriorly towards the ipsilateral nipple. Normally the internal jugular lies
anterior and lateral to the carotid artery; however, it may be unilaterally absent in up to
2.5% of patients. In 5.5% of patients the internal jugular lies outside the path predicted
by anatomical landmarks.
Coagulopathy
Although insertion of CVCs in the presence of a coagulopathy is a relative
contraindication, a recent series of 658 cannulations in patients with liver disease
and coagulopathy demonstrated a low incidence of haemorrhagic complications. The
presence of a raised international normalized ratio alone is not a contraindication to
CVC insertion, and there is little evidence that transfusion of fresh frozen plasma
is required before insertion. Nevertheless, caution is recommended in patients with
combined coagulopathies, thrombocytopenia, or those on haemofiltration.
Aids to successful CVC insertion

Correct positioning of a patient, and the use of various manoeuvres, during central
vein cannulation may increase the chances of success. The diameter of the internal
jugular vein can be increased by using a Valsalva manoeuvre, abdominal binder and
increasing head-down tilt. Carotid artery palpation and full neck extension reduce the
veins diameter.
Venography reduces the number of attempts to insert CVCs in patients with
occluded or absent central veins.
Hand-held Doppler probes avoid multiple attempts in patients with unilateral
absence or narrow diameter veins.
Portable ultrasound machines the use of two-dimensional (B-mode)
ultrasonography allows visualization of the anatomy both before and during cannulation.
100% success has been reported if a portable ultrasound machine is used as a bale-
out technique after failed attempts at blind cannulation. It has recently been suggested
that blind attempts at venous cannulation should be replaced by ultrasound-guided
techniques. The use of a longitudinal view enables the operator to monitor the passage
of the needle throughout the procedure as the needle enters the vein.
Complications
Complications may occur in up to 10% of central vein cannulations. Common
complications are listed in Figure 3.
Complications of central venous catheterization
Local complications
Failure to cannulate
Arterial puncture
Haematoma
Local infection
Thrombosis of vessel
Distant complications
Perforation
Haemorrhage
Cardiac tamponade
Pneumothorax
Arrhythmias
Damage to thoracic duct (subclavian)
Brachial plexus damage (subclavian)
Air embolism
Catheter embolism
Thrombus formation
Bacteraemia, sepsis
Respiratory obstruction
Line infection: catheter-related infections are potentially avoidable, yet account for
about 25% of all nosocomial infections and 50% of nosocomial bloodstream infections
in ICU patients. Consequently, there is considerable interest in determining whether
CVCs need to be changed regularly in ICU patients, even in the absence of evidence
of infection, and whether they should be changed routinely when an ICU patient has a
persistent fever.
Recent data demonstrate that removal of the CVC in patients with suspected line
infection is unnecessary in up to 90% of cases. In the absence of obvious infection at
the skin entry site, one expedient would be merely to change the line over a guidewire
with antibiotic cover and await microbiological advice following culture of the removed
CVC tip. Replacement of the second catheter is recommended if the first is found to be
significantly colonized. However, the first CVC is still often unnecessarily sacrificed to
enable the diagnosis of catheter-related sepsis. To avoid this, using the very sensitive
and specific technique of endoluminal brushing may be an alternative. The use of
endoluminal brushing is regarded as safe and simple and eliminates the need for
recatheterization with its attendant complications. This is particularly important in
patients with long-term Hickman lines.
Catheter-related sepsis may also occur in the absence of pyrexia, leucocytosis
and localized erythema at the insertion site. Line removal may be essential if severe
systemic illness is to be avoided. Regular bacteriological surveillance with endoluminal
brushing or by a technique known as time to positivity of hub-blood versus peripheral
blood cultures (in this technique an earlier positivity of central compared with peripheral
venous blood cultures may be associated with catheter-related bacteraemia) may prove
to be useful surveillance methods.
The incidence of bacteraemia due to infected CVCs has been estimated at 5.3
episodes per 1000 catheter days (ranging from 2.8 in cardiac surgical patients to 12.8
in patients in the burns units). The organism most commonly cultured is coagulase-
negative Staphylococcus, though Candida is often reported. Colonization of lines
may be associated with death, morbidity and a prolonged hospital stay. The essential
elements of a strategy to prevent CVC-related infections include barrier precautions
during insertion, strict aseptic technique during manipulation of lines, avoiding
systematic change of dressings and catheters, and continuous surveillance.
Advances in catheter design
Material: the use of polyurethane virtually eliminates kinking. Soft catheter tips prevent
vessel perforation.
Adjustable hubs permit the insertion distance to be altered after chest radiograph
checks have been performed. In adults, the use of 15 cm CVCs often eliminates the
need for hubs if the internal jugular vein site is used. Suturing the hub may not always
ensure that a CVC is securely sited; it is preferable to suture the catheter itself.
Multilumen catheters reduce the possibility of drug interaction and bolusing of

vasoactive drugs, allow rapid volume replacement and permit the introduction of a
pulmonary artery catheter through the same catheter, thereby reducing the need for
more than one venous puncture.
Heparin and antibiotic coating: non-thrombogenic lining of CVCs was described in

1971 as a method of preventing catheter blockage by fibrin deposits and avoiding
bacterial growth on catheters. Some catheters are now coated with a combination
of antimicrobial agents (e.g. minocycline, rifampicin) and heparin.
FURTHER READING
Scott D H T. In the Country of the Blind, the One-eyed Man is King. Erasmus (1466
1536). Br J Anaes 1999; 82: 8201.
Seldinger S I. Catheter Replacement of Needle in Percutaneous Arteriography; A New
Technique. Acta Radiologica 1953; 39: 36876.

Cardiac Arrhythmias in the
Critically Ill
Kirsten J C Richards
Andrew T Cohen
Kirsten J C Richards is Specialist Registrar in General Medicine at St Jamess

University Hospital, Leeds, UK. She qualified from Sheffield University and trained in
general and emergency medicine in Sheffield and Leeds. She has also worked in
intensive care medicine in Leeds. Her interests lie in acute and intensive care medicine.
Andrew T Cohen is Consultant in Anaesthesia and Intensive Care in the 14-bedded

ICU at St Jamess Hospital, Leeds, UK. He is an examiner for the final FRCA and chairs
the Trust Drug and Therapeutics Committee.
Cardiac arrhythmias are a common cause of potentially life-threatening, haemodynamic

compromise in critically ill patients. This article describes a systematic approach to
the management of the four general characteristics of arrhythmia broad or narrow
complex and tachycardia or bradycardia because it is important to treat the patient
and the general type of rhythm rather than considering each disturbance in detail.
Factors that predispose to the development of arrhythmias in peri-operative or
critically ill patients include:
cardiac disease
hypoxia and hypercarbia
electrolyte imbalance (particularly hypo- or hyperkalaemia, hypomagnesaemia)
hypovolaemia
extremes of temperature
elevated catecholamine levels (endogenous and exogenous)
pulmonary artery catheterization
systemic inflammation (e.g. systemic inflammatory response syndrome)
drugs.
Successful management should be approached in stages:
rapidly assess the haemodynamic status of the patient
identify the origin of the arrhythmia
correct predisposing factors (e.g. hypoxia, electrolyte imbalance)
consider specific therapy (e.g. drugs, DC cardioversion)
prevent further arrhythmias.
Identification of the arrhythmia
A 12-lead ECG should be performed before treatment in all cases of arrhythmia except
pulseless rhythms occurring during cardiac arrest. Identifying the precise rhythm is
unnecessary but it is important to determine whether the complex width is narrow or
broad, whether the patient is haemodynamically compromised, and in certain situations,
whether the patient has known underlying structural heart disease.
A pulseless narrow complex tachycardia should be treated as pulseless electrical
activity (electromechanical dissociation) if the rate is less than 200 beats per minute
(bpm). However, if the rate is greater than 200 bpm, the initial treatment should be
synchronized DC cardioversion (100 J, 200 J, 360 J). The Resuscitation Council (UK)
Advanced Life Support guidelines for pulseless electrical activity should be followed if
there is no response to initial DC cardioversion.
If a pulse is present, determine whether the rhythm is a tachycardia (> 100 bpm)
or a bradycardia (< 60 bpm) and whether the complexes are broad (> 0.12 second)
or narrow (< 0.12 second). Examples of the four types of arrhythmia are given in
Figure 1.
Types of arrhythmia
Narrow complex bradycardias

Sinus bradycardia
Slow atrial fibrillation
Mobitz type II heart block
Broad complex bradycardias

Sinus bradycardia with pre-existing bundle branch block
Mobitz type III heart block (complete heart block may be present if the
ventricular rate is 3040 bpm with complete dissociation of atrial activity)
Narrow complex tachycardias

Irregular: atrial fibrillation
Regular: supraventricular tachycardia (e.g. atrial tachycardia, atrial flutter,
junctional tachycardia, supraventricular tachycardia with accessory pathway)
Broad complex tachycardias

Ventricular tachycardia
Supraventricular tachycardia with aberrant conduction (pre-existing inter-
ventricular block)
Management of arrhythmias
Drug treatment
All antiarrhythmic drugs are also potentially rhythmogenic.
Electrolytes
Potassium hypokalaemia commonly causes arrhythmias, especially ventricular
tachycardia (VT). Patients at particular risk of hypokalaemia include those
taking diuretics, post-operative patients, patients undergoing treatment for diabetic
ketoacidosis, and those receiving intravenous fluid replacement therapy. An infusion of
potassium chloride, 60 mmol in 60 ml normal saline, should be given via central access
at a maximum rate of 30 mmol/hour.
Magnesium magnesium deficiency tends to occur concurrently with
hypokalaemia. Magnesium correction should be considered in all patients with VT.
Intravenous magnesium sulphate, 2.5 g (5 ml 50%), should be given over 30 minutes.
In patients with shock and refractory ventricular fibrillation (VF) an initial dose of
magnesium sulphate, 12 g (24 ml 50%) may be given peripherally over 12 minutes.
Other antiarrhythmic drugs are listed in Figures 2 and 3.
Antiarrhythmic drugs
Uses Dose Important side-effects
Adenosine
Blocks specific cardiac receptors Terminates SVT 612 mg via central access or large Bradyarrhythmias
Slows conduction across AV node Facilitates diagnosis peripheral vein (can repeat 12 mg x 3) Bronchospasm (should be
Slows rate Differentiation of broad Immediately flush with saline. Monitor administered in high dependency
Very short half-life (810 seconds) complex SVTs patient in a high dependency setting facility and used with extreme
from VT hroughout administration. Reduce initial caution in asthmatics)
Identification of arrhythmia by dose to 3 mg in heart transplant patients Transient chest tightness, nausea,
revealing the underlying atrial who are more sensitive to adenosine flushing
rhythm (e.g. atrial flutter/ and to 0.51 mg in patients receiving Avoid in heart block and sick sinus
fibrillation/tachycardia) dipyridamole. Effects are antagonized by syndrome
theophylline and coffee
Amiodarone
Blocks repolarizing potassium Refractory VF Refractory VF/pulseless VT: 300 mg Hypotension, photosensitivity, slate-
channels Pulseless VT in 20 ml 5% dextrose grey skin discoloration, corneal
Prolongs AP, refractory period Haemodynamically stable Stable tachyarrhythmias: 150 mg in microdeposits, peripheral
and QT interval VT, SVT and AF 20 ml 5% dextrose over 10 minutes, or neuropathy, bradycardia, conduction
Long half-life (50 days) 300 mg in 100 ml 5% dextrose over 1 hour disturbances of thyroid and liver,
Minimally negatively inotropic followed by maintenance infusion of 900 mg dysfunction of pulmonary and
in 250 ml 5% dextrose over 23 hours retroperitoneal deposits
Ideally use central access but large- Decrease digoxin and warfarin doses
bore peripheral vein may be used Avoid in heart block
Atropine
Antimuscarinic Bradyarrhythmias 0.51 mg i.v., increasing to a Tachycardia, constipation, reduced
Blocks vagus nerve Asystole maximum total dose of 3 mg bronchial secretions, urinary retention,
dilated pupils
Digoxin
Cardiac glycoside Slows ventricular rate in AF 250500 g in 50 ml 5% dextrose Nausea, diarrhoea, dizziness, anorexia
Inhibits Na/K-ATPase Positive inotrope in over 30 minutes i.v. Repeat once if Toxicity (nausea, arrhythmias)
Increases intracellular calcium congestive cardiac failure necessary increased by hypokalaemia,
Increases vagal tone Oral loading dose 11.5 mg over hypomagnesaemia, hypoxia,
Decreases sympathetic drive 24 hours in divided doses hypercalcaemia, hypothyroidism
Prolongs AV nodal conduction Maintenance 62.5250 g/day Avoid in heart block, WolffParkinson
Positive inotrope Therapeutic plasma range 0.82 ng/ml White syndrome, hypertrophic
Reduce dose in renal impairment, obstructive cardiomyopathy,
old age, low body mass recurrent ventricular arrhythmias
Antagonized by verapamil
Treat overdose with digoxin-specific
antibody fragments
Esmolol
-blocker Second-line therapy of SVT 500 g/kg i.v. over 1 minute Bradyarrhythmias, heart failure,
Short half-life (9 minutes) after adenosine Follow with infusion of 50100 hypotension
Cardioselective at low doses g/kg/minute Avoid in impaired LV function,
Decreases AV node conduction heart block, haemodynamic
Antagonizes circulating collapse
catecholamines Administer with care in asthmatics
Decreases myocardial contractility
Flecainide
Sodium channel blocker AF 2 mg/kg i.v. over 10 minutes to Hypotension, bradycardia, blurred
Slows conduction SVT with accessory pathway maximum of 150 mg vision, paraesthesia
Negatively inotropic Follow with infusion of 1.5 mg/kg/hour Avoid in heart block, sinoatrial
Metabolized in liver for 1 hour, then 0.10.25 mg/kg/hour for disease, heart failure and pace-
24 hours makers (pacing threshold may rise)
Lidocaine (lignocaine)
Sodium channel blocker Haemodynamically stable VT 1.52 mg/kg i.v. as a bolus (effective for Dizziness, paraesthesia, hypotension,
Shortens action potential if amiodarone is unavailable 10 minutes only) bradycardia, respiratory depression
Metabolized in liver Follow with infusion of 4 mg/minute for Toxicity leads to anxiety, metallic
1 hour, then 2 mg/minute for 2 hours, taste, confusion and convulsions
then mg/minute Avoid in severe myocardial depression,
Decrease dose in liver or cardiac failure AV block, porphyria
Verapamil
Calcium channel blocker Established SVT with good 510 mg i.v. over 2 minutes followed by Flushing, hypotension, arrhythmias,
Slows AV nodal conduction LV function further 5 mg bolus if needed headache, gastrointestinal upset,
Peripheral and coronary allergic reactions
vasodilatation Avoid in hypotension, broad complex
Significantly negatively inotropic tachycardias, history of heart failure
or significantly impaired LV
function, heart block, cardiogenic
shock, WolffParkinsonWhite
syndrome, porphyria or i.v. in
conjunction with blockers
Abbreviations: AF, atrial fibrillation; AP, action potential; AV, atrioventricular; LV, left ventricular; SVT, supraventricular tachycardia; VF, ventricular fibrillation; VT,
ventricular tachycardia.
Vaughan-Williams classification of antiarrhythmic drugs

Class and site of action Examples Extra cardiac side-effects
Ia Block fast sodium channels, moderately Quinidine Gastrointestinal upset, thrombocytopenia,

prolongs conduction and repolarization haemolytic anaemia, hepatic toxicity, lupus-
like syndrome, psychosis
Procainamide Gastrointestinal upset, lupus-like syndrome,
agranulocytosis, psychosis
Ib Block fast sodium channels, minimal Lidocaine Confusion, seizures, dizziness, paraesthesia, respiratory
effect on conduction and repolarization (lignocaine) depression, reduce dose in hepatic failure
Ic Block fast sodium channels, marked Flecainide Dizziness, visual disturbances, headache, photosensitivity,
prolongation of conduction ataxia, jaundice, peripheral neuropathy, pulmonary fibrosis
Propafenone Blurred vision, dry mouth, gastrointestinal upset, dizziness,
headache
II -blockers (decrease sympathetic stimulation Propranolol Bronchospasm, lethargy, attenuated hypoglycaemic

on the cardiac muscle) Sotalol response, peripheral vasoconstriction, gastrointestinal upset
Esmolol
III Block repolarizing potassium channels Amiodarone Vasodilatation, hypotension, photosensitivity, slate-grey skin
discoloration, corneal microdeposits, tremor, ataxia,
pulmonary fibrosis, liver and thyroid dysfunction,
optic neuritis, peripheral neuropathy, gastrointestinal upset,
metallic taste, dizziness, paraesthesia, benign intracranial
hypertension
Bretylium Hypotension, gastrointestinal upset, tissue necrosis with
intramuscular injection
Sotalol
IV Calcium channel blockers Verapamil Hypotension, constipation, gastrointestinal upset, flushing,

Diltiazem dizziness, headache, myalgia, paraesthesia, fatigue, ankle
Nifedipine oedema, abnormal liver function tests, rash
3
Temporary pacing
The indications for temporary pacing are given in Figure 4.
Indications for temporary pacing
Temporary pacing indicated

Asystole
Complete heart block
Symptomatic bifascicular block (right bundle branch block + left axis
deviation (LAD)
Symptomatic trifascicular block (right bundle branch block + LAD +
prolonged PR interval)
Mobitz type II second-degree heart block
Symptomatic bradycardia refractive to pharmaceutical therapy
Temporary pacing may be considered

Mobitz type I second-degree heart block with hypotension not responsive to
atropine
Recurrent sinus pauses not responsive to atropine
Atrial or ventricular overdrive pacing for recurrent ventricular tachycardia
Sinus bradycardia with hypotension not responsive to atropine
Broad complex tachycardias
The management of broad complex tachycardias is summarized in Figure 5.
Ventricular tachycardia (VT)

It is safe to assume that any broad complex tachycardia is ventricular in origin unless
the cardiac history suggests otherwise. Causes of VT include:
ischaemic heart disease
ventricular scarring following myocardial infarction or previous cardiac surgery
right ventricular failure
electrolyte disturbances in patients with a prolonged QT interval (drugs that prolong
the QT interval include antiarrhythmic agents, erythromycin, antihistamines, tricyclic
depressants and phenothiazines).
Features in the history and ECG that point to a diagnosis of VT rather than
supraventricular tachycardia (SVT) with aberrant conduction include:
history of ischaemic heart disease
irregular cannon waves or variable S in V1 (atrioventricular dissociation)
independent p waves, fusion or capture beats
positive concordance in all precordial leads
deep S wave in V6
RSR pattern in V1
QRS width greater than 0.14 seconds with right bundle branch block morphology
QRS width greater than 0.16 seconds with left bundle branch block morphology
extreme left axis deviation (90 to 180).
The patient should be assessed clinically for features of haemodynamic compromise
including chest pain, heart failure, low systolic blood pressure (< 90 mm Hg), ventricular
rate greater than 150 bpm, and decreased consciousness.
Management of broad complex tachycardias
If in doubt assume all regular broad complex tachycardias to be ventricular in

origin
The differential diagnosis of a broad complex tachycardia is ventricular

tachycardia (VT) or supraventricular tachycardia (SVT) with aberrant
conduction. An irregular broad complex tachycardia is likely to be atrial
fibrillation with bundle branch block
Avoid verapamil in any broad complex tachycardia it may cause

haemodynamic collapse
Intravenous adenosine may be used safely in broad complex tachycardia as

a diagnostic aid. VT will be unaffected but an SVT with aberrant conduction
will probably be terminated. Transient AV-nodal blockage will reveal the
underlying rhythm in atrial flutter or atrial tachycardia
The drug of choice in VT is amiodarone
Potassium and magnesium deficiencies should be corrected where possible
Synchronized DC cardioversion under sedation should be considered if there

is any evidence of haemodynamic compromise
Treatment of torsade de pointes should include magnesium and pacing

rather than antiarrhythmogenic drugs
Treatment
If haemodynamic compromise is present:
DC synchronized cardioversion under sedation (100 J, 200 J, 360 J)
correct any potassium or magnesium deficiencies using potassium chloride, 60
mmol in 60 ml normal saline at a maximum rate of 30 mmol/hour, and magnesium
sulphate, 5 ml 50% over 30 minutes
if patient remains in broad complex tachycardia, administer amiodarone, 150 mg i.v.
over 10 minutes
consider repeated DC synchronized cardioversion
consider other pharmacological agents (e.g. sotalol, lidocaine (lignocaine),
amiodarone); overdrive pacing is a further possibility
seek cardiological opinion if neccesary.
In the absence of haemodynamic compromise:
correct potassium and magnesium deficiencies
administer intravenous amiodarone, 150 mg over 10 minutes, or intravenous
lidocaine (lignocaine), 50 mg over 2 minutes, repeated to a maximum of 200 mg
consider synchronized DC cardioversion under sedation
consider repeating amiodarone administration
consider repeated DC cardioversion.
Torsade de pointes
Torsade de pointes is a polymorphic form of VT. It is characterized by beat-to-beat
variation and a constantly changing axis. It may be self-limiting but can progress to
VF. It may be caused by antiarrhythmic drugs associated with QT prolongation (e.g.
Class Ia and Ic drugs, phenothiazines, butyrophenones, tricyclic antidepressants and
antihistamines), congenital QT prolongation, electrolyte disturbances (hypokalaemia,
hypomagnesaemia, hypocalcaemia), profound bradycardia, myocardial infarction or
ischaemia, arsenic poisoning and neurological insults (e.g. subarachnoid haemorrhage,
stroke, encephalitis).
Treatment:
intravenous magnesium (even in patients without suspected magnesium deficiency)
correct other electrolyte disturbances (e.g. hypokalaemia)
withdraw precipitating drugs
consider overdrive pacing at rate of 100 bpm, increasing the rate if needed
consider use of -blockers
DC cardioversion in the event of haemodynamic collapse.
Narrow complex tachycardias
The management of narrow complex tachycardias is summarized in Figure 6.
Management of narrow complex tachycardias
If the patient is haemodynamically compromised, proceed immediately to

synchronized DC cardioversion under sedation
When considering treatment options in a patient with uncompromised atrial

fibrillation, consider whether the arrhythmia has been present for less than
24 hours
Cardioversion of atrial fibrillation carries a significant risk of

thromboembolism
Intravenous adenosine should be administered rapidly via a large vein in a

monitored patient, and followed immediately by a flush of normal saline
Avoid adenosine in patients with asthma, atrioventricular block or known

WolffParkinsonWhite (WPW) syndrome
In addition to adenosine, avoid verapamil and digoxin in patients with WPW

syndrome. Flecainide or amiodarone may be used in WPW syndrome
WPW syndrome may give rise to atrial fibrillation or atrioventricular re-entrant

tachycardia. Signs of WPW syndrome on a 12-lead ECG in sinus rhythm
include delta-waves and a short PR interval. The delta-wave is positive in
lead V1 in left-sided accessory pathways, and positive in V6 in right-sided
accessory pathways
Consider the possibility of drug-induced myocardial depression, particularly

with polypharmacy
Consider digoxin toxicity as a cause of atrial tachycardia
Irregular narrow complex tachycardia

Atrial fibrillation often occurs in the critically ill patient, particularly in the presence of
sepsis, inotropic support, underlying heart disease and in the elderly. Other causes of
atrial fibrillation include impaired left ventricular function, hypertension, hypovolaemia,
pulmonary embolism, cor pulmonale, thyrotoxicosis, pericarditis, cardiac trauma
and toxins (e.g. alcohol). Although many patients tolerate rapid atrial fibrillation with
few adverse symptoms, decompensation leading to cardiac failure is common. If
the arrhythmia has been present for longer than 48 hours, thrombi may form in the
fibrillating atria leading to the complication of systemic embolism. ECG evidence to
support a diagnosis of atrial fibrillation includes an irregularly irregular rhythm with
absence of p waves.
Choice of therapy depends on haemodynamic compromise and the duration of
atrial fibrillation. In most patients, the aim of treatment should be cardioversion, using
pharmaceutical or electrical methods. It is important to try to minimize the risk of
systemic embolism.
Treatment
Avoid precipitating factors (e.g. alcohol) and correct electrolyte imbalances. Treat
underlying problems such as thyrotoxicosis, cardiac failure and sepsis.
If there is severe cardiovascular compromise (rate > 150 bpm; systolic blood
pressure < 90 mm Hg; critical perfusion or continuing chest pain), immediately give
intravenous heparin or subcutaneous low molecular weight heparin, and attempt DC
synchronized cardioversion under sedation (100 J, 200 J, 360 J). Amiodarone, 300
mg i.v. over 1 hour, may be given if electrical cardioversion is unsuccessful, repeat
if necessary.
If atrial fibrillation has been present for less than 24 hours in a haemodynamically
stable patient, give heparin and attempt cardioversion. Pharmacological cardioversion
should be attempted if there is no underlying structural heart disease. Amiodarone, 300
mg i.v. over 1 hour, or flecainide, 100150 mg i.v. over 30 minutes, are the agents of
choice. If pharmacological cardioversion fails or if structural heart disease exists, DC
cardioversion with intravenous amiodarone if necessary should be used.
If atrial fibrillation has been present for over 24 hours and the patient is
haemodynamically stable, formal anticoagulation should be commenced and
pharmaceutical agents (e.g. digoxin, -blockers, verapamil or diltiazem) should be
used to control the ventricular rate. Four weeks after anticoagulation, DC cardioversion
should be attempted in patients without significant mitral valve disease or left atrial
impairment. If cardioversion is successful, it is recommended that anticoagulation
is continued for a further 4 weeks to avoid thromboembolism. Patients in whom
cardioversion is unsuitable and those in whom cardioversion is unsuccessful should be
maintained on digoxin and anticoagulation.
Regular narrow complex tachycardias

Sinus tachycardia is the most common rhythm disturbance in critically ill patients.
Generally it requires no specific drug therapy, but it is usually one of the first
warning signs of systemic illness. Common causes include hypoxaemia, hypercapnia,
haemorrhage, thyrotoxicosis, pain, anxiety, infection, pulmonary embolism, cardiac
tamponade, pneumothorax and drug or alcohol withdrawal.
SVT: although critically ill patients often develop a sinus tachycardia or atrial
fibrillation, regular narrow complex tachyarrhythmias may also occur. These are
likely to be caused by atrial flutter, atrial tachycardia, junctional tachycardias
(atrioventricular nodal re-entry tachycardia) or the involvement of an accessory
pathway (atrioventricular re-entry tachycardia). Management is principally the same,
irrespective of the exact type of regular narrow complex tachycardia.
Treatment
If the patient is haemodynamically compromised, immediate synchronized DC
cardioversion under sedation should be considered (100 J, 200 J, 360 J).
In the absence of cardiovascular compromise, vagal man-oeuvres should be
attempted to abolish the arrhythmia or slow the conduction through the AV node in
order to reveal atrial flutter. These include the Valsalva manoeuvre, application of cold
water to the face and carotid sinus massage (avoid if patient has a carotid bruit).
If there is no response to vagal manoeuvres, adenosine, initial dose 6 mg given
rapidly followed immediately by a flush of 20 ml saline, should be administered via
a central vein or large- bore peripheral cannula. The patient should be monitored
closely during administration and should be warned to expect transient feelings of chest
tightness, nausea and flushing. If the arrhythmia persists, adenosine, three doses of
12 mg, every 2 minutes, may be repeated. Adenosine should be avoided in patients
with atrioventricular block and asthma, and care should be taken in patients with
chronic obstructive pulmonary disease because it may provoke bronchospasm. Its use
is contraindicated in patients with WolffParkinsonWhite (WPW) syndrome because
blockade of the artioventricular node may precipitate rapid atrial fibrillation. The effects
of adenosine are potentiated by dipyridamole and antagonised by theophylline.
If the patient has heart failure, chest pain, heart rate over 200 bpm or hypotension,
synchronized DC cardioversion under sedation should be attempted (100 J, 200 J, 360
J). Amiodarone, 150 mg over 10 minutes, may be administered before repeating DC
cardioversion if the initial three shocks are unsuccessful.
If the patient remains cardiovascularly stable, alternative pharmacological therapy
should be considered including esmolol, amiodarone, digoxin or verapamil. Verapamil
should not be used in the presence of WPW syndrome, previous -blockade or if signs
of impaired LV function exist. Be wary of using multiple pharmacological agents.
If the arrhythmia continues despite the above measures, a cardiological opinion
should be sought regarding the possible indication for atrial overdrive pacing.
Bradyarrhythmias
The definition of a bradyarrhythmia is a heart rate less than 60 bpm. However, it should
include patients whose heart rate is proportionally slow for their haemodynamic state.
Causes of bradyarrhythmia include :
acute myocardial infarction
age-related degenerative disease of the conduction system
atrioventricular nodal blocking drugs
hypothyroidism
hypothermia
head injury.
Treatment: the management of bradyarrhythmias is summarized in Figure 7.

Assess the patient for adverse signs including chest pain, heart failure, hypotension
or a heart rate less than 40 bpm.
If adverse signs are present administer atropine, 500 g i.v. This may be repeated
to a maximum total dose of 3 mg.
If there is no response to atropine, consider an adrenaline (epinephrine) infusion at a
rate of 210 g/minute.
Consider the need for temporary pacing. This may be initially in the form of external
pacing leads with mild sedation but should subsequently be via an intravenous
temporary pacing wire.
If adverse signs are absent, it may be appropriate to monitor the patient in a high
dependency environment.
Patients with Mobitz type II atrioventricular block, complete heart block, ventricular
pauses greater than 3 seconds, symptomatic bifascicular or trifascicular block or recent
asystole may require pacing to avoid the risk of asystole.
Management of bradyarrhythmias
Treat the patient rather than the ECG. If the patient is not haemodynamically
compromised it may be appropriate to observe them in a monitored high dependency
setting while removing any precipitating factors
External pacing may save lives in patients whose bradyarrhythmias do not respond to
atropine or adrenaline (epinephrine).
FURTHER READING
Advanced Life Support Course Subcommittee of the Resuscitation Council (UK).
Advanced Life Support Course Provider Manual.4th ed. London: Resuscitation Council
(UK), 2000.
Hammil S, Hubmayr R. The Rapidly Changing Management of Cardiac Arrhythmias.

Am J Respir Crit Care Med 2000; 161(4): 10703.
Mark P E. Handbook of Evidence-based Critical Care. New York: Springer-Verlag,

2001.
McConachie I, Hesketh Roberts D. Handbook of Cardiac Emergencies. London:

Greenwich Medical Media, 2000.
Nolan J, Greenwood J, Mackintosh A. Cardiac Emergencies, A Pocket Guide. Oxford:

Butterworth-Heinemann,1999.

Cardiogenic Shock and
Congestive Cardiac Failure
Henry G W Paw
Henry G W Paw is Consultant in Anaesthesia and Intensive Care at York District

Hospital, York, UK. He qualified from Newcastle University and trained in Newcastle
and Cambridge, UK. He is also a qualified pharmacist.
Cardiac failure occurs when the heart is unable to maintain an adequate cardiac output
to meet the demands of the body despite adequate ventricular filling. A diagnosis of
cardiac failure alone is inadequate and the cause and any precipitating factors should
be determined (Figure 1).
Cardiogenic shock is a severe form of cardiac failure characterized by the triad of
hypotension (systolic blood pressure < 90 mm Hg), low cardiac output, and signs of
poor tissue perfusion (e.g. oliguria, delayed capillary return, cold extremities, impaired
cerebral function). It may be differentiated from other forms of shock by having an
elevated pulmonary capillary wedge pressure (PCWP). Even with intensive care, it has
a high mortality (> 90%) because pump failure causes impaired coronary perfusion that
further reduces cardiac contractility.
Causes of heart failure
Volume overload
Left ventricular failure Right ventricular failure
Aortic regurgitation Tricuspid regurgitation
Mitral regurgitation Atrial septal defect
Ventricular septal defect
Pressure overload (obstruction to cardiac output)

Left ventricular failure Right ventricular failure
Hypertension Pulmonary hypertension
Aortic stenosis Pulmonary embolus
Coarctation of aorta Mitral stenosis
Cor pulmonale
Myocardial dysfunction
Hypoxia
Electrolyte imbalance
Acidosis
Septic shock (cytokines e.g. myocardial depressant factor, tumour necrosis
factor-)
Primary myocardial disease

Cardiomyopathy
Myocarditis
Amyloidosis
Mechanical disadvantage
Large ventricular aneurysm
Prevention of ventricular filling

Pericardial tamponade
Constrictive pericarditis
Restrictive cardiomyopathy
Diastolic dysfunction
High cardiac output

Septicaemia
Thyrotoxicosis
Arteriovenous fistula
Systemic-to-pulmonary shunt
Pagets disease
Beri beri
Factors aggravating or precipitating cardiac failure

Arrhythmias
Anaemia
Fluid overload
Corticosteroids, non-steroidal anti-inflammatory drugs
Hypoxia
Electrolyte imbalance
Acidosis
Infections
Thyrotoxicosis
1
Aetiology
Although there are several causes of heart failure, the most common is ischaemic
heart disease. Left heart failure is most often associated with left ventricular myocardial
infarction or systemic hypertension. The causes of right heart failure include left
heart failure and pulmonary disorders such as chronic obstructive pulmonary disease,
pulmonary hypertension and pulmonary embolus. These pulmonary disorders cause an
increased pulmonary vascular resistance against which the right ventricle must pump.
Myocardial infarction of the right ventricle is uncommon (< 3%). Depressed cardiac
function may be precipitated or exacerbated by infection, anaemia, fluid overload or
dysrhythmias.
Regulation of cardiac function

Maintenance of an adequate cardiac output depends on stroke volume and heart rate
(Figure 2). The essential factors that determine the performance of the heart are
venous return (preload), inotropic state or contractility, outflow resistance (afterload)
and heart rate.
Determinants of cardiac output
2
Venous return (preload): the increase in ventricular stroke volume (ventricular
performance) that occurs with an enlargement of ventricular diastolic volume (preload)
is known as the FrankStarling relationship. In clinical terms, this represents the
increase in cardiac output that accompanies an increase in PCWP. In the failing heart,
the ventricular function curve is flattened and shifted to the right. Small degrees of
myocardial depression are not necessarily associated with a reduction in cardiac output
because it is maintained by an increase in venous pressure and tachycardia. However,
the ejection fraction is reduced early in cardiac failure. In more severe myocardial
dysfunction, cardiac output can be maintained only by a large increase in venous
pressure and marked tachycardia. This eventually results in a further reduction in
contractility. Despite symptoms caused by increased venous pressure, the cardiac
output at rest may be only minimally depressed, but myocardial reserve is so
compromised that cardiac output cannot be increased on exertion. In cardiogenic
shock, the cardiac output at rest is depressed despite high venous pressures.
Inotropic state or contractility: increased contractility can result from increased

sympathetic drive or the administration of inotropic agents. In the critically ill patient,
contractility is often reduced, either as a result of pre-existing myocardial disease or
the acute disease process itself (e.g. acidosis, hypoxia, sepsis). Changes in myocardial
contractility alter the slope and position of the FrankStarling curve (Figure 3).
3
Outflow resistance (afterload): the afterload is the load or resistance against which
the ventricle contracts. For the left ventricle it is determined by the resistance imposed
by the aortic valve and the peripheral vasculature (systemic vascular resistance) and
influenced by the elasticity of the major blood vessels. Decreasing the afterload can
increase stroke volume at any given preload (Figure 4), while also reducing ventricular
wall tension and myocardial oxygen consumption. The reduction in wall tension may
lead to an increase in coronary blood flow, thereby improving the myocardial oxygen
supply:demand ratio. On the other hand, an increase in afterload can cause a fall in
stroke volume and an increase in myocardial oxygen consumption.
Decreasing
afterload
4
Heart rate: extreme bradycardia or tachycardia can reduce cardiac output. When
the heart rate falls, the increase in stroke volume eventually becomes insufficient to
compensate for the bradycardia and cardiac output falls. When a tachycardia occurs
the duration of systole is unchanged, whereas diastole, and thus the time available for
ventricular filling and coronary blood flow, becomes progressively shorter. In the healthy
heart this occurs above 160 beats/minute, but in those with cardiac pathology, stroke
volume may fall at much lower rates. Alterations in heart rate are often caused by
disturbances of rhythm. For instance, in atrial fibrillation or complete heart block, the
absence of atrial contraction reduces stroke volume.
Clinical features
The clinical presentation depends on which ventricle is failing. The division of heart
failure into syndromes of left, right and congestive cardiac failure is clinically useful,
though it is uncommon for any part of the heart to fail in isolation. The left and right
ventricles function in series and left heart failure may lead to right heart failure, the
combination being termed congestive cardiac failure. In congestive cardiac failure there
is a combination of the signs and symptoms of left and right heart failure.
Left heart failure (Figure 5) causes raised hydrostatic pressure within the pulmonary
veins and capillaries. Fluid is forced from the capillaries into the interstitial and
alveolar spaces, causing pulmonary oedema. Interstitial or alveolar oedema results
in breathlessness and interferes with alveolarcapillary gas exchange, leading to
hypoxaemia. Initially, dyspnoea occurs on exercise or lying flat (orthopnoea and
paroxysmal nocturnal dyspnoea) but later occurs at rest.
Right heart failure (Figure 6) results in congestion in the systemic venous system,
leading to raised jugular venous pressure, hepatomegaly, ascites, and dependent
subcutaneous pitting oedema.
In congestive cardiac failure, the features of both pulmonary and systemic venous
congestion are present.
Clinical features of left heart failure
Symptoms Signs
Anxiety Tachycardia
Dyspnoea Pulmonary crepitations
Tachypnoea Wheeze (cardiac asthma)
Orthopnoea Cough productive of pink frothy sputum
Paroxysmal nocturnal dyspnoea Cyanosis
Reduced exercise Third heart sound (gallop rhythm)
tolerance Displaced apex beat
Pulsus alternans
Clinical features of right heart failure
Symptoms Signs
Breathlessness Elevated jugular venous pressure
Fatigue Dependent pitting oedema
Confusion Tender and smooth enlargement of liver
Ascites
Right ventricular heave
6
Investigations
Blood tests: a full blood count should be carried out to identify anaemia. Urea
and electrolytes, magnesium and phosphate should be measured. This is especially
important in patients taking diuretics and angiotensin-converting enzyme (ACE)
inhibitors, which may affect potassium and magnesium handling. Hypophosphataemia
can aggravate heart failure. The cardiac enzymes should be assessed. The myocardial-
bound isoenzyme fraction of creatine kinase and troponin I or T are specific for
myocardial damage. Thyroid function tests should be carried out to identify hypo- and
hyperthyroidism.
12-lead ECG is invaluable to detect either full-thickness or subendocardial infarction,

left ventricular hypertrophy and dysrhythmias. In myocardial ischaemia, the ECG may
be normal between attacks.
Chest radiography: the initial findings include upper lobe blood diversion, perihilar
haze and peribronchial cuffing. Later, septal lines (Kerley A and B lines), bat's wing
perihilar shadowing and pleural effusions occur. Depending on the cause, the heart size
may be normal (acute failure) or enlarged (chronic). Although pulmonary oedema is
usually a manifestation of left-sided heart disease, it can be caused by other pathology
in critically ill patients (e.g. over-vigorous fluid replacement or pulmonary endothelial
damage for example in the acute respiratory distress syndrome (ARDS) or acute lung
injury (ALI).
Arterial waveform: in severe heart failure, pulsus alternans, characterized by

alternately strong and weak beats in the presence of a regular rhythm may occur
(Figure 7). There is absence of bigeminy on the ECG monitor. This is due to the
prolonged recovery time of damaged myocardium and indicates a poor prognosis.
150

100
50
Central venous pressure (CVP) and PCWP monitoring: measurement of the CVP
provides an assessment of right artial pressure and is used as an indirect estimate of
right ventricular end diastolic pressure. However, factors such as intravascular volume,
intrathoracic pressure and venous tone also affect CVP. Elevated left atrial pressure is
a common finding in left heart failure and can be estimated by measuring PCWP using
a pulmonary artery catheter. This may be useful in differentiating cardiogenic (high
PCWP) from non-cardiogenic pulmonary oedema (e.g. ARDS) and also permits rational
use of vasoactive drugs and intravenous fluids. As with CVP monitoring, responses
to treatment and trends are more important than absolute values, which are often
influenced by intermittent positive-pressure ventilation (IPPV), positive end-expiratory
pressure (PEEP), pulmonary disease and myocardial ischaemia.
Echocardiography: transthoracic echocardiography (TTE) and transoesophageal

echocardiography (TOE) may provide useful information regarding valvular or other
cardiac abnormalities (e.g. ventricular aneurysm, pericardial effusion), regional wall
motion and ventricular ejection fraction. An estimation of the ejection fraction in a
patient on inotropes, lying in bed doing very little does not provide a true picture of the
actual state of the failing heart. However, TTE may not provide adequate views of the
aorta and atria and may be unsuitable in patients with COPD or in the obese. TOE
is useful in the diagnosis of endocarditis, left atrial pathology (e.g. thrombus), aortic
dissection and in patients with mechanical valves.
Oesophageal Doppler monitoring provides flow-based rather than pressure-based

monitoring by measuring blood flow in the descending thoracic aorta. It provides
good correlation with other estimates of cardiac output and allows assessment of left
ventricular filling (preload), contractility and afterload. Changes in waveform provide
beat-by-beat visualization of trends and the effects of dynamic challenges to the
circulation with fluids, vasodilators or inotropes. It requires repositioning from time to
time and is not practical in the non-sedated patient.
Coronary angiography provides a diagnostic tool and allows therapeutic intervention.
Management of acute heart failure
Severe heart failure is a medical emergency, and effective management requires an

assessment of the underlying cause, improvement of the haemodynamic status, relief of
pulmonary congestion and improvement in tissue oxygenation.
Underlying aetiology
When the diagnosis of heart failure is made, treatment should be directed at the
underlying aetiology. For instance, coronary ischaemia should be identified and
revascularization considered using percutaneous coronary angioplasty or coronary
artery bypass grafting because revascularization may improve ventricular function.
Other life-saving treatments include mitral valve surgery for acute mitral regurgitation or
closure of a ventricular septal defect caused by myocardial infarct.
Aggravating factors
Regardless of the cause, any aggravating factors should be identified and treated. For
example, supraventicular tachyarrhythmias (e.g. atrial fibrillation), should be controlled
using appropriate antidysrhythmic drugs.
General measures
The patient will be most comfortable in the sitting position because this encourages
blood pooling in dependent parts. Hypoxaemia should be treated initially using high-
concentration oxygen (> 60%) by face mask. Unless there are contraindications,
subcutaneous low molecular weight heparin (e.g. dalteparin 2500 units) should be
administered daily.
Drugs
The drugs used in the treatment of heart failure may be considered in terms of their
effects on factors that influence cardiac output (preload, contractility, afterload and
heart rate). In severe heart failure, drugs may be best administered intravenously
because gut oedema may reduce the absorption of orally administered drugs.
Opioids: morphine, 2 mg i.v. bolus, acts by relieving the distress of dyspnoea and
reducing preload by vasodilatation.
Loop diuretics: drugs such as furosemide (frusemide), 40 mg, and bumetanide, 1

mg, act by reducing preload and as potent loop diuretics. Loop diuretics are most
effective when the pulmonary oedema is a component of congestive cardiac failure
and if the volume of the extracellular fluid compartment is generally increased. When
left ventricular failure is acute, pulmonary oedema is a result of fluid shift from the
systemic circulation and there is minimal fluid retention. Overzealous use of diuretics in
this situation risks hypovolaemia and hypotension.
Nitrates: glyceryl trinitrate and isosorbide dinitrate (infusion rates of up to 12 mg/hour)

are useful in the treatment of acute left ventricular failure because they reduce venous
return and left ventricular work. Being potent coronary vasodilators they are also useful
in myocardial ischaemia. Tolerance rapidly develops with continuous high-dose infusion
but reducing the dose for 4 to 8 hours each day usually maintains effectiveness.
Phosphodiesterase inhibitors: enoximone and milrinone are potent inodilators

that do not act via adrenergic receptors. Consequently, they may be effective
when catecholamines have failed. Their main use is the short-term treatment of
severe congestive heart failure, especially in patients with diastolic dysfunction.
Phosphodiesterase inhibitors increase cardiac output by 3070% in patients with heart
failure without increasing heart rate significantly because they reduce systemic vascular
resistance and pulmonary vascular resistance.
Inotropes: inotropic support with agents such as dopamine and dobutamine (both
520 g/kg/minute) may be required in patients with heart failure or cardiogenic shock.
At lower doses (2.5 g/kg/minute) dopamine may have additional direct renal effects
but these have been challenged as being secondary to improvements in cardiac
output. Both drugs have inotropic and chronotropic actions via 1-adrenergic receptors,
though at higher doses, dopamine may also stimulate receptors causing increased
systemic vascular resistance. Dobutamine reduces preload and afterload, which may
reduce blood pressure. Dopamine also depresses prolactin, luteinizing hormone,
growth hormone and thyroid function, thereby obtundingthe bodys endocrine response
to stress. It may alter immuno-logical function, causing humoral and cell-mediated
immunosuppression.
Ventilatory support
If hypoxaemia is resistant to high-concentration oxygen delivered by simple face
mask, or hypercapnia develops, non-invasive positive-pressure ventilation such as
continuous positive airway pressure or bilevel positive airway pressure may be required.
These may obviate the need for tracheal intubation and IPPV. Positive-pressure
ventilation improves arterial oxygenation, increases functional residual capacity and
lung compliance, reduces the work of breathing, and improves V/Q matching. It
also improves cardiac function by reducing left ventricular afterload and decreasing
myocardial oxygen consumption. In severe pulmonary oedema, with copious pink frothy
sputum, repeated bronchial aspirations are required, but removal of PEEP during
aspiration should be of limited duration.
Other measures
Venesection still has a role to play in acute pulmonary oedema resistant to other
therapies. Continuous veno-venous haemofiltration may be useful in the presence of
oliguric renal failure resistant to diuretic. Circulatory assist devices such as intra-aortic
balloon pump and left ventricular assist devices can be useful in certain patients
with cardiogenic shock resistant to vasoactive therapy. Indications include peri-partum
cardiomyopathy, myocarditis or as a bridge to corrective valve surgery, coronary artery
bypass surgery or heart transplantation.
Management of chronic heart failure
Once acute heart failure has been stabilized, management is directed at improving
prognosis and reducing hospital admissions. Despite the large number of drugs used
in the treatment of heart failure, only the ACE inhibitors (e.g. captopril) and -blockers
improve survival. Recently, low-dose spironolactone, 25 mg/day, has also been shown
to improve survival in patients with severe congestive cardiac failure (ejection fraction <
35%), when combined with loop diuretics and ACE inhibitors.

Cardiopulmonary Resuscitation
Jerry Nolan
Jerry Nolan is Consultant Anaesthetist and Lead Clinician in Intensive Care at the
Royal United Hospital, Bath, UK. He qualified from Bristol University and trained in
anaesthesia and intensive care in Bristol, Bath, Plymouth, Southampton and Baltimore,
USA. He is Chairman of the Advanced Life Support Course Sub-committee of the
Resuscitation Council (UK) and is a member of the Executive Committee of the
European Resuscitation Council.
Successful resuscitation from cardiac arrest requires the prompt application of a

sequence of interventions known as the chain of survival. The chances of survival
are highest for patients in ventricular fibrillation (VF) for whom defibrillation is required
as rapidly as possible. After the onset of cardiac arrest, the chances of successful
defibrillation decline by about 10% per minute. For this reason, the focus is on rapid
defibrillation. The first link in this chain is activation of the emergency services. Out of
hospital this implies a telephone call to emergency medical services; inside hospital,
the cardiac arrest team should be alerted. The second link, basic life support (BLS) is
required unless defibrillation (the third link) can be attempted immediately. The fourth
link in the chain, early advanced life support (ALS), maximizes the opportunity for long-
term survival.
Resuscitation guidelines
Cardiac arrest teams work more efficiently if all members follow standardized
protocols. Following an extensive evaluation exercise, the science supporting the first
internationally accepted cardiopulmonary resuscitation (CPR) guidelines was published
in August 2000.
Basic life support
The purpose of BLS is to maintain adequate circulation and ventilation until the
underlying cause of the cardiorespiratory arrest can be reversed. Failure of the
circulation for 34 minutes (less if the patient is hypoxaemic initially) will lead to
irreversible cerebral damage, and any delay in starting BLS will reduce the chances of
a successful outcome.
Classically, BLS implies that no equipment is employed. However, in a health
care environment, the professional rescuer will have access to additional personnel
and equipment. In particular, adjuncts to airway management are normally available.
Nevertheless, the health care professional may have to perform CPR away from a
health care environment and therefore should be competent in BLS with no additional
equipment.
Mechanism for the production of blood flow during BLS: chest compressions
produce forward blood flow by a combination of two mechanisms:
direct compression of the heart (cardiac pump)
a generalized increase in intrathoracic pressure (thoracic pump); venous collapse
at the thoracic inlet prevents backflow of blood. Even when performed optimally, chest
compressions achieve less than 30% of the normal cerebral perfusion.
BLS sequence of actions: brief outlines of the sequence of BLS actions for the lay
person are given in Figures 1 and 2.
Basic life support
1 Ensure safety of rescuer and patient
2 Check to see if the patient responds to gentle shaking of the shoulders

(shake and shout)
3 If he does not respond:

Shout for assistance
Open his airway (head tilt and chin lift manoeuvre). If there is any possibility
of a cervical spine injury, avoid head tilt
Check for breathing for up to 10 seconds
4 If he is breathing:
Turn him into the recovery position
5 If he is not breathing:
Send someone for assistance or, if you are on your own, leave the patient
and go for assistance yourself
Give two effective rescue breaths
Ensure head tilt and chin lift, and pinch the patients nose
Blow steadily into his mouth over about 1.52 seconds, watching for clear
chest rise
6 Assess the patient for signs of a circulation (taking no more than 10

seconds):
Look for any movement
Check the carotid pulse (if adequately trained to do so)
7 If you are confident that you can detect signs of a circulation:

Continue rescue breathing, until the patient starts breathing on his own
About every minute recheck for signs of a circulation
8 If there are no signs of a circulation:

Start chest compressions using the heel of your hand placed over the
middle of the lower half of the sternum
Interlock the fingers of both hands and ensure that pressure is not applied
over the patients ribs
Compress the sternum by 45 cm
Release the pressure, then repeat at a rate of about 100 times a minute.
Compression and release should take an equal amount of time
Continue compressions and breaths in a ratio of 15:2
Basic life support algorithm
Check responsiveness Shake and shout
Open airway Head tilt/chin lift

If breathing
recovery Check breathing Look, listen and feel
position
Breathe Two effective breaths
Assess (10 seconds only) Signs of circulation
Circulation present No circulation

Continue rescue Compress chest
breathing
Check circulation 100 per minute
every minute 15:2 ratio
Send or go for help as soon as possible

according to guidelines
When to go for assistance: it is vital for rescuers to get assistance as quickly as

possible. When more than one rescuer is available, one should start resuscitation while
another goes for assistance. Advice on how the lone rescuer should proceed depends
on the likelihood of the casualty being in VF.
In trauma, drowning, or if the patient is a child, the rescuer should perform
resuscitation for about 1 minute before going for assistance, because the arrest rhythm
is less likely to be VF.
If the patient is an adult, and the cause of unconsciousness is not trauma or
drowning, the rescuer should seek assistance once it has been established that the
patient is apnoeic.
No ventilation CPR: the standard method of performing basic CPR is difficult for the
lay person to learn and there is evidence that skill retention is poor. During the first few
minutes of cardiac arrest, the use of chest compressions alone may be as effective as
chest compressions combined with mouth-to-mouth ventilation. In the presence of a
patent airway, it likely that chest compressions result in some alveolar ventilation; this
may be supplemented by the patients spontaneous gasps.
BLS in hospital: following cardiac arrest within the hospital, it is likely that more than
one health care professional will be available, making it possible to undertake several
actions simultaneously. A defibrillator should be close at hand; in the pulseless patient
the priority is to bring this to the patient. If the patient has a pulse, urgent medical
assessment will be required. In the intervening period, the patient should be monitored,
oxygen administered and intravenous access secured.
Airway management and ventilation should be undertaken with the most appropriate
equipment immediately at hand. The level of staff training will influence the choice
of equipment. A pocket mask, which may be supplemented with an oral airway and
oxygen, a laryngeal mask airway and bagvalve apparatus, or a bagvalvemask
device are all suitable.
BLS with defibrillation: traditionally, defibrillation has been viewed as an ALS

intervention. However, the increasing availability of simple automated external
defibrillators (AEDs) has moved defibrillation into the domain of BLS. Health care
personnel and lay people can use AEDs safely and effectively after a short training
programme (typically about 4 hours). It is no longer acceptable for nursing staff to have
to await the arrival of a cardiac arrest team before attempting defibrillation of a patient
in VF, because any delay reduces the chance of survival.
Advanced life support
Treatment algorithm: cardiac arrest rhythms can be divided into two main groups:
ventricular fibrillation/pulseless ventricular tachycardia (VF/VT)
other rhythms asystole, pulseless electrical activity (PEA).
The only difference in the management of these groups is the need for defibrillation in
patients who are in VF/VT. Maintenance of BLS, airway management, venous access,
the administration of adrenaline (epinephrine) and the identification and correction of
contributing factors are common to both groups. The algorithm for the management
of cardiac arrest (Figure 3) is used in conjunction with either manual or automated
defibrillators.
VF/VT: in adults, the most common rhythm at the onset of cardiac arrest is VF. This
may be preceded by a period of pulseless VT. Most long-term survivors of cardiac
arrest fall into this group. In order to achieve success, patients must be defibrillated
promptly.
BLS should be started if there is any delay in obtaining a defibrillator, but it must
not delay defibrillation. If the arrest was monitored, a single precordial thump may
be appropriate. If delivered early enough, this may provide enough kinetic energy to
convert a fibrillating myocardium to sinus rhythm.
Defibrillation the initial three shocks are given with energies of 200 J, 200 J
and 360 J (or their equivalent see below). The aim should be to administer all three
shocks (if required) in less than 1 minute. After delivery of a shock, there is a delay of
a few seconds before an ECG display of diagnostic quality is obtained. Even when a
rhythm normally compatible with a cardiac output is obtained, there is often a period
of temporary impairment in cardiac contractility, resulting in a pulse that is too weak
to palpate. For this reason, if the rhythm following a shock is asystole or PEA, only 1
minute of CPR is given before reassessing the rhythm.
For defibrillators using a conventional damped sinusoidal waveform, the rationale
for starting defibrillation at 200 J is that it will cause little myocardial injury and, in most
recoverable situations, is adequate to defibrillate the patient successfully. The second
shock should also be at 200 J, because the first shock lowers the chest impedance,
thereby increasing the current reaching the heart. Third and subsequent shocks are
given at 360 J. A number of new defibrillators deliver shocks with biphasic waveforms
(polarity is reversed midway through shock delivery). These appear to be more effective
than conventional sinusoidal waveform defibrillators; defibrillation is more successful
at a lower energy (typically 150 J). Many defibrillators also incorporate impedance
compensation (i.e. the shock waveform is adjusted according to the impedance of
the patients chest). The optimal energy level and waveform for biphasic defibrillation
remains to be determined.
Airway and ventilation management if VF persists after three shocks, 1 minute
of BLS at a compression:ventilation ratio of 15:2 is undertaken in an attempt to preserve
cerebral and myocardial viability. In expert hands, tracheal intubation provides the most
secure airway. Attempted intubation by unskilled personnel will delay more important
interventions such as chest compressions and further shocks. Furthermore, there is
a significant possibility of unrecognized oesophageal intubation. In the absence of a
skilled intubator, a laryngeal mask airway or a Combitube are useful alternatives; these
devices are less likely to cause gastric inflation and regurgitation than a face mask.
The highest possible concentration of oxygen, preferably 100%, should be delivered to
the patients lungs. Once the patient has been intubated, chest compressions should
continue throughout ventilation. It takes at least 1 minute for chest compressions to
generate the maximal coronary perfusion; this optimal perfusion pressure has to be re-
established each time that chest compressions are interrupted.
Drugs intravenous access should be established as soon as possible. The chosen
route will depend on the skills and equipment available. Adrenaline (epinephrine), 1
mg i.v., should be given every 3 minutes. Alternatively, adrenaline, 23 mg diluted in
10 ml, can be given via the tracheal tube. Although used universally, the evidence that
adrenaline improves outcome following cardiac arrest is weak. There are preliminary
data supporting the use of a single dose of vasopressin, 40 units, instead of repeated
doses of adrenaline, but long-term outcome data are awaited.
If the patient remains in VF after 1 minute of CPR, three further shocks of 360 J are
given. The left-hand loop of the algorithm (Figure 3) is continued with each sequence
of three shocks followed by 1 minute of CPR. Potentially reversible causes (4 Hs and 4
Ts see Figure 3) must be excluded, because each can impair the ability to defibrillate
VF successfully.
Universal algorithm for the management of

cardiac arrest
Cardiac arrest
Precordial thump if appropriate
BLS algorithm if appropriate
Attach defibrillator monitor
Assess rhythm
Check pulse
VF/VT Non-VF/VT
Defibrillate x 3 as necessary CPR 3 minutes

(1 minute
if immediately
CPR 1 minute after defibrillation)
During CPR
Correct reversible causes
If not already done:
Check electrodes, paddle position and contact
Attempt/verify airway and oxygen i.v. access
Give adrenaline every 3 minutes
Consider:
Antiarrhythmics
Atropine
Pacing
Buffers
Potential reversible causes

Hypoxia
Hypovolaemia
Hypo/hyperkalaemia and metabolic disorders
Hypothermia
Tamponade
Toxic/therapeutic disorders
Thromboembolic and mechanical obstruction
If VF persists, the use of an antiarrhythmic drug should be considered. Historically,

despite the lack of robust data, lidocaine (lignocaine) has been recommended after 12
unsuccessful shocks. Compared with placebo, amiodarone produces an improvement
in short-term survival from refractory VF. In the International Guidelines 2000,
amiodarone replaces lidocaine as the antiarrhythmic of choice in refractory VF. The use
of bicarbonate during cardiac arrest remains controversial. A dose of 50 mmol can be
considered if the arterial pH is < 7.1, but there is no good evidence to support this. The
generation of carbon dioxide may cause a temporary intracellular acidosis.
Non-VF/VT: the outcome from non-VF/VT is poor unless a reversible cause can be
found and treated effectively. With time, VF will degenerate to PEA and asystole.
Asystole the possibility of a misdiagnosis must be considered; lead disconnection,
incorrect gain setting, or equipment failure will give the appearance of asystole despite
underlying VF. If there is any doubt, the patient should be treated as for VF. Otherwise,
BLS is commenced (or restarted) for 3 minutes, the airway is secured and the patients
lungs are ventilated. Adrenaline, 1 mg, is given every 3 minutes. Although atropine, 3
mg i.v., or 6 mg via the tracheal tube, is traditionally given to block vagal activity, there
is no proof that it alters outcome.
Whenever a diagnosis of asystole is made, the ECG should be checked carefully
for the presence of P waves or slow ventricular activity. These may respond to cardiac
pacing, either external or transvenous. Reversible factors should be identified and
treated promptly. The use of high-dose adrenaline is no longer recommended.
PEA is cardiac arrest in the presence of a rhythm normally associated with a cardiac
output. The patients best chance of survival is prompt identification and treatment of
any underlying cause (4 Hs and 4 Ts). CPR is started immediately, and a patent airway,
ventilation and venous access are secured. Adrenaline, 1 mg i.v., is administered every
3 minutes.
Post-resuscitation care
Patients resuscitated after a short period of cardiac arrest and who have adequate
spontaneous ventilation may be managed in a coronary care unit. After more than a
few minutes of circulatory arrest, followed by restoration of spontaneous circulation, the
patient is likely to require a period of ventilatory and cardiovascular support on an ICU.
The duration and level of ventilatory support should be tailored to the requirements of
the individual patient.
Outcome
Despite developments in the emergency services, the outcome from prehospital

cardiac arrest remains poor, with a survival to hospital discharge rate of about 5%. After
cardiac arrest within the hospital, the survival to hospital discharge after VF is as high
as 40%. After an initial rhythm of asystole or PEA, this figure is just 6%.
At least two-thirds of in-patients sustaining a cardiac arrest display signs of
significant deterioration (e.g. hypoxia, tachypnoea, hypotension) before they arrest.
If medical and nursing staff are trained to recognize and treat these physiological
abnormalities at an earlier stage, cardiac arrest may be prevented. This strategy is
infinitely more sensible than waiting to call a cardiac arrest team after the patient has
effectively died.
FURTHER READING
Advanced Life Support Course Sub-Committee of the Resuscitation Council (UK).
Advanced Life Support Course Provider Manual. 3rd ed. London: Resuscitation Council
(UK), 1998.
Colquhoun M C, Handley A J, Evans T R. ABC of Resuscitation. 4th ed. London: BMJ
Publishing Group, 2000.
Hallstrom A, Cobb L, Johnson E, Copass M. Cardiopulmonary Resuscitation by Chest
Compression Alone or with Mouth-to-mouth Compression. N Engl J Med 2000; 342:
154653.
International Guidelines 2000 for Cardiopulmonary Resuscitation and Emergency
Cardiovascular Care. A Consensus on Science. Resuscitation 2000; 46: 1448.
Paradis N A, Halperin H R, Nowak R M. Cardiac Arrest. The Science and Practice of
Resuscitation Medicine. Baltimore: Williams & Wilkins, 1996.

Chronic Obstructive Pulmonary
Disease and Chronic
Respiratory Failure
Liz Spencer
Liz Spencer is Consultant in Anaesthesia and Intensive Care Medicine at Gloucester

Royal Hospital, UK. She qualified from Southampton University and trained in
anaesthesia in Trent and the South West of England. She spent 2 years as a Research
Fellow at the Intensive Care Unit at the Bristol Royal Infirmary. Her interests are non-
invasive ventilation and multidisciplinary education.
Chronic obstructive pulmonary disease (COPD) describes a spectrum of diseases

that are characterized by airflow limitation due to intrinsic airways disease (e.g.
chronic bronchitis), bronchospasm (e.g. asthma) and/or parenchyma destruction
with associated loss of elastic recoil (e.g. emphysema). Airflow limitation is generally
progressive, may be accompanied by airway hyperactivity and may be at least
partially reversible. Risk factors for COPD include cigarette smoking and 1-antitrypsin
deficiency (AAT). Most patients with COPD have a combination of the three conditions
described below.
Chronic bronchitis is defined as the presence of a chronic cough with sputum

production that occurs most days of the week, at least 3 months of the year, for more
than two consecutive years in the absence of other specific causes (e.g. asthma,
cystic fibrosis, bronchiectasis). Most patients with chronic bronchitis do not have any
significant airflow limitation and should not be classified as having COPD. There is
mucosal and submucosal oedema and inflammation, with an increase in the number
and size of the submucosal mucous glands.
Asthma is an inflammatory disease of the airways that results in reversible airflow

limitation. Unlike the minority of asthmatics with poorly reversible airflow limitation, most
patients respond well to therapy and therefore do not have COPD.
Emphysema is defined pathologically as a permanent, abnormal air-space

enlargement that occurs distal to the terminal bronchiole and includes destruction of
alveolar septa.
Diagnosis
COPD is primarily a clinical diagnosis. However, severe emphysema and lung
hyperinflation can be diagnosed on a chest radiograph. The lung fields are enlarged
and hyperlucent, the diaphragms flattened and the cardiac shadow is narrow. On the
lateral film the volume of retrosternal air space is enlarged.
Measurement of the forced expiratory volume in 1 second (FEV1) and the ratio of
FEV1 to forced vital capacity (FVC) is critical to assess the severity of the disease,
to predict prognosis and to follow progression. An FEV1/FVC ratio of less than 70%
is diagnostic of airways obstruction. It falls progressively as the severity of COPD
increases.
As patients with COPD deteriorate, respiratory failure (a partial pressure of carbon
dioxide in arterial blood (PaCO2) greater than 6.7 kPa or a partial pressure of oxygen
in arterial blood (PaO2) less than 8 kPa breathing air at sea level) often ensues and
is frequently chronic and progressive. Hypercapnia is not usually seen until FEV1 falls
below 1 litre. Polycythaemia is seldom seen until PaO2 is less than 7.2 kPa.
Long-term treatment
As COPD is an irreversible and progressive process, treatment is symptomatic and

cannot alter the underlying pathology or improve survival.
Stopping smoking
Smokers with COPD have an accelerated fall in FEV1. Stopping smoking reduces the
rate of decline of FEV1 at any stage of the disease.
Medications
Bronchodilators provide the mainstay of therapy for most patients. They act by reducing
bronchomotor tone and the level of pulmonary hyperinflation. Inhaled agents are as
effective as oral agents.
Short-acting 2-agonists (e.g. salbutamol) have a rapid onset of action and are either
used regularly or as required. They activate specific 2-adrenergic receptors on smooth
muscle cell surfaces, which leads to an increase in intracellular cyclic adenosine
monophosphate (cAMP) and smooth muscle relaxation. 2-agonists are available as
liquids for nebulization, in aerosol form delivered by pressurized metered-dose inhalers
and as dry powders that can be inhaled via special self-actuated devices. Pressurized
metered-dose inhalers are the most widely used, but dry powder delivery methods are
likely to increase because they do not use chlorofluorocarbon (CFC) propellants.
Anticholinergic agents compete with acetylcholine at postganglionic muscarinic

receptors, thereby decreasing cholinergically mediated bronchomotor tone and
leading to bronchodilatation. Although muscarinic receptors are more numerous in the
larger airways, anticholinergic bronchodilatation occurs at all levels of the bronchial
tree. Anticholinergic agents also block vagally mediated reflex arcs that cause
bronchoconstriction thereby inhibiting airway reactivity. Anticholinergics have a slower
onset of action than 2-agonists and are best given regularly. Anticholinergics and 2-
agonists may act synergistically.
Theophyllines have been widely used since the early 1900s but their use has
diminished owing to their narrow therapeutic range and toxicity. In COPD, theophyllines
are only modest bronchodilators with a variable effect on exercise tolerance and
symptoms. They are metabolized in the liver but the extent varies between patients
because metabolic enzymes are affected by other drugs and disease states (Figure 1).
Theophyllines were thought to produce bronchodilatation by increasing intracellular
cAMP, but the precise mechanism is unknown and may involve increased intracellular
calcium transport, adenosine antagonism or prostaglandin E2 inhibition. Theophyllines
also appear to increase mucociliary clearance, reduce pulmonary vascular resistance
and may improve diaphragm and cardiac muscle contractility. Side-effects include
nausea, vomiting, tremor, nystagmus, seizures, gastro-oesophageal reflux and
arrhythmias. Plasma theophylline levels should be monitored and maintained in the
therapeutic range.
Factors that affect theophylline dose

Need to increase dose Need to decrease dose
Cigarettes Congestive heart failure
Hyperthyroidism Liver dysfunction
Marijuana Viral/acute illness
Barbiturates Age > 60 years
Phenytoin PaO2 < 6 kPa
Rifampicin Allopurinol
Carbamazepine Cimetidine
Ciprofloxacin
Erythromycin
Propranolol
Oral contraceptives
Verapamil
1
Corticosteroids: the presence of inflammatory changes in the airways of patients with
COPD provides a rationale for the use of corticosteroids. However, the relationship
between inflammatory changes, pulmonary function and therapeutic response is not
clearly established. Long-term oral corticosteroid therapy may slow the decline of FEV1
but is not recommended because of the side-effects. On present evidence, inhaled
corticosteroids (e.g. beclomethasone, up to 800 g/day, budesonide, 1600 g/day,
or fluticasone, 2 mg/day) should be given to patients with an objective response to
corticosteroids.
Other agents: there is no evidence to support the use of prophylactic antibiotics,

other anti-inflammatory drugs (e.g. sodium cromoglycate, nedocromil, antihistamines)
pulmonary vasodilators or mucolytics in COPD.
Management of acute exacerbation of COPD
Infections, cardiac failure and pulmonary embolism are the most common factors to
precipitate acute respiratory failure in patients with COPD. Signs and symptoms include
increasing dyspnoea, increased sputum production (often purulent) and wheeze.
Worsening gas exchange is the initial presentation. Stable COPD patients usually
have altered ventilationperfusion (V/Q) matching that worsens when acute respiratory
failure develops. For instance, increased airways resistance reduces ventilation in some
areas of the lung, thereby increasing low V/Q units; additionally, hyperinflation reduces
blood flow in distended alveoli which increases high V/Q units. These alterations are
the main reason for the increase in PaCO2 that occurs in COPD despite maintenance
of minute ventilation. Worsening of V/Q mismatch is limited by hypoxic pulmonary
vasoconstriction but high concentration oxygen may abolish this reflex, causing a
deterioration in V/Q mismatch and a further increase in PaCO2.
Presenting history: consider the following:

previous exercise tolerance (how independent is the patient under normal
circumstances and during exacerbation?)
assess current treatments (use of nebulizers and long-term oxygen therapy)
time course of current exacerbation
current symptoms (sputum volume and purulence, dyspnoea, wheeze, chest
tightness)
previous admissions over the last 5 years (any to ICU?)
smoking history
social circumstances and quality of life.
Examination: look for the following:

signs of infection (e.g. pyrexia, purulent sputum)
signs of airway obstruction (tachypnoea, use of accessory muscles, pursed-lip
breathing, audible wheeze)
peripheral oedema, cyanosis or confusion.
Investigations: the following investigations may be helpful.

Arterial blood gas analysis and inspired oxygen concentration hypoxaemia may
be severe (less than 4 kPa). The extent of hypercarbia depends on the severity of the
condition but PaCO2 levels greater than 10.6 kPa are uncommon. Arterial pH is usually
well maintained because bicarbonate is chronically retained. A respiratory acidosis
suggests a recent exacerbation and a pH below 7.26 predicts a poor outcome.
Chest radiograph, preferably a posteroanterior view to check for pneumonia and
pneumothorax.
Full blood count polycythaemia and leucocytosis occur in severe disease.
Urea and electrolytes hypokalaemia is common due to 2-antagonist,
corticosteroids and diuretic therapy.
ECG right heart hypertrophy and strain suggest cor pulmonale.
Initial FEV1 and peak flow should be assessed.
Microbial culture of purulent sputum and blood is required.
Treatment
Oxygen therapy all critically ill patients require 100% oxygen in the emergency
situation while the initial assessment is made and therapy commenced. Subsequently
many patients with an acute exacerbation of COPD will continue to benefit from high
flow oxygen and the aim of oxygen therapy is a PaO2 of at least 8 kPa. However, when
given high inspired oxygen concentrations, a few patients may increase their PaCO2
through complex mechanisms involving altered V/Q mismatch, the Haldane effect and
decreased minute ventilation. This acute rise in PaCO2 may cause carbonarcosis with
agitation, drowsiness or coma. Monitoring by serial arterial blood gas measurements is
essential and when the pH is less than 7.26 the inspired oxygen concentration should
be titrated to relieve severe hypoxaemia while maintaining a level of consciousness that
retains the patient's ability to cough and cooperate. The level of carbon dioxide is not
of prime importance. Once stable, the patient can be monitored using pulse oximetry,
but repeat arterial blood gases should be performed at any time if the patient's clinical
condition deteriorates.
Some patients with COPD are chronically hypoxaemic and develop counter-
regulatory mechanisms such as increased haematocrit and increased oxygen
extraction from the tissues. These patients can tolerate acute hypoxaemia better than
others.
Bronchodilators nebulized bronchodilators should be given at least every 46
hours. For moderate exacerbations either a 2-agonist (e.g. salbutamol, 2.55 mg)
or an anticholinergic (e.g. ipratropium, 0.250.5 mg) is appropriate, but for severe
exacerbations both should be given because they have a synergistic effect. Although
some practitioners power nebulizers using the wall-mounted oxygen supply, the use of
compressed air may be preferable in COPD patients with hypercapnia or a respiratory
acidosis. Oxygen can be given by nasal prongs at 12 litres/minute during nebulization.
Intravenous bronchodilators can be used if the patient fails to respond to nebulizers.
There is no place for intravenous 2-agonists but aminophylline, 0.5 mg/kg/hour, is
proven to be of benefit.
Antibiotics infection often worsens COPD and antibiotics should be administered
to any patient with acute-on-chronic respiratory failure (pH < 7.35) and two or more of
the following:
increased breathlessness
increased sputum volume
purulent sputum.
Likely pathogens include Haemophilus influenzae, Streptococcus pneumoniae and
Moraxella catarrhalis. Atypical pathogens are seldom a problem though Chlamydia
pneumoniae may be found. Some infections are viral. For moderate exacerbations,
oral antibiotics (amoxicillin (amoxycillin) or tetracycline) should be used but in severe
exacerbations, an intravenous broad-spectrum cephalosporin with the addition of a
macrolide, if necessary, will be required.
Corticosteroids it is unclear if systemic corticosteroids alter the course of an
acute exacerbation of COPD, but it is common practice to use a 714 day course of
prednisolone, 0.5 mg/kg/day, or hydrocortisone, 200 mg/day, especially if:
the patient usually takes corticosteroids
there has been a previous response to corticosteroids
the airflow obstruction is resistant to bronchodilators
this is the first presentation of airways obstruction.
Diuretics should be given if there is peripheral oedema or a raised jugular venous
pressure.
Respiratory stimulants hypercapnia during COPD exacerbations may be due to
respiratory muscle fatigue or a blunted ventilatory drive. Doxapram may be used if the
respiratory rate is less than 15/minute and acts centrally to increase respiratory drive
and respiratory muscle activity. Its effect is significant for only 2448 hours; the main
factor limiting its use is side-effects that can lead to agitation. It should not be used if
non-invasive ventilation is being considered.
Anticoagulants pulmonary emboli are probably more common than
previously recognized in severe COPD but full anticoagulation treatment is
not currently recommended. Nevertheless, prophylactic subcutaneous heparin
must be prescribed for all patients with acute-on-chronic respiratory failure.
Nutrition many patients with COPD have an increased resting metabolic rate
and nearly 50% of those admitted to hospital with acute respiratory failure have some
degree of protein calorie malnutrition. Feeds high in carbohydrate should be avoided
because they increase carbon dioxide production and oxygen consumption.
Physiotherapy there are few data to suggest that chest physiotherapy reduces
sputum retention in acute exacerbations of COPD and so it cannot be recommended
routinely. However, it seems appropriate to provide physiotherapy in those patients who
have large volumes of retained sputum in the acute phase.
Managing respiratory failure with mechanical ventilation
Ventilatory support, either as non-invasive ventilation or intermittent positive-pressure

ventilation (IPPV) via a tracheal tube, may be necessary for patients who fail to respond
to supportive treatment and controlled oxygen therapy. The main goal of mechanical
ventilation is the support of gas exchange and fatigued respiratory muscles while
the precipitating cause of acute respiratory failure is treated. A trial of non-invasive
ventilation should be performed in all patients with respiratory failure and intubation
should be reserved for non-responders and those unable to cooperate.
Non-invasive positive-pressure ventilation (NIPPV)

NIPPV avoids the morbidity and mortality associated with IPPV (e.g. sedative drugs,
nosocomial chest infections, ventilator dependence) and may reduce intubation rates,
mortality, and length of hospital stay. It can be applied intermittently, avoids the need for
sedation, and allows the patient to eat, talk and drink. It can also be used outside the
ICU, thereby reducing the demand for ICU beds. NIPPV is most beneficial when used
early and it has been suggested that all COPD patients with a respiratory acidosis (pH <
7.35) after initial treatment are offered NIPPV.
NIPPV uses two ventilatory techniques continuous positive airway pressure and
inspiratory assist (pressure support) (see page 343). On non-invasive ventilators these
pressures are set as expiratory positive airways pressure (EPAP) and inspiratory
positive airways pressure (IPAP). The pressure support delivered is IPAPEPAP.
Patient selection for NIPPV is important. Confused patients and those with a large
volume of secretions are less likely to respond well. The prerequisites for success are:
patient cooperation
patient can maintain airway and expectorate secretions
adequate cough reflex
patient can breathe unaided for several minutes
functioning gastrointestinal tract
haemodynamic stability.
Negative non-invasive ventilation

The application of intermittent subatmospheric pressure to the chest wall generates the
same gradient of pressure between the peripheral and central veins as a spontaneous
breath. Various devices have been used including tank ventilators, cuirasses and jacket
ventilators. These techniques are used, mainly to provide long-term support for
patients with limited respiratory reserve and nocturnal hypoventilation due to
restrictive disorders such as kyphoscoliosis, thoracoplasty, and residual paralysis from
poliomyelitis. More recently, non-invasive high-frequency oscillation has been shown
to increase carbon dioxide elimination. Consequently the Hayek oscillator has been
developed. It consists of a cuirass that surrounds the chest and which maintains
subatmospheric pressure with superimposed oscillations.
IPPV
In certain situations NIPPV is unsuccessful and IPPV should be considered (Figure 2).
Many medical and ethical issues surround the use of IPPV for COPD patients including
the patient's wishes, the likelihood that the patient will survive to leave hospital with a
good quality of life and the availability of resources. The provision of IPPV may also
cause unnecessary distress to the patient and their relatives. NIPPV can be useful in
supporting the patient until the appropriateness of tracheal intubation and mechanical
ventilation can be determined. Senior medical staff must be involved in this discussion.
Indications for tracheal intubation and ventilatory support are:
severe respiratory distress
failure to cough
decreasing level of consciousness
agitated, confused patient.
Determining when to use intermittent positive pressure ventilation (IPPV)
Factors to encourage use of IPPV

Reversible reason for current decline
First episode of respiratory failure
Good quality of life
Factors to discourage use of IPPV

Previously documented severe chronic obstructive pulmonary disease found
to be unresponsive to relevant therapy
Poor quality of life
Severe co-morbidity (e.g. congestive heart failure, cancer)
Management as the patient recovers
As the patient's condition improves (less dyspnoea, better peak expiratory flow rate
(PEFR), improved oxygen saturation in arterial blood) the nebulized bronchodilator can
be changed to the patients usual inhaler. Antibiotics and corticosteroids can usually
be stopped after 1 week. PEFR should be recorded twice daily until clinically stable
and both FEV1 and arterial blood gases (on air) should be recorded before hospital
discharge. Before discharge the patient's inhaler technique should be assessed and
advice given on the treatment regimen and on how to stop smoking.
FURTHER READING
Albert R, Spiro S, Jett J. Comprehensive Respiratory Medicine. London: Harcourt
Brace, 1999.
British Thoracic Society. The British Guidelines on COPD Management. Thorax 1997;
52 (Suppl 5): S1S28.

CNS Infections in Intensive
Care
Marcia McDougall
Ian S Grant
Marcia McDougall is Specialist Registrar in Anaesthetics and Intensive Care

in Edinburgh. Her areas of interest include nutrition in intensive care and high
dependency, and glucose control in intensive care.
Ian S Grant is Consultant Intensivist at the Western General Hospital, Edinburgh. He

qualified from Edinburgh University, and trained in general medicine and anaesthesia
in Glasgow, before taking up consultant posts in anaesthesia and intensive care in
Dundee and Edinburgh. His interests include neurointensive care and long-term
ventilation.
Many CNS infections can be treated in a general ward, but prolonged seizures, coma,
septic shock or airway compromise are indications for ICU admission for treatment and
supportive care. In the UK, severe CNS infections fall into three categories: meningitis,
encephalitis and cerebral abscess.
Acute bacterial meningitis

This pyogenic infection of the subarachnoid space and cerebral ventricles is the most
common intracranial infection in the UK (incidence 35/100,000). The usual causative
organisms are:
Streptococcus pneumoniae (40%)
Neisseria meningitidis
Haemophilus influenzae
Staphylococcus aureus.
In post-transplant, alcoholic, diabetic, immunosuppressed or HIV-positive patients, the

organism may be atypical (e.g. Listeria monocytogenes).
Pathophysiology bacteria colonize the bloodstream via the nasal or oropharyngeal

mucosa, and cross the bloodbrain barrier. Direct spread from trauma, sinusitis
or mastoiditis, or haematogenous spread from distant infection also occurs.
Lipopolysaccharide and teichoic acid produced by Gram-negative and Gram-
positive bacteria, respectively, induce meningeal inflammation and cause leucocyte
chemoattraction and vascular endothelial damage. This results in cerebral oedema and
ischaemia, disruption of the bloodbrain barrier and failure of cerebral autoregulation.
Blockage of CSF flow may cause hydrocephalus.
Clinical features include:

a prodromal period of malaise, myalgia, upper respiratory tract symptoms, joint pains
and fever
severe headache
vomiting
photophobia
neck stiffness
decreased conscious level
rash: petechial or purpuric (meningococcal infections); maculopapular
(staphylococcal or pneumococcal infections)
cranial nerve lesions
seizures
papilloedema
septic shock (meningococcal and pneumococcal disease).
Signs in the very young and old may be more subtle. The differential diagnosis of acute
bacterial meningitis includes viral meningitis, encephalitis, subarachnoid haemorrhage,
subdural empyema, brain abscess and legionnaires disease.
Investigations the diagnosis is primarily clinical when a rash is present; otherwise

it rests on detecting organisms from blood culture or CSF. Lumbar puncture is
contraindicated in the presence of focal neurological signs, papilloedema or depressed
conscious level unless raised intracranial pressure (ICP) has been excluded by CT
scan. Early lumbar puncture (i.e. within 2 hours of antibiotic treatment) may yield
diagnostic information from a Gram stain, culture, polymerase chain reaction (PCR) or
latex agglutination test. CSF is characteristically turbid, with over 1000 neutrophils/mm3,
low glucose and raised protein levels. Viral meningitis may also cause a neutrophil
leucocytosis early in the illness, though it normally leads to a lymphocytosis.
There may be a coagulopathy, peripheral neutrophilia and renal impairment, the latter
especially if shock is present.
Management recommended antibiotics are cefotaxime, 2 g 46 hourly i.v., or

ceftriaxone, 2 g 12 hourly i.v. Vancomycin, 1 g 12 hourly adjusted according to levels,
should be considered in areas with a high prevalence of resistant pneumococci,
or if the infection arises after neurosurgery. Different therapy is required in the
immunosuppressed, elderly or neonates. Close contacts of patients should receive
prophylactic rifampicin, 600 mg 12 hourly for 2 days (10 mg/kg 12 hourly for children).
Corticosteroids are beneficial in children with Haemophilus meningitis. Early treatment
with dexamethasone, 10 mg continued 6 hourly for 4 days, has been shown to improve
outcomes in adults with acute bacterial meningitis. If Listeria meningitis is considered a
possible diagnosis, ampicillin, 12 g 6 hourly i.v., should be added.
Intensive care management focuses on supportive care and prevention of secondary

brain injury due to ischaemia and hypoxia. Specific guidance includes:
intubation and ventilation for patients with a Glasgow Coma Score of 8 or less, loss
of airway protection or persistent seizures
avoid factors that increase ICP
adjust ventilation to maintain a PaCO2 of 4.04.5
nurse the patient in a head-up position
tape, rather than tie, tracheal tubes
maintain a normal plasma sodium and euglycaemia
there should be a low threshold for repeating a CT scan
if hydrocephalus is present, ventricular drainage may be required
enteral nutrition should be commenced early
fever should be treated (active cooling and/or paracetamol)
treat syndrome of inappropriate secretion of antidiuretic hormone (SIADH) and
diabetes insipidus.
Raised ICP should be treated with mannitol, furosemide (frusemide) or hypertonic

saline. The cerebral perfusion pressure (mean arterial pressure (MAP) ICP)
should be kept above 70 mm Hg with fluid and vasopressors (e.g. noradrenaline
(norepinephrine)). Fluid resuscitation should be guided by arterial blood pressure,
central venous pressure and, where appropriate, pulmonary artery pressure monitoring.
If cerebral oedema is severe, a thiopental (thiopentone) infusion may decrease cerebral
oxygen demands and ICP.
Complications status epilepticus should be treated with phenytoin, loading dose

of 15 mg/kg given over 3060 minutes, if benzodiazepines fail. If it is persistent,
thiopental (thiopentone) or propofol infusion may be required. Continuous full or
processed EEG monitoring may be required to detect subclinical status epilepticus
or to optimize the thiopental (thiopentone) infusion rate to achieve burst suppression.
Neurological deterioration may indicate worsening cerebral oedema or the development
of hydrocephalus, subdural empyema or sagittal sinus thrombosis. Long-term
complications include cranial nerve palsies, hemiparesis and deafness. Skin loss and
digital or limb ischaemia are complications of meningococcal sepsis.
Outcome mortality is about 25%. It is worse in children and the elderly, in those with
a delayed diagnosis, comatose on admission or with raised ICP.
Viral encephalitis
Encephalitis is inflammation of the brain parenchyma, often with meningeal involvement
(meningo-encephalitis). It is caused by:
herpes simplex virus (HSV) I (the most common cause in Europe; annual incidence
1/250,000) 30% of cases are associated with herpes labialis or genitalis
HSV II (neonates, immunosuppressed patients)
other viruses (measles, mumps, rubella, varicella zoster, polio, HIV,
cytomegalovirus, rabies and EpsteinBarr viruses).
Pathophysiology virus reaching the brain via the nasal mucosa, or from respiratory
or enteral infections causes direct cerebral cytotoxicity by lysis, and excites an
inflammatory response leading to cerebral oedema, vascular obstruction, cerebral
ischaemia, infarction and atrophy.
Clinical features and diagnosis in herpes encephalitis, a 710-day prodrome of

fever, malaise, headache, upper respiratory tract infection, myalgia and personality
change leads to focal seizures, confusion, irritability and focal neurological deficits. In
severe cases, coma ensues. The differential diagnoses include:
infectious encephalitides of non-viral origin (e.g. Lyme disease)
viral meningitis
acute bacterial meningitis
sagittal sinus thrombosis
metabolic and toxic encephalopathies (cocaine and chemotherapeutic agents)
carcinomatous meningitis
cerebrovascular accident
cerebral abscess
connective tissue disease causing cerebral vasculitis
cerebral malaria.
In immunosuppressed patients, progressive multifocal leucoencephalopathy,

Toxoplasma, cryptococcal meningitis, tertiary syphilis, CNS lymphoma, or tuberculous
meningitis are alternative diagnoses.
Investigations include:
a full travel history
blood culture
blood for viral and fungal serology; blood films for malaria parasites
EEG (bilateral periodic lateralized epileptiform discharges are pathognomonic of
HSV encephalitis)
CSF examination, if lumbar puncture is not contraindicated (lymphocytic pleocytosis
501500/mm3, low or normal glucose and a mildly elevated protein)
CT or MRI if there are focal neurological signs or a decreased conscious level
(Figure 1). MRI is more sensitive in detecting the changes of HSV encephalitis
PCR for HSV and cytomegalovirus (sensitivity > 95%).
Brain biopsy may be required if there is deterioration despite aciclovir, if CT suggests

an alternative diagnosis, or in the immunosuppressed. Viruses are detected by
immunohistochemical staining of brain tissue.
a b
a Acute herpes encephalitis. T2 axial MRI of the brain showing
hyperintensity and swelling of the grey and white matter of the pole
of the left temporal lobe (arrowed). b Post-herpetic atrophy. CT scan
showing marked atrophy and gliosis of both temporal lobes (arrowed)
following herpetic infection. Herpes encephalitis is more often bilateral 1
than unilateral. Scans courtesy of Dr D Collie, Western General Hospital,
Edinburgh.
Intensive care management is similar to that for acute bacterial meningitis, although
if HSV encephalitis is suspected, aciclovir, 10 mg/kg/over 1 hour i.v. then 8 hourly for
10 days (adjusted in renal failure), should be started. Cytomegalovirus encephalitis is
treated with ganciclovir, 5 mg/kg 12 hourly i.v. for 1421 days. If treatment for retinitis
has already been given, add foscarnet, 90 mg/kg 12 hourly. There is no specific
treatment for other viral encephalitides; supportive care is indicated.
Complications worsening cerebral oedema and necrosis may occur, especially

in HSV encephalitis. Repeat CT scan may show hydrocephalus or severe oedema;
craniotomy with decompressive temporal lobectomy may be life-saving. However, if the
swelling is in the dominant hemisphere, residual disability is severe. CSF drainage may
relieve hydrocephalus. Bilateral brain swelling with failed response to ICP treatment
leads to tentorial herniation and brain death. Such patients are unsuitable as organ
donors owing to viraemia.
Outcome in HSV encephalitis is worse in patients over 30 years of age, if treatment
with aciclovir is delayed beyond 4 days from onset, and if coma and cerebral oedema
are present. Sequelae include amnesia, cognitive deficits, personality change and
epilepsy. Secondary brain injury due to hypoxia and infarction may cause physical
disability. The mortality is 1030%, and 60% of survivors who present in coma have
neurological sequelae.
Parasitic intracranial infection

Epidemiologically, the most important parasitic infection is cerebral malaria caused by
Plasmodium falciparum. In the UK, there are up to 2000 cases of malaria every year
(usually in the pyrexial traveller or immigrant).
Cerebral malaria: obstruction of cerebral blood vessels by parasitized erythrocytes

causes decreased cerebral blood flow, tissue hypoxia and inflammation. The clinical
features include:
coma
seizures
hypertonia
extensor posturing
hypoglycaemia
haemolytic anaemia
coagulopathy
dysconjugate gaze
raised ICP
brainstem herniation.
A mortality of 1525% can be reduced to 5% with intensive care. Investigations include:

peripheral blood smears show malarial parasites
antigen detection with the ParaSight F test
lumbar puncture may yield parasites in the CSF.
Treatment should be started if clinical suspicion is high, even if tests are negative.
Treatment involves quinine, 20 mg/kg over 4 hours i.v. then 10 mg/kg over 4 hours
repeated 8 hourly thereafter. Supportive intensive care and ICP management may be
required. Exchange transfusion is indicated if parasitaemia reaches 510%.
Cerebral abscess and subdural empyema

A localized suppurative infection of the brain parenchyma may arise by direct spread
(e.g. sinusitis, mastoiditis, penetrating head trauma, meningitis) or by haematogenous
spread (e.g. endocarditis, skin or soft tissue infections, pneumonia, dental abscesses,
otitis media). Infecting organisms are often a mixture of aerobic and anaerobic,
including streptococci, staphylococci, Bacteroides, and less commonly Klebsiella and
Pseudomonas. In the immunocompromised patient, causal organisms may be atypical.
Pathophysiology a localized area of cerebritis undergoes necrosis and liquefaction.

A fibrous capsule with surrounding vasogenic oedema develops. Subdural empyema
is the result of spread of infection from sinuses, or following trauma or neurosurgery.
Abscess formation may cause rapid deterioration with fever, mass effect, cerebral
oedema and tentorial herniation.
Clinical features and diagnosis clinical features include:

headache
fever (50%)
focal neurological deficits
behavioural changes
decreased conscious level (50%)
seizures (30%).
Rapid onset and deterioration may indicate rupture into the ventricles. Multiple
abscesses carry a higher risk of severe cerebral oedema. Brainstem abscesses may
cause cranial nerve palsies, nystagmus, ataxia, swallowing difficulties, abnormal
breathing patterns and airway compromise. The differential diagnoses include:
any cerebral space-occupying lesion
meningitis
encephalitis
cerebrovascular accident
multiple sclerosis
cerebral sarcoid.
Investigations white cell count and ESR are raised. Blood, urine and sputum
cultures should be sent for viral, fungal and Toxoplasma serology. CT or MRI with
contrast should be carried out (MRI is more sensitive for detecting multiple small
abscesses and cerebritis; enhancement with contrast favours Toxoplasma or cerebral
lymphoma, Figure 2). Lumbar puncture is contraindicated in the presence of a space-
occupying lesion.
a b
a Cerebral abscesses. Contrast-enhanced CT scan showing multiple thin-

walled ring-enhancing lesions (arrowed) in the right cerebral hemisphere
with surrounding oedema, and mass-effect with effacement of the right
lateral ventricle. Radiologically it may be impossible to distinguish cerebral
abscesses from multiple cerebral metastases. b Subdural empyema. MRI
scan showing a large subdural empyema in the right parietal region (arrowed)
causing mass-effect and midline shift, with thickened and inflamed dura
mater. Scans courtesy of Dr D Collie, Western General Hospital, Edinburgh.
2
Management for early, small, multiple, inaccessible, brainstem and some multilocular
abscesses, medical treatment with antibiotics is first-line therapy (ceftazidime, 2 g
8 hourly i.v., and metronidazole, 500 mg 8 hourly i.v., the latter to cover anaerobes).
Vancomycin, 1 g 12 hourly i.v. adjusted according to levels, is given in the case of post-
surgical infection, staphylococcal infection or cephalosporin allergy. Serial CT scans
can monitor the size of the abscess to determine the need for drainage. Antibiotics
should be continued for 68 weeks.
Aspiration is indicated for abscesses over 2.5 cm in diameter, deterioration due to

cerebral oedema, diagnostic culture or failure of medical treatment. Abscesses should
be drained stereotactically under general anaesthesia. Rapid increase in size with
worsening neurological function may necessitate urgent craniotomy and excision.
General intensive care management follows the principles of neurointensive care
outlined above. Dexamethasone, 10 mg bolus followed by 4 mg 6 hourly, is indicated for
worsening cerebral oedema.
Outcome complications include seizures, hydrocephalus and ventriculitis. Mortality is

1525%, worse in the elderly and immunosuppressed, those with multiple abscesses
and those with rapid deterioration. Brainstem abscesses are associated with a good
outcome and resolution of deficits.
Post-surgical infections
Neurosurgical patients in ICU are at risk of infection via ventriculostomy catheters and
ICP monitoring devices. Meticulous attention to asepsis during insertion and dressing
of such devices must be observed. CSF should be sampled regularly for surveillance
culture, or if the temperature or white cell count are raised.
Shunt infections require high dose antibiotics, removal of the shunt and later
replacement in a separate location. Common organisms are staphylococci and Gram-
negative organisms. Antibiotics may be administered directly into the CSF if the
infection proves persistent. Patients with a CSF leak are susceptible to meningitis; there
should be a low threshold for CSF examination and antibiotic treatment. u

DIC and other Coagulopathies
in the ICU
Colin Green
Colin Green is Consultant in Intensive Care and Anaesthesia at Gloucestershire Royal

Hospital, Gloucester, UK. He qualified from St Bartholomews Hospital, London, and
trained at the Hammersmith Hospital, St Georges Hospital and Great Ormond Street
Hospital, London.
Disseminated intravascular coagulation (DIC) and other disorders

of the clotting mechanisms are common in the ICU. They are usually the manifestation
of a diffuse disease state, which must be treated in conjunction with the clotting defect
to break the cycle (Figure 1).
Cessation of bleeding following trauma to blood vessels depends on:

contraction of the vessel wall
formation of a platelet plug at the break
formation of a fibrin clot.
The relative importance of these elements varies with the site and size of the vessels
involved.
Consequences of coagulopathy
Precipitating
disease
Impaired
resistance Coagulopathy
Organ Impaired
dysfunction perfusion
Platelet breakdown or tissue damage produces thromboplastin, which, in the presence

of calcium ions, results in the formation of thrombin from prothrombin. As a continuation
of the clotting cascade, fibrinogen is converted to fibrin, which forms a clot (Figure 2).
The coagulation cascade creates a stable fibrin clot. This cascade is an integrated
sequence of enzyme reactions, which amplifies a small stimulus into a large response.
If this amplification is inappropriate to the clinical requirements, the cycle described
in Figure 1 may be set in motion. The sequence begins when factor VII is exposed
to tissue factor released at the injured endothelium. A complex forms, which acts on
factors IX and X to produce thrombin. Thrombin causes formation of fibrin, which
becomes cross-linked, forming a clot. The sequence is nominally divided into intrinsic
and extrinsic components (Figure 3). Thrombin also interacts with thrombomodulin,
producing a protein conformation that activates protein C. This is an anticoagulant
protein involved in the control of the coagulation response to injury. It is a vitamin K-
dependent plasma protein, which is synthesized in the liver and circulates as a pro-
enzyme. Activated protein C reduces fibrin production and platelet activation, and has
a negative feedback effect on thrombin generation. It also prevents activation of factors
Va and VIIIa.
Plasmin is an enzyme that breaks down fibrin and clot, thus re-establishing circulation
in small vessels. It is present in the plasma as a precursor (plasminogen). Streptokinase
is a therapeutic activator of plasminogen.
Clotting cascade
Platelet breakdown
Thromboplastin
Tissue damage Ca2+
Prothrombin Thrombin
Fibrinogen Fibrin
2
Cross-linked fibrin
Tissue factor
XIIIa
IX XI
Fibrinogen Fibrin
VII
VIIIa

XIa
Tissue factor/VIIa
IXa Prothrombin Thrombin
Inactive Active Va
factor X factor X
3
DIC
DIC is the most common coagulopathy in the ICU. It is a patho-logical phenomenon
involving pan-activation of haemostasis and intravascular formation of fibrin. Sepsis
(particularly if caused by Gram-negative organisms) is the most common stimulus but
others include:
trauma (surgery, burns, crush injury, fat embolism)
obstetric causes (abruptio placentae, amniotic fluid embolus, pre-eclampsia)
shock (hypovolaemia)
liver disease (cirrhosis, cholestasis)
malignancy
immunological disease (ABO incompatible transfusions).
Activation may be via:
the extrinsic pathway by tissue factor released from damaged endothelium or
leucocytes
the intrinsic pathway
a pathway bypassing normal activation
direct effects on endothelium or platelets.
Complement activation and cytokine release may amplify the effects. These activities
usually produce DIC in its acute or fulminant form, however, it is possible for DIC to
appear in a subacute or chronic form. The result is excessive release of thrombin and
the deposition of fibrin in the microvasculature. This prothrombic state leads to organ
dysfunction and failure. At the same time, excessive plasmin levels lead to clot lysis
(fibrinolysis) and the patient presents with haemorrhage, either spontaneously from
mucosal surfaces or provoked by intravascular cannulation. Therefore, DIC depends
on a balance between thrombosis and fibrinolysis and these opposing elements are
represented by the extremes of DIC. The clinical diagnosis of DIC may be inferred by
overt haemorrhage or by organ dysfunction, particularly in the presence of one of the
common stimuli.
Investigations should include:

platelet count (decreased)
prothrombin time (prolonged)
activated partial thromboplastin time (prolonged)
fibrin degradation products (elevated); however, this measures only plasmin-cleaved
fibrinogen or fibrin (if positive it does not indicate thrombin formation)
fibrinogen levels (depressed).
The pattern of changes in these tests is often variable. D-dimer assay of plasma
samples may be more useful. This is an antigen formed when plasmin breaks down the
cross-linked fibrin. It distinguishes between fibrinolysis and fibrinogenolysis. A positive
test indicates the presence of thrombin and plasmin.
Treatment is often difficult and controversial. The first step is elimination of the
stimulus. Secondary treatment involves replacing deficient clotting factors, though some
believe that this exacerbates the situation. Also, it is often argued that plasma protease
inhibitors are always present in sufficient concentrations to halt increased coagulation
caused by enriched component concentrations. Correction of coagulopathy involves:
platelet transfusions if there is thrombocytopenia
fresh frozen plasma to replace clotting factor deficiencies
cryoprecipitate infusions to maintain fibrinogen levels at 100150 mg/dl.
Tertiary treatment may involve heparin, but this is potentially dangerous and should be
undertaken only after seeking haematological advice. Heparin potentiates antithrombin
and therefore inhibits thrombin, factor Xa and other coagulation factors. In the presence
of adequate levels of antithrombin, it may inhibit thrombin formation. Heparin is
advisable if there are obvious signs of thrombosis or if there is protein C or protein S
deficiency. In these circumstances, heparin is usually started as an infusion without a
loading dose and its rate of infusion is adjusted according to the level of coagulation
component measured (e.g. fibrin degradation products, D-dimer or fibrinogen).
Outcome: DIC is associated with a high mortality rate, mainly due to the underlying
cause, rather than to DIC itself. The morbidity associated with DIC is largely related
to thrombotic events and the resultant organ dysfunction, although catastrophic
haemorrhage is certainly possible.
Other coagulopathies occurring in critical care
Platelet dysfunction
Coagulopathy caused by platelet defects occurs because of a decrease in the absolute
number of platelets in circulation or a reduction in their ability to function properly.
Platelet adhesion and aggregation are primary events in normal coagulation. Platelets
are first activated by adenosine diphosphate (ADP) (released by damaged endothelial
cells), collagen (exposed by endothelial damage) and thrombin. The platelet surface
is then modified, binding plasma fibrinogen with extracellular calcium to form an
aggregate. The platelets then provide a phospholipid platform, which allows further
plasma factor activation. Some inherited conditions affect the absolute number of
platelets (e.g. idiopathic autoimmune thrombocytopenia), their adhesion (e.g. Bernard
Soulier syndrome) or their reactivity to collagen or abnormalities in prostaglandin
pathways. These are rare and unlikely to be the cause of haemorrhage in most
critical care settings. Abnormalities in platelet numbers or activity induced by disease
processes or drugs are more common.
Many of the precipitants of DIC result in consumption of large numbers of platelets,

rendering the patient thrombocytopenic. This fuels the haemorrhagic element of DIC.
Treatment in these cases is aimed at eliminating the cause of DIC and increasing
platelet numbers by transfusion.
Iatrogenic platelet dysfunction is common in the ICU. Massive transfusion without

platelet transfusion decreases platelet numbers by dilution. Aspirin is the most common
drug causing platelet dysfunction. It inhibits cyclo-oxidase and thus inhibits the ability of
the platelets to adhere to subendothelial components and aggregate. Long-term aspirin
therapy in high doses or self-inflicted overdose thus interferes with clotting.
Heparin is commonly used in extracorporeal circuits (e.g. cardiopulmonary bypass

or haemofiltration circuits) to prevent thrombin formation. However, it does not
prevent sequestration of platelets. For this reason, low-molecular-weight heparins are
commonly used in extracorporeal circuits because they have less effect on platelets.
Cardiopulmonary bypass circuits reduce platelet numbers by sequestration and may
be a common cause of postoperative haemorrhage in cardiac ICUs. The induced
hypothermia which accompanies cardiopulmonary bypass depresses thromboxane A2
synthesis and causes platelet dysfunction.
Platelet dysfunction is also seen in renal failure, due to the effect of urea. The defect
lies in the interaction between platelets and the vessel wall.
Liver disease
Liver dysfunction is common in the ICU because of diffuse disease (e.g. septicaemia) or
as a primary presentation (e.g. alcoholic cirrhosis, paracetamol overdose). Coagulation
factors II, VIII, IX and X are produced by the liver; all except factor IX are involved in
the extrinsic system. The synthesis of these factors relies on a vitamin K-dependent
carboxylase which causes partial carboxylation and lowered activity. Deficiency is
detected by prolongation of the prothrombin time. Vitamin K is poorly absorbed if there
is intestinal malabsorption (common in many systemic illnesses), biliary obstruction or
an enteric fistula, because bile salts are required for vitamin K absorption. Vitamin K is
antagonized by coumarins (e.g. warfarin).
Fresh frozen plasma is used to treat coagulopathy due to liver disease.
Inherited disorders
Other specific, inherited disorders of clotting are uncommon and require haematological
advice. u
FURTHER READING
Bernard G R, Vincent J-L, Laterre P-F et al. For the Recombinant Human Activated
Protein C Worldwide Evaluation in Severe Sepsis (PROWESS) Study Group. Efficacy
and Safety of Recombinant Human Activated Protein C for Severe Sepsis. New Engl J
Med 2001; 344: 699709.

Ethical Issues in Resuscitation
and Intensive Care Medicine
Gary Smith
Gary Smith is Consultant in Intensive Care Medicine at Portsmouth Hospitals

NHS Trust. He qualified from Southampton University Medical School and trained in
anaesthesia and general medicine in Gloucester, Bristol and Southampton, and at Yale
University, USA. His interests include the organization of intensive care services,
outcome prediction and the training of doctors, nurses and paramedics.
An ethic is a moral principle or a set of principles considered by an individual, group

or society to be correct. All areas of healthcare raise moral and ethical dilemmas, but
those concerning resuscitation and intensive care medicine (Figure 1) often appear
more acute. There are several reasons for this.
Patients are often unconscious, making it impossible for them to give consent or
provide opinions regarding whether treatment should be administered.
Patients relatives are more often directly involved in decision-making on behalf of
the patient than in other areas of healthcare.
Intensive care resources are limited and rationing inevitably occurs.
Ethical issues often involve life and death decisions. Open and honest discussion
of difficult ethical matters by patients (where possible), their relatives and healthcare
workers usually permits their resolution, however, very rarely, this leads to conflict. This
article describes the principles of ethical decision-making and considers some areas
that provide dilemmas for intensive care staff. The rights of children and of the unborn
child are not considered here.
Examples of ethical issues in resuscitation and intensive care medicine

Informed consent
Blood transfusion and Jehovahs Witnesses
The unconscious patient
Withholding or withdrawal of treatment
Research into resuscitation and intensive care medicine
Decisions not to attempt resuscitation
Brain death, organ donation and transplantation
Quality of life
Costbenefit
Patient confidentiality
Advance statements
Human immunodeficiency virus infection testing
Principles of ethics
It is generally accepted that there are at least four, equally weighted, principles to
consider when making ethical decisions.
Respect for autonomy: this is the right of a fully informed individual to choose
a certain course of action for him/herself. It encompasses decisions regarding the
acceptance or refusal of treatment. The traditional paternalistic approach to healthcare
delivery, in which doctors and nurses know best and are the sole decision-makers,
is increasingly seen as inappropriate. Consequently, a model of partnership between
healthcare professionals and patients is now recommended. In general, provided a
patient is competent, and the decision is rational, there is an obligation for healthcare
professionals to respect the patients voluntary decision, even if they disagree (e.g.
respecting the decision of a Jehovahs Witness to refuse blood transfusions). Ethically,
such an obligation is deemed to be binding, unless it is overridden or outweighed by
competing moral obligations. If competent patients make irrational decisions, this may
impact on the autonomy of other patients or healthcare workers. However, the courts
have ruled that doctors are not obliged to provide treatment contrary to their clinical
judgement.
Beneficence is the obligation to do good and is the basis for all medical and nursing
care. The end point of beneficence has traditionally been interpreted as preserving life.
However, in situations where life is of such poor quality (e.g. because of pain or severe
disability) that it is considered less beneficial for the patient than death, the principle of
beneficence may include palliation and ensuring a good death.
Non-maleficence is the obligation to avoid doing harm (primum non nocere). Conflicts
may arise if beneficial medical interventions also cause harm. The potential for the
double effect of treatment is well recognized when morphine is administered for
palliation, but inadvertently causes respiratory depression or even death.
Justice is the right of a patient to receive an equal share of the distribution of

healthcare. Healthcare should not be distributed on the basis of arbitrary criteria (e.g.
age, gender, race, sexual orientation) but should be apportioned fairly. Therefore, the
principle of justice implies equity (fairness) and equality, and is manifest in arguments
over the rationing of healthcare. Discussions about the principle of justice inevitably
include the concepts of utilitarianism bringing about the greatest good to the greatest
number of patients and deontology, which relates to the duty of healthcare workers
to individual patients.
Dilemmas
Some examples of dilemmas in intensive care and resuscitation are discussed below.
Patient consent
Informed consent is required prior to medical or surgical intervention (e.g. clinical
examination, surgical operation, teaching session, entry into a research trial, medical
photography) on a competent adult. Although there is generally no legal obligation
to obtain written consent, it is regarded as good practice. Nevertheless, verbal or
implied consent (i.e. acquiescence to the intervention in full knowledge of what the
intervention entails) may suffice. Failure to obtain consent may result in charges of
assault; inadequate counselling may result in charges of negligence. Informed consent
demands that the patient understands the nature and purpose of the intervention,
receives a full explanation of the benefits and risks of the procedure and is provided
with a similar description of the alternative measures available. Consequently, the
doctor obtaining consent (usually the person undertaking the procedure) must have
a thorough knowledge of these matters, otherwise truly informed consent cannot be
obtained. For informed consent to be valid, the patient must consent voluntarily and
freely.
In intensive care and during resuscitation, it may be impossible to obtain the patients
consent if they are unconscious. Doctors must then act in good faith by providing
care that is required to save life or prevent significant clinical deterioration. However, if
there is evidence (e.g. a legally binding advanced directive) that a previously competent
adult would wish to refuse all or some forms of treatment, this should be respected.
In England, Wales and Northern Ireland, no one (not even a relative with enduring
power of attorney) may consent legally on behalf of another adult, even though
there is an increasing tendency for family members to believe that they have this
authority. Consequently, the relatives of an unconscious adult cannot give consent for
an operation or any other intervention. It is, however, good practice to discuss the
intention to operate with them to establish that they understand the actions about to be
taken and the reasoning behind them. This is termed informed assent and is done, in
part, to diminish risks of subsequent litigation by relatives who claim that procedures
were undertaken without their knowledge. Informed assent has no legal status and has
the risk of conflicting with the patients right to confidentiality.
Consent for human immunodeficiency virus (HIV) infection testing: informed

consent must be obtained from any competent patient in whom an HIV test is
contemplated. This applies even when the test is being considered because a
healthcare worker feels at risk of disease transmission following a needle-stick injury
from a potentially HIV-infected patient. If a patient is unconscious, an HIV test may be
undertaken without consent, if the test result confers a specific benefit to the patient
(e.g. helps to make a diagnosis). If a healthcare worker has a needle-stick injury from
an untested, unconscious patient, and the patient is unlikely to regain consciousness
within 48 hours, patient testing may be justified but should be discussed with the Trusts
Occupational Health Service. If a healthcare worker has a needle-stick injury from a
patient who subsequently dies, and there is good reason to suspect that the patient was
HIV-positive, it is advised that the dead patients blood is tested.
Advance statements
Competent persons may state in advance their choices for treatment in the event
of becoming incapacitated. This legally binding opinion is known as an advance
statement or living will. Such statements may include clear instructions regarding
the refusal of certain therapies (advanced directive), may describe the degree of
irreversible deterioration beyond which no life-sustaining support should be given and
may nominate another person who should be consulted at the time that such decisions
must be made. Advanced statements may be written or in the form of a witnessed
oral statement.
Withholding and withdrawal of treatment

Modern medicine brings both benefits and dilemmas. In the ICU, the availability
of technology does not imply that it is correct for it to be used for all patients.
Unfortunately, it may have limited efficacy in some patients and may merely prolong
the dying process rather than prolonging life. For instance, physiological stability may
be easily obtained using vasoactive drugs and intermittent positive-pressure ventilation,
but this does not guarantee hospital survival. In such circumstances, decisions may be
made to withhold or limit the extent of treatment offered, or to withdraw that already
being provided. Generally, treatment is withdrawn when it has ceased or failed to
achieve the benefits for which it was used.
Occasionally, even a treatment that might produce short-term benefit may be
withheld or withdrawn if the patient is suffering from a terminal illness. Factors usually
taken into account in the decision to withhold or withdraw treatment include the
diagnosis, severity of disease, co-existing illnesses, prognosis, response to current
treatment, physiological reserve, anticipated quality of life and the patients wishes, if
known.
There is an important distinction between withdrawing or withholding treatment in
patients in whom no clinical benefit can be obtained and a deliberate act to end a
patients life (e.g. euthanasia or murder). Withholding or withdrawal of treatment raises
several ethical dilemmas, including:
the wishes of the (often unconscious) patient
the validity and legality of opinions or decisions made by a surrogate
the diversion of limited resources from patients with a good chance of survival to
those who are unlikely to benefit, if treatment is not withheld or withdrawn
the definition of futility and who defines it
the nature of medical treatment (legally, the use of artificial nutrition and hydration
constitutes a medical treatment, thus, the principles that cover the withdrawal of any
other artificial organ support equally apply to artificial nutrition and hydration)
withdrawal involves a physical act (e.g. turning off a vasoactive drug) that often
brings about the rapid demise of the patient; some healthcare workers find this
psychologically unacceptable.
Decisions not to attempt resuscitation

A specific area in which treatment may be withheld is cardiopulmonary resuscitation
(CPR). CPR may be attempted whenever cardiac or respiratory function ceases.
However, as cardiopulmonary failure is an inevitable part of dying, healthcare workers
should identify patients for whom it is a terminal event in their illness and for whom a
prior do not attempt resuscitation (DNAR) decision may be appropriate. Guidance on
DNAR decisions has been published recently in a combined statement by the British
Medical Association, Resuscitation Council (UK) and the Royal College of Nursing. In
addition, the Department of Health has mandated that NHS Trusts must have an agreed
resuscitation policy that gives respect to patients wishes. Trusts must also identify a
Non-Executive Director to be responsible for overseeing implementation of the policy
and its audit.
DNAR decisions cannot be generalized and should always be made on an individual
basis, ideally as part of an overall care plan for the patient and in advance of
cardiopulmonary arrest. Discussions with the patient, and their family, are potentially
distressing and must be handled sensitively; senior, experienced members of the
medical team should undertake these. The overall responsibility for DNAR decisions
rests with the consultant in charge of the patients care. Any discussions about whether
to attempt CPR should be documented, signed and dated in the patients record. If the
clinical decision is challenged and agreement cannot be reached, legal assistance may
help to clarify the appropriate course of action.
Overall survival to hospital discharge following cardiac arrest is about 15%, but
may be considerably lower for certain patients (e.g. those with sepsis or cancer).
Inappropriate use of CPR makes death undignified and may have ethical implications
for others. For instance, repeated attempts that provide only short-term clinical success
can be emotionally draining for the patients family and may mean that resources are
diverted from patients with a potentially better outcome. Additionally, failed CPR can
lower the morale and enthusiasm of the healthcare team.
The public often has the misconception that a DNAR decision is analogous with
a decision not to treat. In fact, a decision not to perform CPR is entirely consistent
with the full provision of medical and nursing care up to that point. Consequently,
patients and their families should be reassured that all other treatment and care (e.g.
analgesia, antibiotics, physiotherapy) may continue to be offered. Finally, decisions
about resuscitation must be reviewed regularly and in the light of changes in the
patients condition and wishes.
Research in intensive care patients
Research performed on intensive care patients or those under-going CPR poses
several ethical difficulties. For instance, the heterogeneity of patients in ICUs limits the
generality of research outcomes. Additionally, the ability to obtain a patients consent
is limited by disease-induced coma or pharmacological sedation. If a patient is unable
to give consent to entry into a trial, it is customary to obtain informed assent from the
patients next-of-kin, although deferred consent (consent after patient recovery) is an
alternative approach for some studies. Particular problems arise for research into areas
of CPR where consent cannot be obtained from the patient and there is insufficient time
to obtain informed assent from relatives. Finally, the ethical principles of beneficence
and non-maleficence are important here because patients entering into trials do not
necessarily benefit from doing so, and may actually be harmed by it. In general, it is
advisable to discuss all research into areas of resuscitation or intensive care with the
Local or Regional Research Ethics Committees.
Human Rights Act 1998
The Human Rights Act 1998 came into force in October 2000, bringing into UK law
many of the rights set out in the European Convention on Human Rights. The Act
includes numerous Articles, some of which have implications for healthcare (especially,
Articles 2, 3, 5, 6, 8, 9, 10, 12 and 14). For instance, Article 2, which covers the
right to life, has implications for withholding or withdrawing treatment. This Article does
not mean that healthcare workers must always strive to save life. Rather, it implies
that the medical decision-making process must consider the patients right to life and
that the NHS must act reasonably in its decision-making. Withholding or withdrawing
treatment does not breach Article 2 if non-treatment is in the patients best interest
(e.g. withdrawing nutrition in a patient with persistent vegetative state). Other Articles of
the Act that may have implications for critical care include Article 3 (treatment without
consent), Article 8 (the right to be provided with sufficient information to give valid,
informed consent) and Article 9 (the right to refuse life-prolonging therapy).
FURTHER READING
The Impact of the Human Rights Act 1998 on Medical Decision Making. London: BMA
Publications, 2000.
Decisions Relating to Cardiopulmonary Resuscitation. A Joint Statement from the

British Medical Association, the Resuscitation Council (UK) and the Royal College of
Nursing, 2001. London: British Medical Association, 2001.
Withholding and Withdrawing Life-prolonging Medical Treatment. Guidance for

Decision-making. London: BMJ Books 1999.
Reference Guide to Consent for Examination or Treatment. London: Department of

Health, 2001.

Fever in ICU Patients
Raj Isaac
Bruce L Taylor
Raj Isaac is Clinical Fellow in Critical Care Medicine at the Queen Alexandra Hospital,
Portsmouth, UK.
Bruce L Taylor is Consultant in Critical Care Medicine and Anaesthesia at Portsmouth

Hospitals NHS Trust, UK. He studied at the Universities of St Andrews and Manchester,
and trained in anaesthesia and intensive care in Gloucester, Southampton, Cambridge,
Exeter, Bristol, and Brisbane, Australia. He returned to Melbourne, Australia, to train in
paediatric intensive care and to complete specialist training in intensive care medicine.
Fever is one of the most common physical signs in critically ill patients. The Society of
Critical Care Medicine defines body temperature over 38.3 C as clinically significant
fever. This figure is a conversion of 101 F to centigrade, and in general a temperature
over 38 C is considered significant.
Fever may indicate infective or non-infective inflammatory processes. Both are

common in ICUs and attempts to correlate different processes with temperature ranges
and timing have limited clinical value. Prolonged fever is associated with a higher
mortality. The causes of fever vary, but ventilator-associated pneumonia, catheter-
related sepsis, urinary tract infection and acute myocardial infarction are ubiquitous.
Surgical patients have additional potential causes of fever.
Infection is the most common cause of death in critically ill patients, therefore fever
should always be taken seriously. Rigorous efforts should be made to identify the
sources of sepsis at an early stage. Critically ill patients often have complex underlying
illness, therefore it is essential that a detailed history is obtained and that there is
access to hospital records. Physical examination should be thorough and include
all sites of potential infection. Because of the increasing risk of developing multiple-
resistant infection, antibiotic therapy should be based on microbiological cultures;
empirical therapy is occasionally necessary. A diagnosis of non-infectious fever should
be made only in the appropriate circumstances and in the absence of clinical evidence
of sepsis.
Pathophysiology: fever occurs when thermoregulatory mechanisms produce and

sustain an elevated body temperature. Exogenous pyrogens (microorganisms,
immunological mediators, toxic agents) trigger cytokine release (interleukins 1 and
6 and tumour necrosis factor- ) from monocytes, lymphocytes, macrophages and
endothelial cells. These bind with receptors in the preoptic anterior hypothalamus,
releasing prostaglandins (PGs), predominantly PGE2 causing local cyclic-AMP release.
This decreases the activity of local warm-sensitive neurons, increasing heat production,
activating heat conservation and modifying the thermoregulatory set point of the
hypothalamus.
Hypermetabolic states (e.g. malignant hyperpyrexia) cause fever by increased heat

production.
Fever patterns: a reliable diagnosis cannot be made from the pattern of fever. Most
patients have remittent or intermittent fever with or without rigors that usually follow
diurnal variation when due to infection.
Sustained fevers may occur in patients with infectious or non-infectious causes.
Patients with severe sepsis may be afebrile or hypothermic.
Septic afebrile patients have a higher mortality.
The cooling effect of continuous veno-venous haemofiltration may mask latent
fever.
Aetiology
Non-infectious: in non-infectious fever the temperature is usually less than 38.9 C.
Drug or transfusion reactions may cause higher temperatures (Figure 1). Postoperative
patients who develop fever in the first few days may have no infective source.
General anaesthesia affects anterior hypothalamic thermoregulation (similar patients
receiving regional or local anaesthesia remain apyrexial).
Cytokine release from tissue injury or blood transfusion may be implicated.
Acute adrenal insufficiency may present as fever.
Malignant hyperthermia (see later), is usually detected intraoperatively, but its onset
may be delayed.
Non-infectious causes of fever
Acute respiratory distress HIV-related non-infective

syndrome (ARDS) fever
Adrenal insufficiency Hypersensitivity reactions
Alcohol/drug withdrawal Hyperthyroidism
Aspiration pneumonitis Myocardial infarction
Bowel ischaemia Neoplastic fevers
Deep venous thrombo- Pancreatitis
phlebitis Pulmonary atelectasis
Dissecting aortic aneurysm Pulmonary/fat embolism
Giant cell arteritis Post surgical (first 2 days)
Gout and pseudogout Reaction to blood
Haemorrhage into CNS, products
lung, retroperitoneum, Reaction to drugs
adrenals Rheumatoid arthritis
Heat stroke Seizures
HenochSchoenlein purpura Systemic lupus erythematosus
Transplant rejection
Drug-induced fever (e.g. by antibiotics, anticholinergics, streptokinase) is easily

overlooked, little reported and its incidence unknown. High spiking temperatures, chills,
leukocytosis and eosinophilia are characteristic. Relative bradycardia is rare.
Fever occurring in a patient receiving blood or blood products may signify a transfusion
reaction. Platelet reactions are most common. Fever may be a sign of clinically
unsuspected acute myocardial infarction.
The combination of prolonged fever, leukocytosis and pulmonary infiltrates is often

inappropriately diagnosed as nosocomial or ventilator-associated pneumonia.
Diagnosis may be improved by semiquantitative culture of non-bronchoscopic lavage
specimens. Fever may be a feature of the chronic fibroproliferative stages of acute
respiratory distress syndrome (ARDS).
Infectious: a temperature over 38.9 C for more than 2 days usually indicates infection
(Figure 2). Critically ill patients are vulnerable to nosocomial infections owing to
prolonged hospitalization, antibiotic therapy, invasive devices, co-morbidity and debility.
There are particular concerns in surgical patients.
Delayed resolution of fever despite definitive intervention and antibiotic therapy
(e.g. appendix abscess, peritonitis, ascending cholangitis) does not necessarily imply
continuing sepsis.
Fever following trauma may indicate bacterial contamination of wounds, joints or
bone; tetanus should also be considered.
Clostridial myonecrosis or streptococcal cellulitis may cause fever within 72 hours of
elective surgery.
Fever and pain may be presenting symptoms of necrotizing fasciitis in susceptible
patients (e.g. the obese, those with diabetes).
Infectious causes of fever in intensive care
Respiratory
Sinusitis
Lung abscess
Empyema
Pneumonia
Tracheobronchitis
Invasive devices
Intravenous/arterial lines (phlebitis, bacteraemia, fungaemia)
Cardiac valve prosthesis or pacemaker
Urinary catheter (pyelonephritis, prostatitis, prostatic abscess, urinary
infection)
Gastrointestinal
Antibiotic-associated colitis
Cholecystitis/cholangitis, acalculous cholecystitis
Infections due to transfusion (hepatitis B and C, cytomegalovirus)
Diverticulitis
Surgical
Wound infection
Peritonitis
Deep infection/abscess
Neurological
Meningitis/encephalitis
Cerebral/epidural abscess
Tetanus, poliomyelitis
Cardiovascular
Endocarditis
Infected arterial graft
Viral myocarditis
Skin, soft tissue and bone

Cellulitis
Decubitus ulcer
Necrotizing fasciitis
Septic arthritis/osteomyelitis
2
Common infective causes

Catheter-related sepsis: about 25% of central venous catheters become colonized;
5% of patients with a central venous catheter develop catheter-related sepsis. The
incidence is related to:
technique of catheter insertion
length of time in situ
number of ports
quality of sterile precautions during handling.
Common causal organisms include Staphylococcus aureus and coagulase-negative

staphylococci, enterococci, Gram-negative bacteria and Candida spp. The incidence of
catheter-related sepsis can be reduced by strict aseptic precautions during insertion and
handling and the use of antimicrobial-bonded catheters.
Ventilator-associated pneumonia is said to occur in 25% of ventilated patients, but

is probably overdiagnosed. Focused antibiotic policies guided by non-bronchoscopic
lung lavage investigation may improve the outcome of suspected ventilator-assisted
pneumonia.
Nosocomial sinusitis is an important, often unrecognized source of infection. It is:

associated with use of nasogastric/nasotracheal tube (incidence lower with oral
tubes)
diagnosed on clinical or radiological suspicion or transnasal puncture
treated by removing nasal tubes, sinus drainage and antibiotics.
Radiological abnormalities of sinuses do not necessarily imply infection.
Urinary tract infection: urinary tract colonization is common, but clinically significant
urinary tract sepsis is rare in patients with normal urine flow. Obstruction or other
abnormalities of the urinary tract increase the risk. Urine may yield positive bacterial
cultures until the catheter is removed. The use of unnecessary antibiotics risks inducing
multiple-resistant bacteria.
Treatment
Thorough clinical examination is essential.
The cause (e.g. abscess drainage, potentially infected lines) should be removed or
treated.
Investigations and microbiological surveillance should be performed and repeated
as required.
The diagnosis of non-infectious fever is one of exclusion.
Antipyretics are generally best avoided because fever is an important component of

the host response. The response to treatment is more difficult to assess in patients
taking antipyretics and temperature enhances the host defences and increases
pathogen susceptibility. However, high temperatures are symptomatically unpleasant
and other effects (e.g. increased cardiac output, oxygen consumption, carbon
dioxide production and energy expenditure) may be deleterious. Antipyretics may be
appropriate for some patients, for example those with limited cardio-respiratory reserve
or neurological injury. If the body temperature is over 41 C it is important to prevent
further escalation because of the increased risk of cerebral injury.
Cooling methods: the use of sponging, fans and hypothermia blankets is controversial
and may be no more effective than antipyretics. Core cooling methods, such as
intravenous cooling cannulae, body cavity irrigation or extracorporeal methods are
probably more effective. Muscle relaxants may be beneficial to prevent shivering.
Large temperature fluctuations, hypermetabolism, increased oxygen consumption and
rebound hyperthermia may occur after cooling.
Specific indications for fever reduction: moderate fever may offer physiological
advantage, but there is no evidence that very high temperatures (over 40.5 C) are
beneficial. The risk of thermal cerebral injury increases with duration as temperature
exceeds 41 C. Seizures induced by hyperpyrexia and hypoglycaemia multiply this
risk and further increase heat production. Fever reduction is therefore indicated in
conditions in which hyperpyrexia occurs, including malignant hyperpyrexia, heat stroke,
neurolept-malignant syndrome and viral encephalitis. The role of induced hypothermia
following traumatic head injury remains unconfirmed, but because persistent pyrexia is
associated with a worse outcome, antipyretics and active cooling may be indicated.
Relative indications for fever reduction

Septicaemia/septic shock in patients with severe sepsis and hyperpyrexia,
continuous veno-venous haemofiltration may improve haemodynamic stability and
reduce vasopressor requirements although the benefits remain unproven. Whether the
effect is secondary to cytokine removal, cooling or both is unknown.
Postcardiac arrest induced hypothermia may improve outcome and antipyretics or

active cooling may be beneficial.
Febrile fits in children cooling to normothermia may reduce the seizure threshold,
but antipyretics should be reserved for children with severe discomfort or high fever.
Patients with critical oxygenation in patients with refractory hypoxaemia, reducing

the oxygen demand is logical, though not evidence-based. u
FURTHER READING
Bouchama A, Knochel J P. Heat Stroke. New Engl J Med 2002; 346: 197887.
Circiumaru B, Baldock G, Cohen J. A Prospective Study of Fever in the Intensive Care

Unit. Intens Care Med 1999; 25: 66873.
Cunha B A. Fever in the Intensive Care Unit. Intens Care Med 1999; 25: 64851.
Davies D M. Neuroleptic Malignant Syndrome. In: Textbook of Adverse Drug Reactions.

4th ed. Oxford: Oxford Medical Publications, 1991.
George M J, Glew R H. Approach to Fever in the Intensive Care Patient. In: Rippe J
M, Irwin R S, Fink M P, Cerra F B. Intensive Care Medicine. 3rd ed. New York: Little,
Brown and Company, 1996.
Grogan H, Hopkins P M. Heat Stroke: Implications for Critical Care and Anaesthesia.
Br J Anaesth 2002; 88(5): 7007.
Marik E P. Fever in the ICU. Chest 2000; 117: 85569.
Miller R D. Malignant Hyperthermia. In: Anaesthesia. 4th ed. New York: Churchill
Livingstone, 107589.

Fluid and Electrolyte Balance in
Intensive Care Patients
Mark A Hamilton
Andrew R Webb
Mark A hamilton is Anaesthetic Specialist Registrar at University College Hospital,

London, UK. He qualified from St Georges Hospital, London. He is currently
training in anaesthesia and critical care at University College Hospital, London.
His research interests include optimization of the surgical patient and exercise
physiology.
Andrew R Webb is Medical Director at University College Hospital, London. His

research interests include fluid management and monitoring of the critically ill.
Fluid and electrolyte balance is one of the basic principles of management of the
critically ill patient. Attaining this balance can be achieved only with a good working
knowledge of the underlying physiology of body fluid compartments coupled with
practical management strategies including accurate record keeping and appropriate
interpretation.
Body fluid compartments
In a 70 kg man about 60% of body weight is made up of water (42 litres), for women
the value is 55% and declines with age. The total body water is not distributed evenly
throughout the body. It is divided into two major components: the intracellular fluid
(ICF) and extracellular fluid (ECF), which contain about 28 and 14 litres, respectively.
The extracellular space is divided into intravascular and interstitial compartments (see
Anaesthesia and Intensive Care Medicine 2:2: 69). The intravascular fluid is the plasma
volume, which constitutes about 3 litres, and the interstitium holds the remaining 11
litres (Figure 1). Each compartment contains different concentrations of electrolytes
and proteins (Figure 2).
Distribution of body water in the three major body

fluid compartments
Distribution of electrolytes, water and protein between body fluid compartments
Intravascular Interstitial Intracellular Typical plasma Daily requirements

(mmol/litre) (mmol/litre) (mmol/litre) (mmol/litre) (mmol/kg/day)
Sodium 140 145 10 135150 11.5

Potassium 3.7 3.8 155 3.55.0 11.5
Chloride 102 115 3 98107 11.5
Calcium 1.2 1.2 0.01 2.22.6 0.070.14
Magnesium 0.8 0.8 10 0.71.0 0.140.17
Phosphate 1.1 1 105 0.81.4 0.280.56
Bicarbonate 28 30 10 2230
Water 3 11 28 22.4 litres/day
Physical principles
Several physical principles govern the distribution of fluid and electrolytes between
body fluid compartments.
Diffusion
Electrolytes move from a region of high concentration to a region of lower concentration
in an attempt to achieve equilibrium by diffusion. If diffusion occurs across a
membrane then the permeability of that membrane to the electrolyte influences the
rate of diffusion. Diffusion is commonly accompanied by bulk flow through biological
membranes (when the concentration difference is high) with ordered flow of particles
rather than the unordered movement of diffusion alone.
Osmosis
Osmosis is the diffusion of water through a semipermeable membrane from a region
of low osmolality to a region of higher osmolality. It leads to the movement of water
through all body fluid compartments. The osmotic pressure generated by particles
(electrolytes and proteins) is proportional to their number and not their mass.
Active transport
Active transport is an energy requiring process that regulates sodium and potassium
exchange at the cell membrane. This gives rise to electrochemical imbalance across
the membrane and helps to maintain the resting membrane potential and cell volume.
Colloid osmotic pressure

Any particle (electrolyte or protein) can exert an osmotic pressure, but the free diffusion
of electrolytes across the capillary wall negates their osmotic effect. Passage of
proteins across the capillary wall is impeded in the normal state. For this reason
they exert an osmotic effect within the capillary, commonly referred to as the colloid
osmotic pressure or oncotic pressure. The osmotic effect of these proteins is about
50% greater than would be expected for the proteins alone. The reason for this is that
most proteins are negatively charged, attracting positively charged ions such as sodium
(the GibbsDonnan effect). These positively charged ions are osmotically active and
therefore increase the effective osmotic pressure.
Starling equation
In health, the movement of fluid across the capillary wall can be described by the
Starling equation:
Jv = Kfc [(Pc Pi) (p i)]
where: Jv, solvent flux; Kfc, filtration coefficient; Pc, capillary hydrostatic pressure; Pi,
interstitial hydrostatic pressure; , reflection coefficient; p, protein osmotic pressure
(oncotic) of plasma; i, protein osmotic pressure (oncotic) of interstial fluid.
The reflection coefficient is 0 if the capillary is freely permeable to the protein or
colloid in question and 1 if it is impermeable.
In most capillaries the Starling equation is positive, indicating some net movement
of fluid to the interstitium. This fluid is normally absorbed by the lymphatic system and
returned to the intravascular space. In disease, the permeability of the capillary often
increases and more protein and fluid is lost to the interstitium. This decreases the
plasma oncotic pressure and, despite an up-regulation of the absorptive capacity of the
lymphatic system, interstitial oedema results when interstitial fluid is formed faster than
it can be removed by lymphatics. It is for this reason that colloids are given to
restore the plasma oncotic pressure and retain fluid within the intravascular space.
However, oncotic pressure is dependent on the number of osmotically active particles
and not their size or mass. The ideal choice of colloid is therefore a compromise
between intravascular retention (dependent on the size of the colloid particles and the
rate of their metabolism) and osmotic pressure potential. The lower molecular weight
succinylated gelatins are suitable for intravascular expansion if there is a low suspicion
of capillary leak. The medium molecular weight hydroxyethyl starches are more suitable
for conditions such as sepsis where there is a greater degree of capillary leak.
Crystalloids distribute according to their predominant electrolyte or particle. Fluids
such as 5% glucose distribute evenly through all three compartments because the
glucose is rapidly metabolized to water. 0.9% saline distributes evenly between the
intravascular and interstitial spaces (ECF) because the capillary endothelium is freely
permeable to sodium, hence their similar sodium content. There will be some entry of
sodium into the cell but this is returned to the interstitial space by the sodiumpotassium
pump to regulate cell volume and electrochemical balance.
Water and electrolyte balance
The principal electrolytes are sodium, potassium, chloride, calcium, magnesium and
phosphate. Many of these electrolytes and minerals are integral constituents of enteral
and parenteral feeds and can be adjusted easily for individual patients. However,
deficiencies and excesses are common in critical care. It is routine to measure the
plasma concentrations of these electrolytes, though they are poorly reflective of total
body stores. Excessively high or low values may induce deleterious effects and should
be corrected on an as-required basis. All deficiencies or excesses of electrolytes are
the result of an imbalance in supply and loss, redistribution and disordered regulation.
Where possible, it is important to identify the cause of the abnormality in order
to correct the problem. Patients in ICU are subjected to a wide range of noxious
stimuli and exhibit an up-regulation in their neuroendocrine response. This results in a
tendency to retain water and sodium.
Water
Water and sodium balance are difficult to separate because of their linked regulation
mechanisms. The average daily water requirement is 22.4 litres/day, generally
achieved via parenteral or enteral feeding and drug carriage volume. If these volumes
are not achieved they can be supplemented with a crystalloid. The daily fluid loss
varies depending on the patients condition, and it is usual for electrolytes to be lost
in proportion to water. However, conditions such as excess sweating, hyperthyroidism,
fever, diabetes insipidus and hypercalcaemia cause more water than electrolytes to be
lost. 5% glucose may be used to supply intravenous water. In general, there is a further
insensible loss of 500 ml/day from the lungs and skin, which must be taken into account
in fluid balance calculations.
Sodium
The normal concentration of sodium in plasma is 135150 mmol/litre. Its principal
route of excretion is via the kidney and is mainly regulated by the renin-angiotensin-
aldosterone system. The distribution of water and sodium throughout the extravascular
space means that they are inextricably linked when considering maintenance and
replacement. For the most part, 11.5 mmol/kg/day of sodium is required and is usually
met from the maintenance fluid or administered feed. Hyper- and hyponatraemia are
common and it is important to establish the cause before embarking on treatment.
Oedematous patients generally have high body sodium stores but may have relative
water deficiency. It should be established if body sodium stores are high, normal or
low and whether body water is normal or low. The rate and degree of correction also
differs in hyper- and hyponatraemia depending on whether the aetiology is acute or
chronic.
Potassium
Potassium is predominantly an intracellular ion, the excretion of which is mainly via
the kidney. The normal plasma concentration is 3.55.0 mmol/litre. Potassium is
exchanged in the kidney for sodium and hydrogen ions and redistributed across cell
membranes depending on the acidbase status of the plasma. It is important to
maintain potassium because of its effects on membrane stabilization.
Hypokalaemia is a potent stimulus for arrhythmias and promotes muscular
weakness. Potassium supplementation is commonly required and should not exceed
40 mmol/hour because the rate of change of potassium is also a potent arrythmogenic
stimulus.
Hyperkalaemia can cause life-threatening dysrhythmias and is common in patients
with renal impairment. Treatment options include ion exchange resins, glucose and
insulin infusions, intravenous bicarbonate, calcium chloride and dialysis.
Magnesium
Magnesium is primarily an intracellular ion and is involved in energy production,
utilization and membrane stabilization most often as an enzyme cofactor. It is regulated
mainly by the influence of parathyroid hormone (PTH) and aldosterone on the kidney.
The normal plasma concentration is 0.71.0 mmol/litre. Deficiency is common and a
potent source of arrhythmias. It should be corrected with 2040 mmol infused over
12 hours.
Calcium
Calcium is widely distributed with normal plasma concentrations of 2.22.6 mmol/litre.
PTH and calcitriol regulate its concentration. Only the ionized fraction is active and
when it is less than 0.8 mmol/litre may cause tetany, convulsions and a prolonged QT
interval. If symptomatic, 510 ml of 10% calcium chloride can be administered over 5
minutes.
Phosphate
Phosphate and calcium regulation are linked but calcitriol predominantly regulates
phosphate. Severe hypophosphataemia, especially when below 0.3 mmol/litre, can limit
ATP formation. Symptoms and signs include muscle weakness, myocardial depression
and platelet dysfunction. Supplementation, although empirical, can be achieved with a
maximum rate of infusion of 9 mmol over 12 hours.
Fluid management strategies
Maintenance
In general, most maintenance requirements are met from enteral or parenteral feeding
and drug carriage fluid. These may be supplemented with a crystalloid. For those who
are not fed and/or receiving colloid solutions, a salt containing crystalloid (e.g. lactated
Ringers solution or 0.9% saline) may be required at about 80100 ml/hour.
Replacement
In general, replacement of fluid should be like for like. Most of the solutions lost from
the body contain salt and should be replaced as such. However, it is important to
take into account the type of fluid being lost when considering its replacement (e.g.
blood, large or small bowel fluid, ascitic fluid, pleural fluid) because they have differing
water and electrolyte concentrations. Blood is generally given in a reactionary fashion
to maintain haemoglobin at 810 g/dl, though a liberal transfusion practice has recently
been questioned.
In critical care patients, the correction of hypovolaemia is important to maintain
oxygen delivery to the tissues and for removal of waste products.
It is difficult to gain information on the adequacy of resuscitation of the interstitial and
intracellular compartments. Many soft endpoints, such as thirst, tissue turgor and
fluid balance charts offer at best empirical estimates. The intravascular compartment
has in comparison harder end points such as heart rate, central venous pressure,
stroke volume, blood pressure and pulmonary artery wedge pressure which, when
challenged dynamically, allow an assessment of the adequacy of resuscitation of the
circulating volume. Static pressure measurements are a poor guide to the adequacy
of intravascular volume replacement. The most efficient way to achieve adequate
circulating volume is to use a fluid challenge approach with a colloid. There is
controversy as to whether a colloid or crystalloid is most suitable for resuscitation.
Colloids are retained in the intravascular space long enough for adequate change in
the haemodynamic end points to be assessed and exert a persisting colloid osmotic
pressure. Crystalloids do not exhibit this effect, making colloids the logical choice. Fluid
may be administered as boluses of 100200 ml and their effect on haemodynamic
end points such as central venous pressure or stroke volume must be observed.
Fluid challenges should be repeated until there is no rise in stroke volume or there
is a rise in central venous pressure greater than 3 mm Hg. The distribution of the
administered fluid is then largely predictable according to its properties and the nature
of the underlying illness.
FURTHER READING
Guyton A C. Textbook of Medical Physiology. 7th ed. Philadelphia: WB Saunders, 1989.
Marshall W J. Clinical Chemistry. 2nd ed. London: Gower Medical Publishing, 1992.
Webb A R, Shapiro M J, Singer M, Suter P M. Oxford Textbook of Critical Care. Oxford:
Oxford Medical Publications, 1999.

Gastrointestinal Tract
Haemorrhage and Ulcer
Prophylaxis in ICU
Matthew Williams
Paul J Sadler
Matthew Williams is Specialist Registrar in Anaesthesia at the Queen Alexandra

Hospital, Portsmouth, UK. He qualified from Bristol University and is training at the
Wessex School of Anaesthesia. His interests include intensive care medicine and
medical education.
Paul J Sadler is Consultant in Critical Care and Anaesthesia at the Queen Alexandra
Hospital, Portsmouth, UK. He qualified from Sheffield University and trained in
anaesthesia and intensive care medicine in Guys Hospital, Leicester, Nottingham and
Birmingham.
Gastrointestinal tract haemorrhage is classified as upper or lower depending on the

source of bleeding (about 20% are lower). Acute gastrointestinal bleeding is a common
cause of hospital and ICU admission and has a mortality of about 10%. Risk factors
that increase the likelihood of death include old age, co-morbidity, coagulopathy
and the magnitude of bleeding. Ulcers involving arteries, such as those close to the
left gastric artery on the lesser gastric curve, or on the posterior duodenal wall, are
particularly problematic. Figure 1 lists the common causes of bleeding.
Common causes of gastrointestinal haemorrhage
Upper gastrointestinal haemorrhagePercentage (%)

Duodenal ulcer 40
Gastric ulcer 17
Acute erosions (gastritis, oesophagitis, 12
duodenitis)
Varices 10
MalloryWeiss tear 5
Cancer 3
Other 13
Lower gastrointestinal haemorrhage

Colon 74
Diverticular disease 16
Angiodysplasia 30
Carcinoma of the colon 11
Rectal lesion 4
Upper gastrointestinal tract 11
Small bowel 9
Inflammatory bowel disease
Meckels diverticulum
Arteriovenous malformation
1
Clinical features
Upper gastrointestinal bleeding is characterized by haemat-emesis and the
passage of melaena (stools blackened by altered blood). Bleeding ulcers are often
painless, especially in the elderly. Signs of massive blood loss are hypovolaemia, pallor,
tachycardia, sweating, cyanosis, altered mental sensorium and oliguria. A more occult
presentation is possible with pallor, fatigue and the development of anaemia. A history
of vomiting before haematemesis suggests a MalloryWeiss tear.
Lower gastrointestinal bleeding arises from a distal source and is characterized

by the passage of fresh blood per rectum (haematochezia). However, bleeding
from the small bowel or right colon may manifest as melaena. Abdominal pain
suggests ischaemia or inflammatory bowel disease, whereas painless lesions include
diverticulosis, angiodysplasia and Meckels diverticulum. Haemorrhoids (which become
swollen in portal hypertension) can be a profound source of bleeding. An occult
presentation with anaemia is more likely with lower than with upper gastrointestinal
bleeding.
Investigations may include combinations of:

blood (urgent to include full blood count, coagulation screen, urea and electrolytes,
cross-match)
endoscopy
angiography
radiolabelled red cell scan.
Investigations and management are often concurrent, depending on the severity of the
case. Blood tests and endoscopy are essential. Barium studies have been superseded
by endoscopy. Angiography and radionuclide tests are useful only in lesions that are
bleeding briskly at the time. These lesions are usually best managed with surgery, but
these techniques may be considered in surgically high-risk patients.
Management
Non-variceal upper gastrointestinal bleeding

Resuscitation severe hypovolaemia leads to a depressed conscious level and is
therefore a potential risk to airway patency, especially when associated with vomiting.
The patient should be resuscitated using clear fluids, colloids and blood, guided by
regular monitoring of vital signs (including postural blood pressure, conscious level
and urine output) and repeat blood investigations. This is best achieved in a high
dependency nursing area where invasive monitoring can be instituted; particularly for
elderly patients in whom co-morbidity and existing drug therapies make resuscitation
more difficult.
Assessment and management patients who require early intervention (endoscopy

or surgery) include those at high risk and those with evidence of significant bleeding
(e.g. presence of postural hypotension, cardiovascular instability and blood loss
requiring 4 or more units of red cells to be transfused in 12 hours). Rockall devised
a scoring system (Figure 2) to stratify the risk of re-bleeding and death following
gastrointestinal haemorrhage. This system can help to identify at-risk patients, possibly
triggering management decisions at a certain score (e.g. 3, central venous pressure
monitoring; 5, surgical referral).
The Rockall score for stratifying risk of re-bleeding and death following upper gastrointestinal
haemorrhage
Contributor Score
0 1 2 3
Age (years) < 60 6080 > 80
Shock None Pulse > 100 Blood pressure < 100

Blood pressure > 100
Co-morbidity None Ischaemic heart disease, Renal/liver failure,
congestive heart failure disseminated
malignancy
Diagnosis None, All others Upper gastrointestinal

MalloryWeiss tract malignancy
tear
Endoscopic None Blood in upper gastro-

findings intestinal tract, adherent
clot, visible vessel
Pharmacological intervention includes the early use of proton-pump inhibitors to aid

ulcer healing. These can be given intravenously in the first instance. Bleeding due to
coagulopathy should be managed with the administration of blood products (as guided
by investigations) and antifibrinolytic agents (e.g. tranexamic acid).
Endoscopic therapy can stop haemorrhage from some sources of upper

gastrointestinal bleeding (see below). Endoscopic techniques include adrenaline
(epinephrine) injection, electro-coagulation, thermal probes and laser photocoagulation.
The initial haemorrhage is usually stopped in over 90% of cases; but 90% of arterial
bleeds re-bleed. Endoscopic treatment is more effective than medical treatment alone
at reducing the rate of re-bleeding and subsequent transfusion requirements.
Surgery is the definitive treatment for upper gastrointestinal bleeding, but the
mortality is 1520%. Procedures include under-running of bleeding ulcers to secure
haemostasis, vagotomy or partial gastrectomy. Results are better when surgery is
performed early; therefore, there must be close liaison between senior members of the
medical, intensive care and surgical teams.
Variceal bleeding
Acute variceal bleeding is a complication of portal hypertension and has a high
mortality. Management includes fluid resuscitation concurrent with medical, endoscopic
and/or surgical intervention. Guidelines for management are shown in Figure 3.
Guidelines for management of variceal bleeding

Variceal bleeding
Balloon
Endoscopic therapy
Vasopressin/ tamponade/
Injection sclerotherapy
octreotide medical
Variceal ligation
therapy
Bleeding Continuing
control bleeding
Repeat Transjugular intrahepatic Surgery

endoscopy portosystemic
shunt (TIPSS)
3
Resuscitation gastrointestinal haemorrhage with a background of liver disease can

precipitate an encephalopathy; therefore attention to airway, breathing and circulation
is required. Bleeding can be torrential, but care must be taken not to over-transfuse
because rebound portal hypertension risks re-bleeding.
Medical management the reversal of coagulopathy using blood products is

paramount. Antidiuretic hormone (ADH) analogues (vasopressin, terlipressin) are
used to lower portal pressure, but can cause cardiac ischaemia and coagulopathy.
Somatostatin analogues given as an infusion (e.g. octreotide) are safer but reports of
efficacy are varied. Long-term non-selective -adrenergic receptor blocking agents can
decrease portal hypertension and re-bleeding.
Endoscopic therapy endoscopic injection of a sclerosing agent into varices causes

venous thrombosis and tissue fibrosis allowing about 85% of bleeds to be controlled.
Complications (ulceration, chest pain, mediastinitis) are common. Gastric lesions are
more difficult to inject and control than oesophageal varices. The use of rubber bands
to ligate varices is as effective as injection sclerotherapy with fewer complications.
Balloon tamponade using a balloon to exert direct pressure on the bleeding point
can control variceal bleeding. The SengstakenBlakemore tube has been replaced
by the Minnesota (oesophageal and gastric balloons and aspiration ports) (Figure 4)
and Linton (gastric balloon with oesophageal and gastric ports) tubes. Pressure on the
gastric veins feeding the varices seems to be more important than direct pressure on
the oesophageal varices. Limiting the duration of inflation and pressure is likely to be
important in preventing pressure necrosis of the oesophageal mucosa, but definitive
advice regarding the precise time to initiate balloon tamponade and the duration of
placement is difficult to find. Complications of balloon tamponade include:
incorrect placement
aspiration pneumonia
airway obstruction
oesophago-gastric rupture
tissue pressure necrosis.
Tamponade is successful in about 85% of cases, but re-bleeding occurs in about 45%
following balloon deflation. Successful tamponade should be followed by re-endoscopy
and further intervention as required.
Distal end of Minnesota tube
Aspiration ports
Oesophageal aspiration site

Balloon ports
Oesophageal balloon
Varices
Gastric balloon
Stomach
Gastric
aspiration port
Transjugular intrahepatic portosystemic shunt (TIPSS) using a catheter placed

via the jugular vein into the hepatic vein under radiological guidance, a stent can be
introduced to create an intrahepatic portosystemic shunt. This reduces portal blood
pressure and the risk of bleeding. Complications of TIPSS include intra-abdominal
haemorrhage, stent occlusion and hepatic encephalopathy. TIPSS has little impact on
long-term survival.
Surgery the control of bleeding can be achieved by staple transection of the

oesophagus or by forming a portocaval shunt. However, long-term survival is not
improved.
Lower gastrointestinal bleeding

Lower gastrointestinal bleeds are seldom immediately life-threatening. However, careful
resuscitation and monitoring are required.
Endoscopy electrocoagulation and heater probes can stop bleeding vascular points.
Bleeding polyps can be removed.
Angiography injecting embolizing agents into the vessel identified at angiography

can stop vascular bleeding points.
Surgery surgical removal of bleeding diverticular lesions or vascular abnormalities

is indicated when other measures have been unsuccessful. Surgery may also be
indicated if the source of bleeding is not identified.
Acute stress ulceration in ICU patients

Patients may present with peptic ulceration caused by pre-existing disease, as part of
their critical illness, or secondary to drug therapy (e.g. steroids or non-steroidal anti-
inflammatory drugs). In each case, an imbalance between mucosal protection and acid
production results. ICU patients are prone to acute stress ulceration, especially those
with sepsis, shock, burns, multiple trauma, head injury, spinal injury, respiratory failure,
renal failure or hepatic failure.
The incidence of acute stress ulceration has decreased but

remains about 20%. Presentation may be occult or overt, with lesions most commonly
found in the gastric fundus. Potential sequelae include:
cardiovascular collapse
anaemia (requiring blood transfusion)
increased urea load in the gut
aspiration of regurgitated or vomited gastric contents.
Prophylaxis and treatment

Significant bleeding should be managed as above. The incidence of stress ulceration is
lowered by prophylactic therapy aimed at alkalinizing the gastric contents (gastric pH >
3.5). However, ulceration can occur despite these measures and there is no guarantee
of reduced mortality. Alkalinization of the stomach contents may cause overgrowth of
gastric bacteria with the potential to lead to nosocomial pneumonia.
Supportive treatment includes optimizing oxygenation and perfusion.
Enteral feeding may reduce ulceration by improving local tissue perfusion and
maintaining local protective mechanisms.
Antacids (e.g. magnesium, aluminium) have to be given often to alkalinize the gastric
contents effectively. They can lead to ileus or diarrhoea and are seldom used.
H2-receptor antagonists (e.g. cimetidine, ranitidine, famotidine) act by blocking acid

production by the gastric parietal cells. Ranitidine is the most commonly used agent; it
can be given intravenously or via a nasogastric tube. The dose should be decreased for
patients with renal impairment.
Mucosal strengtheners sucralfate is a basic aluminium salt of sucrose octasulphate

that protects the gastric mucosa against acidity by adhering to the gastric mucosal
surface and increasing mucus production. It does not alter gastric acidity and
therefore causes no disruption to the normal gastric flora. Problems with its use
include constipation, aluminium toxicity and the formation of bezoar when mixed with
nasogastric feeds. Bismuth chelate may act in a similar way to sucralfate. It also helps
to eradicate Helicobacter pylori.
Proton-pump inhibitors (e.g. omeprazole, lanzoprazole) irreversibly inhibit the H +/K+ -

ATPase (proton pump) enzyme to reduce the amount of H + transported to the gastric
lumen by the parietal cells.
Other drugs antibiotics may be used to eradicate H. pylori. Misoprostol, a

prostaglandin E1 analogue, helps to decrease acid production and improve healing but
causes diarrhoea and can only be given orally. u
FURTHER READING
Galley H F. Critical Care Focus Vol 9 The Gut. London: BMJ Publishing, 2002.
Oh T E. Intensive Care Manual. Oxford: Butterworth-Heinemann, 1997.

Generalized Convulsive Status
Epilepticus
George Thomas
Nicholas Hirsch
George Thomas is Specialist Registrar at the National Hospital for Neurology and
Neurosurgery, London. He qualified from Manipal, India, and trained in anaesthetics in
Manipal, University College London and the Royal Free Hospital. His interests include
neurosurgical anaesthesia and chronic pain.
Nicholas Hirsch is Consultant Anaesthetist at the National Hospital for Neurology and
Neurosurgery, London. He is Director of the Neuromedical Intensive Care Unit and has
a special interest in respiratory failure due to neurological disease.
Generalized convulsive status epilepticus (GCSE) is the most common form of status
epilepticus and affects about 14,000 people annually in the UK. It is a medical emer-
gency and failure to recognize and treat it effectively results in major morbidity
and mortality. It is traditionally defined as continuous seizure activity lasting 30 minutes
or intermittent seizure activity lasting 30 minutes during which consciousness is not
regained.
Clinical features: GCSE is usually diagnosed easily by observation alone and is

characterized by unconsciousness, tonic-clonic muscle activity, tongue biting and
urinary incontinence. However, as the duration of seizure activity increases, clinical
signs of abnormal muscular activity may become subtle (e.g. restricted to minor
twitching of the fingers or eyelids). There is seldom doubt about the diagnosis, but
other conditions that should be considered include rigors due to sepsis, myoclonic
jerking, generalized dystonia and pseudostatus epilepticus.
Aetiology: determining the aetiology of GCSE is of fundamental importance and may

be divided into acute and chronic processes (Figure 1). In 50% of cases of GCSE
presenting to non-specialized centres, status epilepticus is the first manifestation of
epilepsy. The aetiology also affects the prognosis of GCSE.
Aetiological factors of GCSE
Acute processes Chronic processes

Electrolyte disturbance Pre-existing epilepsy
(e.g. sodium, calcium imbalance) Poor anti-epileptic drug compliance
CNS infection Alcoholism (especially withdrawal)
(e.g. encephalitis, meningitis) Cerebral space-occupying lesion
Cerebral trauma
Cerebrovascular accident
Drug toxicity
(e.g. alcohol, cocaine)
Hypoxic cerebral damage
Generalized sepsis
Renal failure
1
Pathophysiology: two distinct phases with specific neurophysiological changes occur

during the progression of GCSE. In phase I, the increased metabolic requirements of
abnormally discharging neurons are adequately met. The increased cerebral
activity results in a coupled increase in cerebral blood flow and an increase in
autonomic activity. The latter results in tachycardia, hypertension and an increase
in blood glucose levels. After about 30 minutes of seizure activity, the compensatory
mechanisms that have maintained adequate cerebral perfusion begin to fail. This stage
(phase II) is characterized by a failure of cerebral autoregulation, a rise in intracranial
pressure, systemic hypotension, hypoglycaemia and a rise in systemic and intracranial
lactate levels. When this occurs, cerebral oxygen requirements exceed supply and
electromechanical dissociation occurs in which cerebral seizure activity may be
accompanied by minimal visible muscular twitching.
The disruption of normal cerebral physiology is further compounded by many of the

systemic derangements that are seen during GCSE. These include CNS pathology
(cerebral anoxia, haemorrhage, oedema, hippocampal damage, cerebral venous
thrombosis), respiratory system pathology (respiratory failure, pneumonia, pulmonary
hypertension, pulmonary oedema, pulmonary embolus), cardiovascular system
pathology (arrhythmias, hyper/hypotension, myocardial infarction, cardiac arrest),
metabolic disorders (electrolyte imbalance, metabolic acidosis, hyperpyrexia, renal and
hepatic failure, acute pancreatitis) and other complications (rhabdomyolysis, fractures,
sepsis syndromes, disseminated intravascular coagulation).
Management
GCSE requires decisive and rapid treatment. The longer GCSE continues, the greater
the likelihood of neuronal damage, systemic complications, unresponsiveness to
treatment and the development of chronic epilepsy. The mortality of GCSE is also
related to its duration. Management falls into three categories that need to be instituted
simultaneously:
emergency medical management
identification and investigation of aetiological factors that have precipitated status
epilepticus
drug treatment of the seizures.
Emergency medical management

Monitoring of ECG, blood pressure and pulse oximetry should be started immediately.
Generally, patients in GCSE require early tracheal intubation and mechanical
ventilation to protect the airway from aspiration of gastric contents and to ensure
adequate ventilation and oxygenation while seizures are being controlled. A rapid
sequence induction of anaesthesia should be performed using thiopental
(thiopentone) or propofol followed by suxamethonium. Before induction, intravenous
access is often required to allow fluid resuscitation. The administration of fluids is often
all that is needed to restore normotension, but patients who have experienced
prolonged status epilepticus may also require inotropic therapy. Blood pressure should
be maintained at normal or supranormal levels to ensure an adequate cerebral
perfusion pressure. Following intubation, the use of long-acting non-depolarizing
neuromuscular blocking drugs is seldom necessary and obscures the clinical
manifestations of continuing seizure activity.
Blood should be taken for determination of electrolytes, full blood count, blood
glucose, toxicology screen, liver function tests and arterial blood gas analysis. Patients
with pre-existing epilepsy should have their anti-epileptic drug levels measured.
A bedside test for glucose should be performed immediately and, if hypoglycaemia is

present, 50% glucose, 50 ml, should be given. The theoretical danger of exacerbating
cerebral ischaemia by an increased blood glucose level is outweighed by the correction
of hypoglycaemia. If there is evidence of alcoholism or malnutrition, intravenous
thiamine, 100 mg, should be given before administration of glucose to avoid
precipitating Wernickes encephalopathy.
Metabolic acidosis is common during uncontrolled status epilepticus, but acidbase

balance is usually restored with control of seizures and with adequate resuscitation.
There is experimental evidence that acidosis in GCSE may be neuroprotective.
High temperatures may occur in status epilepticus due to the increased muscle activity
and may exacerbate or prolong seizure activity. Where possible, normal body tempera-
ture should be maintained using surface cooling and antipyretic agents.
Identification and investigation of aetiological factors

A careful history often provides a clue to the aetiology of the status epilepticus (e.g. a
known epileptic who has failed to take his medication, an alcoholic who has been on a
binge, a patient with a previously diagnosed cerebral tumour). Similarly, a general and
neurological examination of the patient often reveals a systemic or neurological cause of
the seizures. Further investigations (e.g. CT, MRI, examination of CSF, blood cultures)
may be required.
Drug treatment of seizures

Drug treatment of seizures must be instituted early and should proceed during
resuscitation. All anti-epileptic drugs used in the treatment of status epilepticus are
sedative and their effect on the conscious level of the patient needs to be monitored
closely. There have been few well-conducted trials of the optimum treatment for GCSE,
however, Figure 2 shows a widely used and accepted regimen.
Treatment algorithm for status epilepticus
Urea and electrolytes

Full blood count
Cardiopulmonary resuscitation, Creatine kinase
monitoring i.v. access, Glucose
blood samples, check glucose LFTs, Ca2+, PO4-
Mg2+
Toxicology
Lorazepam
0.1 mg/kg i.v. at < 2 mg/min
Seizures and Yes

their cause rapidly
corrected?
30 minutes
No
Phenytoin
20 mg/kg i.v. at < 50 mg/min
or
Fosphenytoin
20 mg phenytoin equivalent/kg
i.v. at < 150 mg/min
Maintain recovery
position in a
Seizures Yes
safe environment
terminated? while conscious
No level improves
Phenytoin
further doses of 510 mg/kg i.v.
up to total 30 mg/kg
or
Fosphenytoin
510 mg phenytoin equivalent/kg
i.v. up to 30 mg phenytoin
equivalent/kg
Seizures Yes
terminated?
No
Intensive care
setting or major Yes General anaesthesia
systemic propofol or thiopental
disturbance? (thiopentone)
No
Phenobarbital (phenobarbitone)
1020 mg/kg i.v. at < 50 mg/min
may give additional 510 mg/kg i.v.
Seizures No
terminated?
2
Benzodiazepines act by enhancing -aminobutyric acid (GABA)-mediated inhibition

in the CNS by increasing chloride conductance at the post-synaptic ligand-gated
GABAA receptor. Lorazepam, 0.1 mg/kg i.v., is the benzodiazepine of choice in GCSE.
Although it is less lipophilic than diazepam, it terminates seizures as rapidly as the
latter. Its main advantage is its long duration of action (over 12 hours) and it is often
effective as the sole agent in terminating GCSE. In contrast, diazepam has a short
duration of action due to rapid redistribution to body fat stores and is less effective than
lorazepam.
Hydantoins (phenytoin and fosphenytoin): if seizures continue following

administration of lorazepam, phenytoin, 20 mg/kg i.v., is the drug of choice as a
second-line treatment. It acts by blocking neuronal sodium channels and inhibiting
repetitive firing of neurons. The range of normal therapeutic plasma levels is
4080 g/litre.
Phenytoin should be given only via a large vein, because of its high alkalinity. It should
be made up in saline and concurrent administration of other drugs should be avoided
because of the risk of precipitation. The maximum rate of infusion is 50 mg/minute, but
even lower rates carry the risk of hypotension and arrhythmias. Meticulous monitoring
of ECG and blood pressure is mandatory.
Fosphenytoin is a recently introduced water-soluble prodrug of phenytoin and its dose
is expressed in phenytoin equivalence (75 mg of fosphenytoin is labelled 50 mg
phenytoin equivalent). Its main advantage over phenytoin is that it can be administered
more rapidly. However, serious cardiovascular sequelae may occur and careful
monitoring during and after administration is vital.
Phenobarbital (phenobarbitone): if seizures persist despite adequate plasma levels

of phenytoin, phenobarbital (phenobarbitone), 1020 mg/kg i.v., should be given. This
barbiturate acts on a receptor site associated with GABAA chloride channels. Its main
side-effects include excessive sedation, respiratory depression and hypotension.
General anaesthesia: refractory status epilepticus that has not responded to

hydantoins and/or phenobarbitone requires general anaesthesia using either
thiopental (thiopentone) or propofol. This should be carried out in a specialist unit
where the anaesthetic agents can be titrated against continuous EEG monitoring.
Most authorities aim for a burst suppression pattern on EEG though evidence that
outcome is improved is sparse. Optimum levels of phenytoin and phenobarbital
(phenobarbitone) should be maintained during this period. Patients are intermittently
woken while being monitored for evidence of clinical or electroencephalographic
seizures.
Prognosis
Adult GCSE carries an overall mortality of about 25%. Over 85% of those who die do
so as a result of the aetiology of the status epilepticus; only about 2% of deaths are
due to the GCSE itself. The aetiology also determines outcome; 90% of patients with
status epilepticus secondary to drug withdrawal have a good outcome compared with
only 30% of patients with status epilepticus due to stroke. Duration of seizures is also
an important factor; GCSE lasting over 1 hour has a mortality of 35% while seizures
lasting less than 30 minutes have a mortality of 3.7%. u
FURTHER READING
Chapman M G, Smith M, Hirsch N P. Status epilepticus. Anaesthesia 2001; 56: 648
59.
Shorvon S. Management of Status Epilepticus. J Neurology Neurosurgery Psychiatry

2001; 70(Suppl 2): 227.

Immune Dysfunction,
Immunodeficiency and
Immunotherapy
Jonathan B Salmon
Jonathan B Salmon is Consultant Physician at the John Radcliffe Hospital, Oxford,

UK. He qualified from Cambridge University and the Middlesex Hospital, London,
and trained in general medicine and intensive care in the army and at UCL Hospitals,
London.
Critical illness produces multiple defects in immune function with impairment of all
components of the immune response. The most common cause of death in patients
who have been in the ICU more than 7 days is sepsis. Particular care is required in
patients who are immunosuppressed; the emphasis should be on prevention, early
detection and aggressive treatment of infection. Although these patients have a worse
prognosis than immunocompetent patients, it is not hopeless. However, those who
require prolonged intubation and ventilation without return of immune function almost
invariably die.
Immune dysfunction due to critical illness

Intravascular catheters and tracheal tubes bypass the normal barriers to infection.
Mucosal barrier function may be reduced by ischaemia, trauma or ulceration. Sedation,
recumbency, acid suppression and antibiotic use contribute to pooling of secretions,
bacterial overgrowth and selection of resistant organisms.
Immune function, particularly cell-mediated immunity and neutrophil function, is

depressed following shock or trauma and may persist for days or weeks. Causes
include poor nutrition, direct effects of the inflammatory response on immune function,
drugs, and metabolic and endocrine effects, particularly uraemia and hyperglycaemia.
Specific immunodeficiencies
Most immunodeficient patients in ICU have acquired rather than congenital disease.
The most important clinical groups are neutropenia, T cell deficits (including HIV), and
broad-spectrum immunodeficiency related to haematological or other malignancy,
chemotherapy and the post-transplant patient. Less important (but significant) are
hypogammaglobulinaemias, splenectomy and complement deficiencies. Patients may
have more than one immune defect (e.g. lymphoma causing T cell dysfunction and
cytotoxic-induced neutropenia).
Neutropenia occurs following decreased production, increased use or decreased

survival of neutrophils. It is considered mild if the total neutrophil count is 11.8 x 109 /
litre, moderate if 0.51.0 and severe below 0.5.
Acquired neutropenia is usually caused by viral infections or drugs but severe bacterial
sepsis is an important cause (Figure 1). Automated blood analysers may occasionally
read falsely low neutrophil counts and unless neutropenia is an expected part of the
patients illness, a blood film should be checked to confirm the count.
Causes of acquired neutropenia
Infection
Viruses (influenza)
Severe sepsis (damage to myeloid precursors and adherence of
neutrophils to endothelium)
Chronic infections (splenic sequestration, brucella, kala-azar, malaria,
tuberculosis)
Drugs
Direct toxicity
Dose related (cytotoxic drugs)
Idiosyncratic (chloramphenicol, carbimazole, phenothiazines work by
enzyme blockade; usually presents within 12 weeks and resolves
over similar period)
Immunogenic
Antibody to complex between drug neutrophil surface proteins
(phenytoin, chlorpropamide, levamisole, clozepam; reversible within
2 weeks of stopping drug)
Marrow infiltration/obliteration
Tumour infiltration, radiation damage, myelofibrosis, osteosclerosis
Nutritional defects
Protein malnutrition, B12 or folate deficiency, copper or zinc deficiency
Auto-immune
Idiopathic or associated with other autoimmune disease
Neutrophil autoantibodies
Rheumatoid arthritis, systemic lupus erythematosus, Feltys syndrome
Splenomegaly
Sequestration (chronic infections (as above), Gauchers disease,
sarcoidosis, lymphoma; usually associated with low haemoglobin and
platelet count)
Haemodialysis
Lung sequestration
Functional disorders
Chronic granulomatous disease
Decreased phagocytic function (many systemic diseases e.g.
diabetes mellitus, uraemia, malnutrition, alcohol abuse, steroids)
1
Qualitative or quantitative defects in neutrophil function lead to impaired bacterial and

fungal killing. Bacterial infections predominate initially. Traditionally, Gram-negative
infections have been the most common and remain the most lethal. 50% of neutropenic
patients with Pseudomonas bacteraemia die within 24 hours unless treated. With
increasing use of long-term intravascular cannulae and prophylactic antibiotics, Gram-
positive organisms are more common and account for over 50% of isolates in febrile
neutropenia. With increasing duration of neutropenia, fungal infections become more
common.
Prevention of infection scrupulous attention to hygiene and isolation in side-rooms

with positive pressure and, preferably, high efficiency particulate air (hepa) filtration
are important. Cross-infection rates increase as the staff:patient ratio falls, particularly
when infectious and immunosuppressed patients are being cared for by the same
personnel. As antibiotic resistance increases, these precautions become more vital.
Diagnosis the symptoms and signs of sepsis may be subtle or absent. Fever may be
the sole indicator of infection. However, absence of fever or hypothermia does not rule it
out.
Consider why the patient is neutropenic and for how long. What symptoms are there
to suggest a source of infection? Was the infection acquired in the community or in
hospital? Has the patient had previous infections? Are there any relevant, contributory
drugs?
Examination is often unrewarding but should be thorough with particular attention to

head and neck, pharynx, ears, optic fundi, chest, abdomen, skin and perineum.
Investigations should include full blood count and film, routine biochemistry (including
liver function), cultures of blood, urine, stool if there is diarrhoea and aspirates from
vesicles or pustules. Sputum is unreliable; bronchoscopic lavage should be performed if
respiratory infection is likely (or blind broncho-alveolar lavage if the patient is intubated).
Any suggestion of intracranial pathology should prompt a CT of the brain followed by
lumbar puncture. Chest radiographs should be performed routinely. Consider sinus
radiographs (but CT is better). CT of chest, abdomen and pelvis may be required if
there are no obvious clinical clues.
Treatment if the neutrophil count is less than 0.5 x 109 /litre or there is haemodynamic
compromise or organ dysfunction, empirical treatment should be started with broad-
spectrum antibiotics. If the neutrophil count is more than 0.5 x 109 /litre and the patient is
well, relevant cultures should be performed and the patient observed closely. Antibiotics
should be directed primarily at Gram-negative organisms (especially Pseudomonas) but
the choice of antibiotic should be discussed, at the time, with the microbiology service,
unless there is a unit protocol. Treatment for Gram-positive organisms can usually
be delayed pending culture results unless the patient is unwell or there is high clinical
suspicion. Meropenem or Tazocin an aminoglycoside often suffices. Metronidazole
should be added if there is severe mucositis, necrosing gingivitis, perianal tenderness
or abdominal pain.
If fever persists and cultures are negative, re-evaluation is required. The empirical
addition of vancomycin or teicoplanin is required to cover Gram-positive infections,
many of which are due to cell-wall-deficient organisms, which do not survive
conventional culture techniques. With appropriate antimicrobial treatment, the mean
time to defervescence is 5 days. Empirical antifungal treatment should be considered in
patients who remain febrile after this.
It is common to continue antibiotics until the neutrophil count recovers (often 14 days)
but this increases the risk of fungal and resistant bacterial infections. It may be safe and
produce fewer complications if antibiotics are stopped 35 days after defervescence,
provided the patient is monitored closely.
Fungal infections about 30% of patients who fail to respond to antibiotics have
Candida or Aspergillus infection. Fluconazole has few side-effects and is active
against Candida albicans and Cryptococcus spp. but is ineffective against some other
Candida species and Aspergillus. Amphotericin B has been the mainstay of treatment
for these latter organisms but its side-effects include fever, rigors, hypotension and,
especially, nephrotoxicity. Lipid-based preparations are less toxic but more expensive.
Caspofungin and Voriconazole, new antifungals with a broad spectrum of activity and
apparently a better safety profile, are promising.
Viruses herpes simplex, zoster, cytomegalovirus (CMV) and adenovirus infections

are common in neutropenia, especially if there is co-existent depression of cell-
mediated immunity. Treatment is described below.
Deficiency of cell-mediated immunity: worldwide, the most common cause of T cell

deficiency is HIV infection, although in
the UK, antiretroviral drugs have reduced its impact. Immunosuppressive treatments
(e.g. corticosteroids, ciclosporin (cyclosporin)) are also important causes. Infections are
most common with intracellular pathogens (Mycobacteria spp., Listeria), viral infections,
fungi and parasites.
Mycobacteria Mycobacterium tuberculosis usually occurs due to re-activation of old

infection. It is common in myelodysplasia, chronic lymphocytic leukaemia and hairy
cell leukaemia. Presentation is often atypical, progress rapid and extrapulmonary
and disseminated infections are common. Non-tuberculous mycobacteria (especially
Mycobacterium avium-intracellulare and kansasii) are more common in HIV.
Viral infections are common, particularly herpes simplex, zoster, CMV and
adenoviruses. Hepatitis B, EpsteinBarr virus and papillomavirus may cause problems.
Measles can cause life-threatening infections, especially in children. Herpes simplex
and zoster are usually responsive to aciclovir but some simplex isolates are now
resistant. Foscarnet is usually effective, but is toxic (renal impairment in 50%).
Ganciclovir remains first-line treatment for CMV; some resistance is emerging and
foscarnet is an alternative treatment for CMV retinitis in AIDS. Mortality remains
high, especially in CMV pneumonitis. Susceptible patients exposed to measles or
herpes zoster should receive passive protection with human normal immunoglobulin
or varicella-zoster immunoglobulin, respectively. Live-attenuated vaccines should not
be used (nor should live-attenuated polio vaccine be given to siblings of susceptible
patients because of the risk of intrafamilial transmission).
Fungi superficial fungal infections are uncommon (except oropharyngeal candidiasis

in HIV) but deep-seated or disseminated infections occur due to organisms such as
Histoplasma capsulatum. Cryptococcal infections are uncommon except in HIV or in
patients on high-dose corticosteroids.
Parasitic infections include pneumocystis, toxoplasma and cryptosporidiosis. More

rarely, re-activation of malaria, strongyloidiasis or babesiosis may occur.
Pneumocystis pneumonia (PCP) usually presents as progressive respiratory failure

with characteristic widespread pulmonary crackles and alveolar shadowing on a
chest radiograph. First-line treatment is high-dose co-trimoxazole, 120 mg/kg/day.
Steroids are beneficial if pneumonia is severe. Toxoplasmosis often presents as a CNS
infection with multiple space-occupying lesions; pyrimethamine/sulphadiazine is usually
effective.
Cryptosporidiosis presents as non-resolving diarrhoea. The organism is naturally

resistant to most antibiotics and treatment is mainly symptomatic.
The diagnostic approach, initial cultures and imaging are similar to those for
neutropenia but the search for infection must be more extensive. As well as routine
surveillance cultures, CSF, bone marrow and tests for specific parasites (e.g.
strongyloidiasis) should be considered if past exposure is possible.
Other causes of immunodeficiency

Hypogammaglobulinaemia occurs in common variable immunodeficiency (congenital,
but mainly presents in the third decade). Functional hypogammaglobulinaemia may
occur in multiple myeloma and chronic parasitic infections (e.g. trypanosomiasis).
Patients present with recurrent respiratory and gastrointestinal infections.
Complement deficiency leads to recurrent pyogenic infections. Recurrent

meningococcal or overwhelming pneumococcal infections may occur. Systemic lupus
erythematosus is the most common cause of acquired complement deficiency.
Splenectomy is followed by an annual risk of serious sepsis of 0.51%. The risk

diminishes over time, but is never eliminated. Functional asplenia (e.g. sickle cell
disease) carries similar risks. Streptococcus pneumoniae is the most common
organism (66% of cases). Haemophilus influenzae and Escherichia coli are also
important, as is malaria, which may be fulminant. Patients should receive long-term
antibiotic prophylaxis and immunization against S. pneumoniae and H. influenzae.
Infections in transplant patients these patients are at particular risk, not only do
they have the underlying disease that made transplantation necessary, those who
have had solid organ transplantation have suffered a major surgical insult followed by
powerful immune suppression. Bone marrow transplant patients have a particularly
intense immunosuppression: before transplantation they undergo ablative treatment
leading to absent immune function. However, provided they survive the acute period,
the transplanted marrow gradually recovers and much of its immune function is
regained.
Organ support in immunodeficiency management of organ failures in

immunosuppressed patients is no different from that in patients with preserved immune
function.
Immunotherapy
Attempts to modulate the immune response in critically ill patients have been
disappointing. Broad-spectrum immunosuppression with corticosteroids at various
doses has produced no convincing benefit (and possible harm at high doses). Specific
treatments of individual components of the inflammatory response using monoclonal
antibodies have failed to show benefit. The exception is activated protein C, primarily
an antithrombotic agent with anti-inflammatory properties which appears to produce an
absolute reduction in mortality in severe sepsis.
Other forms of immunotherapy, including intravenous immunoglobulin and, to a lesser

extent, plasma exchange have been effective in a limited number of conditions such
as GuillainBarr syndrome and thrombotic thrombocytopenic purpura, respectively.
Colony-stimulating factors have been shown to reduce the duration of neutropenia in
non-critically ill, haematology patients but have not been shown to produce a clear
reduction in mortality. There is no evidence that they are effective in the critically ill. u

The Intensive Care
Management of Acute Severe
Asthma
Kathleen Nolan
Kathleen Nolan is Consultant in Anaesthesia and Intensive Care at Southampton

General Hospital, Southampton, UK.
In Western industrial countries, asthma affects about 5% of adults and 1015% of

children. Its prevalence, severity, and mortality are rising, due to a redefinition of
diagnostic criteria and increased exposure to allergens and atmospheric pollutants.
Asthma is characterized by partially reversible airway obstruction, airway
inflammation and airway hyperresponsiveness.
The diagnosis is often made clinically on a history of episodes of reversible
airflow obstruction, often precipitated by factors such as environmental allergens, viral
respiratory infections, irritants, drugs or food additives, exercise and cold air.
Pathophysiology
The primary defect in asthma is airflow obstruction with resultant lung
hyperinflation and increased work of breathing and oxygen consumption.
Eventually, hyperinflation cannot be maintained and there is a reduced total lung
capacity, airway closure, alveolar hypoventilation and deteriorating gas exchange.
Bronchial obstruction causes a low ventilation:perfusion (V/Q) ratio, while alveolar
overdistension raises the ratio; these lead to hypoxaemia and an increase in dead
space.
Pulmonary artery pressure rises owing to hypoxic pulmonary vasoconstriction and
the pressure of overdistended alveoli on pulmonary vasculature. High pulmonary artery
pressures may impair right ventricular performance and cause leftward displacement
of the interventricular septum and impaired left ventricular function. Pulmonary oedema
may occur, due to left ventricular dysfunction, or the high negative intrathoracic
pressures generated to overcome severe airway obstruction.
Signs and symptoms

The typical signs and symptoms of an acute asthma attack are listed in Figure
1. Risk factors for death include a long history of the disease in young to
middle-aged patients, previous life-threatening attacks or hospitalizations, delay
in obtaining medical aid, and sudden onset with a rapidly progressive course.
Criteria for admission to ICU include:
deteriorating peak flow, worsening or persisting hypoxia, or hypercapnia
exhaustion, feeble respiration, confusion, or drowsiness
coma or respiratory arrest.
On physical examination, there is hyperinflation, accessory muscle use (in
inspiration and expiration) and widespread wheeze. Patients with acute asthma usually
have a combination of hypoxaemia, hypocapnia and respiratory alkalosis on arterial
blood gas analysis. A normal or increased partial pressure of carbon dioxide in arterial
blood (PaCO2) is a danger sign, although observing the trend in PaCO2 is more
useful. Monitoring should include continuous ECG and oximetry, frequent estimations
of respiratory rate, level of consciousness, blood pressure, temperature and peak
expiratory flow rate measurements. Regular examinations of the chest should evaluate
air entry, accessory muscle use and evidence of subcutaneous emphysema.
Indicators of a severe asthma attack1
Potentially life-threatening features

Unable to complete sentences in one breath
Respiratory rate > 25 breaths/minute
Heart rate > 110 beats/minute
Peak expiratory flow rate < 50% of predicted normal or if best normal if
known
Peak expiratory flow rate < 200 litre/minute if best normal not known
Immediately life-threatening features

Peak expiratory flow rate < 33% of predicted normal or best normal if known
Silent chest, cyanosis, or feeble respiratory effort
Bradycardia or hypotension
Exhaustion, confusion, or coma
1
Statement by the British Thoracic Society, 1997.
Treatment
Initial treatment is directed at the relief of bronchospasm and airway inflammation, using
oxygen, 2-adrenergic agonists, corticosteroids and other agents (Figure 2).
Oxygen almost all patients have hypoxaemia during acute exacerbations of
asthma. Humidified oxygen is administered in high concentrations as determined by
pulse oximetry (SpO2) or arterial blood gas analysis.
-sympathomimetic agents the inhaled 2-adrenergic agonists (salbutamol,
terbutaline) have a rapid onset of action and are the first-line treatment for the relief
of bronchoconstriction. Salbutamol has more side-effects including hyperglycaemia,
hypokalaemia and lactic acidosis. One empirical approach is to start nebulized 2-
agonists as first-line treatment and then to use the intravenous form if the response is
poor or the patient is moribund.
Corticosteroids are the most effective treatment for chronic inflammation of
asthma. The peak response occurs 612 hours after an intravenous dose. Intravenous
corticosteroids should be given early and continued until the life-threatening phase is
over; oral and inhaled corticosteroids are then appropriate.
Anticholinergic agents block muscarinic receptors, inhibit vagal tone and promote
bronchodilatation. They are medium potency bronchodilators and produce substantively
less bronchodilatation than sympathomimetics. Nebulized ipratropium is indicated when
asthma is severe on presentation, or when 2-adrenergic agonist therapy fails.
Intravenous aminophylline is regarded as a second-line drug because of its
narrow therapeutic range and high incidence of side-effects (cardiac arrhythmias and
seizures). Its mechanism of action is unclear, because at therapeutic concentrations
phosphodiesterase inhibition is minimal and bronchodilatation is weak There are wide
variations in the elimination of aminophylline and plasma concentrations should be
checked regularly. The dose is reduced in the elderly and those with hepatic or cardiac
disease.
Medical therapy for life-threatening acute asthma1
Oxygen
Use the highest concentration available and set a high flow rate
High-dose inhaled 2-agonists
Salbutamol, 5 mg, or terbutaline, 10 mg, nebulized with oxygen or with a
metered dose
inhaler into a large spacer devise (two puffs 1020 times)
High-dose systemic corticosteroids
Prednisolone, 3060 mg orally, or hydrocortisone, 200 mg i.v., or both,
immediately
If life-threatening features are present
Add ipratropium, 0.5 mg, to the nebulized 2-agonist
Give aminophylline, 250 mg i.v. over 20 minutes, or salbutamol, 250 g i.v. over
10 minutes. Continue with infusion. Do not give bolus aminophylline to patients
already taking oral theophyllines
1
Statement by the British Thoracic Society, 1993.
MechanIcal ventilation
13% of patients admitted to hospital with acute asthma require intermittent positive-
pressure ventilation (IPPV). It is indicated in asthmatic patients who exhibit:
decreasing or decreased level of consciousness
decreasing PaO2
increasing PaCO2
increasing arterial paradox (fall in systolic blood pressure on inspiration)
increasing heart rate
increasing respiratory rate
decreasing peak expiratory flow rate
decreasing ability to speak.
Even patients presenting with gross hypercarbia may be managed without IPPV, if
medical therapy produces rapid improvement. In contrast, a patient with a low but rising
PaCO2 may require IPPV. Other indicators of the severity of an attack will aid decision
making (Figure 1).
At the time of intubation, patients with severe asthma are often tachycardic,
tachypnoeic, hypoxic, hypercarbic, acidotic, hypovolaemic and hypokalaemic. Unless
a difficult intubation is anticipated, rapid sequence induction is appropriate. For
potentially difficult intubations, inhalation induction (sevoflurane in oxygen), or an awake
blind nasal or fibre-optic intubation with topical anaesthesia may be used. Following
intubation, the patient should be given sedatives and, if necessary, muscle relaxants;
control mode ventilation is preferable. The chosen ventilatory mode should achieve
adequate oxygenation and ventilation at the lowest possible airway pressures, thereby
minimizing the risk of barotrauma. This involves the delivery of low tidal volumes (68
ml/kg) at a slow rate (< 10 cycles/minute), aiming to keep peak airway pressures below
35 cm H2O. A prolonged expiratory phase is preferred (I:E 1:21:4). Hypercapnia is
tolerated (PaCO2 up to 15 kPa) in the belief that it is less harmful than barotrauma.
Severe ventilationperfusion mismatch may be improved using bronchial lavage to
remove mucous plugs and, more controversially, positive end expiratory pressure.
Complications of IPPV in asthma are related to barotrauma (e.g. pneumothorax,
pneumomediastinum, subcutaneous emphysema) or cardiac depression (e.g.
hypotension).
Additional bronchodilators
Inhalation anaesthetics treatment of ventilated asthmatics with volatile
inhalational agents often reduces peak airway pressures and improves arterial blood
gases. Halothane (0.53.0%) has a low therapeutic ratio in the acidotic, hypovolaemic
patient and its prolonged use is associated with bromide toxicity. Isoflurane (0.53.0%)
is safer and probably as effective. Adequate gas scavenging facilities must be available
in the ICU.
Intravenous anaesthetics ketamine, infusion 1040 g/kg/minute, is a potent
bronchodilator. It increases catecholamine levels and directly relaxes bronchial
smooth muscle, however, it is not licensed for use as a sedative or bronchodilator.
Magnesium sulphate anecdotal evidence suggests that magnesium sulphate
provides useful bronchodilatation, however, this is not confirmed by controlled studies.
Helium-oxygen mixtures the inclusion of helium, a low density gas, in inhaled
gas mixtures lowers airway resistance and decreases respiratory work.
Nitric oxide is a short-acting, endogenous vasodilator and bronchodilator. Its
bronchodilatory may be useful.
Weaning: the duration of IPPV in acute severe asthma varies considerably.

Complications of mechanical ventilation, such as barotrauma and infection, tend to
prolong the duration of ventilation and may be associated with reduced survival.
Reversal of bronchospasm is indicated by the absence of wheeze, and a fall in peak
inflation pressures, dynamic compliance or the alveolar to arterial oxygen difference.
Mortality in asthma patients undergoing IPPV: reported rates are as high as

38%, but include cases of brain injury from cardiorespiratory arrest prior to ventilatory
support. In over 10,000 children with acute asthma, 27 (0.3%) needed IPPV. The single
death associated with asthma and IPPV represents 4% of ventilated cases. Death
in asthmatics receiving IPPV usually results from barotrauma, hypotension, cardiac
arrhythmias or sepsis.
Extracorporeal support
There are several reports of extracorporeal lung assist (ECLA) in severe asthma. With
modern ICU management, acute severe asthma has such a low mortality that the
additional survival afforded by ECLA is probably marginal.
Outcome
An increase in the mortality rate from asthma has been observed despite improvements
in pathophysiological findings and the introduction of new effective therapeutic agents.
Patients who have previously required ICU admission and IPPV are at significant risk
during subsequent exacerbations of asthma.

Intensive Care Management of
Pulmonary Embolism
Brid McGrath
Simon J Fletcher
Brid McGrath is a final year Senior Registrar at the Norfolk and Norwich Hospital,
Norwich. She has an interest in intensive care and teaching.
Simon J Fletcher is Consultant in Anaesthesia and Intensive Care at the Norfolk and
Norwich Hospital. He qualified from Guys Hospital, London, and subsequently trained
at St Thomas Hospital, London, University of Mayland, Baltimore, USA, Norwich, and
Addenbrookes Hospital, Cambridge.
Incidence and natural history

Pulmonary embolism is not an isolated disease of the chest but a complication of
venous thrombosis. Determining the true incidence of pulmonary emboli is problematic
because the presentation is often silent or clinically ambiguous, the diagnosis is difficult,
and the intensity of post-mortem examination for pulmonary embolism varies.
The incidence in the USA is estimated to be at least 500,000 per year with a
mortality rate of 10%. The incidence is highest in those undergoing emergency surgery
following trauma (e.g. hip fractures) and pelvic surgery. Following total hip replacement,
5% of elderly patients develop a pulmonary embolism; nearly half of these cases
are fatal. Clinical presentation ranges from the haemodynamically stable patient with
pleuritic chest pain to the patient presenting with no cardiac output. The fatality rate is
less than 5% in treated patients who are haemodynamically stable at presentation but
about 20% in those with persistent hypotension. The mortality from massive pulmonary
embolism is high and many patients die before treatment can be initiated. Greater
emphasis on prophylaxis is needed if mortality and morbidity are to be reduced in those
presenting with cardiorespiratory arrest or severe hypotension.
Pathogenesis
Pulmonary emboli occur as a result of thrombi at a distal site, therefore it is important to
consider the whole disease process. Most thrombi form at the site of venous valves in
the calf and most of them resolve spontaneously (80%). The other 20% of calf thrombi
extend proximally to the ilio-femoral veins. Thrombi that remain confined to the calf
pose little risk of embolization, while thrombi in the ilio-femoral systems pose a 50%
risk of embolization.
Over 90% of pulmonary emboli originate from the lower extremities. Less
common causes of embolization include, axillosubclavian thrombosis, which may occur
spontaneously or be related to indwelling central venous catheters. Septic emboli may
develop from infected peripheral thrombi; common in intravenous drug abusers.
Pathophysiology
When venous thrombi become dislodged from their site of formation they travel
proximally to the heart and lodge in the pulmonary arterial tree. A large
embolus will settle at the bifurcation of the pulmonary artery, forming a saddle
embolus, which is invariably fatal. The effects of an embolus depend on:
the extent of pulmonary vascular obstruction
the pre-existing function of the cardiopulmonary system
the time over which the obstruction accumulates.
If an embolus obstructs less than 50% of the pulmonary circulation, it may cause
no symptoms in a previously fit patient, but cause compromise in a patient with pre-
existing cardiopulmonary disease. When more than 50% of the pulmonary circulation
is suddenly occluded the patient presents with haemodynamic instability ranging from
hypotension to cardiorespiratory arrest.
Obstruction of the pulmonary vascular bed acutely increases right ventricular
afterload. The thin-walled right ventricle is designed to work against a low resistance
pulmonary circulation and hence functions poorly against a sudden increase
in pulmonary vascular resistance. As the right ventricle dilates it pushes the
interventricular septum to the left, impeding filling of the left ventricle compounding the
fall in cardiac output. The fall in aortic pressure and the rise in right ventricular pressure
may cause ischaemia of the right ventricle due to coronary hypoperfusion. The cardinal
pulmonary effect is altered gas exchange. The main causes are:
ventilationperfusion mismatch normal parts of the lung become overperfused but
have inadequate ventilation to oxygenate the extra blood flow fully
low mixed venous oxygen saturation caused by decreased cardiac output
accentuates hypoxaemia because there is insufficient time for the desaturated blood to
become oxygenated as it passes through the over-perfused part of the lung. Carbon
dioxide elimination is nearly always normal because there is a compensatory increase
in minute ventilation.
Clinical manifestations
The clinical features of acute life-threatening pulmonary embolism can be explained
in terms of the pathophysiological changes. The patient presenting to the ICU team
will often have severe cardiorespiratory compromise. Patients will be acutely distressed
with dyspnoea and tachypnoea. The physical signs are those of reduced cardiac output,
namely, sinus tachycardia, hypotension, cool clammy peripheries, and confusion. There
will be both central and peripheral cyanosis and signs of acute right heart strain: a
raised central venous pressure, a palpable right ventricular heave, and a gallop rhythm.
Finally, patients may present in atrial fibrillation due to a dilated right heart.
The symptoms and signs described above are not specific to pulmonary embolism;
they are often the manifestation of any critical illness.
Investigations
Non-imaging diagnostic methods
ECG the ECG is abnormal in over 70% of patients with pulmonary embolism
but these changes are nonspecific. Common findings are sinus tachycardia and ST
segment abnormalities. In massive pulmonary embolism, evidence of right heart strain
may be seen (right axis deviation, T wave inversion in V13). The classic S1-Q3 -T3
pattern seldom occurs (Figure 1). The ECG is useful in excluding other conditions such
as myocardial infarction.
Arterial blood gases the characteristic changes are a reduced partial pressure of
oxygen in arterial blood (PaO2) and a normal or low partial pressure of carbon dioxide.
An abnormal PaO2 is nonspecific.
Plasma D-dimer enzyme-linked immunosorbent assay (ELISA) relies on the
principle that endogenous fibrinolysis is occurring in an effort to break down thrombus
to fibrin degradation products (D-dimers). Although elevated levels of D-dimers are
sensitive for the presence of pulmonary embolism they are not specific. A variety of
clinical conditions encountered in the ICU can result in accelerated fibrinolysis (e.g.
recent surgery, myocardial infarction, sepsis).
ECG of a 28-year-old patient who died from a massive pulmonary embolism

1
Imaging diagnostic methods
Chest radiography most patients with a pulmonary embolism have an abnormal
chest radiograph. In massive embolism a plump pulmonary artery shadow can be seen
in the presence of oligaemia in those parts of the lung affected by emboli. There may be
signs of pulmonary infarction; a wedge-shaped area along the pleural surface.
Echocardiography transthoracic echocardiography can detect right ventricular
dilatation and may reveal thrombus floating in the right ventricle or atrium.
Transoesophageal echocardiography is particularly useful in the ICU because the patient
is often too unstable for transportation. It allows detection of emboli involving the main
trunk and the right and left pulmonary arteries.
Pulmonary angiography remains the diagnostic gold standard. It is expensive,
invasive, and carries a 0.3% risk of mortality. Angiographic interpretation relies heavily
on image quality and the observers experience. Risks include vasodilatation due to
contrast and the possibility of pushing clot in the right heart into the lungs.
Contrast-enhanced spiral CT is emerging as a first-line investigation. The
technique is faster, less complex, and less operator dependent than angiography. The
procedure has over 90% specificity and sensitivity in diagnosing pulmonary embolism
in the main, lobar and segmental pulmonary arteries (Figure 2).
Ventilationperfusion scanning is the most common imaging method used in the
diagnosis of pulmonary embolism, but it cannot be performed in intubated patients.
2 Spiral CT scan of the same

patient as in Figure 1. There is
a filling defect in the left main
pulmonary artery consistent with
a large pulmonary embolism.
Management
Diagnostic uncertainty is often accentuated in the critical care setting where the
complexity of safe transport often becomes a major determining factor in the diagnostic
approach. Subsequently, management decisions are often based on incomplete clinical
data.
Resuscitation
Oxygen therapy oxygen should be administered in high concentration by mask.
Patients with a decreased level of consciousness and/or severe respiratory distress
require ventilation. Attention should be paid to full monitoring of resuscitation efforts
in the form of ECG, invasive blood pressure, and central venous pressure monitoring.
Arterial blood gas values can be used to assess the degree of hypoxaemia and indicate
the presence of a metabolic acidosis due to hypoperfusion.
Haemodynamic support the aim of treatment is to restore tissue perfusion to
maintain end organ perfusion. It is imperative to maintain right heart filling pressures.
The central venous pressure is raised in patients with pulmonary embolism; often
as high as 20 mm Hg, this should not prevent fluid administration. A pulmonary
artery catheter is not essential but may be useful in monitoring the response of
fluid challenges. If hypotension exists after fluid-loading, inotropes should be started
(e.g. adrenaline (epinephrine), 0.31.5 g/kg/minute), and the dose titrated to blood
pressure.
Definitive treatment
Heparin remains the mainstay of therapy for pulmonary embolism. A loading dose
of 10,000 units i.v. or 100150 units/kg followed by an infusion of 1525 units/kg/hour
is administered as soon as possible. The activated partial thromboplastin time (APTT)
ratio should be checked every 6 hours and the infusion adjusted to maintain an APTT
ratio of 22.5 normal.
Warfarin can be started early because it takes 5 days to achieve its full effect.
Heparin should be continued for at least 5 days or until the international normalized ratio
(INR) is 23. Warfarin without intravenous heparin depresses protein S and C activity at
the onset, thus creating a thrombogenic potential.
Thrombolysis the use of thrombolytic agents in acute pulmonary embolism
remains controversial. Trials have failed to show any benefit over conventional
treatment. Thrombolytics can increase the rate of thrombolysis in the first 24 hours
but there is no convincing evidence that it decreases morbidity or mortality. There is a
substantial risk of bleeding including intracranial haemorrhage (0.52%).
On this basis, thrombolytic agents should be reserved for those in whom accelerated
thrombolysis may be considered lifesaving. Tissue plasminogen activator (tPA), 100 mg
as an intravenous infusion over 2 hours is the thrombolytic of choice (less allogenic). It
can be administered peripherally or into a pulmonary artery catheter. Heparin infusion is
started after thrombolysis to maintain the APTT ratio at 22.5.
Pulmonary embolectomy is limited to centres with cardiothoracic surgeons. It has
a high mortality rate and should be considered only in particular circumstances, for
example in those in whom thrombolysis is contraindicated or who fail to respond.
Other therapies: low molecular weight heparin (LMWH) is licensed for the treatment
of pulmonary embolism. It has little use in the compromised patient because
subcutaneous LMWH takes 24 hours to reach therapeutic effect. Balloon-tipped
catheters under fluoroscopy have been used to extract emboli; further investigation is
required before their use becomes widespread.
Nitric oxide has been used as an adjunct to critical care management. It is a
selective pulmonary vasodilator used to increase oxygenation by improving ventilation
perfusion matching. There are case reports advocating its use because it allows life-
threatening hypoxaemia to be improved while instituting definitive therapy.

Intensive Care Myopathy and
Neuropathy
Francis J Andrews
Richard D Griffiths
Francis J Andrews is Lecturer in Medicine (Intensive Care) at Liverpool University

and Specialist Registrar at Whiston Hospital, Prescot, UK. He qualified from Leeds
University and trained in accident and emergency medicine in West Yorkshire. His
research interests include muscle wasting and the effect of nutrition on the immune
system in critically ill patients.
Richard D Griffiths is Professor of Medicine (Intensive Care), University of Liverpool,

and Honorary Consultant Physician Intensive Care, Whiston Hospital, Prescot, UK. He
has research interests in muscle, nutrition and the rehabilitation of the post-ICU patient.
The effects of the systemic inflammatory response syndrome (SIRS) on the main
organs are widely known, but the effects on peripheral nerve and muscle in the critically
ill have only recently begun to be recognized and understood.
Definitions
Recovery from critical illness may be followed by critical illness neuropathy and/or
critical illness myopathy. Critical illness neuropathy is an acute axonal neuropathy
developing in critically ill patients which remits spontaneously when the critical illness
has passed. Critical illness myopathy is an acute myopathy developing during a critical
illness. The incidence of myopathy and polyneuropathy varies among studies, but
it is estimated that 7080% of patients with severe sepsis or multiple organ failure
develop some form of critical illness neuropathy or myopathy. Various neuropathies and
myopathies have been described.
Neuropathies
Critical illness polyneuropathy (CIP) is a common, diffuse, axonal motor and
sensory neuropathy, which develops while patients are critically ill in the ICU and,
generally, remits spontaneously as the patient recovers from their underlying critical
illness. There is a primary axonal degeneration of peripheral motor and sensory
fibres, but no evidence of inflammation. Muscle shows scattered atrophic fibres with
occasional necrotic fibres.
Acute motor neuropathy is a variant of CIP associated in some cases with the
administration of competitive neuromuscular blocking agents (e.g. pancuronium
bromide, vecuronium) given for more than 48 hours. There is severe primary axonal
degeneration of predominantly motor fibres, demonstrable with nerve conduction
studies and electromyography (EMG). Muscle biopsies are non-specific and may show
denervation, and atrophic and necrotic changes. Electrophysiological testing may show
defects in neuromuscular transmission consistent with a postsynaptic defect.
Transient neuromuscular blockade refers to the prolonged effect of competitive

neuromuscular blocking agents in liver and kidney failure. Repetitive nerve stimulation
studies are abnormal. Recovery occurs in a few days following cessation of the drugs.
Myopathies
Thick filament myopathy occurs in patients with acute asthma and is associated with
the use of high-dose corticosteroids and neuromuscular blocking agents. Creatine
kinase is often markedly elevated and needle EMG motor unit potentials are polyphasic,
low amplitude and of short duration (conduction and repetitive nerve stimulation studies
are normal). Recovery is often rapid. Muscle biopsy shows characteristic loss of central
structure in muscle fibres, due to thick myosin filament destruction. Muscle denervation
from CIP or the use of neuromuscular blocking agents predisposes patients to this
condition.
Critical illness myopathy: mild myopathic changes are often seen in patients with CIP
and motor neuropathy. In many patients, myopathic changes are more pronounced,
consistent with a hypercatabolic myopathy. Biopsies show loss of myosin but relative
preservation of structural proteins, with ubiquitin proteolysis.
Acute necrotizing myopathy is rare; it occurs following insults that cause

myoglobinuria. Electrophysiology shows abnormal spontaneous activity, highly elevated
creatine and myoglobinuria. Muscle biopsy shows widespread necrosis. Recovery is
variable.
Pathophysiology
The pathophysiology of critical illness neuropathy and myo-pathy is poorly understood.
There is often a marked discrepancy between the results of electrophysiological and
histological studies. Early in critical illness, there is often marked atrophy of type I and II
muscle fibres, with necrosis being rare; at this stage electrophysiological investigations
are normal. Electron microscopy shows early loss of myosin but retention of structural
proteins (Figure 1). However, when critical illness neuropathy and myopathy become
clinically apparent later during illness, histological examination of peripheral nerves is
often normal, despite abnormal EMG and nerve conduction studies as seen in CIP.
Electron micrograph of skeletal muscle taken

from a normal muscle and b a patient with
multiple organ failure. Between the Z lines, where
the actin is attached there is almost complete
loss of the double-ended myosin filaments
(arrowed) that form the characteristic central
A band.
1
It has been speculated that axonal degeneration is a consequence of the circulating

mediators of SIRS, resulting in a common endothelial and vascular pathology that leads
to nerve and muscle damage. In this theory, blood vessels supplying peripheral nerves
are susceptible to disruption of the microcirculation in critical illness. The resulting
increase in vascular permeability and oedema may result in hypoxic neural damage,
not manifesting histologically until severe energy deficits occur. In these circumstances,
neuromuscular drugs could also have a direct toxic effect on axons. Studies have failed
to show any convincing evidence for nutritional deficiencies, medication, Guillain
Barr syndrome, or types of primary illness or injury as primary causes of critical
illness myopathy or neuropathy. Severe CIP is asssociated with prolonged ICU stay,
hyperglycaemia and hypoalbuminaemia.

These patients appear to be recovering from sepsis and multiple organ failure, often
following prolonged ventilation, but have difficulty weaning from the ventilator and have
limb weakness. Lung or cardiac causes of respiratory insufficiency need to be excluded
before considering the diagnosis of neuropathy or myopathy.
Aside from weakness and muscle wasting, neurological signs of neuropathy or

myopathy may not always be present. In particular, tendon reflexes may be normal
instead of decreased in some patients, and even exaggerated if the patient has a co-
existing CNS disorder. A useful sign is that deep painful stimulation of limbs may show
weak movements but strong facial grimacing.
Differential diagnosis
It is important to exclude conditions that would have begun before admission to the
ICU, such as acute infective, traumatic or neoplastic spinal cord compression, Guillain
Barr syndrome, myasthenia gravis or muscular dystrophy. Usually these conditions are
obvious before admission, but deterioration is often so rapid that diagnosis before ICU
admission is impossible.
Investigations
Depending on the clinical variables, involvement of the high cervical spinal cord,
peripheral nerves, neuromuscular junctions and muscles should be investigated.
Patients with weakness following trauma should be investigated for spinal cord trauma
before investigations for critical illness neuropathy or myopathy. EMG is the most
useful initial investigation. EMG evidence of denervation activity consistent with axonal
degeneration is diagnostic of CIP in the absence of other more plausible causes. If
performed, nerve conduction studies in CIP show normal speed of impulse conduction
but decreased compound motor and sensory nerve action potential amplitudes. Nerve
conduction studies may be useful in diagnosing acute motor neuropathy, evidenced
by markedly reduced compound motor but normal sensory nerve action potential
amplitudes. Repetitive nerve stimulation studies are helpful in establishing the diagnosis
of transient neuromuscular blockade. Serum creatine kinase is often elevated in
thick filament and necrotizing myopathy but may be normal. Muscle biopsy is the
investigation of choice for suspected myopathy and should be performed on all critically
ill patients with new onset of weakness and the absence of electrodiagnostic findings
suggestive of CIP or transient neuromuscular blockade.
Management
There is no specific therapy for critical illness neuropathy and myopathy. However, it is
important to limit or prevent them because of their variable prognosis. The severity of
critical illness neuropathy correlates with prolonged sepsis and catabolism, therefore
sepsis must be treated aggressively, with attention to adequate nutrition. Evidence also
suggests that tight glycaemic control reduces the incidence of CIP. Muscle relaxants
and corticosteroids should be used sparingly, especially in acute asthma and in the
presence of renal or liver failure. Prolonged physio-therapy and rehabilitation therapy is
the mainstay of treatment for established conditions. Careful positioning of the patient is
essential to avoid further nerve damage due to pressure areas.
Prognosis
The degree of recovery from critical illness neuropathy and myopathy is related to the
severity of the condition. Milder cases of neuropathy are associated with recovery in
weeks whereas more severe forms may take months to recover. Some patients with
severe neuropathy, especially with evidence of slowing of nerve conduction may not
recover. Generally, there is a rapid recovery following thick filament myopathy, but the
prognosis may be poorer for some cases of necrotizing myopathy. u
FURTHER READING
Bolton C F. Sepsis and the Systemic Inflammatory Response Syndrome:
Neuromuscular Manifestations. Crit Care Med 1996; 24: 140816.
Griffiths R D. Management of Muscle Pathology in the Critically Ill. In: Preedy V, Peters
T, eds. Skeletal Muscle: Pathology, Diagnosis and Management of Disease. London:
Greenwich Medical Media, 2002; 57384.
Hund E. Neurological Complications of Sepsis: Critical Illness Polyneuropathy and

Myopathy. J Neurol 2001; 248: 92934.
Lancomis D, Giuliani M J, Van Cott A et al. Acute Myopathy of Intensive Care: Clinical,
Electromyographic and Pathological Aspects. Ann Neurol 1996; 40: 64554.
Latronico L, Fenzi F, Recupero D et al. Critical Illness Myopathy and Neuropathy.

Lancet 1996; 347: 157982.

Management of the Poisoned Patient
Cliff Reid
Gary Smith
Cliff Reid is Specialist Registrar in Pre-hospital Care for the London Helicopter
Emergency Medical Service. He qualified from Southampton University and completed
training in emergency medicine at North Hampshire Hospital followed by training in
intensive care medicine in Portsmouth. His interests include the interface between
emergency medicine and intensive care, and emergency airway management.
Gary Smith is Consultant in Intensive Care Medicine at Portsmouth Hospitals NHS

Trust, and Honorary Senior Lecturer in Critical Care in the School of Postgraduate
Medicine, University of Portsmouth, UK. He qualified from Southampton University
Medical School and trained in anaesthesia and medicine in the South of England and
Yale University, USA. His interests include the organization of intensive care services,
outcome prediction and the training of doctors, nurses and paramedics
Poisoning is a common cause of hospital attendance, but seldom requires admission to

the ICU. In many cases the poison is known and the patient requires only supportive
care. Occasionally, the history is unclear or unobtainable; in such cases, the recognition
of certain toxicological syndromes or toxidromes (Figure 1) and the selective use of
investigations may help. The management of all poisoned patients is summarized in
Figure 2.
Recognizable clinical toxidromes
Toxidrome Features Causative agents

Anticholinergic Agitation, hallucinations, coma Antihistamines (diphenhydramine)
Tachycardia Anticholinergic plants such as Atropa
belladonna (deadly nightshade)
Large pupils Tricyclic antidepressants
Dry skin Atropine
Urinary retention Antiparkinsonian agents
Warm, flushed peripheries
Cholinergic Lacrimation Organophosphate carbamate insectides

Salivation
Bradycardia
Increased respiratory tract secretions
Diaphoresis
Vomiting
Diarrhoea and urinary incontinence
Fasciculations
Opiate Respiratory depression Heroin and other opiates

Depressed conscious level
Small pupils
Sedative-hypnotic Depressed conscious level Benzodiazepines

Mild respiratory depression Some sedative hypnotics
Hypotension in large ingestions
Serotonergic Confusion, agitation, restlessness Serotonergic antidepressants especially in

Myoclonus, hyperreflexia combination (e.g. serotonin reuptake
Diaphoresis inhibitors, monoamine oxidase inhibitors and
Tremor, rigidity tricyclic antidepressants)
Hyperthermia
Sympathomimetic Tachycardia Cocaine

Hypertension Amphetamines,
Hyperthermia methylenedioxymethamphetamine
Agitated delirium (MDMA; ecstasy)
Large pupils Alcohol or sedative hypnotic withdrawal
Diaphoresis
Management sequence for the poisoned patient
Primary survey
A
Oxygen
Manual airway opening manoeuvres
Simple airway adjuncts
Rapid sequence intubation for airway protection
B
Assist ventilation as required
C
Intravenous access 12-lead ECG
Correct arrhythmias and hypotension
Monitor urine output
D
Glasgow Coma Score, pupils, cranial nerves, lateralizing signs (CT scan), blood glucose
E
Exclude hypothermia
Fully expose
Monitoring
Respiratory rate, ECG, non-invasive blood pressure, pulse oximetry
Secondary survey
Track marks, pressure areas, co-existing injuries, characteristic odour, recognizable toxidrome
History
Investigations
Radiographic
Chest radiograph for evidence of pulmonary aspiration or non-cardiogenic pulmonary oedema
(opiates, salicylates)
Abdominal radiograph for ingested metals (e.g. iron, lead, zinc)
Laboratory
Full blood count, urea and electrolytes, arterial blood gases
Anion gap, plasma osmolality
Urinalysis: blood, glucose, ketones, urine osmolality
Advice: Toxbase on-line
Levels: paracetamol; others as indicated (salicylate, iron, lithium)
Gastric decontamination
Activated charcoal
Whole bowel irrigation
Antidote
Diagnostic naloxone
Treatment N-acetylcysteine
Increased elimination
Multiple dose activated charcoal
Haemofiltration or haemodialysis
Supportive
Follow-up/referral
Primary survey and resuscitation

Airway and breathing: many drugs taken in overdose cause a variable depression of
conscious level that leads to airway obstruction, depressed airway reflexes and reduced
ventilatory drive. Patients are at risk of aspiration of gastric contents, hypoxaemia,
hypercapnia, and aspiration of vomit. Indications for tracheal intubation include: the
inability to maintain a patent airway; a Glasgow Coma Score of 8/15 or less; agitation
or combative behaviour that risks harm to the patient; hypoxaemia; and hypoventilation.
Careful thought should also be given to the anticipated clinical course of the patient.
For example, patients with a fluctuating conscious level, those requiring interhospital
transfer and those in whom future deterioration can be predicted should be intubated
electively.
A rapid sequence induction technique minimizes the adverse consequences
of airway manipulation and intubation, such as pulmonary aspiration, arrhythmias
and raised intracranial pressure. The temptation to intubate a comatose patient
without providing anaesthesia must be resisted, because this could exacerbate the
arrhythmogenic effects of certain poisons. The presence or absence of a gag reflex
does not correlate with conscious level or true airway protective ability and should not
influence the decision to intubate.
Circulation: some poisons have direct negatively chronotropic or inotropic effects

(e.g. -blockers, calcium antagonists), while others (e.g. tricyclic antidepressants)
cause severe tachydysrhythmias that reduce contractility indirectly or precipitate
cardiac arrest. CNS depression or drugs with an effect on the peripheral circulation
(e.g. -blockers) may also cause hypotension, whereas sympathomimetics (e.g.
amphetamines) may result in tachycardia and severe life-threatening hypertension.
Hypotension will sometimes respond to intravenous crystalloid alone, but a failure
to reverse hypotension or oliguria may necessitate central venous or pulmonary artery
catheterization to guide volume therapy and vasoactive support.
Arrhythmias should be corrected, though standard advanced life-support guidelines
may require modification, because tachyarrhythmias are likely to be refractory to
anti-arrhythmic agents or cardioversion. Initial attention must be paid to correcting
hypoxaemia, hypercapnia, and electrolyte and acidbase disturbances. For instance,
the use of deliberate hyperventilation or intravenous sodium bicarbonate (12 mmol/kg
body weight) to produce alkalaemia appears to reduce the risk of dysrhythmias, and
possibly seizures, in tricyclic antidepressant poisoning.
Disability (neurological assessment): some agents (e.g. insulin, alcohol,

hypoglycaemic agents) lower blood glucose and, thus, conscious level; therefore blood
glucose measurement should form part of the neurological examination. The presence
of lateralizing signs such as hemiparesis may indicate coexisting pathology. Ataxia,
nystagmus and seizures may provide clues to toxin ingested.
Exposure and full examination (secondary survey) of the skin may reveal track
marks suggesting intravenous drug abuse. Patients who remain unconscious for
many hours before being found may develop hypothermia, skin blistering, peripheral
neuropathy and rhabdomyolysis.
History
Where possible, the amount and type of poison ingested, as well as the exact
time of exposure, should be identified. Co-morbid conditions and the patients usual
medications may influence the progress of the poisoning or the patients recovery.
In patients who have no apparent cause for their condition, consideration should be
given to the possibility of body packing or stuffing, in which large quantities of illegal
drugs are hidden within body cavities. Such suspicion necessitates rectal and vaginal
examination, abdominal radiology and enteroscopy.
Investigations
Blood: routine blood count and urea and electrolyte tests are important to assess
the impact of poisoning on electrolyte homeostasis and renal function. An elevated
serum creatine phosphokinase may suggest rhabdomyolysis due either to pressure-
induced myonecrosis or from a direct toxic effect on myocytes. Arterial blood gas
analysis permits assessment of ventilation and identifies acidbase disturbances.
Modern blood-gas analysers also provide quantitative evidence of carbon monoxide
or abnormal haemoglobin complexes. Other useful investigations include calculation of
any anion or osmolar gap. If the anion gap exceeds 16 + 4 mmol/litre, it may support
the diagnosis of poisoning by salicylates, iron or toxic alcohols. An osmolar gap (the
difference in measured and calculated serum osmolality) indicates the presence of
unmeasured osmotically active substances (e.g. ethylene glycol).
Urine: the presence of pigment in the urine (haemoglobin or myoglobin), in the

absence of RBCs on urine microscopy, suggests myoglobinuria and diagnosis of
rhabdomyolysis.
Toxicological investigations: there is seldom an indication for a blanket toxicology

screen, because they are expensive, often unavailable during the patients
hospitalization and seldom alter the clinical management. Nevertheless, paracetamol
levels should be requested, since the demonstration of toxicity necessitates the
administration of N-acetylcysteine to prevent hepatocellular injury. Further advice on
specific poisons can be obtained:
on-line at www.spib.axl.co.uk
by telephone in the UK from the National Poisons Information
Service on 0870 600 6266.
Gastrointestinal decontamination
There are several ways to prevent the further uptake of poison present in the
gastrointestinal tract, including emesis, lavage and activated charcoal, but few have
sound evidence for their use. In particular, the role of gastric lavage is now reserved for
patients with life-threatening poisoning presenting to hospital within 1 hour of ingestion.
Specific antidote therapy

Most patients improve with supportive care alone, though some require the
administration of specific antagonists or antidotes. The response to the administration
of the opiate antagonist naloxone (0.40.8 mg i.v. or 0.8 mg i.m. or s.c.) can assist in
the diagnosis of opiate overdose. However, the benzodiazepine antagonist, flumazenil,
should not be used empirically, because it can induce an acute withdrawal reaction in
chronic benzodiazepine users, and may induce seizures if the toxic effects of a tricyclic
antidepressant overdose are being masked by concomitant benzodiazepine ingestion.
Enhanced elimination
Activated charcoal, 1 g/kg every 4 hours, may increase elimination of poisons that
have an enterohepatic circulation. In addition, the gut wall acts as a semipermeable
membrane and assists removal of the drug by an intestinal dialysis.
Forced alkaline or acid diuresis: now seldom used, these methods involve
the manipulation of urine pH in order to maintain weak acids (e.g. salicylates,
phenobarbitone) or weak bases (e.g. amphetamine, phencyclidine) in their ionized,
lipid-insoluble form to limit renal tubular reabsorption. Careful monitoring of acidbase
status, electrolytes, and fluid balance is required.
Dialytic techniques: haemodialysis is effective at removing toxins that are poorly

protein bound, and have a molecular weight less than 500 Da. Drugs with a high
volume of distribution such as tricyclic antidepressants are not cleared effectively.
Continuous haemofiltration methods can remove larger molecules than haemodialysis,
and continuous methods may be more suitable for drugs with a high volume
of distribution (e.g. lithium). In charcoal haemoperfusion, blood is passed via
an extracorporeal circuit over a cartridge of activated charcoal. This method
is more suitable than haemodialysis for the removal of large or protein-bound
molecules. However, it can result in thrombocytopenia, coagulopathy, hypothermia and
hypocalcaemia, and in many cases provides no greater clearance of poison than
multiple doses of activated charcoal.
Follow-up
Many poisoned patients are young, otherwise fit, adults who often have treatable
underlying psychiatric illness. Referral for psychiatric assessment should always be
undertaken when they have recovered from acute poisoning.
FURTHER READING
Anonymous. Advanced Challenges in Resuscitation. Section 2: Toxicology in ECC.
Resuscitation 2000; 46: 2616.
Henderson A, Wright M, Pond S M. Experience with 732 Acute Overdose Patients
Admitted to an Intensive Care Unit over Six Years. Med J Aust 1993; 158: 2830.
Manoguerra A S. Gastrointestinal Decontamination After Poisoning: Where is the
Science? Crit Care Clin 1997; 4: 70925.
Rosen P, Barkin R. Emergency Medicine: Concepts and Clinical Practice. St Louis:
Mosby, 1998.
Vernon D D, Gleich M C. Poisoning and Drug Overdose. Crit Care Clin 1997; 3: 647
67.

Nosocomial Bacterial
Infections
Aodhn S Breathnach
Aodhn S Breathnach is Consultant Medical Microbiologist in the PHLS Collaborating

Centre and Department of Medical Microbiology, St Georges Hospital, London, UK.
Nosocomial infections are those acquired in or associated with hospitals. Any infection
can, in theory, occur in hospital, but there are many factors in the hospital environment
that lead to a particular spectrum of infective problems (Figure 1). Nosocomial
infections are common, and may be serious or fatal. Some are unavoidable, but doctors
must remember that their duty of care to their patients extends to fundamental matters
such as basic hygiene and avoidance of unnecessary antibiotics, which may prevent
patients becoming infected.
Typical hospital organisms
Usual Risk factors Typical Comments

location for acquisition infections
Methicillin-resistant Nasal or Antibiotic use Skin/wound Occasional case reports

Staphylococcus cutaneous Skin lesions Orthopaedic of isolates developing
aureus Overcrowding, Intravenous resistance to glycopeptides,
poor infection devices which are the agents
control Bacteraemia of choice for
Endocarditis invasive infections
Respiratory tract
Prosthetic devices
Enterococci and Gut Antibiotics Low virulence Vancomycin-resistant

vancomycin- Hospital particularly Typically, enterococci are more
resistant environment cephalosporins, vulnerable ICU correctly, but rarely,
enterococci glycopeptides patients, or renal termed glycopeptide-
patients in whom resistant enterococci
glycopeptide Heat and disinfectant
antibiotics tolerant, so survive well in
are commonly hospital environment
used
Clostridium Gut Antibiotics Antibiotic- Large outbreaks with fatal

difficile Hospital Chemotherapy associated cases reported
environment Lack of hygiene diarrhoea/
Elderly care pseudomembranous Predisposed by loss of
wards colitis native bowel flora, hence a
number of suggested
alternativeremedies based
on the principle of replacing
this flora (e.g. live yoghurt,
donor faeces)
Multi-resistant Gut Antibiotics Intra-abdominal, Various species (e.g.

Gram-negatives Hospital Lack of hygiene respiratory and Acinetobacter, Klebsiella,
environment High-dependency bloodstream Enterobacter,
units infections Stenotrophomonas)
in vulnerable Many are indolent
patients opportunists, but some
(e.g. Klebsiella,
Pseudomonas aeruginosa)
can cause aggressive,
virulent infections
NB:Most nosocomial infections are caused by the patients own flora or by cross-infection with more sensitive
organisms not listed above
Background
It is reasonable to expect medical and nursing care to be safe, but hospitals have
always been hazardous places until the 20th century, they were avoided by those
who had the option of being treated elsewhere. Paradoxically, with the advent of
modern medicine and large urban hospitals in the 19th century, overcrowding,
squalor and ignorance increased the danger to patients, and there was a significant
risk of death from nosocomial infection following many procedures, from childbirth to
amputation.
The current situation is much improved, but hospital-acquired infections still cause
considerable illness and some mortality. It has been estimated that, at any one time,
9% of in-patients in the UK have a nosocomial infection; the incidence is highest in
surgical wards and ICUs, and lowest in medical units. Apart from the obvious ethical
significance of harm resulting from medical or nursing care, nosocomial infections
cause a financial burden to hospitals, patients and society. A recent estimate of the cost
in the UK was up to 1000 million/year. This figure does not include costs of litigation
and compensation; courts increasingly tend to assume that hospital staff are at fault in
cases of nosocomial infection.
Predisposing factors for nosocomial bacterial infection

Underlying patient factors (Figure 2) many patients are intrinsically vulnerable
to infection; they are at the extremes of age, are debilitated, or have an underlying
illness causing immunodeficiency (e.g. HIV). Neurological illness may lead to aspiration
pneumonia; immobility and dehydration may encourage urinary tract infection (UTI).
Skin disease and bedsores allow organisms to enter subcutaneous tissue. In addition,
and importantly, the normal flora of all patients includes potential pathogens such as
Escherichia coli in the gut and Staphylococcus aureus in the nose.
Predisposing factors in nosocomial infection
Patient factors
Debility
Extremes of age
Impaired gag reflex (e.g. cerebrovascular accident)
Trauma
Immunosuppressive illness (e.g. HIV)
Normal flora potential pathogens
Medical and surgical interventions

Surgical incisions
Intravascular devices
Urinary catheters
Prostheses
Antibiotic use
Immunosuppression
Anaesthesia and ventilation
Hospital environment
Other patients organisms
Cross-infection transient staff carriage
Environmental organisms
Lack of hygiene
Overcrowding
Understaffing
Hospital pathogens
2
Medical and surgical interventions surgical incisions and intravascular devices

provide means of entry for pathogens. Urinary catheterization often causes UTIs.
Prosthetic joints and heart valves provide a protected niche for bacterial growth, which
usually results in loss of the prosthesis. Immunosuppressive therapy allows even low-
virulence organisms to assume a dangerously pathogenic role.
Less obvious ways in which medical therapy can facilitate infection include anaesthesia
and ventilation (may lead to nosocomial pneumonia) and antibiotics (alter normal flora,
reducing resistance to colonization by hospital organisms). Inadequate disinfection
of endoscopes can transmit pathogens such as Mycobacterium tuberculosis and
Salmonella.
Hospital environment patients may become infected with new organisms, usually
from other patients, or more rarely from staff or the inanimate environment. Transient
hand carriage by medical or nursing staff is thought to be the main route of spread,
but occasionally other routes are involved, such as the airborne route for respiratory
pathogens. Overcrowding, understaffing and lack of hygiene, particularly lack of
handwashing, increase the risk of cross-infection.
Antibiotic use in hospital has selected resistant organisms, which readily colonize
and infect patients. Many (e.g. coagulase-negative staphylococci, enterococci) are
of relatively low virulence, but can cause severe illness in compromised patients;
some (e.g. methicillin-resistant Staph. areus, MRSA) can be as virulent as their more
sensitive counterparts.
Common syndromes and problems of nosocomial bacterial infection

Most nosocomial infections fall into a small number of common categories (Figure 3).
Specialist units (e.g. burns, transplant, neurosurgery) see different infections, in addition
to the following syndromes. The importance of nosocomial viral and fungal infections
should not be overlooked.
Foci of nosocomial bacterial infections

Gastrointestinal 5%
Other 13%
Unknown 5%
Lower respiratory tract 23%
Urinary tract 23%

Surgical wound 11%
Skin 10%
Bacteraemia 6%
Intravascular device 4%
3
Line-associated infections and bacteraemia: one-third of cases of nosocomial

bacteraemia are associated with an intravenous device, 25% are from an unknown
source, and the remainder have various sources, including the urinary tract, the
gut and ventilator-associated pneumonia. Almost 50% of isolates are staphylococci
(MRSA proportion increasing), and these are most likely to be line-associated.
The remainder are mostly Gram-negative (E. coli, Klebsiella, Enterobacter, Proteus
and Pseudomonas), with small numbers of enterococci and Candida (not bacteria,
but generally included in reviews of bacteraemia). Gram-negatives may be line-
associated, but are more likely to have a urinary source, or to arise from the gut in
patients with intra-abdominal pathology or neutropenia.
Intravenous lines provide both a break in the skin, allowing entry of organisms, and
a protected site for bacterial growth shielded from immune defences by a biofilm of
platelets, fibrin and bacterial slime. The risk is greater with increasing age of the line,
central and multi-lumen lines, and poor insertion technique or line care, leading to
infection of the insertion site or hub. Pre-existing skin disease and colonization with
pathogens such as MRSA, also increase the risk of infection. The heavy normal flora
of the groin means that femoral lines are often infected, despite careful insertion
technique.
Presentation and diagnosis line infections present with septicaemia or obvious

infection of the exit site or tunnel, or are silent. Other sequelae (which may manifest
only after line removal) include endocarditis and disseminated abscesses (e.g. spinal,
ophthalmic). Blood cultures and culture of the line tip, or exit site if clinically infected, are
the usual means of diagnosis. There has been interest in diagnostic methods that avoid
line removal (e.g. line brushings, quantitative line blood cultures), but these have yet to
gain wide acceptance.
Management line infections (except some caused by coagulase-negative

staphylococci) are almost never eradicated by antibiotics without line removal. Infected
lines are sometimes left in situ, particularly when intravenous access is difficult, but this
increases the risk of septicaemic complications.
Nosocomial chest infections: pneumonia is responsible for about 25% of all
nosocomial infections, but the precise diagnosis is often uncertain; in severely ill
patients, there may be other explanations for fever, hypoxia and pulmonary infiltrates on
radiography (e.g. pulmonary oedema, shock lung, segmental collapse). Furthermore,
the respiratory tract of hospitalized patients is often colonized with various organisms,
and it is difficult to distinguish colonization from genuine pneumonia, even when
deep sample collection techniques (e.g. broncholaveolar lavage) are used. The
approach must therefore be pragmatic. Microbiology of respiratory samples should
guide treatment in those with clinical and radiological evidence of lung sepsis, but the
possibility of under-treatment and over-treatment should be acknowledged.
Most studies implicate a variety of Gram-negative organisms as the predominant

causative agents, with doubts over the significance of culture results as described
above. Staph. aureus, particularly MRSA, is the only commonly implicated Gram-
positive organism; pneumococci are seldom isolated, but may be under-diagnosed.
Thus, empirical treatment guide-lines for nosocomial pneumonia assume Gram-
negatives to be the likely cause, and generally recommend agents with Gram-negative
activity (e.g. broad-spectrum cephalosporins).
Hospital-acquired tuberculosis and legionnaires disease are rare, but important

because of their severity and because of the possibility of outbreaks. Any smear-
positive TB patient who is not adequately isolated may spread the organism to other
patients; unrecognized multidrug-resistant TB poses the greatest risk, because
these patients are likely to remain infectious for longer. All non-immune contacts are
theoretically at risk, but the greatest risk of progression to disease is in HIV-positive and
other severely immunosuppressed contacts.
Legionella infection is acquired from the environment; transmission between patients

does not occur. The organism normally inhabits water, preferably at 2040C, and is
spread to patients via airborne droplets. Sources within hospitals include water-cooled
ventilation systems (formerly the cause of large outbreaks), shower heads and tap
water. Patients most at risk include the elderly, those with chronic respiratory disease,
and the immunosuppressed, particularly recent transplant recipients. The infection
presents as severe pneumonia; the organism grows poorly, so diagnosis usually
depends on serology or urinary antigen detection.
Surgical site infections: despite asepsis and antibiotic pro-phylaxis, surgical site
infections remain common. It is believed that infection usually arises from the patients
own skin flora, inoculated into the wound during surgery; hair follicles and sweat
glands cannot be completely sterilized during skin preparation, so no surgical field is
completely sterile. Other possible sources include theatre staff (who inevitably shed
skin flakes and respiratory droplets during the procedure), perforated gut and
contaminated traumatic wounds. These infections usually manifest soon after surgery.
The incidence of infection varies between hospitals and types of surgery. In a recent
large English survey, the lowest rates (23.5%) were in orthopaedic procedures, and
the highest (1015%) in amputations and abdominal surgery. Severe underlying illness
and lengthy operations increase the risk more than 35% of severely ill patients
undergoing prolonged large bowel surgery develop infection. Staphylococci (mostly
Staph. aureus, 50% of which are MRSA) cause almost 50% of infections; most of the
remainder are caused by Gram-negatives, including E. coli and Pseudomonas.
Most infections are superficial and easily treatable. Deeper infections are rarer, and
may be catastrophic, particularly when surgery involves bone, brain, a prosthesis, a
vascular graft or a transplant. Group A Streptococcus can cause rapidly spreading,
often fatal necrotic infections (necrotizing fasciitis).
Urinary tract infections (UTIs): urinary cathers are used routinely in the care of
acutely and chronically ill patients, and are responsible for most cases of nosocomial
UTI. It is said that bacteriuria develops in 5% of catheterized patients per day;
unhygienic insertion technique probably increases the risk, and also increases the risk
of cross-infection with other patients organisms. Greater age, debility and dehydration
also increase the risk of UTI. It is important to distinguish asymptomatic bacteriuria from
symptomatic infection; the latter occurs in only a minority.
It is reasonable to treat symptomatic infection with anti-biotics, but unless the catheter
is removed, the urinary tract will not be sterilized, and may become colonized with
antibiotic-resistant organisms. For this reason, it is not recommended to investigate
urinary samples from asymptomatic chronically catheterized patients. u
FURTHER READING
Ayliffe G A J, Fraise A P, Geddes A M, Mitchell K, eds. Control of Hospital Infection: A
Practical Handbook. 4th ed. London: Arnold, 2000.
Wenzel R P, ed. Prevention and Control of Nosocomial Infections. 2nd ed. Baltimore:
Williams & Wilkins. 1993.
www.cdc.gov/ncidod/hip/default.htm (CDC Hospital Infection Program; US

government website dealing with all aspects of hospital infections.)
www.phls.co.uk/ (UK National Nosocomial Infection Surveillance Scheme reports on

surgical site infections and hospital-acquired bacteraemia.)

Nutrition in Critical Illness
Frankie Dormon
Frankie Dormon is Consultant in Anaesthesia and Intensive Care in Poole, Dorset,

UK. She qualified and trained in anaesthesia on the North Thames Circuit and was
Consultant in Charge of Intensive Care at Lister Hospital, Stevenage, Hertfordshire, for
10 years. Her main non-clinical interests are teaching PALS, ALERT and CCrISP.
Patient nutrition is an often neglected aspect of the overall management of patients,

but 50% of surgical patients suffer protein energy malnutrition. Sepsis, injury and
starvation are the main contributors to postoperative morbidity and mortality. Following
the initial resuscitation of the critically ill patient, the nutritional status should be
assessed and a plan of nutritional management made. It is best to use the enteral route
if possible, however adequate calorie intake is often difficult to achieve. The currently
available intravenous feeding regimens present a confusing array of mixtures of fat,
carbohydrate, amino acids, vitamins and minerals and there are several steps to follow
to initiate treatment safely. Many hospitals have a nutrition team, which assists with
the management of enteral feed or total parenteral nutrition and helps with monitoring
during treatment, but the clinician should have a working knowledge of patient nutrition
to initiate a good management plan.
Nutritional requirements
The average 70 kg man requires about 2000 kcal/day. Without food, the body uses
glycogen stores and then muscle protein, to provide energy. In the healthy person, the
metabolic rate is reduced and stores are conserved. In illness or after surgery, burns or
trauma, the following sequence occurs.
Energy requirements are increased by up to 30%.
Metabolism is affected by altered levels of catecholamines and cortisol.
Blood sugar control becomes deranged as patients develop an apparent increased
resistance to insulin.
There are major fluid and electrolyte losses from diarrhoea, vomiting or nasogastric
losses, excessive sweating, stoma losses and surgical drains.
Fluid shifts, caused by leaky membranes or fluid moving into the third space, create
difficulties in assessing fluid balance.
Assessing nutritional status

The following identify patients at risk of protein energy malnutrition:
clinical history (e.g. nausea, vomiting, diarrhoea, abdominal distension, previous
surgery, weight fluctuations)
dietary history (types and amounts of food taken, dysphagia)
physical examination (weight: height, body mass index (BMI),
general appearance).
The following tests can be used to establish the severity of protein energy malnutrition
and the response to nutritional intervention:
anthropometric (skin fold thickness)
biochemical (albumin, transferrin and pre-albumin)
immunological (lymphocyte count).
However, they are unspecific, and similar abnormalities may be found in other
conditions. In particular, albumin can fall rapidly with sepsis.
Enteral feeding
If the patient has any functional bowel, the enteral route should be used if possible.
The best nutrition comes from a balanced diet that is chewed, swallowed and digested.
Gut motility is influenced by hormones released during mastication. Stomach emptying
controls the delivery of food to the jejunum to maximize absorption. The gut mucosa is
more likely to retain its normal function if it is bathed in the correct nutrients. The large
bowel requires an adequate amount of fibre to ensure regular soft bowel actions. As
soon as any of these aspects of feeding are defective, the absorption of nutrients is
affected. Factors that reduce the chances of successful enteral feeding are shown in
Figure 1. Problems associated with enteral feeding are listed in Figure 2.
Factors that reduce the chances of successful enteral

feeding
Inadequate swallow due to:

Sedation
Intubation/tracheostomy
Pharyngeal dysfunction
Oesophageal disease
Surgery
Reduced gastric emptying and/or gut motility

Opioids
Pain/anxiety
Postoperative gastric stasis
Pyloric swelling
Suture lines perceived risk of anastomotic leak
Paralytic ileus
1
Problems associated with enteral feeding
Problem Management
Large gastric aspirates Use prokinetics (e.g. metoclopramide,
erythromycin)
Diarrhoea Give fibre feed, examine stool specimen for

Clostridium difficile, check for faecal
impaction and overflow
Patient cant or wont have Use gastrostomy

a nasogastric tube
Distended abdomen Check for constipation, paralytic ileus
Aspiration/regurgitation of Monitor gastric residual 4-hourly Limit volume

feed causing lung of feed used or use parenteral route
contamination
Failure to deliver target volume Follow local unit protocol, avoid stopping feed
unless absolutely necessary 2
Routes of enteral feeding

Nasogastric feeding is the most commonly used route, but it relies on adequate
gastric emptying. Sometimes it is impossible to pass the nasogastric tube or maintain
its position. Feed is usually started at about 30 ml/hour via a continuous infusion pump
and increased slowly, provided the gastric residue after 4 hours does not exceed
200 ml. Regimens aim for a maximum calorie intake that is dependent on weight and
general condition.
Nasojejunal feeding avoids the pylorus and is used in patients with gastric stasis.
Nasojejunal tubes are more difficult to pass and often require insertion under direct
fibre-optic observation. Feeds are started at about 30 ml/hour. Absorption is assessed
by checking for abdominal discomfort and distension.
Percutaneous gastric feeding using an endoscopic technique, a tube is passed

percutaneously into the stomach to avoid the discomfort of a nasogastric tube. These
can be used for continuous or bolus feeds. They are commonly used in patients
requiring long-term enteral feeding, such as those with cerebral palsy, after head injury
and following major maxillo-facial surgery.
Percutaneous jejunal feeding the percutaneously placed tube passes from the
stomach into the jejunum. This route is sometimes used for postoperative feeding if
gastric stasis is likely and a nasojejunal tube cannot be passed.
Type of enteral feed

Most enteral feeds are a mixture of fat, carbohydrate, protein, water, electrolytes,
minerals and fibre (Figure 3). Standard feeds have about 1 kcal/ml, but more
concentrated versions are available with about 1.5 kcal/ml. Energy is delivered as fat
and carbohydrate.
Approximate combinations of nutrients in enteral feeds
Elderly/Frail Normal Sepsis
Protein (nitrogen) 810 g 1016 g 1620 g
Carbohydrate 700 cal 1000 cal 1200 cal
Fat 700 cal 1000 cal 1200 cal
Total calories (non-nitrogen) 1400 cal 2000 cal 2400 cal
Total volume 2.5 litres 2.5 litres 3.0 litres

3
Some specialist feeds (e.g. Pulmocare) provide a greater percentage of calories as fat
(by providing fewer calories derived from carbohydrate, the amount of carbon dioxide
produced is reduced, thereby assisting ventilatory weaning in some patients). Other
specialized feeds (e.g. elemental solutions of amino acids or peptides) are available
for patients with short-bowel syndrome, malabsorption or severe inflammatory bowel
disease. Extra food supplements can also be used to provide extra fat or carbohydrate.
Weaning off enteral feed

Many patients return to general wards on established enteral feed. Weaning back to
a normal diet can be best achieved by its introduction during the day and continuing
with enteral feed at night, reducing the night feeds as the daytime feed increases. The
normal daytime diet can be supplemented by sip feeds comprising sachets of easy-to-
digest, milk-based, flavoured feed. Ward nursing staff should be encouraged to keep
a clear record of nutritional intake, remembering that nutrition stops for surgery and
investigations. Intake is also affected if patients do not like the food offered, are unable
to open the packaging or incapable of feeding without assistance. Ward dietitians have
an important role in advising on nutritional requirements and can be helpful in finding
suitable food supplements to suit an individual patients needs.
Parenteral feeding
When the bowel is not functioning, unable to be used or all attempts at feeding using
this route have failed, parenteral nutrition is indicated. A multidisciplinary nutrition team
including doctors, nurses, pharmacists and dietitians can improve the efficacy of total
parenteral nutrition (TPN). Insertion of a feeding line is usually undertaken by doctors
and cared for by nurses; the dietitian can advise on nutritional requirements and the
pharmacist can recommend nutritional preparations and additives. The whole team
has a role to play in the continuing care of the feeding line, monitoring of response to
therapy and audit of complications.
Patient selection
Common reasons for requiring TPN are:
post surgery if bowel function is likely to be disturbed
short-bowel syndrome
gastrointestinal fistulae
prolonged paralytic ileus
inflammatory bowel disease
preoperatively in malnourished patients with ineffective bowel function.
Sepsis, severe burns and pancreatitis were also considered reasons for using the
parenteral route, but enteral nutrition is now recognized as more appropriate. In some
cases, a combination of parenteral nutrition and enteral feed may be used.
Venous access
Ideally, TPN should be given via a tunnelled subclavian vein central line. The incidence
of catheter-associated infection can be reduced by meticulous care during insertion,
using a full aseptic technique. A post-insertion, chest radiograph should be taken to
exclude a pneumothorax and to check that the catheter tip lies in the inferior vena cava
(such positioning reduces the risk of thrombosis). To reduce the risk of catheter-related
sepsis, the feeding line should be used for TPN only, and no other drugs or fluids
should be given through the catheter nor should the line be used for blood sampling.
Some mixtures of TPN are specially formulated to be given peripherally for short-term
treatment, but intravenous lines used for such a purpose generally have a short life.
Choice of mixture
TPN solutions should contain a balanced mix of protein, carbohydrate and lipid,
together with water, vitamins, electrolytes and minerals. Generally TPN is produced
in large bags containing all the requirements for 24 hours. Protein is provided as a
balanced solution of essential (40%) and non-essential (60%) amino acids.
Lipid emulsions are used because it is possible to supply a large amount of energy
in a small volume (9 kcal/g), which is non-irritant to veins. Glucose (4 kcal/g) is used
as the main source of carbohydrate, but requires close control of blood sugar. Feeds
with a high proportion of glucose may delay weaning from ventilation in some patients,
because they sometimes cause excess carbon dioxide production. Other micronutrients
must be added to mixtures to avoid deficiency after a few days. These include vitamins
and trace elements, which are usually added to the bags in the pharmacy. Electrolytes
can be added if required. Phosphate supplements may be required in considerable
amounts in patients with malnutrition.
Monitoring
when the intravenous route is chosen for feeding, it is important that the correct
nutrients are given in the correct proportions to avoid serious derangement of
electrolytes, blood sugar and fat metabolism. Figure 4 lists the routine investigations
that should be undertaken.
Monitoring for patients being given parenteral feeding
Investigation Frequency Comment
Blood sugar 4 hourly until stable Patients may require insulin therapy
612 hourly when stable good glycaemic control is important
in critical illness
White cell count Daily Rising white count may be first sign of
developing sepsis
Electrolytes Daily May need additional potassium in

daily bag
Urea/creatinine Daily Initially to ensure renal function,

longer term to guide nitrogen
requirements
Calcium/phosphate Twice weekly Phosphate can fall dramatically at

start of treatment. Hypocalcaemia
is common in pancreatitis and sepsis
Plasma lipidaemia Twice weekly Liver may not clear lipid infusions
Liver function tests Twice weekly Albumin may indicate efficacy of

treatment, total parenteral nutrition
can cause fatty liver and raised liver
enzymes
Plasma transferrin and pre-albumin Weekly Assessment of efficacy of treatment
Urinary urea Alternate weeks To aid assessment of nitrogen

balance
Trace elements (e.g. zinc, copper,

iron, selenium) Alternate weeks These may become deficient after
several weeks treatment
Recent advances
The constituents of TPN have been modified and simplified over the past few years.
The use of a single bag every 24 hours reduces the infection risk by reducing the
need to handle the line connections. Several companies have special bags that allow
mixing of the constituents immediately before use without the risk of contamination, this
increases the shelf-life of the product and enables the pharmacy to supply TPN almost
on demand. The vitamins and minerals required are available in single-day vials for
addition immediately before use.
Recent research on immunotherapy suggests that the addition of substances such as

glutamine, arginine and the omega-3 fatty acids, may enhance the immune response
during critical illness. Recent work suggests that blood sugar control in a tight range
reduces mortality in critical care patients. u
FURTHER READING
Anderson I D. Care of the Critically Ill Surgical Patient. London: Arnold, 1999.
British National Formulary. Appendix 7 Borderline Substances.
Goldhill D R, Withington P S. Textbook of Intensive Care Part 4. Nutrition. London:

Chapman & Hall, 1997.

Organ Donation and
Maintenance of the Multiple
Organ Donor
Suzie J Tanser
Gary B Smith
Suzie J Tanser is Specialist Registrar in Anaesthesia, Royal Navy Southampton

General Hospital. She qualified from St Bartholomews Hospital, London, then joined
the Royal Navy. She trained in anaesthesia and intensive care in Plymouth, Exeter,
Portsmouth, Southampton and London and completed advanced training in intensive
care in 2001.
Gary B Smith is Consultant in Intensive Care Medicine at Portsmouth Hospital NHS

Trust and Honorary Senior Lecturer in Critical Care in the School of Postgraduate
Medicine at the University of Portsmouth. After qualifying from the University of
Southampton, he trained in anaesthesia and medicine in the South of England
and at Yale University, USA. His main interests are multiprofessional education,
cardiopulmonary resuscitation and pre-hospital trauma care.
The first reported human-to-human transplant involved corneal grafting and was
carried out in Czechoslovakia in 1905. Today, corneas can be stored in an eye bank
for up to 30 days, enabling over 2000 transplants to take place in the UK every year.
The first successful kidney transplant was performed between two identical twins in
the USA in 1954. Improvements in surgery and anti-rejection therapy have led to 75%
5-year functional survival for transplanted kidneys. In 1983, the first combined heart
and lung transplant was performed at Harefield Hospital, UK. Today, there are nine
UK heart and lung transplant centres and seven UK liver transplant centres. There is
a shortage of all human organs for transplantation, partly because of reduced death
rates from road-traffic accidents and the loss of public confidence following scandals
regarding organ removal. Consequently, it is vital that when suitable organs become
available, they are maintained and used appropriately.
Criteria for donation

Living donors (usually first-degree relatives) can donate one kidney, a lung or liver lobe
without adverse clinical effect. Corneas, heart valves, bone and skin can be donated
up to 24 hours after asystole. The need to maintain structural and functional integrity
in other organs dictates that they are usually removed from beating heart donors (i.e.
those with brainstem death whose breathing is maintained on a ventilator), though
kidneys are occasionally removed in asystole. General criteria for donation are:
the donor should be 075 years (age ranges change regularly)
diagnosis of brainstem death must have been made according to current criteria
respiratory support is being maintained (not always necessary for kidney donation)
no evidence of malignancy (except certain primary brain tumours)
no evidence of transmittable infection (Figure 1)
no objection by the Coroner or, in Scotland, the Procurator Fiscal.
If the potential donor fulfils the above criteria, an adequately trained and informed
member of staff should approach the family for informed assent to remove organs.
The family may decline the offer or stipulate which organs can be removed. Tissues for
research may be taken only if this has been agreed by the family or the deceased. Most
major religious and cultural groups support transplantation, but some have specific
objections. The involvement of a religious leader may be helpful. Once assent has been
obtained, the transplant co-ordinator begins the process of organizing the donation
process.
Contraindications to organ donation
Infections Malignancies
HIV/AIDS Leukaemia
Hepatitis Lymphoma
CJD Myeloma
Malaria Any tumour affecting the
Syphilis organ to be transplanted
Tuberculosis
Rabies
Major systemic sepsis
CNS disease of unknown aetiology
1
Donation process
Potential contraindications to donation must be identified at an early stage. This often
involves detailed, sensitive and explicit questioning of the potential donors family to
exclude the possibility of communicable diseases and to identify possible risk factors
(Figures 1 and 2). A full medical and social history should be obtained and a range of
supporting laboratory tests undertaken:
tissue typing
virology (hepatitis B and C, HIV infection, cytomegalovirus)
haematology (blood group, cross-match, full blood count, coagulation screen)
biochemistry (urea and electrolytes, creatinine, liver function tests)
arterial blood gas analysis
12-lead ECG
chest radiograph
microbiology (culture and sensitivity results).
Risk factors for communicable disease
People at risk include those:

who have ever injected themselves with drugs
who have ever worked as prostitutes
men who have ever had sex with another man
who have ever had sex with anyone living in Africa
who have been treated for haemophilia
who received human growth hormone before 1985
who have a family history of CJD
who have had malaria, rabies or tuberculosis
who have ever had a neurological disorder of unknown origin
who have ever had sex with anyone from the above list
Organ removal occurs in the referring hospital; the operating theatre co-ordinator
should be informed. The transplant co-ordinator organizes the arrival of the retrieval
team(s). The donation process may take 1218 hours, therefore the family may require
considerable psychological support.
Physiological changes following brainstem death

Following brainstem death, there is loss of autonomic and endocrine homeostasis. If left
untreated, these eventually lead to asystole, usually within 72 hours.
Cardiovascular instability ischaemia of the brainstem causes an increase in

sympathetic outflow to maintain cerebral perfusion. This sympathetic storm may
cause arrhythmias, myocardial ischaemia or infarction. Brainstem death results in a
loss of sympathetic tone and progressive hypotension. Hypovolaemia due to use of
diuretics, mannitol or diabetes insipidus may compound this problem. Arrhythmias due
to previous infarction, electrolyte imbalance or hypothermia are common.
Pulmonary effects the sympathetic storm may cause pulmonary capillary damage;
pulmonary oedema occurs in up to half of brainstem-dead patients. Progressive
hypoxaemia due to aspiration or infection is also common.
Endocrine failure there is dysfunction of the hypothalamicpituitary axis, leading

to a fall in circulating cortisol, insulin and free triiodothyronine. This causes electrolyte
imbalance, abnormal cellular metabolism, hyperglycaemia and myocardial depression.
Diabetes insipidus, due to loss of posterior pituitary function, occurs in about 65% of
brainstem-dead patients and results in hypovolaemia and electrolyte abnormalities.
Temperature regulation the thermoregulatory centre is situated in the

hypothalamus; brainstem death causes poikilothermia. Hypothermia results from loss of
heat by conduction, convection and radiation, combined with lack of muscular activity, a
low metabolic rate and loss of vasomotor tone.
Clinical management of the organ donor

Once brainstem death is diagnosed, the management of the donor is directed to
maintaining optimal organ perfusion and oxygenation with a normal fluid, electrolyte
and acidbase balance.
Cardiovascular and electrolyte management particular attention is required if

diabetes insipidus occurs, because incorrect replacement of hypotonic urine with salt-
containing isotonic solutions causes hypernatraemia. Care should be taken with the
choice of site for vascular cannulae. Where possible the arterial cannula is best situated
in the left arm and the central venous catheter in the right internal jugular vein. The use
of adrenaline (epinephrine) may result in organ ischaemia and preferably is avoided.
Dopamine, dobutamine or noradrenaline (norepinephrine) may be used in low doses;
suggested goals are:
mean arterial pressure over 60 mm Hg
central venous pressure 612 mm Hg
urine output 12 ml/kg/hour
potassium greater than 4.5 mmol/litre.
Respiratory support the lowest possible fraction of inspired oxygen (FiO2) should
be used. Positive end-expiratory pressure (PEEP) of 5 cm H2O or over improves
oxygenation, prevents airway collapse and limits pulmonary oedema. Carbon dioxide
production falls after brainstem death, therefore a reduction in delivered minute volume
may be appropriate (best achieved by reducing rate, rather than tidal volume, to prevent
airway collapse). Strict asepsis should be maintained when undertaking tracheal toilet,
and sputum samples should be sent for microbiological surveillance. Suitable targets
are:
partial pressure of oxygen in arterial blood (PaO2) over 10 kPa
PaCO2 4.55.5 kPa
PEEP 57.5 cm H2O
FiO2 less than 40%.
Endocrine replacement improves haemodynamic instability, reduces inotrope

requirements and delays asystole. Suggested regimens for adults include:
antidiuretic hormone (ADH) (vasopressin): bolus 1 unit, infusion 1.54 units/hour
triiodothyronine (T3): bolus 4 g, infusion 3 g/hour
hydrocortisone, 5 mg/kg, or methylprednisolone, 30 mg/kg
insulin to maintain blood glucose at 46 mmol/litre.
Other management issues the donors temperature should be maintained using

warmed fluids, warmed humidified gases and forced air, and warming blankets. Up to
one-third of patients may develop disseminated intravascular coagulation owing to the
release of plasminogen activators from dead brain tissue. Coagulopathies may require
corrective treatment with blood products; the haematocrit should be maintained at 30%.
Anaesthetic considerations brainstem-dead patients do not require analgesia

or sedation, but may have intact spinal reflexes that cause hypertension or muscular
contractions during surgery. Neuromuscular blocking agents and anaesthetic agents or
opiates should be used to prevent reflex contractions and perioperative hypertension,
respectively. Temperature may fall rapidly following skin incision, predisposing to
ventricular fibrillation. Blood loss may be considerable and this should be replaced until
circulatory arrest occurs.
Follow-up the final care of the donor should be identical to that of any other patient
who has died. The time of death is recorded as the time of completion of the first set
of brainstem death tests. The transplant co-ordinator usually writes to the donors
family within 2 weeks of donation to thank them and inform them of the outcome of the
recipient operations. u
FURTHER READING
Buckley T A. Management of the Multiorgan Donor. Intensive Care Manual. Oxford:
Intensive Care Society. Donation of Organs for Transplantation. The Management of

the Potential Organ Donor. London: Intensive Care Society, June 1999.
Jonas M. Brain-stem Death and Management of the Multiple-organ Donor. In: Goldhill
D R, Withington P S, eds. Textbook of Intensive Care. London: Chapman & Hall, 1997.

Organization of and Admission
Criteria for High Dependency
and Intensive Care Units
Simon Mackenzie
Simon Mackenzie is Consultant in Anaesthesia and Intensive Care at the Royal

Infirmary, Edinburgh, UK. His research interests include cardiovascular support, acute
liver failure and the use of severity scoring systems in critical illness.
The term critical care is increasingly used to encompass both intensive and high
dependency care, but there are important differences between them in terms of
organization, patients and treatments.
Intensive care is a service for patients with potentially reversible conditions who
can benefit from more detailed observation and invasive treatment than can safely be
provided in general wards or high dependency areas.
High dependency units (HDUs) provide a level of care intermediate between an
ordinary ward and an ICU.
In some hospitals, one area may fulfil both roles: this may be appropriate when
separate units would be small and lack flexibility.
Organization
Intensive care
ICUs require a nurse:patient ratio of 1:1, a resident doctor without other duties and
consultant cover throughout 24 hours. Few consultants are full-time intensivists, but
they should not have other duties while covering the ICU. Most ICUs are general,
though some support a specific specialty. In the UK, a typical unit contains six beds;
this is small in comparison with those in other European countries and the USA.
Larger UK units may have greater flexibility to cope with fluctuating demand, but do not
necessarily have better outcomes or lower costs. An ICU where care is provided by a
team of intensivists, supported by other clinicians when requested, is described as a
closed unit. A unit in which patient care is delivered by more than one group of doctors
is termed an open unit. In the UK, the latter is more common, though the former may
be associated with better outcomes.
High dependency care

For most hospitals, HDUs are a recent development. Many are specialty, usually
surgically, based though general units are preferable. HDUs provide greater monitoring
and nursing input than is given on general wards, may provide support for single-organ
failure (but not ventilation) and can act as a step down area for patients between
the ICU and the general ward. The nurse:patient ratio on an HDU is 1:2. There is
seldom a resident doctor. Patients are admitted and cared for by their referring team,
the members of which will have duties elsewhere. The ICU staff may be involved in
aspects of management, but will not be the principal caring team.
Admission criteria
Admission criteria must be practical and ethical. The precise indications for admission
depend on the particular unit and the other acute care facilities available. The decision
about admission to ICU is a clinical one for the ICU consultant. It is based on the
patients present condition, the treatment possible, the likely response, co-morbidities
and the patients wishes. Scoring systems used for ICU audit (e.g. APACHE, SAPS or
MPM, see page 94) cannot be used for individual patient prognostication or admission
decisions. Chronological age influences survival after intensive care, but should not be
the sole arbiter for ICU admission. Indeed, limited physiological reserve means that
elderly patients may require admission to the ICU or HDU in cases where younger
patients would not. Similar considerations apply to patients with chronic disease, but
patients with irreversible progression of chronic disease should not be admitted.
When to admit
In principle, patients should be referred early and by a consultant. The working
arrangements of many hospitals make this difficult to achieve. Many patients are
referred late in their illness, after potentially avoidable deterioration, which may include
cardiac arrest. To overcome this, some hospitals have developed an emergency team
that accepts calls from nursing or medical staff in an attempt to ensure early referral.
Typical criteria for referral are given in Figure 1. Late admission may be partly the result
of a lack of ICU beds, but staff attitudes are also important. Doctors outside the ICU
may fail to appreciate what an ICU can offer or may see ICU referral as an admission
of failure. Doctors within the ICU may give the impression that they are too busy to be
bothered with patients who are not really sick.
Specific criteria for ICU referral
Airway
Actual or threatened airway obstruction
Impaired ability to protect airway
Breathing
Respiratory rate < 8 or > 30
Respiratory arrest
Oxygen saturation < 90% on 50% oxygen
Worsening respiratory acidosis
Circulation
Pulse < 40 or > 140
Systolic blood pressure < 90 mm Hg
Cardiac arrest
Metabolic acidosis [H+] > 62 nmol/litre
Urine output < 0.5 ml/kg/hour
Neurological
Repeated or prolonged seizures
Decreasing conscious level
General
Patient causing concern to medical, nursing, physiotherapy staff
Note
Much depends on whether there is an identified and easily remediable cause. It
is the start of an adverse trend despite treatment that is important
Source: McQuillan et al. BMJ 1998; 316: 18538.
Who to admit and where

Patients who require tracheal intubation and ventilation should be admitted to an ICU,
as should patients who require support for two or more organ systems (Figure 2), even
if they do not require ventilation (Figure 3). Patients who require close monitoring rather
than organ support can usually be managed in an HDU, as can many with single-organ
failure (except those who require ventilation).
Classification of organ system monitoring and support
Advanced respiratory support

Mechanical ventilatory support (excluding mask continuous positive airway
pressure or non-invasive ventilation)
Possibility of sudden, precipitous deterioration in respiratory function
requiring immediate tracheal intubation and mechanical ventilation
Basic respiratory monitoring and support

Need for more than 40% oxygen via a fixed performance mask
Possibility of progressive deterioration to the point of needing advanced
respiratory support
Need for physiotherapy to clear secretions at least 2-hourly
Patients recently extubated after prolonged intubation and ventilation
Need for mask, continuous positive airway pressure or non-invasive
ventilation
Patients intubated to protect the airway but not requiring ventilation
Circulatory support
Need for vasoactive drugs to support arterial pressure or cardiac output
Support for circulatory instability due to hypovolaemia from any cause which
is unresponsive to modest volume replacement
Patients resuscitated after cardiac arrest where intensive or high
dependency care is considered clinically appropriate
Neurological monitoring and support

CNS depression, from whatever cause, sufficient to prejudice the airway and
protective reflexes
Invasive neurological monitoring
Renal support
Need for acute renal replacement therapy
Notes
Patients requiring advanced respiratory support should be admitted to ICU
Patients requiring support of two or more organ systems should be admitted
to ICU
Patients requiring single-organ support may be suitable for high dependency
rather than intensive care
Source: DoH. Guidelines on Admission to and Discharge from Intensive Care

and High Dependency Units. London: HMSO, 1996.
3 Intensive care treatment of a patient with multiple organ failure.

Respiratory: patients may be referred with hypoxaemia or ventilatory failure. The
decision to ventilate a patient may be based on blood gas results, but is usually
made on clinical criteria. Patients who are clearly exhausted (e.g. confused, unable to
talk, using accessory muscles) and not responding to treatment should be ventilated
before respiratory arrest ensues, irrespective of their blood gases. Some patients with
hypoxaemia and dyspnoea may respond well to continuous positive airway pressure
in the HDU.
Cardiovascular: patients with deteriorating tissue perfusion (e.g. cool peripheries,

peripheral cyanosis, reduced skin turgor, slow capillary refill, oliguria, reduced
conscious level and metabolic acidosis) should be referred to ICU. Metabolic acidosis is
often overlooked when interpreting blood gas or biochemistry results. Patients in shock
may have surprisingly normal blood pressure. Although oxygen and fluids are almost
invariably required, the underlying cause of shock must be diagnosed and treated.
Patients requiring large-volume fluid replacement, central venous pressure monitoring
or vasoactive drugs should be admitted to an HDU or ICU.
Neurological: many patients with impaired consciousness caused by head
injuries, intracranial haemorrhage, meningitis, encephalitis, drug overdose, hepatic
encephalopathy, hypoxia or other causes require admission to the ICU or HDU. Airway
obstruction, absent airway reflexes, hypoxaemia, and hypoventilation are all indications
for intubation and controlled ventilation. Patients with severe head injuries require
ventilation with intracranial pressure monitoring.
Intravenous anaesthetic agents may be used to control recurrent seizures, but they
should be administered in an ICU.
Patients with neuromuscular diseases (e.g. GuillainBarr, myasthenia gravis) may
require ventilatory support if airway reflexes are impaired or vital capacity is reduced
(< 1000 ml).
High-risk surgery: the perioperative risk of major non-cardiac surgery is high, as is

the risk of more modest surgery in patients with significant cardiorespiratory disease.
Surgery produces a predictable, but temporary, physiological stress, and such patients
can benefit greatly from admission to HDU or ICU postoperatively. Some advocate
admission before surgery for pre-optimization, aiming for a cardiac index of 4.5
litre/minute/m2 and oxygen delivery of 600 ml/minute/m2. Although pre-optimization
remains controversial, the value of good perioperative care is established.
Who not to admit

Patients should not be admitted to the ICU if they are too well, if they refuse or if they
are too ill to benefit. Admitting patients who are too well wastes resources and exposes
the individuals to potential complications.
Patients have the same right to refuse intensive care as they do any other treatment.
If they are unable to express a view (e.g. because of coma), discussion with the
relatives may be helpful in ascertaining the patients wishes. Any advance directive
should be respected, but, in practice, these are uncommon and may be ambiguous.
Patients should not be admitted if further treatment is futile, whether this is because
of co-morbidity or the acute illness. This is often difficult to judge and may be best
resolved by a trial of therapy. There is increasing concern that patients may survive but
have a poor quality of life. However, doctors should be careful not to make decisions
based on their own opinion of another individuals existing or future quality of life.
FURTHER READING
Department of Health. Guidelines on Admission to and Discharge from Intensive Care
and High Dependency Units. London: HMSO, 1996.
Intensive Care Society. Standards for Intensive Care Units. London: Intensive Care
Society, 1997.
Short A I K. Selection of Patients for Intensive Care. In: Tinker J, Browne D R G,
Sibbald W J, eds. Critical Care. Standards, Audit and Ethics. London: Arnold, 1996:
28997.
Smith G, Nielsen M. Criteria for Admission. BMJ 1998; 318: 15447.

Oxygen Delivery and Uptake
Jeremy M Reid
Ravi Gill
Jeremy M Reid is Specialist Registrar in Anaesthetics at Portsmouth Hospitals NHS

Trust. He qualified from Southampton University Medical School. He trained in general
medicine and cardiology in Wessex and the South West of England before deciding on
a career in anaesthetics. He has an interest in intensive care medicine.
Ravi Gill is Consultant Cardiac Anaesthetist in Southampton, UK. He qualified from

Southampton University and trained in anaesthesia at St Thomas Hospital, London and
Southampton, and in critical care in London, Ontario, Canada.
Oxygen is transported from the atmosphere to the tissues where it is used in the
mitochondria to produce high-energy phosphate bonds. The declining partial pressure
of oxygen as it is transported from the atmosphere to the mitochondria is described by
the oxygen cascade (Figure 1).
Oxygen carriage in blood
Oxygen in the alveolus diffuses across the pulmonary capillary membranes; in the
capillaries it is bound to haemoglobin and dissolved in plasma. The amount of oxygen
dissolved in plasma is proportional to its partial pressure (Henrys law) and represents
0.023 ml/100 ml blood/kPa. Oxygen is transported more efficiently when bound to
haemoglobin (an iron-porphyrin compound of four polypeptide chains bound to a
protein globin), forming a readily reversible compound known as oxyhaemoglobin.
The degree of binding depends on the number of polypeptide chains bound to oxygen.
Increased oxygen binding leads to the sigmoid shape of the oxygen dissociation curve
(Figure 2). Oxygen loading and unloading differs according to the shape of this curve.
Oxygen delivery to the tissues is facilitated by a right shift of P50 (the partial pressure of
oxygen at which 50% of haemoglobin is saturated) caused by acidosis, raised partial
pressure of carbon dioxide in arterial blood (PaCO2), increased temperature and
elevated levels of RBC 2,3-diphosphoglycerate.
Oxygen delivery
Oxygen delivery (DO2) = blood flow x arterial oxygen content of blood (CaO2)
CaO2 = (Hb x O2 saturation/100 x 1.39) + 0.023 PaO2
where: Hb is haemoglobin concentration in g/dl (theoretically 1 g of pure Hb can

combine with 1.39 ml of oxygen); PaO2, partial pressure of oxygen in arterial blood
measured in kPa (0.023 PaO2 is the amount of dissolved oxygen in 100 ml blood where
PaO2is measured in kPa).
A worked example concerning oxygen delivery to the body as a whole is given
below.
DO2 = cardiac output x blood oxygen content

Assume Hb = 15 g/dl
Assume blood to be 100% saturated and the partial pressure of oxygen to be 13 kPa
Assume cardiac output to be 5 litre/minute (i.e. 50 dl/minute)
DO2 = 50 x [(1.39 x 1 x 15) + 0.023 x 13] ml/minute
DO2 = 50 x (20.85 + 0.3) = 1056 ml/minute
Therefore DO2 is about 1000 ml/minute
Note that the value for dissolved oxygen under normal conditions is so small (0.3
ml/100 ml of blood) that in most clinical situations it may be discounted
Factors affecting oxygen delivery

The oxygen flux equation shows that the factors affecting oxygen delivery to the tissues
are:
cardiac output or regional blood flow
haemoglobin concentration and abnormal haemoglobin
(e.g. carboxyhaemoglobin, methaemoglobin)
oxygen saturation (related to the partial pressure of oxygen by the dissociation
curve).
Manipulating these factors may alter oxygen delivery. For instance, cardiac output may
be increased by the use of fluids, inotropes or peripheral vasodilators. Haemoglobin
concentration may be increased by the use of RBC transfusion, though transfusion
may cause a drop in cardiac output and may not increase overall oxygen delivery.
The optimum level of haemoglobin varies depending on the clinical circumstance and
remains the subject of great debate. Under normal conditions, blood in the pulmonary
capillaries is almost 100% saturated and therefore increasing the concentration of
inspired oxygen has little effect on global oxygen delivery. However, if the alveolar/
capillary membrane is diseased (e.g. by pneumonia, aspiration) increasing the inspired
oxygen concentration may be beneficial. Manipulation of the above factors may be
important because the outcome of some high-risk surgical patients has been linked to
augmentation of oxygen delivery.
Oxygen uptake
The equation that quantifies single-organ or whole-body oxygen uptake is based on

the Fick principle. Using this formula, the saturation of mixed venous blood (SvO2)
reflects the overall degree of oxygen consumption. A worked example, assuming that
the saturation of mixed venous blood is 75% and that its partial pressure of oxygen is
5.3 kPa, is provided below.
Oxygen uptake (VO2) = cardiac output x (arterial O2 content mixed venous O2 content)
VO2 = 50 x {[(1.39 x 1 x 15) + 0.023 x 13] [(1.39 x 0.75 x 15) + 0.023 x 5.3]}
ml/minute
VO2 = 50 x (21.15 15.76) = 269.5 ml/minute
Therefore global oxygen uptake is about 250 ml/minute
VO2, calculated using SvO2, represents the adequacy of whole- body oxygen
consumption. SvO2 is the 'flow-weighted' average of the venous drainage from various
tissues. Therefore SvO2 may be little changed despite severe hypoxia in a tissue
receiving little blood flow. SvO2 also remains relatively normal if cells are unable to
utilize the oxygen delivered to them. A clinical example is cyanide poisoning. As cardiac
output falls, oxygen is more avidly extracted by tissues and therefore mixed venous
oxygen saturation falls.
Relationship between oxygen delivery and uptake
Oxygen delivery is considerably greater than uptake, providing a large margin of safety. To meet
metabolic demands, oxygen utilization may need to rise 12-fold. In normal subjects, cardiac
output is able to increase only six- or seven-fold, therefore the oxygen extraction ratio (O2ER)
must also be increased if metabolic demands are to be met.
O2ER = VO2/DO2
VO2 seldom exceeds DO2, though it may in a hypermetabolic disease (e.g. sepsis).
Usually DO2 decreases as a result of myocardial failure or haemorrhage and VO2 is
maintained by increasing O2ER until DO2crit is reached. DO2crit is the critical value
of oxygen delivery at which oxygen consumption becomes supply dependent (i.e. the
point of inflexion in Figure 3). At this point, oxygen extraction is maximal. The amount
of oxygen that can be taken up by the tissues is then dependent on the amount of
oxygen delivered.
Many studies have examined the relationship between oxygen delivery and uptake.
Unfortunately many of them are flawed because they calculate both oxygen delivery
and uptake from shared variables with the potential for artefactual results, termed
mathematical coupling. Ideally, studies should use independent methods of measuring
oxygen uptake and delivery. Further work is needed to clarify the relationship between
oxygen delivery and uptake in humans in a clinical setting, before these measurements
can be used to guide treatments aimed at improving clinical outcome.
FURTHER READING
Archie J P. Mathematical Coupling of Data A Common Source of Error. Ann Surg
1981; 193: 296303.
Feldman S, Scurr C, Soni N, eds. Scientific Foundations of Anaesthesia the Basis of
Intensive Care. 4th ed. Oxford: Heinemann Medical Books, 1990.

The Postoperative Patient in
the ICU
Martin Street
Martin Street is Consultant in Intensive Care Medicine at the Royal Sussex County
Hospital, Brighton, UK. He qualified from Birmingham University and trained in intensive
care in Australia.
The major reasons for admitting patients to an ICU in the postoperative period are the
extent of surgery and the presence of significant co-morbidity. This period presents
particular physiological challenges, but with the application of resources available in the
ICU (Figure 1) patient outcome is improved.
Regardless of the surgical procedure, the clinical management of patients in the ICU
has common therapeutic goals.
Resources available in the ICU
Increased nursing staff levels

Increased medical staff levels
Availability of invasive monitoring
Availability of respiratory support
Comprehensive understanding of the complex pathophysiology in the
postoperative period
Early warning of complications
Higher levels of physiotherapy support
Reduction in perioperative morbidity
Maintenance of tissue perfusion
Multiple organ dysfunction syndrome (MODS) is a leading cause of death in non-

cardiac ICUs, with a mortality of more than 50%. Treatment of MODS is largely
supportive, therefore its prevention is vital. Current thoughts regarding its generation
involve the two-hit theory an initial insult primes the host response and a second
insult leads to a massive release of stress hormones, causing profound cardiovascular
and pulmonary changes, and the activation of endothelium complement and clotting
pathways. The initial insult can be multifactorial, including infection, trauma, pancreatitis
and prolonged shock. Second insults include reperfusion injury, hypoxia and infection.
The maintenance of tissue perfusion into the postoperative period is therefore crucial.
It is not clinically possible to measure tissue perfusion at a microvascular level,
therefore there is reliance on whole-body estimations of cardiac output, oxygen
delivery, mixed venous saturation and blood lactate. In the absence of peripheral
vascular disease, estimating the temperature gradient along the limb may give a rough
guide to limb perfusion, but more sophisticated estimations may be made by invasive
monitoring. Careful monitoring of cardiac filling pressures (central venous or pulmonary
capillary wedge pressures) together with cardiac output enables precise titration of
fluids and inotropic drugs.
Renal circulation: adequate urine output (> 0.5 ml/kg/hour) has traditionally been seen
as a marker for adequate renal vascular perfusion. However, previous administration of
loop diuretics may give false reassurance that the patient is adequately hydrated, while
coexisting cardiac failure and oliguria may coincide with water overload. The routine
use of low-dose dopamine has not been shown to prevent renal failure.
Splanchnic circulation: the introduction of gastric tonometry to assess the pH of

the intramucosal cells lining the stomach is believed by some to indicate adequacy of
splanchnic perfusion and is used as a basis for fluid resuscitation. Others have found
this less reliable as an end-point for cardiovascular management and trial evidence
does not support its routine use.
Maintenance of oxygenation
In the immediate postoperative phase, the elimination of nitrous oxide results in falls
in arterial saturation. Increased intrapulmonary shunting and ventilation/perfusion
mismatch should be treated with supplemental oxygen. Patients whose ventilation is
based entirely on hypoxic drive seldom present for elective surgery, but they should be
monitored carefully for hypoventilation and rises in arterial carbon dioxide (PaCO2).
In clinical practice it is difficult to improve arterial oxygenation significantly because
few patients have a haemoglobin saturation below 95% preoperatively. Clinical
management should be directed towards halting any decline in pulmonary function. The
pain associated with large abdominal incisions has a deleterious effect on respiratory
function, causing a reduction in tidal volume and functional residual capacity. The
sudden cessation of smoking postoperatively increases secretion production and small
airways plugging. This, together with the inhibition of coughing, results in alveolar
instability and a tendency to alveolar collapse. Radiographic evidence of basal or plate-
like atelectasis often precedes a further reduction in lower lung zone or lobar (usually
the left lower lobe) aeration. Respiratory physiotherapy promotes the clearance of
secretions and enhances alveolar recruitment in areas of atelectasis.
The combination of poor airway secretion clearance and alveolar instability
increases the risk of nosocomial infection. Gram-negative pathogens usually
predominate; however, the prolonged use of antibiotics perioperatively risks the
selection of more resistant organisms such as Pseudomonas aeruginosa.
Postoperative ventilation: elective ventilation is commonly employed following major

surgical procedures. This reduces both the metabolic demand associated with the
work of breathing and voluntary muscular activity. It allows better matching of oxygen
demand to supply until the effects of fluid shifts and blood loss are overcome (Figure 2).
Balance of tissue perfusion and metabolic demand
Myocardial
Lung function Haemoglobin Fluids
contraction
Arterial oxygen Cardiac output

content
Pain
Shivering
Sepsis
Surgery
Metabolic demand Tissue perfusion
Increased oxygen demand Increased oxygen supply
Analgesia and sedation
Adequate analgesia and sedation maintains patient comfort, ameliorates the metabolic
response to surgery and trauma and halts the postoperative decline in lung function. It
may be achieved by continuous or patient-controlled opiate infusions. However, local
anaesthetic epidural infusions provide better analgesia and improve ability to cough.
Sedation for postoperative ventilation is best achieved with short-acting drugs (e.g.
benzodiazepines, propofol) administered by infusion. Their hypotensive side-effects can
usually be ameliorated by fluid or inotropic support.
Simple clinical end-points (Figure 3) can be used to guide successful weaning from
ventilatory support in the postoperative period.
Clinical management of postoperative ventilation
Warm peripheries Achieve by producing adequate cardiac output with

the administration of fluids and inotropes to ensure
adequate peripheral perfusion
Wake Reduce sedation
Wean Gradually reduce respiratory support
Maintenance of homeostasis
Haemostasis
Bleeding is a common event in the postoperative phase and results from a variety of
causes:
ligature failure
relaxation of vessel wall spasm
hypothermia
coagulation disorder
thrombocytopenia.
Patients requiring transfusions exceeding 1 unit/hour over a 4-hour period should be
assessed, if necessary by laparotomy, to exclude surgical causes. Haemorrhage may
be caused by a combination of surgical bleeding (e.g. slipped surgical ties) and a
coagulopathy in the same patient; these may require simultaneous correction.
Haemoglobin
It has been accepted practice to transfuse patients to a haemoglobin of 10 g/dl both
pre- and post-surgery. Recent studies have called this arbitrary practice into question
and emphasized the disadvantages of supporting a higher haemoglobin in critically ill
patients (Figure 4). Further trials are required to elucidate the risk:benefit ratios of these
two competing strategies. The use of haemopoietic drugs such as erythropoietin, which
offer the benefit of a high haemoglobin without the side-effects of transfusion, may
prove useful. However, they are not currently recommended, primarily on cost grounds.
Relative merits of competing transfusion strategies
Advantages of higher haemoglobin

Improved arterial carriage of oxygen
Decreased risk of coronary ischaemia
Margin of safety for further blood loss
Advantages of fewer transfusions and lower haemoglobin

Improved microcirculatory blood flow and oxygen delivery
Decreased cardiac work from decreased blood viscosity
Decreased immunosuppression
Nutrition
In healthy individuals, the intestinal mucosa is an efficient barrier to the entry of bacteria
and bacterial products into the portal circulation. Atrophy of the mucosa occurs rapidly
after surgery and injury, and is also quantitatively associated with its severity.
Total parenteral nutrition has also been associated with mucosal atrophy and
increased bacterial translocation. The introduction of the amino acid glutamine into total
parenteral nutrition solutions and the establishment of early enteral nutrition have been
shown to inhibit these mucosal changes and to be associated with increased patient
survival. The addition of omega-3 fatty acids, arginine and nucleotides to the enteral
feed may confer additional benefits.
The placement of enteral feed directly into the jejunum, using percutaneous or
endoscopically placed tubes, may be safely instituted in conditions such as pancreatitis
that historically have been managed with intravenous feeding.

Pain Relief in Intensive Care
Sue Smith
Sue Smith is Consultant in Anaesthesia and Intensive Care. Her interests include
pharmacology, nutrition and steroid metabolism in the critically ill.
For patients in the ICU, many aspects of their illness and treatment may lead to
discomfort and pain. However, pain is difficult to assess in ICU patients because
of communication difficulties and because the usual clinical signs of pain (sweating,
tachycardia, hypertension) may be caused by sepsis, stress or catecholamine
administration. Nevertheless, there are opportunities to use analgesic techniques that
would be unsuitable for other hospital patients.
Opiate analgesics
Opiates provide the mainstay for analgesia in critically ill patients. Their systemic effects
(Figure 1) predominantly result from their actions on receptors.
Systemic effects of opiates
Decrease systemic vascular resistance
Decrease blood pressure, partly due to histamine release
Bradycardia in high doses
Respiratory system
Respiratory depression
Decreased ventilatory response to hypoxia and hypercapnia
Antitussive
'Wooden chest' syndrome
CNS
Potent analgesic
Causes drowsiness
Relieves anxiety
Produces euphoria
Miosis is produced by direct stimulation of the EdingerWestphal nucleus
Muscle rigidity
Renal system
Increased tone in the ureters, bladder detrusor muscle and sphincter
Urinary retention
Nausea, vomiting
Constipation due to decreased gastrointestinal motility
Decreased gastric acid, biliary and pancreatic secretions
Metabolic
Increased secretion of antidiuretic hormone leading to impaired water
excretion, hyponatraemia
Other
Mild diaphoresis and pruritus due to histamine release
Side-effects
Hallucinations
Dependence
Morphine
Morphine is a phenanthrene derivative. It is both a and receptor agonist. It can be
administered orally, intramuscularly, intravenously (single dose, infusion or via a patient-
controlled analgesia device), intrathecally or into the epidural space. Age and disease,
especially liver and renal failure, alter its pharmacokinetics.
Morphine is well absorbed when administered orally but is susceptible to first-pass
metabolism. The bioavailability by this route is only 1550%. It is 2040% protein
bound and equilibrates slowly with the CSF. There is no correlation between plasma
drug levels and the degree of analgesia.
Morphine is metabolized in the liver by conjugation to morphine-3-glucuronide,
morphine-6-glucuronide and nor-morphine. The glucuronides are potent analgesics in
their own right and have longer elimination half-lives than morphine.
Excretion of morphine occurs predominantly via the urine, but 710% appears in the
faeces. The clearance of morphine is 123 ml/minute/kg and its elimination half-life is
1.74.5 hours. The elimination half-lives of the glucuronides vary from 4.5 to over 100
hours with declining renal function.
Morphine metabolites are water soluble, renally excreted and are not removed
efficiently by haemodialysis/haemodiafiltration.
Alfentanil
Alfentanil is a highly selective, synthetic, anilinoperidine derivative with agonist
activity. It produces a bradycardia of vagal origin with hypotension, but cardiac output,
systemic vascular resistance and pulmonary capillary wedge pressure are unaffected.
Chest wall rigidity may result from receptor stimulation of GABA-ergic
interneurons. Alfentanil causes minimal histamine release; bronchospasm is not a
feature. The stress response is reduced.
Alfentanil is 1020 times more potent than morphine, but does not produce
hypnosis or sedation. It is 8592% protein bound and is predominantly metabolized
by the hepatic cytochrome P450 enzyme group by N-dealkylation to noralfentanil.
The remainder is metabolized using other reactions, including hydroxylation,
O-demethylation, and amide hydrolysis followed by acetylation. The major phase II
pathway is by glucuronidation. There is evidence for genetic polymorphism in its
metabolism and several pathways are saturable. At low doses (< 2 mg/hour in
adults), the drug exhibits first-order kinetics, but in liver failure, septic shock or when
higher dosing regimens are used, zero-order kinetics operate, thus explaining the long
recovery time from termination of the infusion. Its elimination half-life for first-order
kinetics is 100 minutes but increases exponentially when saturation occurs. Likewise,
the half-life is greatly increased in liver disease and in the elderly. Erythromycin,
cimetidine and ranitidine significantly inhibit its metabolism.
Studies suggest that the higher costs of alfentanil (in com-bination with propofol) are
outweighed by shorter weaning times, shorter stays in ICU, and a lowered incidence of
withdrawal syndromes compared with morphine and midazolam.
Remifentanil
Remifentanil seems to be an ideal analgesic agent for critically ill patients because of its
cardiovascular stability and organ- independent pharmacokinetics. It undergoes rapid
ester hydrolysis by non-specific esterases to a carboxylic acid derivative, which is much
less potent and is excreted by the liver.
Remifentanil is unlicensed, but undergoing trials for ICU use. It does not possess
sedative actions and causes significant nausea and vomiting. Board-like rigidity, due
to GABA-receptor activation in the chest wall can make respiration and ventilation
difficult. Consequently, care must be taken in the flushing of intravenous lines in which
remifentanil has been administered.
Pethidine
Pethidine is of limited use in critically ill patients because its metabolite (norpethidine)
accumulates in renal failure and is excitatory and epileptogenic.
Codeine phosphate
Codeine has a low affinity for opioid receptors. It is less potent than morphine and is
traditionally used for analgesia in patients with head injuries, because of the alleged
reduced risk of respiratory depression.
If the drug is given intravenously or in overdose, cardio-vascular collapse may occur.
Therefore, its use is limited to the treatment of diarrhoea (reduced gastrointestinal
motility) and in managing mild-to-moderate pain. The dose should be reduced in
patients with renal failure.
Non-opioid analgesics
Paracetamol
Paracetamol is an acetanilide derivative that can be administered orally, enterally or
rectally. It is a potent prostaglandin synthesis inhibitor within the CNS; this explains
its antipyretic action (inhibition of pyrogen-induced, prostaglandin synthesis by the
anterior pituitary). It acts peripherally as an analgesic by blocking bradykinin-sensitive
nociceptors. The drug is rapidly absorbed from the stomach, therefore plasma levels
can be used as a measure of gastric emptying. Bioavailability is 7090% owing to
first-pass metabolism in the liver. 80% is metabolized to glucuronide and sulphate
derivatives, and 10% is metabolized via the cytochrome P450 group to a highly reactive
metabolite, which is immediately inactivated by conjugation with glutathione.
Non-steroidal anti-inflammatory drugs (NSAIDs)

NSAIDs are useful for the relief of musculoskeletal pain, as an adjuvant to paracetamol
and for reducing opiate dose. However, all NSAIDs, even the highly selective COX-2
inhibitors, have significant side-effects (Figure 2), especially in critically ill patients.
NSAIDs exert their anti-inflammatory, analgesic and antipyretic actions by reversibly
blocking the conversion of arachidonic acid to PGG2 a reaction catalysed by cyclo-
oxygenase.
NSAIDs are extensively protein bound and a given dose has a greater effect if
hypoproteinaemia exists. NSAIDs increase the anticoagulant effect of concurrently
administered warfarin by displacement from plasma proteins.
Side-effects of non-steroidal anti-inflammatory drugs
Hypertension
Sodium and water retention
Peripheral oedema
Closure of ductus arteriosus
Gastritis
Gastric ulceration and haemorrhage
Small bowel villous atrophy
Diarrhoea
Reversible hepatic dysfunction
Renal system
Interstitial nephritis
Renal vasoconstriction
Cortical blood flow diversion
Acute renal failure with hypovolaemia and ACE inhibitors
Blood
Inhibition of platelet aggregation
Prolongation of the bleeding time
Decreased killer T cell activity
Entonox
The combination of inhaled Entonox (50% oxygen; 50% nitrous oxide) may be of benefit
during physiotherapy or if regular dressing changes are required (e.g. burns, necrotizing
fasciitis).
Antidepressants
Antidepressants have mood-altering properties and permit rapid eye movement (REM)
sleep patterns to be established. Tricyclic antidepressants have analgesic properties
and also block the reuptake of noradrenaline at the postsynaptic nerve terminals.
Noradrenaline is a potent analgesic in the CNS and both pain relief and mood alteration
occur within 37 days.
The high incidence of anticholinergic side-effects and drug interactions may limit the
use of antidepressants.
Epidural blockade
Epidural analgesia is increasing in the ICU because it provides superior pain relief
without sedation. The combination of a dilute local anaesthetic solution with a
preservative-free opioid produces superior analgesia. The use of epidural analgesia
in patients with severe chest injuries has reduced mortality and morbidity by avoiding
the need for intubation and ventilation. Epidurals preserve the cough reflex, allow deep
breathing, preserve functional residual capacity, facilitate chest physiotherapy and
permit early mobilization.
Concerns have been raised about the possible link between epidural anaesthesia
and anastomotic breakdown following bowel surgery. One possible cause is that
hypotension and reduced cardiac output following the epidural may decrease
splanchnic blood flow.
Epidural anaesthesia is useful in reducing the incidence of post-amputation phantom
limb pain, especially if the autonomic blockade is established before amputation.
Regional blockade
The ability to leave a catheter in the femoral nerve sheath makes local anaesthetic,
femoral nerve blocks useful for relieving pain after femoral fractures or mid-thigh
amputations.
Similarly, catheters may be placed in the axillary or brachial plexus sheaths
to provide analgesia for fractures and vasodilatation when extensive reconstructive
surgery has been undertaken. It may also protect against reflex autonomic dystrophies.
For analgesia to be satisfactory with an intercostal nerve block (e.g. for fractured
ribs), it must be repeatedly performed, with the risk of a pneumothorax. This
complication is avoided by the placement of an intrapleural catheter and the use of a
local anaesthetic infusion.
Stellate ganglion blocks may be used in certain situations, such as quinine overdose,
methanol toxicity and inadvertent drug extravasation into the upper limb tissues.
Other therapies
Attention to pressure areas, mobilization, nutrition, mood, prevention of sleep

deprivation and communication will relieve the discomfort of immobility. The pleasure
of touch and massage may also promote well-being. Transcutaneous electrical nerve
stimulation (TENS) machines may also help. Occasionally, other assistance may be
required, such as the specialist advice of neurologists, chronic pain specialists or the
palliative care team.
FURTHER READING
Sasada M S, Smith S P. Drugs in Anaesthesia and Intensive Care.2nd ed. Oxford:
Oxford University Press, 1995.

The Role of Tracheostomy in
ICU
Andrew R Bodenham
Ben N Barry
Andrew R Bodenham is Consultant in Anaesthesia and Intensive Care at Leeds

General Infirmary, UK. He trained in London, Cambridge, Brisbane and Leeds. His
interests include adult intensive care, the airway, vascular anaesthesia and vascular
access.
Ben N Barry is Specialist Registrar in Intensive Care at Leeds General Infirmary, UK.
He trained in London, Sheffield and Leeds and has specialized in anaesthesia and
intensive care. He has recently finished advanced training in intensive care.
Historically the main indication for tracheostomy has been to bypass an upper
airway obstruction, for example that caused by diphtheria. Modern open surgical
tracheostomy techniques were standardized in 1909 by Chevalier-Jackson. In the early
days of intensive care, including the Scandinavian poliomyelitis epidemics of the 1950s,
tracheostomy became the accepted means of airway management for provision of
longer-term assisted ventilation (Figure 1). Tracheostomy provides protection against
aspiration of pharyngeal secretions and access for suctioning pulmonary secretions. In
the following decades, patients requiring intensive care were more commonly managed
initially by translaryngeal intubation with tracheostomy only after 23 weeks. The recent
development of percutaneous tracheostomy techniques has reawakened interest in the
place of tracheostomy in the ICU.
1 Adolescent in the early days of

the Tetanus Unit at Leeds General
Infirmary. Manual ventilation via a
red rubber tracheostomy tube with
carbon dioxide absorption in a Waters
canister. The patient made a full
recovery. Photograph kindly provided
by Professor J Norman.
Indications for tracheostomy in the ICU

The most common indication for tracheostomy in ICU patients is prolonged airway care,
though there are often coexisting problems that favour early tracheostomy in preference
to prolonged translaryngeal intubation (Figure 2). Survivors of prolonged intensive care
are often profoundly weak (e.g. from critical illness neuropathy or myopathy) and are
therefore unable to clear pulmonary secretions unaided until their condition improves.
Acute upper airway obstruction is usually managed initially by translaryngeal intubation
but tracheostomy may be used to secure the airway in patients undergoing head and
neck surgery, for example for obstructing tumours and after laryngectomy. Patients with
laryngeal incompetence, brain injury, cerebrovascular or neuromuscular disease, may
require long-term tracheostomy to reduce the risk of aspiration and facilitate removal
of pulmonary secretions.
Indications for tracheostomy in ICU

Prolonged weaning from assisted ventilation
Acute and chronic neuromuscular conditions
Poor cardiorespiratory reserve
Bulbar dysfunction
Brain injury
Benefits of tracheostomy
Tracheostomy offers the patient significant advantages over prolonged translaryngeal
intubation. The patient is generally more comfortable, allowing a reduction in sedative,
analgesic and muscle-relaxant drugs; clearance of airway secretions, general nursing
care and enteral nutrition are all facilitated. There is a reduced incidence of accidental
extubation and endobronchial intubation. Verbal communication may be possible as
the patient awakens and regains laryngeal competence. A fenestrated (speaking)
tracheostomy tube may be inserted, or the tube cuff may be deflated to allow
phonation. Airway res-istance and anatomical dead space are reduced, reducing the
work of breathing and improving the chances of weaning from assisted ventilation.
Tracheostomy may allow earlier discharge from the ICU to the high-dependency unit
or a general ward.
Timing of tracheostomy
The decision when to convert translaryngeal intubation to tracheostomy remains
controversial. An assessment of the risks and benefits for performing a tracheostomy
should be carried out daily. Tracheostomy is associated with serious complications (see
below). Conversely, the incidence of laryngeal injury and subglottic stenosis increases
significantly over time with prolonged translaryngeal intubation.
It is desirable to minimize the risks of both means of airway maintenance.
The present consensus is that translaryngeal intubation should be converted to
tracheostomy at 714 days, unless rapid improvement is likely. If it is apparent
earlier that the patient will require prolonged respiratory support (e.g. GuillainBarr
syndrome, cervical cord injury or traumatic brain injury) then earlier tracheostomy may
be appropriate. If there is uncertainty about the patients ability to maintain airway and
respiratory function unaided, a trial of extubation is often performed to ascertain the
need for prolonged airway instrumentation.
In children and adolescents, the relative risks of tracheostomy are higher than in
adults, therefore it is usual not to perform tracheostomy unless it is likely to become a
long-term or permanent requirement.
The complications of tracheostomy are common to all insertion techniques (Figure 3).
The distinction between early and late complications is somewhat artificial because
many problems on initial insertion or re-insertion may develop into late complications.
The changing indications, less frequent use of open insertion techniques, use of less
traumatic tubes and better aftercare should reduce the incidence of complications.
However, the overall number of complications is likely to increase as the number of
tracheostomies performed in intensive care patients increases.
Early Late
Haemorrhage Stomal infection
Obstruction by blood clot or Tracheal stenosis
mucous plugs Tracheo-oesophageal fistula
Misplacement Tracheo-innominate artery fistula
Dislodgement Tracheomalacia
Subcutaneous emphysema Obstruction by mucous plugs
Pneumothorax
Injury to adjacent structures
Tracheostomy techniques
Open tracheostomy
Open tracheostomy is well described in standard surgical texts. The neck is extended
and a horizontal or vertical skin incision made over the trachea. The platysma muscle is
incised and the strap muscles are separated in the midline. Further dissection exposes
the thyroid isthmus, which can be retracted or divided to expose the trachea. An incision
is made into the trachea to accommodate an appropriate sized tube. There is little
evidence to help choose which tracheal incision to use. Pressure necrosis from the tube
ultimately makes all incisions circular and of a size dependent on the indwelling tube
used. Adequate haemostasis is crucial to minimize bleeding into the trachea, and thus
to reduce the potential for airway obstruction by blood clot.
Percutaneous tracheostomy
Techniques for percutaneous tracheostomy at the bedside were described in the 1960s
but medical museums contain much earlier instruments for rapid tracheostomy (Figure
4). New techniques based on the Seldinger needle-guidewire method and better
materials have allowed safer percutaneous airway access. Common to all dilatational
techniques are: a superficial skin incision, localization of the trachea by needle with
free aspiration of air, insertion of a guidewire, formation of a tract with blunt dilators
and subsequent insertion of a tracheostomy tube. The technique of dilatation varies
between different kits using one or more serial dilators, or specially designed forceps
(Figure 5).
4 Tracheostomy set from the 19th century. Note fenestrated silver tube
with inner liner. Scalpel and sharp introducing forceps. Kit kindly lent for
photography from Thackray Medical Museum, Leeds.
a b
5 Percutaneous tracheostomy kits. a Cook Ciaglia serial dilators,12 FG to 36 FG (Portex

tube mounted on 24 FG dilator); b Cook Blue Rhino single dilator; c Portex kit dilating
forceps, cannula over needle, guidewire and dilator; d indentations on Portex dilating
forceps marking top of groove through which guidewire runs to allow insertion of forceps
in closed position.
In ICU, procedures are performed at the bedside with the patient in the conventional
position for tracheostomy. Procedures should be performed or supervised by senior
staff in daylight hours when surgical and theatre assistance is readily available if
required. Anaesthesia should be provided as for a conventional surgical tracheostomy
and by a separate anaesthetist. The authors currently use a total intravenous technique
with propofol and alfentanil infusions; a muscle relaxant is not essential but makes the
procedure easier. The procedure can be performed under local anaesthesia alone, but
this is likely to be unpleasant for the patient. The patient is usually already intubated
and ventilated prior to the procedure; a laryngeal mask airway provides an alternative
means of airway control. The anaesthetist withdraws the tracheal tube under direct
laryngoscopy until the cuff is seen to lie within the larynx, avoiding the risk of transfixion
of the tube or cuff with the needle and guidewire.
After preparation with sterilizing solution and the application of drapes to maintain
a sterile field, the area of incision is infiltrated with local anaesthetic (e.g. 1% lidocaine
(lignocaine) with adrenaline (epinephrine) 1:200,000). A superficial 1.52 cm horizontal
skin incision is made over the space between the second and third or third and fourth
tracheal rings. The subcut-aneous and pretracheal fascial layers are opened by blunt
dissection with forceps; on occasion, large anterior jugular veins are identified and may
require ligation. The trachea is palpated through the incision to improve orientation and
confirm anatomy. The thyroid isthmus need not be identified or specifically avoided.
The trachea is entered with a cannula over needle, confirmed by the free aspiration
of air into a partially fluid-filled syringe. A guidewire is passed into the trachea and the
tract dilated to accept an 8 or 9 mm internal diameter tracheostomy tube.
Bronchoscopy using a fibre-optic scope passed through the tracheal tube may be
used routinely to guide correct placement of needle, guidewire and tube or may be
reserved for teaching or difficult cases only. The presence of a fibre-optic scope may
hinder ventilation with consequent risk of hypoxia or elevation in partial pressure of
carbon dioxide in arterial blood (PaCO2) and intracranial pressure. It is also easy to
cause expensive damage to the bronchoscope by needle puncture.
Open versus percutaneous techniques

Studies have tended to favour percutaneous techniques in ICU patients, but operator
experience and aftercare are likely to be as important as individual insertion technique
or reported device malfunction. In many units, dilatational techniques have almost
completely replaced conventional techniques in adult patients. Percutaneous
techniques have the following advantages:
quicker and easier to perform at the bedside
less risk of early bleeding
reduced risk of stomal infection
better cosmetic result by virtue of the smaller incision.
However, there is a higher risk of tracheal damage and other complications related
to insertion.
With experience, percutanous techniques can be successfully performed in more
difficult patients including those with abnormal coagulation, chronic lung disease,
morbid obesity, previous tracheostomy or thyroidectomy, halo-traction and critical
oxygen dependency. Relative contraindications to dilatational techniques include a
large goitre, malignant infiltration or other anatomical abnormalities. Worldwide, many
centres routinely use open techniques because of the cost of percutaneous devices,
lack of experience in such techniques and conservatism in medical practice.
Choice of tracheostomy tube

A large number of different tubes and materials are commercially available (Figure 6)
and some manufacturers provide custom-made tubes. In an adult, 79 mm internal
diameter tubes are typically used. In the patient with an increased distance between
skin and trachea (e.g. obesity, tumour, haematoma) a long-shanked adjustable flange
tracheostomy tube should be used. Tubes are available with fenestrations to allow
speech, removable inner liners for ease in cleaning, plus various other features to aid
communication and suction of secretions.
b c
a
d e
g
h
6 Tracheostomy tubes.
a Portex 9.0 mm profile cuff tube; b Shiley size 8 low pressure cuff tube; c Portex 7.0 mm
adjustable flange tube; d Shiley size 6 fenestrated tube with plain and fenestrated inner
tubes; e Shiley 3.0 neonatal tube; f silver 34 FG tube with plain and speaking valve inner
tubes and trocar; g silver tube speaking valve; h Shiley fenestrated inner tube.
Role of cricothyroidotomy
The larynx lies superficially at the level of the cricothyroid membrane and so this
procedure may be performed rapidly in an emergency to relieve airway obstruction.
Kits are available for rapid insertion of 46 mm tubes using a modified Seldinger
technique or a traditional surgical cut-down may be performed. Cricothyroidotomy in
the non-emergency setting is commonly referred to as minitracheostomy; it has been
used for patients with sputum retention and atelectasis not requiring protection against
pulmonary aspiration or assisted ventilation. The widespread use of percutaneous
tracheostomy has made the use of minitracheostomy for such patients less common.
Aftercare and decannulation
Obstruction is a recurrent problem with all types of tracheostomy tube. Humidification,

tracheal suction and physiotherapy are all essential to avoid accumulation of respiratory
secretions with crusting and subsequent tube blockage. If left untreated, the patient will
suffer respiratory distress, hypoxia and hypercapnoea, proceeding to cardiorespiratory
arrest.
The risk may be reduced by adequate frequency of suction and removal of the
inner tube for cleaning, or changing the tube, as applicable. In the short term, a
spontaneously breathing patient will manage to breathe adequately through a formed
stoma. Never be afraid to remove a tracheostomy tube if there is doubt regarding its
patency and the adequacy of the airway. The stoma will usually be established by 7
days and there should be little difficulty in replacing the tube: alternatively the patient
may be reintubated by the oral route.
In the patient who is recovering following intensive care, there is a general tendency
to leave the tracheostomy tube in place for too long. Once the patient is able to cough to
clear secretions and protect the airway, consideration should be given to removing the
tube, because its presence limits generation of an effective cough and may promote a
tracheitis. There is no ideal way to assess when the patient is ready for decannulation,
though a multidisciplinary approach, in consultation with physiotherapists and nurses is
prudent. The risks associated with a failed decannulation are likely to be minimized if
decannulation is carried out during daylight hours because the patient requires a period
of close observation and may require tube reinsertion. After successful decannulation,
stomas are usually left to granulate and close spontaneously. Recently closed wounds
may be re-opened by blunt dissection if needed. A few patients require late surgery to
release a tethered wound or excise a persistent sinus.
FURTHER READING
Dulguerov P, Gysin C, Perneger T V, Chevrolet J C. Percutaneous or Surgical
Tracheostomy; A Meta-analysis. Crit Care Med 1999; 27: 161725.
Freeman B D, Isabella K, Cobb J P et al. A Prospective, Randomized Study Comparing
Percutaneous with Surgical Tracheostomy in Critically Ill Patients. Crit Care Med 2001;
29: 92630.
Shepherd M P. Tracheostomy. In: Jackson J W, Cooper K C eds. Rob Smiths Operative
Surgery, Thoracic Surgery. 4th ed. 1986; 12434.
Wilson R, Bodenham A. Percutaneous Tracheostomy. Br J Hosp Med 1993; 49: 1236

Secondary Transport of the
Critically Ill
Saxon Ridley
Saxon Ridley is Consultant in Anaesthesia and Intensive Care at the Norfolk and
Norwich Hospital, UK. He qualified from the Royal London Hospital and trained in
London, Whitehaven, Exeter and Glasgow. His research interests include outcome
following intensive care and the cost of intensive care.
Transport of patients may be divided into primary and secondary. Primary transport
refers to the movement of patients from the scene of an accident or the onset of illness
to hospital where their presenting problems can be assessed, stabilized and treated.
Secondary transport refers to the movement of the patient after initial assessment
and may be to specialized diagnostic or therapeutic facilities within the same hospital
(intra-hospital) or another hospital (inter-hospital).
In the UK, the secondary transfer of critically ill patients started under the auspices
of the Clinical Shock Study Group in Glasgow. This specialized transfer team has been
responsible for most of the inter-hospital transfers in the West of Scotland for almost
30 years. Early publications from this group outlined the physiological changes that
could be expected during transfer of critically ill patients and these principles form the
basis of the clinical management of such patients. In the UK, just over 10,000 critically
ill patients require secondary transfer each year. Despite the logistic advantages and
improved patient outcome when transfers are undertaken by specialist teams, there are
few such teams and most transfers are undertaken by the staff of the referring hospital
who do not regularly perform such tasks.
In the UK, where intensive care facilities are relatively sparse, the concept of ICUs
working together as a web to provide a geographical or regional service is being
considered to maximize the use of resources. The recent introduction of the National
Intensive Care Bed Register and biannual census of ICU beds emphasizes the political
interest in this area.
Reasons for transfer
Patients may require transfer to an alternative ICU for several reasons.
Upgrade in care: specialist services may not be available at the base hospital.
Examples include regional centres for cardiac and neurosurgery, burns and renal failure
management. Occasionally, transfer is required because the referring clinician believes
that the patient may benefit from the greater expertise and experience available at a
larger centre.
Special investigations such as MRI under general anaesthesia are available only at
certain large hospitals.
Inadequate facilities at the referring hospital may require the patient to be transferred
to an ICU.
Social: moving a critically ill patient to an ICU nearer home to facilitate family support
and minimize disruption to family life may be advantageous.
Principles
The principles underpinning transfer of the critically ill may be broadly divided into
organizational and clinical. Attention to both is vital if transfer is to be effective and
safe.
Organization
Good communication between the referring and receiving hospitals is essential.
Communication is usually on a regional or geographical pattern. Senior medical staff
should make all transfer decisions.
Nominated consultant: in each hospital a consultant should be responsible for the

transfer of all critically ill patients. The consultant should develop local protocols for
a safe and efficient transfer service that can be maintained on a 24-hour basis. The
consultant should also be responsible for auditing care during transfer and ensuring that
the accompanying staff are adequately trained.
Accompanying personnel: working in the confined space of an ambulance is difficult

and should not be delegated to inexperienced staff because clinical signs are not easy
to recognize and the work is unsupervised. Training of the accompanying staff is vital
to ensure patient safety.
Transfer teams: ideally, movement of critically ill patients should be conducted as

a regionally or geographically based service; however, this would require significant
additional funds and may not be feasible in the short term. Regional teams are probably
best for the semi-elective transfer of patients requiring an upgrade of care or special
investigations. For potentially unstable patients requiring urgent surgery, the regional
teams response time may be too long and the patient may require a more expeditious
transfer.
Clinical principles
The overriding clinical principle is that the intensive care environment should be moved
with the critically ill patient, though active intervention is almost impossible en route.
Preparation and stabilization: anything that may have to be done en route should be
carried out before departure. Resuscitation, stabilization and preparation are mandatory
before departure from the referring hospital. Monitoring is essential to ensure stability or
to detect any adverse physiological changes that may occur during transfer. The systolic
arterial blood pressure must be measured with an intra-arterial cannula because
vibration and movement artefacts make non-invasive methods unreliable. Manipulation
of the cardiac filling pressures may be needed to stabilize the patient before transfer.
Patients must be hypervolaemic and if fluids alone are inadequate to render the patient
hyperdynamic, then inotropes should be added. Modern portable transfer monitors
have at least two pressure channels and so should allow simultaneous measurement of
arterial and central venous blood pressure.
Stabilization of the respiratory system usually involves tracheal intubation and
mechanical ventilation. The effectiveness of mechanical ventilation should be checked
by blood gas analysis before departure and capnography en route. A high inspired
oxygen fraction is required because of changes in ventilation/perfusion mismatch
associated with acceleration and deceleration forces during transfer.
Sedation is vital so that the adrenergic response to transfer is minimized. An
uncontrolled adrenergic response confuses the physiological trends associated with
transfer.
Speed of transfer: a stable ICU patient should be moved at normal speed in an

unhurried fashion. Normalization of physiological parameters before transfer offers
some scope for deterioration as a result of the normal forces experienced during travel.
Speed is required only for specific, initial life-saving interventions such as extradural
haematoma evacuation and aortic aneurysm rupture repair. Relevant case notes,
radiographs, a referral letter and investigation reports should be transferred with the
patient. A record of the patients physiological parameters and interventions undertaken
en route should also be left at the receiving centre.
Personnel
Medical staff: all medical staff involved in transferring critically ill patients should be
competent in intensive care medicine and be familiar with the equipment used in the
care of these patients. Before taking responsibility for a transfer, staff should receive
training and accompany transfers as an observer. Resources are required to achieve
this and to ensure safe transfer systems throughout the UK. At least two personnel
should accompany a patient during transfer; often the second member of the team is
a nurse who should be experienced in the care of the critically ill and specifically in
patient transfer.
Insurance cover: adequate insurance to cover the death or disability of staff

accompanying patients as a result of road traffic accidents is required. In the UK, such
personal accident insurance is one of the benefits of membership of specialist societies
such as the Intensive Care Society and the Association of Anaesthetists.
Equipment
The equipment required during a transfer may be divided into four broad categories
(Figure 1). The first category is the equipment needed for basic care such as the ICU
bed or cot, laundry, sources of warmth and comfort. Life support equipment such as
the ventilator and other respiratory support, including oxygen supply may be considered
as the second category. The third category includes monitoring devices and the fourth
includes equipment required to treat the patient. Two types of treatment equipment
are required: that needed for continuing intensive therapy and that required for
emergencies arising because of physiological deterioration or equipment failure (e.g.
blocked tracheal tube, loss of oxygen, power failure, avulsed intravenous infusion
lines).Equipment required for intra-hospital transfer is similar to that needed for inter-
hospital transfer; to avoid duplication of equipment and to maximize staff familiarity
with one standard apparatus inventory, institutions may elect to use their inter-hospital
mobile ICU for intra-hospital transfers.
Categories
Special of equipment for transfer
cases
Basic care
ICU bed or cot, warmth, comfort
Life support equipment
Airway
Laryngoscopes, spare batteries and bulbs
Sterile cuffed tracheal tubes (various sizes)
Sterile cuffed tracheotomy tubes (various sizes)
Tracheal tube introducers (metal and gum elastic)
Airways, oral and nasal (various sizes)
Suction catheters and suction device
Catheter mounts
Disposable humidifiers
Fixed-performance oxygen masks and piping
Lubricating jelly
Artery forceps
Tape and adhesive dressing
Magill forceps
Breathing
Portable ventilators (ideally capable of volume-controlled ventilation, positive end
expiratory pressure generation, variable inspired oxygen fraction, lightweight,
simple, gas driven, robust and reliable)
Oxygen cylinder with appropriate pressure-reducing valves for ventilator and fresh
gas flow to face mask
Disposable (or autoclavable) ventilator tubing
Self-inflating resuscitation bag with anaesthetic masks (various sizes)
Circulation
Intravenous cannulae (various sizes)
Cannulae appropriate for intra-arterial pressure monitoring
Intravenous fluids and administration sets
Central venous catheters (various lengths and diameters)
Sutures and dressings
Infusion pumps with appropriate syringes
Three-way Luer lock taps and intravenous line extensions
Monitoring equipment
Central venous and pulmonary occlusion pressures, direct measurement
Arterial oxygen saturation
Temperature
Blood pressure (direct intra-arterial and non-invasive)
ECG
End tidal carbon dioxide tension
Treatment
Continuing ICU management
Drugs and intravenous fluids
Emergency treatment needed during transfer
Nasogastric tubes (various sizes)
Scissors and razors
Syringes and needles
Sterile, plain and alcohol-soaked swabs
Gloves and aprons
Defibrillator
1
Children
During the development of paediatric intensive care services, the importance of
regional retrieval teams was appreciated and now most regional paediatric ICUs
support such teams. Adverse events are more common if paediatric retrieval is not
carried out expertly. For example, a study in Birmingham, UK, reported that 75% of
transfers were complicated by an adverse physiological event, equipment failure, or
inadequate documentation of vital signs. In 1995, an American study of 180 paediatric
transfers reported adverse physiology changes occurring in 72% and major equipment
mishaps in 10%. Major interventions were required in 40% of these transfers. In a
subsequent phase, the introduction of a specialist paediatric transfer team resulted in
no adverse events. In another study, it was found that only 4% of 51 critically ill children
suffered preventable physiological deterioration when accompanied by a specialist
transfer team. The patients severity of illness, as judged by the PRISM (Pediatric Risk
of Mortality) score, decreased during transfer, reflecting an improved clinical state as a
result of the pre-transfer and intra-transfer resuscitation.
Neurosurgical
Emergency neurosurgical patients requiring further management at the regional
neurosurgical centre represent a dilemma. The effects of secondary brain damage,
mainly resulting from hypoxia and hypotension, must be minimized. These
complications are best treated by experienced staff who are familiar with the problems
that occur during transfer. However, the response time of any regional transfer team
may limit their effectiveness under such circumstances and staff from the referring
hospital must move the patient. This is best managed if protocols and guidelines
developed in conjunction with the regional neurosurgical centre are followed (Figure 2).
Guidelines used for transfer of patients requiring further neurosurgical

management
Indications for intubation and ventilation before transfer

Coma (Glasgow Coma Score GCS 8)
Loss of airway reflexes
Ventilatory insufficiency
(PaO2 9 kPa on air or 13 kPa on O2)
(PaCO2 6 kPa)
Respiratory arrhythmia
Spontaneous hyperventilation with PaCO2 3.5 kPa
Additional indications for intubation

Deteriorating consciousness (decrease in GCS by 2)
Fractured mandible
Bleeding into the upper airway
Patient fitting
Aeromedical
Road transfer is satisfactory for most critically ill patients. It has the advantages of
low-cost, rapid mobilization, less weather dependency and easier patient monitoring.
Air transfer should be considered for longer journeys (over 50 miles or 2 hours).
Its apparent speed must be balanced against organizational delays and intervehicle
transfer at either end of the flight. Helicopters are recommended for journeys of 50150
miles or where access is difficult, but they provide a less comfortable environment
than road ambulance or fixed- wing aircraft. Helicopters are expensive and have a
poorer safety record than fixed-wing aircraft. Fixed-wing aircraft, preferably pressurized,
should be selected for transfer distances over 150 miles.
The problems associated with aeromedical transfers are altitude, temperature
control, noise, vibration, visibility and unfamiliar environments. Changes in barometric
pressure are hazardous, because a small pneumothorax expands by 20% with an
increase in altitude of 6000 ft.
Quality and audit

Transfer forms are vital to record physiological changes and therapy before and during
transfer. Regular audit of transfers is necessary to maintain and improve standards. The
responsible consultant should review all transfers in and out of the hospital and a similar
process should be established at regional and national level. The referring hospital,
the receiving hospital, the ambulance service and any external auditing system should
retain copies of the transfer documentation.
FURTHER READING
Intensive Care Society. Guidelines for Transport of the Critically Ill Adult. London:
Intensive Care Society, 1997.
Association of Anaesthetists of Great Britain and Ireland. Recommendations for
the Transfer of Patients with Acute Head Injuries to Neurosurgical Units. London:
Association of Anaesthetists of Great Britain and Ireland, 1996.
Runcie C J, Reeve W R, Wallace P G. Preparation of the Critically Ill for Interhospital
Transfer. Anaesthesia 1992; 47: 32731.
Morton N S, Pollack M M, Wallace P G M. Stabilization and Transport of the Critically Ill.
New York: Churchill Livingstone, 1997.

Sedation and Neuromuscular
Paralysis in the ICU
Andrew J Soppitt
Andrew J Soppitt is Specialist Registrar in Intensive Care and Anaesthesia at

Southampton General Hospital, UK. He qualified from Birmingham University
and trained in general medicine in Birmingham and in anaesthetics in Bath and
Southampton, UK.
Patients receiving mechanical ventilation usually require sedation and/or analgesia.

The patients underlying disease state and the indications for mechanical ventilation
should be considered before selecting and administering sedative agents. The risk of
prolonged sedation after discontinuation of drug therapy can be reduced with careful
selection of agents and their dosing regimen. There must be a clear reason for using
muscle relaxants, because there are disadvantages to their use.
Sedation
During intensive care, sedation is required to relieve the discomfort and anxiety caused
by procedures such as tracheal suction, physiotherapy and manual handling, and to
facilitate the tolerance of tracheal tubes and intermittent positive-pressure ventilation
(IPPV). It may also be useful in managing other aspects of intensive care, such as
insomnia, hallucinations and agitation. However, the use of sedation should not be
excessive and, in general, the aim should be to create a cooperative, calm and pain-
free patient who will tolerate the necessary interventions of intensive care and permit
clinically useful assessments to be undertaken.
Inappropriately deep sedation should be avoided, because it has several potential
adverse effects including hypotension, prolonged recovery time, delayed weaning
from IPPV, ileus, the development of drug tolerance or a chronic confusional state.
Occasionally, deep sedation is appropriate, for example in the management of patients
with refractory hypoxaemia or raised intracranial pressure, or in those for whom
neuromuscular paralysis is appropriate (see below). It may also be used to reduce
oxygen consumption and metabolism.
Although pharmacological methods of managing anxiety and discomfort in the ICU
are the mainstay of therapy, other approaches may be useful:
good communication between ICU staff and the patient
control of the environment (e.g. noise, temperature, humidity)
management of thirst, hunger, constipation
attention to ventilation (hypercapnia increases sedative requirements)
aromatherapy and massage
adequate analgesia (may include regional techniques).
Pharmacological methods of sedation

The ideal sedative agent possesses the following qualities:
an easily controllable level of sedation
no effect on major organ functions
a short onset and offset of action
metabolic pathways independent of hepatic or renal function
no accumulation
inactive metabolites
inexpensive
no interactions with other ICU drugs.
Drugs used for sedation include opiates, benzodiazepines, propofol, barbiturates,
butyrophenones and other antipsychotic agents, central-acting 2-agonists, and
the volatile anaesthetic isoflurane. Newer rapidly titratable drugs are also available
including alfentanil and remifentanil (Figure 1).
Sedative drugs may be administered by bolus or by continuous infusion. In general,
sedation is best maintained using an infusion technique, with additional boluses as
required. Bolus administration alone leads to fluctuating sedation levels. The clearance
of most commonly administered drugs relies on metabolism and excretion by the liver or
kidney or both; their duration is prolonged in hepatic or renal failure. Drugs metabolized
at least in part by other mechanisms include propofol and remifentanil.
Opioids are traditionally given to treat pain, but they possess sedative properties
by virtue of their central action on opioid receptors. In the UK, morphine, fentanyl and
alfentanil are the most commonly used, though others (e.g. remifentanil) are being
considered. The specific features of opiates are listed inFigure 2. The adverse effects of
opioids include:
respiratory depression
cardiovascular depression (hypotension and bradycardia are common, secondary to
a decrease in sympathetic tone)
depression of intestinal motility
pruritus.
Benzodiazepines used in the ICU include midazolam, diazepam and lorazepam.
They all exhibit anxiolytic, hypnotic, muscle relaxant and anticonvulsant effects, and
synergy with opioids. Rapid intravenous injection in an unstable patient may produce
airway compromise and cardiovascular depression. Diazepam, and to a lesser extent
midazolam, have active metabolites that can accumulate over days of use and extend
their duration of action. Lorazepam does not accumulate in lipid stores or have an
active metabolite, but its elimination half-life is more than 10 hours. Overdose or
accumulation of benzodiazepines can be reversed by flumazenil. This benzodiazepine-
receptor antagonist has a shorter half-life than agonist benzodiazepines and may need
to be given by infusion.
Propofol (2,6-diisopropylphenol) is a lipid-soluble agent with a rapid onset and
short duration of action. Recovery from sedation usually occurs within 10 minutes
and is not significantly lengthened by prolonged drug administration. However, some
accumulation may occur in obese patients, because the drug is lipid soluble. Propofol
is rapidly metabolized by hepatic and extrahepatic mechanisms. When compared
with midazolam for ICU sedation, propofol has shorter arousal times, but there is no
difference in the quality of sedation. Propofol is a potent vasodilator, and can cause
significant hypotension, especially in the hypovolaemic or septic patient. Prolonged
infusions lead to increased serum triglyceride and cholesterol concentrations. In fluid-
restricted patients, the large volume of infusion may pose problems. Propofol is not
licensed for sedation in children because several deaths have been reported following
its use in very young children. Patients receiving propofol infusions may develop green
or reddish-brown urine.
Ketamine in subanaesthetic concentrations ketamine has analgesic and sedative
properties, but it should not be used as monotherapy because of its excitatory and
hallucinogenic side-effects. These can be avoided if ketamine is administered in
combination with a benzodiazepine or propofol. Ketamine acts at the N-methyl-
D-aspartate (NMDA) receptor. Its catecholamine-releasing properties may have
advantages or disadvantages, depending on the circumstances. It is expensive.
Barbiturates are unsuitable for therapeutic sedation, because they are
cardiovascular depressants and accumulate following prolonged use. Thiopental
(thiopentone) may be useful in managing status epilepticus or raised intracranial
pressure.
Etomidate is not used by infusion on the ICU, because an excess mortality has
been associated with its use, secondary to adrenal suppression.
Butyrophenones and phenothiazines haloperidol and other antipsychotic
agents (e.g. chlorpromazine) have greater antipsychotic than sedative effects at
lower doses, and decrease hallucinations, paranoia and motor activity. They can
be used for promoting calmness and clarity in critically ill patients with delerium or
delerium tremens. Haloperidol may be the preferred agent, because it exhibits less
-adrenoceptor-blocking tendency, but any of these agents may cause vasodilatation,
hypotension, a prolonged QT interval, extrapyramidal symptoms or neuroleptic
malignant syndrome.
Clonidine 2-adrenoceptor agonists (e.g. clonidine) inhibit catecholamine release,
and exert synergistic interactions with opioids and other sedatives. Administration of
2-adrenoceptor agonists results in functional central sympatheticolysis, which may
be useful in withdrawal syndrome from chronic alcohol abuse, during the weaning
from long-term mechanical ventilation and in patients with tetanus. Clonidine doses
are usually 0.91.5 mg/day, but may range up to 15 mg/day. Contraindications include
hypovolaemia (risk of refractory hypotension) and severe arrhythmias.
Isoflurane delivered into the ventilator circuit in concentrations of 0.250.50% has
been used to provide sedation of ICU patients. Problems include vasodilatation and the
need for expired vapour scavenging.
Chloral hydrate is used in paediatric intensive care practice as an adjunct to
intravenous sedation, particularly during weaning from ventilation. It is metabolized
in the liver to the active compound trichloroethanol. The acetate and glucuronide
metabolites accumulate in renal dysfunction
Pharmacology and dose of sedative drugs

Plasma half- Elimination/ Recovery time Active metabolites Loading dose Infusion rate
life (hours) metabolism after prolonged (half-life hours) (mg/kg) (mg/kg/ hour)
sedation
Morphine 24 Liver >> kidney Days Morphine-6- 0.050.15 0.020.1
glucuronide (210)
Fentanyl 1.56 Liver Hoursdays None 0.00010.0004 0.0010.004
Alfentanil 12 Liver Minuteshours None 0.0040.014 0.010.1
Remifentanil 0.71.2 Blood/tissue Unchanged None 0.00050.001 0.00010.0005
Esterases
Midazolam 1.012.31 Liver Hoursdays1 None 0.0250.35 0.0250.2
Diazepam 2050 Liver Days Desmethyldiazepam 0.10.2 0.0070.15
(30200) + others
Lorazepam 1020 Liver Days None 0.020.04 0.0020.05
Propofol <1 Liver/extra-hepatic Minuteshours None 0.532 0.58
1
May accumulate, especially after 48 hours, in the elderly and in obese patients, exacerbated by liver or renal failure. Initial short half-life
results from redistribution into fat, not elimination.
2
Slow intravenous titration until loss of consciousness occurs, because it may cause significant hypotension, especially if the patient
is hypovolaemic or shocked.
Specific features of opiates in the ICU
Morphine
Cheap, gold-standard
Long-acting, slow to reach steady state
Renally excreted, metabolite (morphine-6-glucuronide) accumulates in renal failure
May cause histamine release, risking hypotension
Fentanyl
Initial rapid redistribution, but lipid stores are soon saturated
No additional accumulation in renal failure
Minimal cardiovascular effects
Alfentanil
Relative lack of lipid solubility and short half-life minimize accumulation, except in
severe hepatic failure
Minimal cardiovascular effects
Relatively expensive
Remifentanil
Metabolized by nonspecific blood and tissue esterases, hence short duration of action
unaffected by organ dysfunction
Expensive
Pethidine
Metabolite (norpethidine) accumulates during infusion and may cause convulsions
Monitoring sedation levels

Clinical several sedation scores have been advocated, but none has undergone
rigorous testing or gained widespread clinical acceptance. Ideally, a sedation score for
regular use in a busy ICU must be valid and simple. Most objective sedation scores
based on a single continuum (e.g. the Ramsay scale; Figure 3) are simple to use, but
lack the detail to document the patients mental state accurately. They do not contain
a separate assessment for pain, and fail to distinguish between level of consciousness
and abnormal mental states. In October 1999, the Intensive Care Society published
national guidelines on sedation, concentrating on the principles of management,
applicable to any drug.
Electrophysiological most sedation scores are useless for patients receiving
neuromuscular relaxants in whom an accurate physiological monitor is required.
Possibilities include:
bispectral index, a form of EEG processing
auditory-evoked potentials
oesophageal contractility.
The first two techniques appear reliable at discriminating consciousness from
unconsciousness in the anaesthetized patient, but their role in the ICU has yet to be
established.
Neuromuscular paralysis
The use of muscle relaxants fell from about 90% in the early 1980s to less than 10% in
the 1990s. During this period, ICU practice changed from the use of deep to rousable
sedation. Indications for muscle relaxants in the ICU include:
refractory hypoxaemia (may decrease oxygen consumption)
to allow inverse ratio or prone ventilation
raised intracranial pressure
status epilepticus
tetanus
during patient transport.
Ramsay scale for clinical endpoints for sedation
Level Description
1 Anxious, agitated or restless
2 Cooperative, oriented, and tranquil
3 Responds to commands only
4 Asleep, but brisk response to glabellar tap or loud auditory stimuli
5 Asleep, but sluggish response to glabellar tap or loud auditory stimuli
6 No response
Neuromuscular blockers the ultra-short acting depolarizing agent

suxamethonium (succinylcholine) is predominantly used to facilitate emergency tracheal
intubation. It is unsuitable for prolonged or frequently repeated use in the ICU. Figure 4
shows the features of commonly used non-depolarizing agents.
Monitoring neuromuscular blockade in intensive care is required to avoid overdose.
The degree of neuromuscular blockade can be assessed by stopping the infusion, by
witholding further doses, or by regular measurement of neuromuscular transmission
using a peripheral nerve stimulator (e.g. train-of-four count).
Problems with muscle relaxants
The patient may receive inadequate sedation.
Accumulation of the parent compound or active metabolite may occur with the
aminosteroidal muscle relaxants, especially during hepatic or renal impairment.
Prolonged neuromuscular paralysis may occur after discontinuing relaxant therapy,
as a result of drug accumulation or, in some cases, a myopathy. Myopathy is more likely
in the presence of severe sepsis, or high-dose corticosteroid therapy.
The protective reflexes may be lost.
Hypokalaemia, hyperkalaemia, hypophosphataemia and many drugs (e.g.
aminoglycoside antibiotics) may enhance paralysis.
Features of common non-depolarizing agents
Vecuronium
Chemical analogue of the aminosteroid pancuronium
Intubating dose 0.1 mg/kg, duration 3545 minutes
Infusion dose 12 g/kg/minute
Cardiovascularly stable
Short duration of action makes it suitable for administration by infusion
May accumulate when renal function is impaired
Pancuronium
Long-acting (0.1 mg/kg lasts 90100 minutes)
Possesses vagolytic effects
May accumulate if given by infusion
Rocuronium
Aminosteroid agent, similar to vecuronium but with a slightly longer duration of action
After a bolus dose of 0.61.2 mg/kg, onset time is almost as rapid as suxamethonium.
Satisfactory intubating conditions occur after about 75 seconds (or less with higher
dose)
Atracurium
Benzylisoquinolinium derivative with a duration of action similar to vecuronium; can be
given by continuous infusion
Intubating dose, 0.40.5 mg/kg; infusion, 412 g/kg/minute
Organ-independent metabolism; little tendency to accumulate
Histamine release common if given too rapidly
A metabolite (laudanosine) accumulates in profound hepatic failure; it causes convul-
sions in animals, but not in humans
Cisatracurium
Potent stereoisomer of atracurium; lower doses required, resulting in less generation of
laudanosine
No histamine release in clinical doses
May be the agent of choice on the ICU, for its cardiovascular stability, and organ-inde-
pendent metabolism
Intubating dose, 0.1 mg/kg; infusion dose, 12 g/kg/minute
4
Sepsis
Jonathan M Fielden
Jonathan M Fielden is Consultant in Anaesthesia and Intensive Care Medicine and

Clinical Director of Emergency Services at the Royal Berkshire Hospital, Reading. He
qualified from Bristol, training in general medicine and then anaesthesia and intensive
care in Bristol, Southampton, Portsmouth, and Sydney, Australia. His research interests
include outreach, resuscitation and sepsis.
Sepsis remains a significant challenge to intensive care medicine. It is the cause

of 27.7% of UK adult general ICU admissions. These 23,000 cases represent an
estimated incidence of 0.5/1000 population; mortality is about 45%. In the USA, sepsis
is the thirteenth leading cause of death and is a significant economic burden. Sepsis
kills as many people as acute myocardial infarction. Early recognition and removal
of the source of infection are key factors in management. Until recently, treatment
has been largely supportive but understanding of the sepsis process has allowed the
development of novel interventions that are improving survival.
Definition
Sepsis is part of the bodys response to infection (Figure 1). Early investigations into
treatment for sepsis were hampered by a lack of knowledge about the mechanisms
driving sepsis. Bone et al. clarified this and produced the agreed consensus definitions
(Figure 2). Sepsis is characterized by a systemic inflammatory response (SIRS) to an
infective insult and key abnormalities of the homeostasis of coagulation and endothelial
function. However, only 60% of cases are likely to be confirmed microbiologically and
there is no correlation between severity of sepsis and documented infection. Bone et
al. also categorized the stages of the bodys response to sepsis (Figure 3). Recent
research has revealed the key aspects of the pathophysiological derangement and
allowed targeted research.
Spectrum of response
Other
Systemic Pancreatitis
inflammatory
Severe
Infection response
sepsis Trauma
syndrome
(SIRS)
Sepsis
Burns
ACCP/SCCM consensus conference definitions1
Systemic inflammatory response syndrome (SIRS)

Response to a wide variety of severe clinical insults manifest by two or more of
the following:
temperature > 38 oC or < 36 oC
heart rate > 90 beats/minute
respiratory rate > 20 breaths/minute or partial pressure of carbon dioxide in
arterial blood (PaCO2) < 4.2 kPa (32 mm Hg)
WCC > 12 x 109 /litre or < 4 x 109 /litre, or > 10% immature forms
Sepsis
Two SIRS criteria plus (signs of) infection
Severe sepsis/SIRS
Sepsis/SIRS associated with organ dysfunction, hypoperfusion of hypotension
Sepsis-induced hypotension
Systolic blood pressure < 90 mm Hg or reduction > 40 mm Hg from baseline in
absence of other causes
Septic shock/SIRS shock

Severe sepsis/SIRS with hypotension despite adequate fluid resuscitation with
perfusion abnormalities including those requiring inotropes
Multiple organ dysfunction syndrome (MODS)

Presence of organ dysfunction in an acutely ill patient such that homeostasis
cannot be maintained without intervention
ACCP, American College of Chest Physicians; SCCM, Society of Critical Care

1
Medicine.
2
Reaction to sepsis
Infectious insult
Host factors
Epithelial barrier
Local defence (e.g. pH)
Immune status
Genetic factors
Immunity
T and B cell response
Infecting agent factors
Bacteria (link to epithelium, biofilms)
Gram-negative endotoxaemia
Gram-positive exotoxins
Fungi
Preliminary systemic response

Febrile reaction
Cytokines
Tumour necrosis factor-
Interleukin-1
Interleukin-6
Interleukin-8
Interferon-
Overwhelming systemic response

Endothelial cell dysfunction
Shift of phenotype to thrombotic state
Increased permeability
Vasodilatation
Organ dysfunction
Compensatory anti-inflammatory reaction

Interleukin-4
Interleukin-10
Transforming growth factor-
Immunomodulatory failure
3
Mechanism of sepsis-induced multiple organ failure

The SIRS response in sepsis results in systemic vasodilatation, increased cardiac
output, falling blood pressure and reduced oxygen extraction from the tissues. The
circulatory abnormalities of SIRS and sepsis lead to global tissue hypoxia. The key
advancement in understanding the link between sepsis and multiple organ failure
was the definition of the disturbance of homeostasis of coagulation and fibrinolysis.
The initial insult (infection in sepsis) alters endothelial function with the release of
tissue factors. There is also release of a variety of cytokines (the proinflammatory
agents: tumour necrosis factor- (TNF-), interleukin (IL)-1 and IL-6; the excess
anti-inflammatory cytokines IL-4, IL-10, IL1-receptor antagonist and soluble TNF
receptor I and II) and upregulation of circulating monocytes. This leads to activation
of the extrinsic system of coagulation and formation of thrombin, further amplifying
the thrombotic response via the intrinsic coagulation cascade. The subsequent
microvascular clotting leads to organ dysfunction and failure. There is also a reduction
in some of the natural inhibitors of clotting (e.g. activated protein C) from increased
consumption and endothelial injury. The normal homeostatic balance of fibrinolysis in
the face of thrombosis is also disrupted in sepsis by increased inhibition from cytokine-
induced increases in plasminogen activator inhibitor type 1 and plasminantiplasmin
complexes.
The combination of increased thrombosis and reduced fibrinolysis creates

microthrombi, which lead to multiple organ dysfunction and organ failure. The clinical
manifestations are seen as the development of, for example, acute respiratory distress
syndrome, disseminated intravascular coagulation or renal failure.
Management of the septic patient

The first step in the treatment of sepsis is recognition of the critically ill patient. The
signs are often missed, and delay in referral to ICU and poor management of critically
ill patients is all too common. Maintaining a high index of suspicion, monitoring the
vital signs for the hallmarks of SIRS and identifying the possible sources of infection
are vital. One of the most sensitive markers of deterioration in critically ill patients is
an increase in respiratory rate, a sign often poorly recorded unless emphasized with
the use of Medical Early Warning Scores or a similar system. Careful history and
examination identify possible sources of infection and guide initial therapy.
Initial therapy
Immediate resuscitation based on the ABDCE system is important to stabilize the
patient. At this stage, exact diagnosis is unimportant and treating immediate life-
threatening problems is the goal. Once the patient is stabilized, possible sites of
infection should be examined, including:
all body surfaces and cavities
blood
sputum or bronchoalveolar lavage fluid
aspirated lesions/collections
urine
faeces
CSF should be cultured if there is suspicion of intracerebral infection (provided
raised intracranial pressure can be confidently excluded).
Intra-abdominal signs should prompt early surgical review and operative intervention
unless good reason suggests otherwise. Blood should be taken for blood count,
urea and electrolytes, calcium, magnesium, liver function tests, coagulation tests
(prothrombin time, activated partial thromboplastin time, fibrinogen) and arterial
blood gases including assessment of lactate. Some advocate assessment of other
biochemical markers of infection (e.g. procalcitonin, C-reactive protein, von Willebrand
factor) but this has yet to receive universal acceptance.
Indwelling intravascular catheters should be assessed for signs of phlebitis or infection.

If not required, they should be removed and cultures taken from the insertion site and
per lumen. Chest radiography and imaging of other sites should be arranged. If invasive
monitoring or inotropic support is required, admission to a high dependency unit is
indicated. Patients requiring respiratory support or monitoring beyond the capabilities of
this unit should be admitted to ICU.
Antibiotic therapy
Initial therapy should be guided by a clinical impression of the probable site of infection,
together with guidance from microbiologists on empirical therapy and specific agents,
once microbiological sensitivities are known. Early accurate treatment is important
and should be guided by local knowledge and agreed guidelines to prevent overuse of
broad-spectrum antibiotics and further development of microbiological resistance. As a
guide, use the right drug, at the right dose, at the right time, treat the patient and not the
figures, and avoid toxicity.
Supportive management
Early management to return physiological parameters towards the normal range for
that patient shows promise in improving outcome. Rivers et al. have recently shown
a reduction in hospital mortality for early (i.e. Emergency Department) goal-directed
therapy using a protocol to drive up central venous pressure to 812 mm Hg,
by maintaining mean arterial pressure (MAP) at 6590 mm Hg and keeping central
venous blood oxygen saturation above 70%, using fluids, inotropes and vasopressors.
This contradicts some earlier studies of goal-directed therapy in ICU, but Rivers and
his colleagues argue that early intervention prevents the augmentation of the SIRS
response driven by tissue hypoxia in the uncorrected septic patient. Furthermore, they
were not aiming for supranormal values, which may have been a problem with earlier
studies. The principle of early detection and correction of reduced tissue perfusion
seems logical.
First-line treatment involves fluid resuscitation, aiming for a MAP of 6590 mm Hg.
Central venous pressure can be used as a guide for over filling but aiming for a
specific value, particularly when the patient is ventilated, is difficult. The place of
pulmonary artery catheters is under debate and subject to a multicentre trial. Several
studies promote their use, particularly before high risk surgery but others doubt the
benefit. Initially, the use of the Rivers criteria for central venous pressure, MAP and
urine output (> 0.5 ml/kg/hour) are reasonable aims. This can be supplemented by
using lactate measurements and measurement of oxygen delivery and use.
There is no evidence that the use of any particular inotrope is best in sepsis.
Noradrenaline (norepinephrine) is probably the first vasopressor of choice when aiming
to reverse the vasodilatation and reduced systemic vascular resistance often seen in
sepsis. When increased inotropy and chronotropy are required, dobutamine is often
used. Adrenaline (epinephrine) has the benefit of and sympathetic activity and is often
advocated if simplicity is required (e.g. initial resuscitation, theatre); there is evidence
of detriment from increased hepatic lactate production. There are advocates for other
inotropes (e.g. dopexamine) but the use of dopamine is diminishing because of significant
evidence against its use.
Many patients require ventilation to maximize oxygenation and minimize the work of
breathing. Following work in acute respiratory distress syndrome, most advocate the
use of a protective lung ventilation strategy with tidal volumes limited to 68 ml/kg,
mean airway pressures less than 35 cm H2O, relatively high positive end-expiratory
pressure (PEEP) of 515 cm H2O, and a limitation of fraction of oxygen in inspired air
(FiO2) to a maximum of 0.6.
Early aggressive (high volume 3050 ml/kg) continuous veno-venous haemofiltration

(CVVHF) is advocated in sepsis. It is thought that the removal of inflammatory
mediators aids resolution of the SIRS response. Whether short-term or prolonged
CVVHF is best is unproven. However, the development of renal failure is common
and continued CVVHF is often required. Continuous treatment is more beneficial than
intermittent.
As part of aiming to return physiological parameters to normal, aggressive management

of blood sugar (4.46.1 mmol/litre) levels with insulin is beneficial. In addition, treatment
of the relative adrenal insufficiency often found in sepsis with replacement doses of
hydrocortisone, 300 mg/24 hours, often reduces inotropic requirements.
Novel therapies
Vasopressin the profound vasodilatation seen in sepsis can become refractory to
catecholamine support. Treatment with vasopressin or vasopressin analogues (e.g.
terlipressin) improves MAP and reduces the need for other vasopressors. This matches
the research evidence of the basis of vasodilatory shock in sepsis and SIRS. The
mechanism is thought to be related to the relative naivety of the vasopressin receptors
to stimulus during sepsis, unlike the down-regulated catecholamine receptors.
Methylene blue is known to be an antioxidant. Infusion of methylene blue improves

vascular responsiveness to inotropes in the septic patient.
Activated protein C is one of the most recent treatments available in sepsis. It has
a physiological role in maintaining the coagulation and fibrinolytic balance as well as
in reducing inflammation through inhibiting thrombin-mediated inflammatory activities
and leucocyte attachment to the endothelium. It is reduced during sepsis and levels
correlate to poor outcome. The PROWESS study showed that activated protein C could
significantly reduce (28 day) mortality in sepsis (absolute risk reduction 6.1%), a goal
not achieved by any other inflammatory/coagulation mediator study. Although awaiting
long-term outcome data, and despite its high cost, this seems to be a significant and
cost-effective advance.
Prevention
Close attention to hand washing and skin decontamination with alcohol reduce
nosocomial spread. Efforts to limit antibiotic resistance through careful policies
and surveillance are important. Simple measures to reduce ventilation-associated
pneumonia such as semi-recumbent positioning also have a role, as does careful
insertion and management of indwelling intravenous and urinary catheters. Adequate
and appropriate nutrition, ideally via the enteral route, should be administered.
Outcome
Sepsis carries a high mortality (45%). Until the recent PROWESS trial, most research
showed a mortality of 3060%. It increases by 1520% for each additional organ
failure, and non-survivors tend to consume significant health resources. There is hope
that early normalization of physiology and the appropriate use of agents that reduce the
SIRS response (e.g. activated protein C) will reduce mortality. u
FURTHER READING
Bernard G R et al. Efficacy and Safety of Recombinant Human Activated Protein C for
Severe Sepsis (PROWESS). New Engl J Med 2001; 344: 699709.
Bion J F, Brun-Bruisson C. Infection and Critical Illness: Genetic and Environmental

Aspects of Susceptibility and Resistance. Intensive Care Med 2000; 26 Suppl 1: S12.
Bone R C, Godzin C J, Balk R A. Sepsis: A New Hypothesis for Pathogenesis of the

Disease Process. Chest 1997; 112: 23543.
Rivers E, Nguyen B, Havstad S et al. Early Goal-directed Therapy in the Treatment of

Severe Sepsis and Septic Shock. New Engl J Med 2001; 345: 136877.
Singh N, Yu V L. Rational Empiric Antibiotic Prescription in the ICU. Chest 2000; 117:
14969.
Wheeler A P, Bernard G R. Treating Patients with Severe Sepsis. New Engl J Med 340:
20714.

Severity of Illness Scoring
Systems
John Pappachan
John Pappachan is Consultant in Intensive Care Medicine at Southampton University

Hospitals Trust, UK. He trained in Newcastle, London and Wessex. His research
interests include the epidemiology of intensive care, renal replacement strategies in
sepsis, and the genetic predisposition to sepsis.
This contribution describes systems used to predict the hospital outcome of patients
admitted to an ICU. An acute physiology score is usually derived using values obtained
in the first 24 hours following ICU admission. Hospital outcome is then predicted using
a logistic regression equation. Development and validation, a brief description of the
most popular systems, their applicability in the UK and the standardized mortality ratio
(SMR) are described.
Scoring systems
Data collection on the ICU is necessary to facilitate research, quality assurance and
resource management. Severity of illness scoring systems aid the case-mix adjusted
collection of such data. However, none is perfect and their use to triage individual
patients and to compare the quality of care in different ICUs is severely limited. An
appreciation of their limitations and the statistical methods of assessing their goodness
of fit are vital if the information that they provide is to be used appropriately.
Potential uses for scoring systems include:
case-mix adjustment for entry into randomized controlled trials
audit and comparison of ICU performance
a mechanism to decide resource allocation.
Scoring systems use a logistic regression equation based, variably, on disease severity,
age and diagnosis to derive the probability of hospital death (on a scale of 0 to 1, where
0 = survival and 1 = death). The SMR describes the ratio of expected to observed
deaths. Case-mix variation and the need to derive binary (live or die) data from a
probability estimate, limit the use of such systems to evaluate ICU performance.
System development and validation
Patient variables and the coefficients used to describe their influence on survival
are selected either by clinical consensus or more robust statistical analysis. Typically,
systems are developed from information collected on a cohort of patients admitted to
a group of ICUs over a given period. The predictive equation is then validated on a
subsequent cohort of patients admitted to the same or other units.
Validation is best considered under two headings.
Discrimination describes how well the model distinguishes between survivors and
non-survivors. It can be assessed using either classification matrices or the area under
the receiver operating characteristics curve (ROC). The ROC is a plot of derivatives of
specificity against sensitivity. The area under the ROC (AROC) represents the ability
of a scoring system to distinguish between survivors and non-survivors in the patient
population as a whole. If the AROC is equal to 0.5 then the system is performing no
better than chance, if the AROC is equal to 1 then the system discriminates perfectly.
Calculating the standard error of the mean of each AROC allows comparison between
different systems. Classification matrices are less robust and analyse false-negative,
true-positive and overall correct classification rates at different probability cut offs. A
system will be very sensitive, but not very specific, if a probability of death of greater
than 0.1 is chosen to identify non-survivors. The classification matrix method varies the
cut-off and quotes the best sensitivity and specificity figures generated by the system
under review.
Calibration describes how closely predictions correlate with actual outcome across
the entire range of risk. The first method used to compare expected and observed
mortality is graphical and uses the calibration curve (Figure 1). The data generated
when APACHE III (see below) was applied to ICU patients in the UK demonstrated
the trend for observed mortality to increase as the predicted risk of hospital death
increases. However, there was a significant overestimation of mortality in the lower-risk
bands, which represented most of the sample population. This implies either that the
system does not fit the data, or that the ICUs examined were performing poorly.
In an attempt to answer this question, a statistically more robust method of
assessing calibration is used. The HosmerLemeshow C and H cumulative 2 statistics
compare the actual and expected mortality rates across 10 defined bands of mortality
risk (H2) and 10 deciles, which include equal numbers of patients (C2). A significant
result (p < 0.05) suggests poor system calibration. The only published assessment
of APACHE III in UK patients suggests poor goodness of fit. That for the APACHE
II system (see below) in a selected group of ICUs suggests better, but still imperfect,
calibration. To date, no system has been both developed and validated in UK patients.
Thus it is not possible accurately to assign an observed difference between predicted
and observed outcome to poor ICU performance or poor system fit.
Calibration curve describing the relationship between

observed and expected mortality using APACHE III in
the ICU (UK)
5000 100
Number of patients in each risk group
4500 90
4000 80
Hospital mortality (%)
3500 70
3000 60
2500 50
2000 40
1500 30
1000 20
500 10
0 0
>10 >20 >30 >40 >50 >60 >70 >80 >90 >100
Predicted risk of dying in hospital (%)
APACHE II and other systems
APACHE II used a theoretical approach to the selection and weighting of variables used
in its predictive equation. This was based on consensus opinion and the findings of
previous studies. Other scoring systems, for example the Mortality Prediction Model
(MPM), were developed using a combination of univariate and multivariate logistic
regression techniques. Neither approach has been proven to be superior in terms of the
resulting goodness of fit of the system to target populations.
APACHE II was developed in 1985 from a database of 5815 intensive care admissions
to 13 ICUs in the USA. The severity of illness of patients is assessed using the worst
values of 12 physiological variables in the first 24 hours following admission to the ICU.
These values generate an acute physiology score (APS) by following the weighting
system described in Figure 2. Adding the weightings for chronic disease and age to
the APS generates the final APACHE II score. The probability of hospital mortality is
generated using the logistic regression equation shown in Figure 2. This equation adds
the diagnostic category weight.
APACHE III, the direct successor of APACHE II, uses 17 physiological variables,
comorbidity and age to produce an acute physiology score. In addition, it uses the
diagnostic code and a weighting for source before ICU admission to predict outcome,
length of stay, and the likely intensity of nursing required. It presently represents the
largest published ICU database and has been promoted for use as a management
tool for use in the allocation and evaluation of ICU resources. However, its predictive
equation is not in the public domain, its claimed correction for lead-time bias (the effect
of treatment before ICU admission) is unproven, and it has been shown to fit a UK
database poorly.
There are a variety of simplified, more physiologically based systems available, such
as the MPM and the Simplified Acute Physiology Score (SAPS).
The APACHE II weights for physiological variables
Physiological variable High abnormal range Low abnormal range

+4 +3 +2 +1 0 +1 +2 +3 +4
Temperature rectal (C) 41 3940.9 38.538.9 3638.4 3435.9 3233.9 3031.9 29.9
Mean arterial pressure 160 130159 110129 70109 5069 49
Heart rate (ventricular) 180 140179 110139 70109 5569 4054 39
Respiratory rate 50 3549 2534 1224 1011 69 5

(non-ventilated or ventilated)
Oxygenation: A-aDO2 or
PaO2 (mm Hg)
A: FiO2 0.5 record A-aDO2 500 350499 200349 < 200
B: FiO2 0.5 record only PaO2 > 70 6170 5560 < 55
Arterial pH 7.7 7.67.69 7.57.59 7.337.49 7.257.32 7.157.24 < 7.15
Serum sodium (mmol/litre) 180 160179 155159 150154 130149 120129 111119 110
Serum potassium (mmol/litre) 7 66.9 5.55.9 3.55.4 33.4 2.52.9 < 2.5
Serum creatinine (mg/100 ml) 3.5 23.4 1.51.9 0.61.4 < 0.6
double point score for acute renal
failure
Haematocrit (%) 60 5059.9 4649.9 3045.9 2029.9 < 20
WBC (total/mm3; 1000s) 40 2039.9 1519.9 314.9 12.9 <1
Glasgow coma score (GCS). Score = 15 minus actual GCS

Total acute physiology score (APS) = sum of the 12 individual variable points.
The APS is summed with age points and chronic health points according to APACHE II definitions.
The probability of hospital death (R) is then calculated from the equation:
In (R/1 R) = 3.517+ (APACHE II score x 0.146) + (0.603, only if post-emergency surgery) + (diagnostic category weight).
Source: Knaus W A, Draper E A, Wagner D P, Zimmerman J E. Crit Care Med 1985; 10: 81829.
2
The standardized mortality ratio (SMR)
For a cohort of patients numbering 200 or more, the accepted method of comparing
outcome after adjusting for presenting factors that might influence it (e.g. the severity
of physiological derangement, age and diagnosis i.e. case-mix adjustment), is to use
the SMR. This represents the ratio of observed deaths in the cohort, to the number
of deaths predicted by a scoring system. If the SMR is 1 then the cohort is
acting as predicted; if the SMR is significantly greater than 1 this suggests there
is excess mortality. If scoring systems were perfect, transferable and able to adjust
for case-mix equally well in both development and external datasets, the SMR might
reflect ICU performance. These assumptions are not always valid and there are other
confounding variables, such as lead-time bias and poor treatment in the ICU leading
to a physiological deterioration, that limit the use of the SMR for the audit of ICU
performance.
FURTHER READING
Le Gall J R, Lemeshow S, Saulnier F. A New Simplified Acute Physiology Score
(SAPS II) based on a European/North American Multicenter Study. JAMA 1993; 270:
295763.
Lemeshow S, Teres D, Klar J, Avrunin J S, Gehlbach S H, Rapoport J. Mortality
Probability Models (MPM II) based on an International Cohort of Intensive Care Unit
Patients. JAMA. 1993; 270: 247886.
Knaus W A, Draper E A, Wagner D P, Zimmerman J E. APACHE II: A Severity of
Disease Classification System. Crit Care Med 1985; 10: 81829.
Knaus W A, Wagner D P, Draper E A et al. The APACHE III Prognostic System: Risk
Prediction of Hospital Mortality for Critically Ill Hospitalized Adults. Chest 1991; 100:
161939.
Pappachan J V, Millar B W, Bennett E D, Smith G B. Comparison of Outcome from
Intensive Care Admission after Adjustment for Casemix by the APACHE III Prognostic
System A Study of 17 Intensive Care Units in the South of England. Chest 1999; 115:
80210.
Ridley S. Severity of Ilness Scoring Systems and Performance Appraisal. Anaesthesia
1998; 53: 118594.
Rowan K M, Kerr J H, Major E, McPherson K, Short A, Vessey M P. Intensive Care
Societys APACHE II Study in Britain and Ireland II: Outcome Comparisons of
Intensive Care Units after Adjustment for Case Mix by the American APACHE II
Method. BMJ 1993; 307: 97781.

Ventilatory Modes
Matthew Williams
Martin G Tweeddale
Matthew Williams is Specialist Registrar in Anaesthesia at the Queen Alexandra

Hospital, Portsmouth, UK. He qualified from Bristol University and is training at
the Wessex School of Anaesthesia, based in Southampton, UK. His interests are
anaesthesia for major surgery and intensive care medicine.
Martin G Tweeddale is Consultant in Intensive Care Medicine at Queen Alexandra

Hospital, Portsmouth, UK. He completed a PhD in pharmacology before qualifying in
medicine from Westminster Hospital. He trained in medicine and clinical pharmacology
at McGill University Montreal, Canada, moved to critical care medicine and directed
ICUs in Newfoundland and Vancouver before being appointed at Portsmouth.
Vesalius first discussed tracheostomy and ventilation as a means of resuscitation in

1555 but it was another 300 years before the first ventilator, an iron lung, was built
in Paris by Woillez. Early in the 20th century, positive-pressure ventilation during
anaesthesia allowed the development of more complex surgery, but only in the 1950s
did the early versions of todays ICU ventilators become available.
Over time, ICU ventilators have become increasingly sophisticated and complicated,
so that they now provide intensivists with a variety of modes to use in different clinical
situations. However, the terminology used to describe these modes is not standardized.
For much of this article, the terminology of the Siemens 300 ventilator is used because
of its wide use in the UK.
To avoid confusion, the authors focus on two fundamental characteristics of all the
modes available on ICU ventilators:
the way each breath is delivered (i.e. constant pressure versus constant flow)
whether the breaths are controlled or supported.
In all modes, exhalation is passive. Indications for and complications of mechanical
ventilation are dealt with elsewhere.
Controlled modes
Controlled mechanical ventilation (CMV) is the ultimate controlled mode because

it delivers only a pre-selected tidal volume at a set rate. Apart from alarm settings, the
only other parameter that can be adjusted is the inspiratory flow rate. This is controlled
either directly (which determines the inspiratory:expiratory (I:E) ratio) or indirectly by
altering the I:E ratio. In the latter case, any change in inspiratory time (with tidal volume
and rate fixed) changes the flow rate. A disadvantage of using I:E ratios to govern
inspiratory flow rate (as with the Siemens 300) is that the latter changes whenever rate,
tidal volume or inspiratory time are adjusted. The waveforms are as represented for
volume control in Figure 1a.
In the CMV mode, exhalation commences once the set tidal volume has been
delivered. CMV is suitable only for apnoeic patients (e.g. in the operating theatre or
during transport when the patient is paralysed). It should not be used when there is
any possibility for spontaneous breathing because synchrony between patient/ventilator
is difficult to attain. On some ventilators, 'CMV' is an assist-control (AC) mode (see
below).
Assist-control volume control sets a baseline rate and tidal volume as in CMV,
but allows inspiratory effort by the patient to initiate additional breaths. The patient
can therefore set their own respiratory rate, but all patient-triggered breaths (Figure 2)
will be of the pre-set volume. This encourages better synchrony between patient and
ventilator (and hence reduces the sedation requirements) while markedly reducing the
inspiratory work of breathing. The possibility of weaning can be considered once the
patient starts to trigger the ventilator. Exhalation occurs as in CMV (Figure 2).
In assist-control, the inspiratory flow rate may be adjusted as in CMV. When patient-
triggered breathing occurs, the inspiratory flow should be set to meet, but not exceed,
the patients inspiratory flow demands. This improves synchrony and maximizes the
reduction in work of breathing. Many modern ventilators respond to high respiratory
drive in patients by delivering a tidal volume above the set value in assist-control.
Pressure control (PCV) is also an assist-control mode, but instead of applying a

constant inspiratory flow, the ventilator provides a constant inspiratory pressure that is
applied for a set inspiratory time a square wave of pressure (see Figure 1b). Flow
is provided solely to maintain the set inspiratory pressure. Therefore, initial flow is high
but decreases throughout inspiration. Expiration starts immediately on completion of
inspiration (i.e. is time cycled), so close attention to the I:E ratio is essential in this
mode.
At longer inspiratory times, the flow and pressure curves are different in PCV from
those of volume control or assist-control (see Figure 1). However, at shorter inspiratory
times, the flow and pressure curves are similar to assist-control using a decelerating
inspiratory flow pattern a facility that many ventilators provide in the belief that it is
more natural.
In PCV, the tidal volume delivered is dependent on the respiratory system
impedance as well as inspiratory time, and therefore changes with the changing clinical
situation. Tidal or minute volume alarms should therefore be set to give adequate
warning of excessive or under ventilation.
The main advantage of PCV is its potential to recruit atelectatic lung units while
reducing the risk of barotrauma. When lung compliance is low because of acute
respiratory distress syndrome or acute lung injury (ARDS/ALI), there is a broad
distribution of time constants between different lung units. In assist-control, such a stiff
lung requires high end-inspiratory pressures to inflate units with a longer time constant,
but such pressures applied to normally compliant lung units can result in over-inflation
and barotrauma. By definition, PCV limits the maximum pressure applied to any part
of the lung, and therefore reduces the risk of over-inflation. In PCV, lung recruitment
is achieved by applying this constant pressure for a long inspiratory time, even to the
extent of reversing I:E ratios. With reversed I:E ratios, as frequency rises, expiratory
time progressively shortens and may reach a value that prevents full exhalation during
each cycle. This results in the generation of intrinsic positive end-expiratory pressure
(PEEP) and consequent hyperinflation. Since intrinsic PEEP may be either helpful
or detrimental, its presence should always be sought and its potential consequences
noted, particularly if obstructive airways disease co-exists with ARDS/ALI.
Triggering
Control modes use time cycling to determine the respiratory rate, but during assisted
ventilation, this time cycling is over-ridden by the patients inspiratory efforts. Most
commonly, a set negative pressure must be generated by the patient in order to
trigger the ventilator to deliver a breath. The trigger sensitivity (which uses electronic
logic systems to compare the signal with a reference) is normally set at 12 cm H 2 O
below PEEP but this setting can be altered (if it is decreased, the work of breathing
is increased and vice versa). Once the ventilator detects that the trigger sensitivity
has been exceeded, the demand valve opens and inspiration commences. Too high
a setting can lead to auto-cycling especially if water collects in the breathing circuit.
Because pressure triggering can lead the patient to inhale for a short time against a
closed system (until the demand valve opens), some newer ventilators have established
a flow-triggered system. Here, a constantly monitored flow is delivered to the circuit
(flow-by) during exhalation, and the ventilator initiates inspiration whenever this bias
flow is reduced by the patients inspiratory effort. As with pressure triggering, the level
of inspiratory effort (reduction in bias flow) required by the patient to initiate inspiration
can be adjusted. Although it is claimed that flow triggering can reduce the inspiratory
work of breathing more than pressure triggering, it is difficult to prove an advantage
of one over the other.
Pressure support (PS)
PS is widely used in the ICU, particularly during weaning. It allows excellent matching
of the patients respiratory drive with the ventilator so that less sedation is required. In
addition, the cardiovascular consequences of PS may be less than those of controlled
modes since the maximal inspiratory support pressures are generally lower and are not
maintained throughout inspiration.
PS can be used only in a spontaneously breathing patient because each breath
must be triggered by the patient. Each triggered breath is then supported to a pre-set
pressure level. Support ceases when the inspiratory flow falls to less than 510% of its
peak value, at which point the ventilator opens the expiratory port (see Figure 1c). Thus,
the patient is never faced with attempting to exhale against a closed system. With PS,
the patient can control not only the respiratory rate but also tidal volume and I:E
ratio. PS reduces the work of breathing in proportion to the set pressure, which can
vary from zero (weaned) to full support (equivalent to PCV). As PS is progressively
reduced, the patient takes up an increasing proportion of the inspiratory work until
he is breathing spontaneously (although a low level of PS may be required to
overcome the resistance of the ventilator circuit and tracheal tube). This makes
PS the best available weaning mode in the opinion of many.
In PS, a square pressure waveform is delivered once a breath is triggered. At high
support pressures in a patient with increased respiratory drive, the initial flow required
to generate this pressure can be very high and therefore uncomfortable to the patient.
The rate of rise of inspiratory flow can be adjusted by the slope control to allow a
more progressive achievement of the pre-set pressure and therefore better synchrony
between patient and ventilator. Apnoea and low minute volume alarms must be
available with this mode. Many ventilators now provide an assist-control backup should
apnoea arise.
Hybrid modes
Many modern ventilators provide a variety of hybrid modes, a few of which are
discussed below.
Intermittent mandatory ventilation (IMV) allows the patient to breathe spontaneously

between mandatory breaths. The mandatory breaths are delivered at a pre-set time
regardless of patient effort (Figure 3a). Thus, the mandatory breath may come at any
point in the patients spontaneous respiratory cycle. This may be difficult for the patient
to tolerate and may increase the work of breathing, because the patient is fighting the
ventilator. Inspiratory work may also be increased if the spontaneous respiratory efforts
are inadequate and hence waste energy without ventilatory benefit.
Spontaneous breaths are possible between

mandatory breaths in intermittent mandatory
ventilation (IMV) and synchronized IMV (SIMV)
a IMV
b SIMV

Synchronized intermittent mandatory ventilation (SIMV) was introduced over 20

years ago to avoid the problems of IMV. Modern ventilators invariably have SIMV not
IMV, though they sometimes call it IMV. In SIMV, the patient receives a mandatory
predetermined rate of either volume- or pressure-controlled breaths. The minute is
broken into SIMV periods, determined by the rate set, during which each SIMV breath
will be delivered, either triggered by the patient or time (see Figure 3b). On top of
this the patient may trigger one or more spontaneous breaths between each SIMV
breath; these breaths may be unsupported but, to avoid wasted respiratory effort, are
often assisted by a preset level of PS (also possible in IMV). SIMV is therefore similar
to assist-control in which the mandatory breaths are patient triggered and is hybrid
because it also allows either spontaneous or supported breaths between the mandatory
breaths.
SIMV can potentially be a bridge from assist-control to PS in weaning only if the
patients spontaneous breaths are adequate in rate and depth to tolerate a progressive
reduction in the SIMV rate. Therefore, the patient must be examined to assess the
adequacy of the spontaneous breaths even if arterial blood gases are reassuring.
Volume support (VS) is a pressure support mode in which a minimum tidal and minute
volume are set. The ventilator progressively adjusts the inspiratory support pressure to
whatever level is necessary (limited by the peak pressure alarm) to ensure that both
targets are met or exceeded. In this mode, neither minute nor tidal volume can drop
below the pre-set values. Predictably, if tidal volume decreases, the ventilator
increases the PS until the volume target is again met. If the respiratory rate
drops, tidal volume (i.e. PS) is adjusted to meet the target minute ventilation.
If the rate rises, PS is adjusted to meet the target tidal volume, even if set
minute volume is thereby exceeded. If both minute and tidal volume targets
are exceeded, the PS is reduced until one or other target is again met.
Theoretically, this mode should allow automatic ventilator-controlled weaning.
However, the authors experience suggests that this mode delays weaning, perhaps
because it is difficult to define the right settings for each patient and to follow the
pattern of ventilator changes. If set too high, support is always provided and the patient
cannot be weaned; if too low, the support is withdrawn too soon and weaning fails.
Pressure-regulated volume control (PRVC) attempts to combine PCV and VC. The
ventilator adjusts the pressure control level to give a pre-set tidal volume at the lowest
possible inspiratory pressure. Effectively, the ventilator tests the patients compliance
with an initial breath at 10 cm H 2 O above PEEP. It then varies the delivery pressure
incrementally to find the minimum PC value that delivers the required tidal volume. This
mode is designed to compensate for the unavoidable variation in tidal volume with PCV
as clinical conditions change. Because volume is fixed in PRVC, inflation pressure must
be monitored to give warning of changes in patient compliance or resistance.
Adjuncts to oxygenation
PEEP sets an elevated pressure baseline during mechanical ventilation to prevent

expiratory airway closure and aid oxygenation by increasing functional residual capacity
(FRC) and reducing respiratory workload. Although labelled PEEP, it is applied
throughout the ventilatory cycle. PEEP is achieved by a variety of methods that
function as Starling resistors to raise the expiratory pressure without significantly
increasing expiratory resistance. Excessive PEEP can lead to lung hyperinflation and so
impair cardiac output and increase dead space. It may also contribute to barotrauma.
PEEP must be optimized for each patient.
Continuous positive airway pressure (CPAP) is an elevation in baseline pressure

throughout the respiratory cycle during spontaneous ventilation. It can be applied via
a mask or a tracheal tube, and by a ventilator or a freestanding device. The aim is
to prevent or reverse airway closure, thus maintaining or increasing functional residual
capacity (FRC) and therefore oxygenation. Increasing FRC may place the patients lungs on
a more favourable point on the compliance curve and thus minimize the work of breathing.
CPAP is maintained at a pre-set level during inspiration and expiration.
During ventilator CPAP, inspiratory flow is made available in proportion to the
patients inspiratory efforts, but only to maintain the required CPAP level. If the demand
valve is slow to respond, or the patient has an excessive respiratory drive, flow
delivery may be inadequate initially, leading to a drop in the CPAP level and increased
respiratory work. For external circuits, sufficient flow must be provided throughout the
respiratory cycle so that patient demands are always met.
Other modes of ventilation
Non-invasive ventilation (NIPPV) is increasingly used with a nasal or full face mask in
the management of respiratory failure or acute pulmonary oedema, as an alternative
to tracheal intubation and conventional ventilation. Easily portable, NIPPV has the
advantages of lessening respiratory work and having fewer cardiovascular effects, but
the mask can be difficult to tolerate (pressure sores and necrosis may occur with
prolonged use) and gastric distension can arise. NIPPV is well established for patients
with ventilatory failure secondary to chest wall deformity or neuromuscular disease;
together with CPAP, it has its place in sleep-related disorders.
NIPPV can be delivered by a ventilator with all modes possible, although some
are not well tolerated, or more commonly via a stand-alone machine. These machines
are pressure generators, behaving similarly to PS on mechanical ventilators, in that a
pre-set pressure is delivered to support triggered breaths in addition to having a
baseline PEEP. On some models, the machine can be set for the breaths to be time
cycled, similar to mechanical ventilation. Humidification can be added to the circuit
to prevent the drying of secretions by the gases delivered. To be effective, patient
selection and close monitoring are essential.
Others: in this brief overview, it is not possible to describe recently released modes
(such as proportional assist or pressure release ventilation) or methods that have been
used when conventional ventilation is not succeeding (e.g. high-frequency ventilation
or partial liquid ventilation).
FURTHER READING
Kirby R R, Smith R A, Desautels D A. Mechanical Ventilation. New York: Churchill
Livingstone, 1985.
Nunn J F. Nunns Applied Respiratory Physiology. Oxford: Butterworth-Heinemann,
1994.
Oh T E. Intensive Care Manual. Oxford: Butterworth-Heinemann, 1997.
Siemens. Servo Ventilator 300 Operating Manual. Sweden: Siemens-Elema AB, 1994.
Tobin M J. Principles and Practice of Mechanical Ventilation. New York: McGraw-Hill,
1994.

Neurosurgical
Anaesthesia
on CD-ROM
Acute Head Injury: Initial
Resuscitation and Transfer
Richard Kendall
David K Menon
Richard Kendall is Specialist Registrar in Emergency Medicine at Addenbrookes

Hospital, Cambridge, UK. He qualified from St Georges Hospital Medical School,
London. His main professional interest is in medical education both undergraduate
and postgraduate.
David K Menon is Professor of Anaesthesia at the University of Cambridge and

Consultant in the Neurosciences Critical Care Unit at Addenbrookes Hospital,
Cambridge. He trained at the Jawaharlal Institute, India; Leeds General Infirmary,
The Royal Free Hospital and Addenbrookes Hospital. His research interests include
mechanisms of secondary neuronal injury, metabolic imaging of acute brain injury and
imaging anaesthetic action in the brain.
Initial resuscitation
In the UK each year, about 1 million patients present to hospitals with head
injury. These injuries range from the relatively trivial to the fatal and some form of
classification is necessary. The most useful clinical classification of head injury is by
severity. For adults, the Glasgow Coma Scale (GCS) is the best method for initially
classifying the severity of head injury (Figure 1):
mild GCS 1415
moderate GCS 913
severe GCS 8 or less.
Initial assessment and resuscitation should follow the guidelines suggested by the
ATLS (advanced trauma life support) protocol. The identification of compromised
airway, inadequate ventilation or circulatory insufficiency must take precedence over
detailed assessment of the neurological state.
Glasgow Coma Scale (GCS)
Eye opening response

Spontaneously 4
To speech 3
To pain 2
None 1
Best motor response

Obeys commands 6
Localization to painful stimuli 5
Normal flexion to painful stimuli 4
Spastic flexion to painful stimuli 3
Extension to painful stimuli 2
None 1
Best verbal response

Oriented 5
Confused 4
Inappropriate words 3
Incomprehensible sounds 2
None 1
Normal adult total score 15
Airway management: the priority is to secure, maintain and protect a clear airway.
Remove secretions and foreign bodies by manual extraction or suction. Provide
oxygen by non-rebreathing mask (1012 litres/minute). Hold the neck immobile in
line with the body, apply a rigid or semi-rigid cervical collar and (unless the patient is
very restless) secure the head to the trolley with sandbags and tape. This is achieved
with two sandbags, one on each side of the head, and two pieces of tape, one across
the forehead and one across the chin, to secure the head and the sandbags to the
trolley. Cervical spine injury can be difficult to diagnose in the unconscious patient and
should be assumed to be present until it can confidently be excluded. A normal lateral
radiograph of the cervical spine does not exclude the possibility of important cord injury.
Maintain aligned immobilization of the neck when turning the patient during examination
and treatment. Criteria for tracheal intubation are listed in Figure 2.
Indications for intubation and ventilation after head injury
Immediately
Coma (not obeying, not speaking, not eye opening; GCS < 8)
Loss of protective laryngeal reflexes
Ventilatory insufficiency (as judged by blood gases):
hypoxaemia (PaO2 < 11 kPa on oxygen)
hypercarbia (PaCO2 > 6 kPa)
Spontaneous hyperventilation causing PaCO2 < 3.5 kPa
Respiratory arrhythmia
Before the start of transfer to the neurosurgical unit

Deteriorating consciousness (GCS has decreased by 2 points or more
since admission to A&E, not caused by drugs) even if not in coma
Bilaterally fractured mandible
Copious bleeding into mouth (e.g. from skull base fracture)
Seizures
An intubated patient must also be ventilated:

aim for PaO2 > 11 kPa, PaCO2 4.55.0 kPa
The choice of anaesthetic drugs and neuromuscular blockers used for intubation is
an individual decision that is modified by drug availability and clinical circumstance.
Intravenous anaesthetic agents are indicated before intubation, even in neurologically
obtunded patients, because they attenuate the rises in intracranial pressure associated
with intubation. Most of these patients require a rapid sequence intubation with
cricoid pressure and in-line cervical immobilization with removal of the collar, tape
and sandbags. In such circumstances, the rapid onset of action of suxamethonium
outweighs any theoretical risk that it might cause an increase in intracranial pressure.
The use of opiates in a patient who is intubated and ventilated is not contraindicated,
but large bolus doses of fentanyl or alfentanil may cause reductions in mean arterial
pressure (MAP) and reflex rises in intracranial pressure (ICP), even in the ventilated
patient. Tracheal tubes should be secured with adhesive tape that does not pass round
the neck, or with loosely tied tape (to avoid compressing venous return from the head).
It is advisable to pass an orogastric tube to empty the stomach, which commonly dilates
after trauma. Nasogastric tubes or nasotracheal intubation are best avoided in patients
in whom a basal skull fracture has not been excluded.
Clearing the cervical spine: there is no consensus about how the cervical spine
should be cleared of significant injury when it is safe to remove immobilization. Purists
claim that the cervical spine can only truly be cleared in a conscious patient, not
intoxicated, with normal neurological examination, normal plain radiographs and with no
painful distracting injury. This is impossible in a patient with a moderate or severe head
injury because they will have a decreased level of consciousness. In such patients, it is
acceptable to clear the cervical spine with the aid of plain radiographs and CT. A lateral
radiograph of the cervical spine should delineate all seven cervical vertebrae and the
cervico-thoracic junction. Anteroposterior radiographs of the cervical spine are difficult
to interpret in intubated patients, and when doubt exists a CT is indicated. Radiological
assessment of the cervical spine is discussed in Anaesthesia and Intensive Care
Medicine 3:5: 163. Plain radiographs and CT delineate bony injury only and may miss
significant ligamentous injury. There is increasing interest in using MRI to exclude such
injuries.
Breathing: a mechanical ventilator should be used whenever possible, and the

adequacy of ventilation assessed clinically and by arterial blood gas analysis. If
possible, an indwelling cannula should be inserted when the initial arterial sample
for blood gas analysis is obtained, thus allowing serial blood gas measurement
and continuous recording of blood pressure. Pulse oximetry is valuable for indirect
measurement of how well the patient is being oxygenated, but provides no information
about arterial carbon dioxide tension. Avoid excessive hyperventilation, which can
depress the myocardium and induce cerebral ischaemia.
Circulation: the circulatory management of patients with significant head injury is given
in Figure 3. Hypotension is a late sign of hypovolaemic shock, especially in children and
fit young adults. Pulse rate, respiratory rate and capillary refill time are useful ways of
assessing the circulation after injury. An isolated head injury is almost never the cause
of shock, especially in adults. Maintenance of cerebral perfusion pressures (CPP =
MAPICP) above 60 mm Hg is the intervention that best improves outcome. The ICP
is not measured at this stage, but is certain to be high if the CT scan suggests raised
intracranial pressure. Assume the ICP is greater than 2030 mm Hg, and maintain
MAP above 90 mm Hg. Avoid severe hypertension (MAP > 120 mm Hg).
Systemic and cerebral haemodynamic management in acute

head injury
Suspect hypovolaemia, even in the absence of hypotension

Tachycardia, arterial respiratory swing, delayed capillary refill, source
of bleeding, oliguria
Confirm hypovolaemia
Measure central venous pressure (CVP) if necessary
Find a cause for hypovolaemia (unlikely to be isolated head injury)

Multiple fractures, thoracic or abdominal haemorrhage (consider body
CT)
Correct hypovolaemia
Targets: CVP = 810 cm H2O; haematocrit 30% normal clotting, Na+,
K+
Use 0.9% saline, Hartmanns solution, Gelofusine, Haemaccel, blood,
fresh frozen plasma
Avoid 5% dextrose, hetastarch and hypotonic solutions
Catheterize bladder and measure urine output

Polyuria is usually the consequence of mannitol, and may require
colloid supplements
If polyuria is disproportionate or persistent consider diabetes insipidus
Assume elevated intracranial pressure

Assume intracranial pressure > 20 mm Hg unless
proven otherwise in patients with GCS < 12
Maintain mean arterial pressure at 90100 mm Hg

This will ensure cerebral perfusion pressure > 60 mm Hg; use
vasopressors or inotropes if needed
If resistant hypotension consider

Myocardial contusion, tamponade, tension pneumothorax,
high spinal cord injury, coning
3
It is advisable to set up two large-bore, peripheral, intravenous infusions and rapidly

infuse an electrolyte solution such as normal saline or Hartmanns solution (not
dextrose). Under-infusion is a more common error than overinfusion and the loss of
more than 15% of blood volume must be corrected by blood transfusion. In patients
with obvious hypovolaemia, early direct monitoring of arterial pressure and central
venous pressure is helpful for assessing the adequacy of resuscitation. The sources of
blood loss should be identified and controlled. Delay in recognizing thoraco-abdominal
injuries and major pelvic and limb fractures is common and is associated with a high
incidence of hypovolaemic shock and a poor outcome. A patient in persistent clinical
shock despite fluid resuscitation must not be transported for CT or to the neurosurgical
unit until the source of blood loss has been identified and controlled in theatre if
necessary.
Dysfunction: GCS measurements should be recorded as soon as possible and

repeated frequently (at least every 10 minutes during the first hour in hospital).
In a drunken patient with head injury, never assume the altered conscious level is
simply a result of alcohol. Record any asymmetry of limb movements and compare
the pupils repeatedly for size and reaction to light. Any deterioration in conscious
level or the development of focal neurological signs must be recorded and acted
on; the patient may have become hypoxaemic or shocked, or have an expanding
intracranial haematoma. An infusion of mannitol, 0.251.0 g/kg, may allow transfer to
a neurosurgical unit. Conscious level and limb movements cannot be measured in a
patient who is pharmacologically paralysed and ventilated. Repeated assessment of
pupil size and reaction is important in such neurologically inaccessible patients.
Exposure (other injuries): remove all the patients clothing and check for injuries from
head to toe, front and back. Some injuries do not need treatment at once but will do
later, and all should be documented. Consider the need for abdominal and thoracic CT
scans when the head is being scanned (Figures 4 and 5). Patients with major thoracic
or abdominal injuries may require urgent exploration in theatre. CT of the torso is best
used in patients who are not so unstable as to require exploration, but would benefit
from having such injuries excluded before transfer.
Indications for neurosurgical referral and/or urgent CT scan
GCS < 9 persisting after resuscitation

Deterioration in level of consciousness or progressive focal
neurological deficit
Skull fracture with any of the following
Confusion or deteriorating impairment of consciousness
Seizures
Neurological symptoms or signs
Open injury
Depressed open fracture of skull vault
Base of skull fracture
Penetrating injury
Patient fulfils the criteria for a CT of the head but this cannot be
obtained within a reasonable time (2 hours)
Indications for CT of the head before referral to neurosurgeons
Skull fracture and GCS of 15

Seizures
Confusion or neurological symptoms or signs persisting after initial
assessment and resuscitation
Unstable systemic state precluding transfer to neurosurgery
Diagnosis uncertain
Tense fontanelle or suture diastasis
Significant head injury requiring general anaesthesia
Indications for referral to neurosurgeons after head CT

Abnormal CT
Normal CT but unsatisfactory progress
5
Monitoring: the minimum standards of monitoring for anaesthesia apply equally

to a seriously injured patient during resuscitation and transfer. They are continuous
monitoring of blood pressure, ECG, oxygen saturation and urine output. Ventilated
patients require monitoring of end tidal carbon dioxide concentrations and repeated
arterial blood gas measurement.
Antimicrobial prophylaxis: booster doses of tetanus immunization are indicated in

most patients. A suitable anti-staphylococcal agent is appropriate for patients with
significant open injuries. Specific antimicrobial prophylaxis is ineffective and possibly
harmful if there is CSF leak or a skull fracture.
Referral and transfer

Much time may be saved if the information outlined in Figure 6 is available when
speaking to the neurosurgeon, and at the time of transfer.
What the neurosurgeon needs to know at referral
Patients age and previous medical history (if known)

History of injury
Time of injury
Cause and mechanism (e.g. height of fall, approximate velocity of
impact)
Neurological state
Talked or not after injury
Conscious level on arrival at the A&E Department
Trend in conscious level after arrival (sequential GCS)
Pupil and limb responses
Cardiorespiratory state
Blood pressure and pulse rate
Arterial blood gases, respiratory rate and pattern
Injuries
Skull fracture
Extracranial injuries
Imaging findings
Haematoma, swelling, other
Management
Airway protection, ventilatory status
Circulatory status and fluid therapy (? mannitol)
Treatment of associated injuries (? emergency surgery)
Monitoring
Drug doses and times of administration
6
Patients with head injuries are at risk during intra- and inter-hospital transfer. Adequate
resuscitation and the optimization of systemic haemodynamics can reduce the risks and
allow the maintenance of physiological homeostasis during transfer. Undesirable changes in
the patients homeostasis may be unnoticed or untreated because of inadequate monitoring,
lack of equipment and drugs, or inexperienced escorts. Failures of communication can
compound the problem and it is important that protocols and admission procedures facilitate
a comprehensive handover.
Timing the decision that a patient has been rendered stable for transfer (Figure 7)
requires experience and follows a period of monitoring in the resuscitation room. This
can legitimately delay the transfer, and it is helpful to telephone the neurosurgical unit
as the journey starts to give the estimated time of arrival. Never start a journey with an
unstable patient because of the high risk of complications during the journey.
Checklist before transfer of patient with head injury to a

neurosurgical unit
Respiration
Is the PaO2 > 11 kPa?
Is the PaCO2 4.55 kPa?
Is the airway adequately protected for the journey?
Circulation
Is the mean arterial pressure > 90 mm Hg?
Is the pulse rate < 100/minute?
Is peripheral perfusion adequate?
Is there reliable and adequate venous access?
Has enough volume/blood been given to replace losses?
Is there a suggestion of continuing bleeding?
Is the patient catheterized (essential if mannitol has been
administered)?
Head injury
What is the GCS score?
What is the trend in GCS score?
Is there any focal neurological deficit?
Is there a skull fracture?
Other injuries
Has a cervical spine injury been excluded?
Have broken ribs/pneumothorax been excluded/dealt with (chest
drain)?
Could there be an intrathoracic or abdominal bleed?
Are there pelvic or long bone fractures?
Have extracranial injuries been splinted (cervical collar, limb
splints)?
Imaging
If the patient is sufficiently stable, was the need for CT of thorax,
abdomen or cervical spine considered at the time of head scan?
7
Escort the minimum escort for a patient with severe head injury is a doctor and a
trained nurse or paramedic. They are professionally responsible for the patient until
they hand over at the neurosurgical unit. They must be well informed about the patient
before the journey starts, and ideally should have been involved in the patients care
in the resuscitation room. They must know what can go wrong during the journey and
must have the skills and equipment to identify and deal with these problems. A doctor
competent in airway procedures must escort every intubated and ventilated patient.
Patients who are at substantial risk of deterioration during transfer are best intubated
before leaving the referring hospital. When the risk of deterioration is less, the presence
of an appropriately equipped and skilled doctor during transfer will ensure airway
protection should the patient deteriorate during transfer. If in doubt, intubate before
transfer.
Monitoring it is unwise to rely solely on eyes and ears when monitoring a

patient in the back of a noisy, dark, moving ambulance. The monitoring started in
the resuscitation room should be continued. There must be reliable intravenous
access. The ECG should be monitored continuously as should the blood pressure
(sphygmomanometry is unreliable in a noisy, moving ambulance). Invasive blood
pressure monitoring is ideal; failing this an automated non-invasive blood pressure
machine is mandatory, but may be inaccurate in the back of a fast moving ambulance.
All lines must be secured, and arterial and central venous lines should be clearly
labelled to prevent inadvertent drug injection through them. A pulse oximeter is
mandatory. Capnography during transport is ideal, but is often unavailable. An injured
patient quickly becomes cold in an ambulance and should be wrapped in blankets
(preferably a foil blanket). It is not essential to correct mild hypothermia (> 36.0C)
because it may contribute to cerebral protection. The ventilator should have a pressure
dial to indicate inflation pressure and a blow-off valve to avoid barotrauma. There
should be a system to deliver high-flow oxygen to the patient, and two oxygen cylinders
should be carried, both full and checked before use.
Other equipment and drugs even if the patient has been intubated before transfer
it may be necessary to reposition or replace a tube which obstructs or falls out, and
the ambulance must carry a range of tracheal tubes and two working laryngoscopes.
The oxygen supply can fail, and it is always advisable to carry a self-inflating bag.
Intravenous lines inserted before transfer may block or fall out or may have to be
supplemented for rapid fluid infusion during transfer. A range of cannulas and fluids
should be carried. If blood has been cross-matched before the journey it should travel
in the ambulance, not in a separate taxi. The escorts should carry drugs for cardiac
resuscitation, non-depolarizing muscle relaxants, short-acting analgesics and sedatives
for controlling ventilation, anticonvulsants and mannitol.
Ambulance and trolley modern ambulances do not always offer a smooth, quiet
ride but usually provide reasonable space and lighting. The problems of working in
any moving vehicle make it vital to stabilize the patient and set up monitoring before
transfer. The ambulance seldom needs to travel at great speed, which can worsen
cardiovascular instability; a smooth ride at constant speed is safer. The patient should
be placed in the ambulance head first because this allows better tolerance of any
sudden deceleration during the journey. Most centres suggest that the head is elevated
by about 15 throughout transfer. If life-saving procedures (e.g. tracheal intubation) are
required during the journey it is best to stop the ambulance briefly rather than attempt
heroics under poor conditions.
Handover the escorts should give the neurosurgical staff an accurate description
of all injuries, the trends in conscious level and neurological signs since injury or
admission, and the drugs and intravenous fluids given. They should not leave until this
has been done. The neurosurgical team may need further information later and must
know whom to contact. All medical and nursing clinical notes, observation charts, drug
prescription sheets, radiographs and scans should be left with the neurosurgical team.
u
FURTHER READING
Abrahams M J, Menon D K, Matta B F. Management of Acute Head Injury:
Pathophysiology, Initial Resuscitation and Transfer. In: Matta B F, Menon D K, Turner J
M, eds. Textbook of Neuroanaesthesia and Critical Care. London: Greenwich Medical
Media, 2000; 28398.
Bartlett J et al. Guidelines for the Initial Management of Head Injuries. Br J Neurosurg
1998; 12(4): 34952.
Brain Trauma Foundation. Guidelines for Prehospital Management of Traumatic Brain

Injury.
www.braintrauma.org/index.nsf/pages/guidelines-main.
Gentleman D, Dearden M, Midgley S, Maclean D. Guidelines for Resuscitation and

Transfer of Patients with Severe Head Injury. Br Med J 1993; 307: 50752.
Infection in Neurosurgery. Working Party of the British Society for Antimicrobial

Chemotherapy. Antimicrobial Prophylaxis in Neurosurgery and after Head Injury. Lancet
1994; 344: 154751.
Neuroanaesthesia society of Great Britain and Ireland and the Association of

Anaesthetists of Great Britain and Ireland. Recommendations for the Transfer of
Patients with Acute Head Injuries to Neurosurgical Units. London: Royal College of
Anaesthetists, 1996.

Anaesthesia and the Cervical
Spine: Surgery and Trauma
Ian Calder
Ian Calder is Consultant Anaesthetist at the National Hospital, Queen Square, and the
Royal Free Hospital, London, UK. He qualified from Liverpool University and trained in
Liverpool and London. His research interests lie in airway management.
The main considerations in anaesthesia for cervical spine surgery are the risk of
neurological deterioration and airway problems.
Risk of neurological deterioration (spinal cord injury)

Patients with disease of the cervical spine or spinal cord run an increased risk of
developing spinal cord injury during anaesthesia. The mechanism of the damage is
uncertain. MRI shows that the shape of the spinal cord and the anterior and posterior
spinal arteries changes with posture. People with healthy spines, kept in abnormal
postures for several hours, or exposed to low blood pressure, have developed spinal
cord injury. Prolonged cord deformation can result in spinal cord injury and patients with
an abnormal spine have developed a spinal cord injury after short periods (less than 1
hour) of anaesthesia. The risk of general anaesthesia may stem from the immobility it
induces. A position that would be tolerated only briefly by a conscious patient can be
maintained for a dangerously long time under anaesthesia. Anaesthetists should be
aware that some patients deteriorate neurologically for no discernible reason following
cervical trauma and that absence of radiological evidence of damage does not mean
that a spinal cord injury will not occur. Up to 50% of patients with spinal cord injury after
traumatic neck injuries have no radiological evidence of trauma. Cervical injury may
compromise the homeostatic mechanisms safeguarding the spinal cord.
Instability of the cervical spine is thought to be a risk factor for the development of
a spinal cord injury during anaesthesia. Instability is hard to define. White and Panjabi
defined it as loss of the ability, under normal physiologic loads, to maintain relationships
between vertebrae in such a way that there is neither initial nor subsequent damage
to the spinal cord or nerve roots, and there is neither development of incapacitating
deformity, nor severe pain. The mechanism of injury may involve several factors, such
as deformation of the blood supply of the cord, reductions in spinal cord perfusion
pressure and cord compression. 40% of patients with fractures or dislocations of the
spine have vertebral artery damage.
Direct laryngoscopy may have caused a spinal cord injury in patients with
cervical spine disease but there is no convincing case report in the literature. Direct
laryngoscopy causes the same small amount of movement in cadaver spines
rendered unstable by surgical preparation as jaw thrust or chin lift. A comparative
study of different airway control systems (laryngeal mask airway (LMA), intubating
LMA, lightwand, fibrescope, direct laryngoscopy) showed no significant difference
between the methods, in terms of movement of an unstable C3 vertebra. Flexible
fibre-optic laryngoscopy and intubation is useful in cervical spine disease because
direct laryngoscopy is often difficult. The use of the gum-elastic bougie to minimize the
amount of glottic exposure is deservedly popular in the UK.
Manual in-line neck stabilization: there is conflicting evidence about whether this
practice results in any worthwhile reduction in movement at unstable cervical sites.
Enthusiastic application may make direct laryngoscopy difficult. There is an analogy
with cricoid pressure application because in both situations the airway difficulty induced
could be hazardous for the patient.
Pathology
Spinal cord injury may be associated with spondylosis, herniation of intervertebral
discs, spinal stenosis, tumours, syringomyelia, infections, rheumatoid arthritis,
ankylosing spondylitis or trauma.
Cervical rheumatoid arthritis: spinal involvement in rheumatoid arthritis is common,

with the upper cervical joints being affected most often. There are three main patterns
of involvement in the cervical spine:
atlanto-axial subluxation (Figure 1) (65%)
vertical subluxation (20%)
sub-axial subluxation (15%).
1 Radiograph of the neck showing

tuberculous abscess eroding C2 and causing
atlanto-axial subluxation.
All three types may be present. The amount of atlanto-axial subluxation has been
assessed by measuring the distance between the anterior arch of the atlas to
the odontoid peg on lateral radiographs (Figure 2), the distance being known as
the atlanto-dental interval (ADI). The size of the ADI does not correlate well with
neurological symptoms and signs, or cord compression seen at MRI. Whether there
is any correlation between the size of the ADI and the risk of spinal cord injury during
anaesthesia is unknown. The clinical presentation of cervical rheumatoid disease is
seldom acute. An insidious progression of neck pain, occipital headache, stiffness
and crepitus occurs. LHermittes phenomenon of an electric shock sensation up and
down the spine can occur. Temporomandibular joint and arytenoid joint involvement is
common. Rheumatoid cervical disease may be symptomless, therefore the question
arises whether patients should have flexion/extension lateral radiographs before
anaesthesia for procedures unrelated to the cervical spine. Requesting radiography
demonstrates the anaesthetists concern and appreciation of the possibilities.
Prevention of injury during anaesthesia for cervical surgery

There is an increased risk of spinal cord injury in:
patients with preoperative myelopathy
cranio-cervical junction surgery
multi-level surgery
insertion of fixation devices.
Great care should be taken with positioning. The position should look comfortable.
Hypotension may reduce spinal cord blood flow. Hypertension causes oedema
formation in experimental cord injury models. Normotension is recommended. Many
practitioners avoid muscle relaxant drugs after intubation, so that irritation of the cord or
a nerve root produces limb movement.
Spinal cord monitoring during cervical surgery: there is no evidence that

monitoring improves outcome. Sensory evoked potentials are routine in many centres
(stimulus applied to median nerve and recorded from the scalp over the sensory
cortex). They are reasonably robust to volatile agents, unlike motor evoked potentials,
which are easily abolished with volatile agents. Motor monitoring involves stimulation of
the motor cortex with an electrical discharge, and is not routinely used in many centres.
High-dose steroids: NASCIS I, II and III (North American Spinal Cord Injury Study)
have shown that large doses of methylprednisolone improve outcome after spinal cord
injury. The current recommendation is an initial dose of 30 mg/kg, then 5.4 mg/kg
over 24 hours if the treatment is begun within 3 hours, or over 48 hours if treatment
commences 38 hours after injury. However, whether there is any real benefit is still
debated.
Airway problems
Direct laryngoscopy is often difficult in patients with disease of the upper three
vertebrae. The Mallampati examination is useful in cervical disease; the test can
be regarded as a way of testing cranio-cervical extension. Mandibular protrusion is
often impaired in high cervical disease as temporomandibular joint disease tends to
be associated with cranio-cervical junction pathology. Grade C protrusion is always
predictive of difficult laryngoscopy (see Anaesthesia and Intensive Care Medicine 3:7:
246).
Anterior cervical haematoma can cause airway obstruction after surgery. In some
cases there may be only a small, or even no, haematoma. The obstruction is caused by
swelling of the periglottic tissue, which may make direct laryngoscopy difficult. Both the
LMA and gum-elastic bougie have proved life saving. The wound should be opened as
soon as possible. An inhalational induction with sevoflurane or halothane is generally
regarded as the wisest option. Extubation should be delayed for about 24 hours. u
FURTHER READING
Brimacombe J, Keller C, Kunzel K H et al. Cervical Spine Motion during Airway
Management: A Cinefluoroscopic Study of the Posteriorly Destabilized Third Cervical
Vertebra in Humans. Anesth Analg 2000; 91: 12748.
Calder I, Calder J, Crockard H A. Difficult Direct Laryngoscopy in Patients with Cervical

Spine Disease. Anaesthesia 1995; 50: 75663.
Donaldson W F III, Heil B V, Donaldson V P et al. The Effect of Airway Maneuvers on
the Unstable C1C2 Segment. A Cadaver Study. Spine 1997; 22: 121518.
Lennarson P J, Smith D, Todd M M et al. Segmental Cervical Spine Motion during

Oro-tracheal Intubation of the Intact and Injured Spine with and without External
Stabilization. J Neurosurg 2000; 92: 2016.
McCleod A D M, Calder I. Spinal Cord Injury and Direct Laryngoscopy the Legend
Lives on. Br J Anaesth 2000; 84: 7059.
Nygaard P, Romner B, Thoner J, Due-Tnnessen B. Local Anaes-thesia in Posterior

Cervical Surgery. Anesthesiol 1997; 86: 2423.

Anaesthesia for Posterior
Fossa Surgery
Arun K Gupta
Arun K Gupta is Director of Critical Care and Consultant Anaesthetist at

Addenbrooke's Hospital, Cambridge, UK. He qualified from St Mary's Hospital, London,
and trained in anaesthesia and intensive care in the East Midlands and East Anglian
Regions as well as spending 2 years in Richmond, VA, USA. His research interests are
in mechanisms of secondary brain injury, in particular, regulation of brain oxygenation
and metabolism.
Anatomy
The posterior cranial fossa is a rigid, deep compartment that is almost circular in outline
and contains the cerebellum and brainstem. These structures are covered by a dural
sheet (the tentorium cerebelli) which separates them from the cerebrum superiorly
(Figure 1). Anteriorly lie the dorsum sellae, the clivus, the posterior part of the sphenoid
and the basilar part of the occipital bone. The squamous part of the occipital bone,
the transverse sinus and the superior sagittal sinus lie posteriorly and the petrosal and
mastoid part of the temporal bone, the internal auditory meatus and the sigmoid sinus
lie laterally. The occipital bone, foramen magnum, jugular foramen and hypoglossal
canal lie inferiorly. Compared with the supra-tentorial compartment, the posterior
fossa is small, and a small increase in its volume can rapidly result in life-threatening
brainstem compression.
Relationship of posterior fossa to other intracranial landmarks
Pathology
Tumours primary tumours are the most common indication for posterior fossa
surgery and are more common in children than in adults. Up to 70% of all childhood
brain tumours originate in the posterior fossa and include medulloblastomas,
ependymomas, tumours of the choroid plexus, gliomas and astrocytomas. In contrast,
1520% of adult brain tumours lie in the posterior fossa. Metastatic tumours,
usually from the lung, kidney, breast and skin are the most common posterior fossa
lesion in adults. Other primary tumours include meningiomas, acoustic neuromas
(Schwannomas arise from the VIIIth cranial nerve, often in the cerebellopontine
angle), clival tumours, glomus jugulare tumours, arachnoid and epidermoid cysts.
Haemangioblastomas can develop in the cerebellum and often secrete erythropoietin,
resulting in polycythaemia.
Vascular lesions 15% of aneurysms occur in the posterior circulation with half
of these appearing at the basilar bifur-cation. Haemorrhage or vasospasm from
posterior circulation aneurysms may have a profound effect on brainstem blood flow.
Arteriovenous malformations of the posterior fossa often involve the brainstem with
a haemorrhage rate of 23% per year. Cerebellar haematoma is usually a result of
systemic hypertension and cerebellar infarct may cause swelling and obstructive
hydrocephalus. Both conditions may represent neurosurgical emergencies. Small
vessels impinging on cranial nerves in the posterior fossa can result in symptoms such
as trigeminal neuralgia. Surgical decompression has a good success rate.
Craniocervical abnormalities may require posterior fossa decompression. In the

young this is usually for congenital abnormalities such as ArnoldChiari malformation;
in the elderly, degenerative changes are more common.
Positioning
Patient positioning for optimal surgical access during posterior fossa surgery may have
major implications for the anaesthetist.
Supine position: patients with cerebellopontine angle tumours (e.g. acoustic

neuromas) are often operated on in this position. However, access to the posterior
fossa often requires substantial lateral rotation of the head, resulting in stretching of
the jugular veins and brachial plexus. These problems can be reduced by placing a
sandbag under the ipsilateral shoulder. Maximizing exposure through a relatively small
craniectomy site may require lateral rotation of the operation table, and the use of
safety belts will ensure that patients do not slide off.
The prone position offers good access to midline structures but bleeding can obscure
the surgical field. Head-up tilt is used to reduce haemorrhage but this increases the
risk of air embolism. The chest and iliac crests should be well supported to ensure
free movement of the abdomen during respiration. Obese patients are at particular
risk because of restricted diaphragmatic movement and high intrathoracic pressure.
Pressure on the iliac vessels should be avoided, reducing the risk of deep venous
thrombosis and improving emptying of the epidural venous sinuses. The head is
fixed in clamps in preference to a horseshoe to minimize pressure on the face and
eyes. Pressure points should be well padded and the tracheal tube kept as secure as
possible.
The lateral position is suitable for approaches to lesions not in the midline, particularly
the cerebellopontine angle. This position facilitates gravitational retraction of the
dependent cerebellum and facilitates CSF and venous drainage. A variation called the
park bench position is often used; so-called because of its resemblance to the way
a tramp sleeps on a park bench. A pad should be placed under the body in the axilla
to minimize weight on the lower arm and shoulder. The pelvis should be fixed with
supports in front and behind. The lower leg is flexed at the hip and knee. The upper
leg is kept straight and slightly externally rotated to lock the knee with the foot on a
firm support, which will prevent the patient sliding down the table if significant head-
up tilt is used. A pillow is placed between the legs. The lower arm is flexed across the
body and the upper arm is taped along the upper side of the body. The head is fixed in
pins. Excessive flexion of the neck can obstruct the internal jugular veins. This can be
avoided by ensuring a two or three fingers-breadth gap between chin and sternal notch.
The sitting position provides good surgical access to midline structures, improves
surgical orientation and allows good drainage of blood and CSF. Functional residual
capacity and vital capacity are improved and access to the airway is facilitated.
However, there are increased risks of cord compression, pneumocephalus and venous
air embolism. Macroglossia and peripheral nerve injuries are also more common in the
sitting position. Hypotensive techniques increase the risks of ischaemic damage. Many
authorities now contend that with modern anaesthetic techniques there is no place
for the sitting position in neuroanaesthesia. Excessive head-up tilt in other positions,
however, exposes the patient to similar risks.
In addition to the routine assessment for patients undergoing general anaesthesia
and specific assessment for patients scheduled for craniotomy, information relevant to
posterior fossa surgery needs to be obtained during the preoperative visit. Any cranial
nerve impairment needs to be documented, with particular reference to the lower
cranial nerves, which may affect the gag reflex. Patients with impaired gag reflexes may
have a history of aspiration pneumonia. Furthermore, this may impair airway protection
postoperatively and extubation at the end of surgery may need to be delayed or elective
tracheostomy considered. Patients are often dehydrated with associated biochemical
derangements because of reduced oral fluid intake, or vomiting owing to raised
intracranial pressure. Preoperative fluid replacement may be required.
Consultation with the surgeon will reveal the required position for surgery, and
the patient should be assessed for the proposed position. In some cases, alternative
positioning may have to be considered (e.g. obese patients requiring the prone
position).
Premedication should include all regular medication, with a short-acting

benzodiazepine reserved for those who are neurologically intact and who are
particularly anxious.
Induction: as with any craniotomy, induction is achieved using an appropriate induction
agent, normally an intravenous induction agent in adults, though a smooth inhalational
induction with sevoflurane may be appropriate in children. Neuromuscular paralysis
and an opioid facilitate tracheal intubation. The hypertensive response to intubation
and head-pin insertion can be obtunded by supplementation of appropriate intravenous
agents. If hypotension occurs, it should be treated promptly. An armoured tracheal
tube should be inserted and secured firmly. A nasogastric tube should also be placed
if there is any risk of postoperative bulbar dysfunction or the patient is to be ventilated
postoperatively.
Direct arterial pressure monitoring is essential and can be established before induction
if clinically indicated, or more commonly after induction. A central venous line is
usually required. Access to the internal jugular veins may be difficult, and subclavian
cannulation, or antecubital fossa or femoral long lines are useful alternatives. Core
temperature and urine output must also be monitored during surgery. Especially in
surgery where there is a risk of high venous air embolism, an oesophageal stethoscope
and/or precordial Doppler probes are essential additional monitors.
Maintenance: the choice of particular agents is not critical but stable anaesthesia is
paramount. The effects of a particular drug on blood pressure and neurophysiological
monitoring should be considered. Muscle relaxation is best provided by continuous
infusion of short- or medium-acting agents, which helps ventilation and prevents
movement in a relatively lightly anaesthetized patient. If motor nerve function is
monitored as a guide to resection (e.g. the facial nerve monitoring during acoustic
neuroma surgery), muscle relaxation must be discontinued and sufficient depth of
anaesthesia must be provided to obtund airway reflexes using other agents.
Neurophysiological monitoring is often used. Facial nerve monitoring is routine with all
large acoustic neuroma excisions. Auditory evoked potentials are used as a safeguard
during dissection near the brainstem, particularly during acoustic neuroma surgery.
When somatosensory and motor evoked potentials are monitored, they can be
suppressed during deep anaesthesia. Furthermore, paralysis can occur in the absence
of somatosensory evoked potential changes.
Deliberate hypotension should be employed with caution if significant head-up tilt is

used. It is also important to remember that surgery near the brainstem can induce
further hypotension and bradycardia.
Patients with good preoperative neurology may be extubated at the end of surgery
providing the intraoperative course was uncomplicated. Coughing and straining should
be avoided during the emergence period. Extubation at the end of surgery should not
occur if significant brainstem or cranial nerve injury has occurred. This may manifest as
repeated episodes of intraoperative haemodynamic instability. Pulmonary oedema may
be precipitated by large venous air embolism or after surgery to the floor of the fourth
ventricle. Respiratory failure can occur suddenly, even when awake.
Complications of posterior fossa surgery

Arrhythmias are often caused by manipulation of the brainstem. Bradycardia can
occur when the periventricular grey matter and the reticular formation are stimulated.
Most arrhythmias occur during surgery near the pons and the roots of nerves V, IX
and X. Surgeons should be made aware of bradycardic episodes, which should stop
when the offending surgical stimulation ceases. Anticholinergics should be used only
as a last resort after discussion with the surgical team, because abolition of vagally
induced bradycardia removes a useful indicator of potential brainstem injury. Severe
hypertension can result from stimulation of the trigeminal nerve.
Airway problems: macroglossia and upper airway swelling can occur following
prolonged surgery in the prone position. This is due to obstruction of venous and
lymphatic drainage. Cranial nerve damage can also cause serious airway problems.
Neurological complications: extreme neck flexion can cause midcervical

quadriplegia. Prolonged surgery and hypotension are contributory factors. Surgery near
the roots of nerves VIIX may lead to loss of airway reflexes, dysphagia and dysphonia.
Peripheral nerve damage can result from faulty positioning. The brachial plexus, ulnar
nerve and common peroneal nerve are most vulnerable.
Pneumocephalus: following a craniotomy, an air-filled space between the dura
and arachnoid remains after CSF has leaked away during surgery and brain bulk
is reduced. In the recovery period, brain bulk increases again as cerebral oedema
develops, arterial carbon dioxide concentrations increase and CSF reaccumulates.
The trapped air then comes under increasing pressure and tension pneumocephalus
can occur, which if left untreated can result in brain herniation and cardiac arrest.
Nitrous oxide worsens the situation. Pneumocephalus presents as delayed recovery
or deteriorating neurological state and should always be considered if this occurs.
Pneumocephalus can be reduced by discontinuing nitrous oxide 15 minutes before
surgery finishes and by allowing the arterial carbon dioxide tension to rise towards the
end of the operation. Air may remain within the cranium for 2 weeks postoperatively and
nitrous oxide should be avoided for this period after posterior fossa surgery.
Venous air embolism: a vein cut during surgery will normally collapse, preventing
air being sucked into the circulation. In posterior fossa surgery, cut veins may not
collapse: veins in the skull are held open by the surrounding bone; suboccipital veins
are held open by cervical fascia; and the large venous sinuses are held open by the
dura. Air can thus readily enter the circulation if these veins are opened. The incidence
of air embolism in the sitting position is reported at 2550%. However, recent use
of transoesophageal echocardiography has reported an incidence as high as 75%.
In most cases, the amount of air entering the circulation is small and may have little
clinical importance. When larger volumes of air enter the right heart, cardiac output is
reduced leading to systemic hypotension. Air also passes into the pulmonary arterial
circulation, leading to a rise in pulmonary vascular resistance and an increase in
pulmonary artery pressure. The ECG shows signs of right ventricular strain and right
ventricular failure may occur. Physiological dead space increases as air blocks the
pulmonary circulation with many alveoli ventilated but not perfused. This in turn leads
to a decrease in carbon dioxide excretion and a fall in end-tidal carbon dioxide tension.
Central venous pressure rises as a result of obstruction to right ventricular outflow.
This increase in central venous pressure, together with arrhythmias and the classical
mill-wheel murmur on auscultation are late signs. Occult atrial septal defects or a
probe patent foramen ovale may be present in up to 35% of all individuals in autopsy
studies. The rise in pulmonary pressures associated with venous air embolism that
may predispose to right-to-left shunting in such individuals may result in systemic air
embolism. In practice, though some degree of air embolism occurs in up to 75% of
patients; clinically significant air embolism remains an uncommon complication.
Detection of air embolism

Precordial Doppler device the altered reflection of ultrasonic beams from an
airgas interface means that precordial Doppler probes can detect bubbles of air in
the circulation and can indicate air emboli as small as 1 ml (some critics claim that the
device is oversensitive). An experienced observer is required. Diathermy machines
interfere with probe function.
Capnography a continuous capnograph shows a fall in end-tidal carbon dioxide
concentration as air enters the pulmonary circulation. It is less sensitive than the
Doppler but is much easier to use. However, other causes of a fall in end-tidal carbon
dioxide tensions, such as reduced cardiac output can cause confusion.
End-tidal nitrogen entry of air into the pulmonary circulation results in a rise in
end-tidal nitrogen, which mirrors the decrease in end-tidal carbon dioxide. However,
nitrogen increase is more specific than end-tidal carbon dioxide and is not influenced
by other cardiovascular changes.
Pulmonary artery pressure air embolism increases the pulmonary artery pressure
proportionally to the size of the embolism.
Pulse oximetry detects air embolism that results in significant cardiorespiratory
compromise, but is best viewed as an indicator of the magnitude of circulatory
disturbance and an index of the progress of treatment.
Transoesophageal echocardiography is a highly sensitive method of detecting
intracardiac air and of diagnosing atrial septal defects.
Prevention of air embolism volume loading patients to raise their central venous
pressure reduces the hydrostatic pressure gradient and reduces the likelihood of air
embolism. Similarly, raising end-expiratory pressure may reduce the negative pressure
in an open vein in the posterior fossa. However, positive end-expiratory pressure
reduces venous return and may cause systemic hypotension.
Anti-gravity suits and medical anti-shock trousers help to reduce venous pooling in
the lower limbs. The increase in venous pressure reduces postural hypotension and
decreases the negative hydrostatic pressure in the posterior fossa.
Nitrous oxide diffuses into embolic bubbles and increases their size. If there is a
significant air embolism, nitrous oxide should be discontinued. A central venous
catheter is a useful cardiovascular monitor and is a helpful diagnostic tool if air enters
the circulation. It also provides a useful method of attempting to aspirate air from the
right atrium.
Management of air embolism

Flood the operative field with saline and cover the wound with wet swabs to prevent
further air entrainment.
Ventilate with 100% oxygen, discontinue nitrous oxide.
Raise the venous pressure at the operative site, which can be done by squeezing
the veins in the neck.
Aspirate from the cerebral venous pressure catheter to try to aspirate air from the
right atrium.
If cardiovascular collapse occurs, standard resuscitative measures should be used.
u
FURTHER READING
Drake C G, Friedman A H, Peerless S J. Posterior Fossa Arteriovenous Malformations.
J Neurosurg 1986; 64 (1): 110.
Duffy C. Anaesthesia for Posterior Fossa Surgery. In: Matta B F, Menon D K, Turner J
T, eds. Textbook of Neuroanaesthesia and Critical Care. London: Greenwich Medical
Media, 2000; 26782.
Linden R, Tator C, Benedict D et al. Electrophysiologic Monitoring during Acoustic

Neuroma and other Posterior Fossa Surgery. Can J Neurol Sci 1988; 53: 738.
Porter J, Pidgeon C, Cunningham A. The Sitting Position in Neurosurgery: A Critical

Appraisal. Br J Anaesth 1999; 82: 11728.
Warwick R, Williams P, eds. Neurology. In: Grays Anatomy. 35th ed. Edinburgh:
Longmans, 1973; 26078.

Anaesthesia for Supratentorial
Craniotomy
Ravi Shankar
Arun K Gupta
Ravi Shankar is Specialist Registrar in Anaesthesia at the Addenbrooke's Hospital

NHS Trust, Cambridge, UK. His subspecialty of interest is neuroanaesthesia.
Arun K Gupta is Director of Critical Care and Consultant Anaesthetist at

Addenbrooke's Hospital, Cambridge, UK. He qualified from St Mary's Hospital, London,
and trained in anaesthesia and intensive care in the East Midlands and East Anglian
Regions as well as spending 2 years in Richmond, VA, USA. His research interests are
in mechanisms of secondary brain injury, in particular, regulation of brain oxygenation
and metabolism.
Surgery in the supratentorial region is required for a variety of pathologies including

vascular malformations and space-occupying lesions. This article describes the general
principles of patient management for such surgery and provides specific details about
anaesthesia for mass lesions. Vascular malformations are discussed on pages 1434.
Anatomy
The supratentorial compartment contains the cerebral hemispheres. the floor is formed
by the anterior and middle cranial fossae along with the tentorium cerebelli, and the
cavity is roofed by the calvarium.
Pathology and pathophysiology

Space-occupying lesions comprise:
primary tumours (gliomas, meningiomas of the olfactory groove, medial sphenoidal
wing and the base of the anterior cranial fossa)
secondary tumours, vascular lesions (aneurysms and arteriovenous malformations)
abscesses
haematomas (spontaneous or traumatic).
Patients with anterior fossa lesions may present with seizures, neurological deficits
or signs and symptoms of raised intracranial pressure (headache, nausea, vomiting,
hypertension and bradycardia). The neurological deficits may be visual, caused by
pressure on the optic nerve and chiasma, alteration or loss of smell due to involvement
of the olfactory nerve, compression of the internal carotid artery or middle cerebral
artery. Invasion through the superior orbital fissure may lead to proptosis.
Anaesthesia for supratentorial surgery requires an understanding of intracranial
physiology to facilitate manipulation of intracranial pressure (ICP), cerebral blood flow
(CBF) and cerebral metabolic requirement of oxygen (CMRO2) to optimize perioperative
conditions. The aims of anaesthetic management are listed in Figure 1.
Aims of anaesthetic management in supratentorial craniotomy
Preoperative assessment and optimization of associated medical

conditions
Haemodynamic stability (hypotension can lead to ischaemia in areas of

impaired autoregulation; hypertension increases the risk of haemorrhage
and vasogenic oedema)
Maintain cerebral perfusion and prevent increases in intracranial

pressure
Facilitate surgery by providing a slack brain
Provide cerebral protection if required
Rapid recovery to enable neurological assessment in the immediate

postoperative period
A complete history and clinical examination of the patient provides an opportunity to
identify associated diseases as well as to obtain specific information regarding the
surgery. Underlying cardiac or respiratory disease must be controlled before surgery.
Common associated conditions such as chronic untreated hypertension need to be
controlled to reduce the risk of perioperative myocardial and cerebral ischaemia owing
to the rightward shift in the autoregulatory limits of CBF.
The acute neurological condition must be assessed including the preoperative Glasgow
Coma Score (GCS), an examination of radiological images and an evaluation of
concurrent disease. Preoperative examination of CT and/or MR images provides
information about lesion size, ease of surgical access, positioning of the patient and
indirect information regarding likelihood of blood loss. It also allows assessment of
pathology that may cause intracranial hypertension or reduced intracranial compliance.
It must be remembered, however, that intracranial hypertension may exist in the
absence of imaging signs. A substantial risk of venous air embolism or bleeding may be
associated with lesions encroaching on the sagittal sinus.
A full drug history is important because some drugs affect anaesthetic management.
Steroids, diuretics and anticonvulsants affect plasma biochemistry, glucose
tolerance, the risk of upper gastrointestinal bleeding, intravascular volume and drug
pharmacokinetics. Anticonvulsants and steroids should be continued.
Premedication (e.g. a short-acting benzodiazepine) is only given if the patient is

particularly anxious, provided there is no evidence of raised ICP.
Induction
Induction is performed using an intravenous anaesthetic agent, titrated to minimize
the reduction in blood pressure, together with a nondepolarizing muscle relaxant and
a short-acting opiate. Normotension should be maintained by anticipating stimuli and
preventing haemodynamic responses. The hypertensive response to laryngoscopy and
intubation can be obtunded with an additional bolus of intravenous induction agent,
a short-acting opioid or -blocker, or intravenous lidocaine (lignocaine). Insertion of
skull pins for cranial fixation provides a potent stimulus and the hypertensive response
should be pre-empted by local anaesthetic infiltration, an additional dose of induction
agent and/or a supplemental dose of opiate.
When the airway has been secured with an armoured tracheal tube, the tube should be
carefully taped and secured on the side contralateral to the operation. The eyes should
be taped and padded.
Monitoring
In addition to establishing routine monitoring before induction, invasive arterial blood
pressure monitoring may be established before induction if the patient is unstable
or at high risk, or after induction in patients who are more stable. After induction, a
nasopharyngeal temperature probe and urinary catheter should be inserted. A central
venous line is helpful in most patients, and is mandatory if there is a clinical indication
(e.g. cardiorespiratory disease, large anticipated blood loss). A pulmonary artery
catheter may be required in severe cardiac disease. Other neuromonitoring such
as EEG, somatosensory evoked potentials and a jugular bulb catheter can also be
established if required.
Intra-operative management
Positioning: access is usually through a frontal, parietal or temporal craniotomy, which
allows the patient to remain in the supine position. A neutral position of the head with
a reversed Trendelenburg tilt (15 head up) favours venous drainage from the cranium
and helps to reduce ICP. Extreme head rotation for parietal and temporal access may
impair venous drainage by kinking the internal jugular vein. A shoulder roll placed on the
ipsilateral side reduces the impact of this position on venous drainage. The prolonged
duration of certain neurosurgical procedures demands close attention to pressure
points, nerve compression and thromboembolism prophylaxis. Thromboembolism
deterrent stockings or sequential pneumatic calf compression devices may be used to
reduce the incidence of deep vein thrombosis.
Maintenance of anaesthesia: the anaesthetic technique largely depends on the

ability to control ICP, maintain haemodynamic stability and provide rapid emergence.
Total intravenous anaesthesia with propofol infusion has been used successfully in a
number of studies. Propofol reduces CMRO2, thereby reducing CBF and cerebral blood
volume (CBV) by preserving flow metabolism coupling. This helps to maintain cerebral
perfusion and oxygenation to areas of brain that may be at risk of ischaemia. Propofol
also preserves carbon dioxide reactivity thus allowing manipulation of CBF and CBV
with changes in arterial carbon dioxide levels.
The addition of an opioid contributes to haemodynamic stability and reduces the

requirement for anaesthetic agents. Most short-acting opioids are equally effective
for haemodynamic stability, but remifentanil allows more rapid emergence compared
with fentanyl and alfentanil, probably because its metabolism gives it a short context-
specific half-life. All fluorinated volatile inhalational agents increase CBF and CBV by a
direct intrinsic effect causing vasodilatation. The magnitude of this increase in vascular
diameter depends on the balance between the intrinsic vasodilatory action and the
reduction in blood flow secondary to the dose-related decrease in CMRO2. Reactivity
to carbon dioxide may be impaired with older anaesthetic agents, though it tends to be
better preserved with the newer agents such as isoflurane and sevoflurane. Isoflurane
and sevoflurane also have minimal effects on ICP in concentrations less than 1.5
minimum alveolar concentration, and the vasodilatory effects can be attenuated by mild
hypocapnia. In contrast, nitrous oxide causes an increase in CMRO2 with a coupled
increase in CBF which is unaffected by hypocapnia, which makes its use unfavourable
in patients with raised ICP.
Although there is debate about the most appropriate com-bination of agents for
craniotomy, Todd and colleagues have shown that propofol/fentanyl, high-dose
isoflurane/nitrous oxide and fentanyl/nitrous oxide are equally satisfactory.
An infusion of short- or medium-duration neuromuscular blockers (e.g. atracurium,

vecuronium) facilitates ventilation at lower intrathoracic pressure. The lungs are
ventilated aiming for a partial pressure of carbon dioxide in arterial blood (PaCO2) of
4.04.5 kPa. Many anaesthetists allow body temperature to drift to 3536C when
neural tissue is at risk of ischaemic injury as part of the procedure, though there is no
evidence that this is beneficial. Rewarming should begin as soon as this risk is over,
and certainly by the time dural closure begins.
Optimization of surgical conditions: a slack brain facilitates surgical access with

minimal retraction, which reduces the likelihood of ischaemic damage. The dura should
be observed at the time of craniotomy to ensure that it is not tense or bulging out of
the craniotomy site. Mannitol, 0.51 g/kg, may be infused about 30 minutes before
dural opening to reduce brain bulk. It is an osmotic diuretic that was thought to act
by drawing water from the brain, but it is now also thought to improve the rheological
properties of the blood in the cerebral circulation, increase CBF and reduce CBV and
ICP. Limiting plasma osmolality to 320 mosm/litre reduces the risk of rebound oedema.
Mannitol may also theoretically worsen oedema by crossing a damaged bloodbrain
barrier. Furosemide (frusemide), 0.251 mg/kg, reduces the ICP to the same extent as
mannitol, and lowers cerebral venous pressure, thereby optimizing CSF reabsorption.
Hyperventilation has been used in neuroanaesthesia for many years to reduce ICP.
However, evidence from patients with traumatic brain injuries suggests that it may be
detrimental by causing cerebral vasoconstriction and a reduction in CBF below a critical
threshold. The evidence has lead to guidelines recommending that such patients should
not be hyperventilated prophylactically below an arterial carbon dioxide concentration of
35 mm Hg (4.7 kPa) during the first 24 hours after injury. If hyperventilation is required,
PaCO2 levels should be monitored and maintained above 4.0 kPa, and the use of
jugular oximetry considered, with the aim of maintaining jugular bulb oxygen saturation
above 55%. Intraoperative complications specific to such surgery include haemorrhage
and acute cerebral oedema. The management of intraoperative cerebral oedema is
outlined in Figure 2.
Management of intraoperative cerebral oedema
Optimize ventilation and blood gases

Maximize venous drainage
Deepen anaesthesia bolus intravenous anaesthetic agent, adjust
inhalational agent concentration
Diuretics mannitol, 0.51.0 g/kg
furosemide (frusemide), 0.251.0 mg/kg
CSF drainage
Minimize cerebral metabolic requirement of oxygen bolus lidocaine
(lignocaine); thiopental (thiopentone) or propofol infusion
Consider further doses of diuretic and CSF drainage
2
Fluid management: central venous pressure is used as a guide to maintain
normovolaemia. Reduced osmolality of extracellular fluid results in brain oedema.
Normal saline is slightly hyperosmolar and Hartmanns solution is slightly hypo-
osmolar compared with extracellular fluid. Net transfusion of free water should be
avoided and dextrose-containing solutions should not be used. Fluid replacement
is required if patients are dehydrated (often the case in those who have an impaired
conscious level) or in those who have had a rapid diuresis owing to mannitol. Colloid
solutions are appropriate to restore intravascular volume following diuresis, fluid
deprivation or moderate blood losses. Patients who have lost more than 1 litre of blood
generally require transfusion. It is essential to ensure that haemostasis is monitored
intraoperatively and abnormalities are corrected promptly.
Emergence from anaesthesia

During closure of the craniotomy, the anaesthetic may be reduced with the aim that
the patient rapidly regains consciousness at the end of the procedure. It is important
to normalize mean arterial pressure and PaCO2 before closure to reveal any bleeding
points, and to ensure that intraoperative brain swelling does not increase the likelihood
of intracranial hypertension when the patient is normocapnic. Obvious brain oedema
may prompt a decision to leave the bone flap out, institute ICP monitoring, or opt
for a period of postoperative sedation and ventilatory support. The ideal emergence
should be free from coughing, straining, hypertension and allow rapid and reliable
neurological assessment in the immediate postoperative period. These complications
lead to increased venous or arterial bleeding and oedema formation at the operated
site. In poorly autoregulating areas, hypertension leads to vascular engorgement and
further brain swelling. If the paranasal air sinuses have been breached, coughing after
extubation may lead to tension pneumocephalus. Hypertension during emergence may
be controlled by bolus doses of labetalol or esmolol. Neuromuscular paralysis should
be reversed at the time of dressing application so that coughing and straining are
minimized. Lidocaine (lignocaine), 1.5 mg/kg intravenously, is a useful adjunct to reduce
coughing towards the end of an anaesthetic. Patients with a preoperative GCS
of 1315 can be extubated when they open their eyes to command and have
demonstrated the ability to protect their airway.
Postoperative care
Assessment of pupillary size and its reaction to light should be undertaken soon
after the procedure and documented. The neurological state is assessed as soon as
possible in the recovery room and any gross abnormality should be brought to the
notice of the surgical team. Simple analgesics such as paracetamol or opioids (e.g.
codeine phosphate) are traditional and may be adequate, however, many patients
require more potent analgesia. In patients who have been extubated, any sudden
deterioration in GCS or neurological deficit should be viewed seriously and an urgent
CT scan should be considered. u
FURTHER READING
Algotsson L, Messeter K, Nordstrom C H, Ryding E. Cerebral Blood Flow and Oxygen
Consumption during Isoflurane and Halothane Anaesthesia in Man. Acta Anaesthesiol
Scand 1998; 32: 1520.
Coles J P, Leary T S, Monteiro J N et al. Propofol Anesthesia for Craniotomy: A

Double-blind Comparison of Remifentanil, Alfentanil and Fentanyl. J Neurosug
Anesthesiol 2000; 12: 1520.
Cottrell J E, Robustelli A, Post K, Turndorf H. Furosemide and Mannitol Induced

Changes in ICP and Serum Osmolality and Electrolytes. Anesthesiology 1975; 43: 445.
Todd M M, Warner D S, Sokoll M D et al. A Prospective Comparative Trial of Three

Anaesthetics for Elective Supratentorial Craniotomy. Propofol/fentanyl, Isoflurane/
nitrous oxide and Fentanyl/nitrous oxide. Anesthesiology 1993; 78: 100520.

Anaesthesia for Imaging
Relevant to the CNS
Jonathan P Coles
David K Menon
Jonathan P Coles is a Wellcome Research Training Fellow at Addenbrookes Hospital,

Cambridge, UK. He qualified from Leicester University and trained in anaesthesia in
Leicester before moving to the Anglian Region and Cambridge.
David K Menon is Professor of Anaesthesia at the University of Cambridge, and

Director of the Neurosciences Critical Care Unit at Addenbrookes Hospital, Cambridge.
He trained at the Jawaharlal Institute, India, Leeds General Infirmary, The Royal
Free Hospital and Addenbrookes Hospital, and was an MRC Research Fellow at the
Hammersmith Hospital.
Neuroradiology is an expanding field and likely to involve an increasing input from the
anaesthetist. Many patients need careful anaesthesia and perioperative care during
procedures carried out in sites remote from the normal operating theatre or ICU.
Imaging techniques
CT provides wide access to tomographic structural imaging. Rapid imaging following

administration of intravenous contrast or inhalation of xenon allows computation of
cerebral blood flow and blood volume (Figure 1). Image-guided stereotactic surgery
allows access to intracranial lesions without craniotomy. A mechanical frame is
attached to the patients head, a CT scan is performed, and a computer calculates
three-dimensional co-ordinates within the brain. In frameless stereotaxy, the initial CT
or MRI is stored on computer and fixed points on the skull are mapped on to the image
using a sensor wand.
a b
1a CT and b xenon CT of a patient following surgery for cerebral artery aneurysm. On the
CT there is evidence of oedema within the left hemisphere () with compression of the
ipsilateral ventricle and midline shift. The xenon CT shows low regional cerebral blood
flow, particularly in regions 17 and 18, suggestive of infarction. Scale: ml/100 g/minute.
cameras are commonly used for imaging following the injection of -emitting labels.
Single photon emission CT (SPECT) uses conventional -emitting nuclear medicine
isotopes with multiple detectors to generate tomographic images that are non-
quantitative. Positron emission tomography (PET) uses isotopes such as 15O and 18F,
which emit positrons. The annihilation of these positrons can be localized in space by
pairs of detectors, and provides quantitative images of cerebral physiology.
Interventional neuroradiology (INR): flow-directed microcatheters are introduced

into blood vessels via the femoral artery under local or general anaesthesia and
manipulated through the carotid or vertebral vessels. A variety of devices and drugs
including microcoils, stents, balloons, glues, thrombolytics, sclerosing and
chemotherapeutic agents can be introduced for diagnostic angiography, coiling
or ablation of cerebral aneurysms and arteriovenous malformations, percutaneous
transluminal angioplasty, or intravascular thrombolysis.
MRI and magnetic resonance spectroscopy (MRS): magnetic resonance images

are produced using powerful static magnetic fields and intermittent oscillating
radiofrequency electromagnetic fields that elicit signals from the nuclei of certain atoms.
MRI and MRS allow structural and functional imaging and in vivo biochemical analysis.
Magnetic field strengths are measured in Tesla (1 T = 10000 Gauss (G)). The magnetic
field strength at the surface of the earth is 0.51.5 G. Field strengths of 0.053.0 T
are used in clinical MRI and tend to be based on cryogenic superconducting magnets,
which are maintained at 273oC by immersion in liquid helium.
Safety
Biological safety: all the above techniques, excluding MRI, involve exposure to
ionizing radiation, which is defined by the estimated dose equivalent in milliSieverts
(mSv). In the UK, the range of background radiation is 28 mSv/year (chiefly from
naturally occurring radioactivity). Radiation safety is based on the as low as reasonably
achievable (ALARA) principle. The maximum distance from the X-ray source should
be maintained wherever possible. Lead glass shields, lead aprons and thyroid shields
should be used (together with radiation exposure badges in selected settings) to
assess cumulative radiation burden. The available data generally support the safety of
exposure to magnetic fields, but unnecessary exposure to high magnetic fields should
be avoided, based on general safety principles.
MRI
Projectile risks from ferromagnetic objects ferromagnetic objects (e.g. oxygen
cylinders, identification badges, paging devices) can become dangerous projectiles and
should not be taken into the MR suite unless they are known to be safe.
Implanted devices may be ferromagnetic and move in the magnetic field. Such
movement may be disastrous if the implant is large or in a critical location (e.g.
intraocular foreign bodies, cerebral aneurysm clips). Patients with an intracranial
aneurysm clip should not be imaged using MR, unless the clip has been documented
to be non-ferromagnetic, or the patient has already been imaged at the same field
strength with no problems. Even non-ferromagnetic implants can result in significant
image distortion, or cause local burns because their temperature is increased in the
presence of radiofrequency currents. Fatalities have been reported in patients with
cardiac pacemakers. The magnetic field causes the reed switch on pacemakers to
stick, and revert to fixed rate mode where delivery of a pacing spike on the upstroke of
a T wave can result in an R on T phenomenon and trigger ventricular fibrillation. MRI is
contraindicated in the presence of pacemakers and other implanted electronic devices,
unless it is known with absolute certainty that it will function safely. If there is doubt, the
implants should be tested with a powerful hand-held magnet and checked against the
manufacturers specifications. MR units usually have a checklist for patients and staff
to exclude the presence of implants.
Monitoring devices in addition to the above hazards, monitoring devices may
dysfunction as a consequence of exposure to magnetic fields. Leads from such devices
present a particular hazard because induced currents may result in burns. Simple
precautions can help to ensure safety (Figure 2). Devices are described as MR safe
when they do not represent a risk to the patient, and MR compatible when they also
continue to function in the MR environment without degrading imaging.
Other issues the most commonly used MR contrast agent
(gadopentate dimeglumine Gd-DTPA, Magnevist ), has an ex-cellent safety record.
The helium contained in cryogenic magnets can boil off (quench) rapidly when the
temperature rises. This dilutes room oxygen and the cold vapour gives frostbite and
burns.
Precautions to avoid problems with monitoring devices in magnetic

resonance environments
Check insulation on all monitoring wires and magnetic resonance (MR) cables is
intact
Do not cross cables or form large diameter loops of wire, instead plait leads
around each other
Remove any equipment not in use
Separate all cables from the skin (using padding)
Keep monitoring equipment as far away from the examination area as possible
Use only MR-compatible devices
Ensure limb extremities do not contact each other
Monitoring
Neuroradiology often requires the transport of the patient, and monitoring in an

unfamiliar environment. Minimal monitoring standards outside the operating theatre
should apply:
circulatory function including ECG, blood pressure, and auscultation of heart sounds
or pulse oximetry
oxygenation, including oxygen analyser, and pulse oximetry
ventilation if general anaesthesia is induced, ideally by capnography
temperature, if changes in body temperature are intended, anticipated or suspected.
Monitoring in MRI suites

Integrated monitoring systems based on technology developed for the MRI environment
are widely available, and represent the standard of care (Figure 3). Even
MR-compatible devices should be used with special attention to ensure their safe
application (see Figure 2). Other monitoring problems include ECG distortion. Changes
occur in early T waves and late ST segments that mimic hyperkalaemia or pericarditis
and radiofrequency currents produce ECG artefacts (Figure 4). Intracranial pressure
can be measured accurately via a ventriculostomy. Several intra-parenchymal sensors
are MR safe, but not MR compatible.
Magnetic resonance compatible monitoring and anaesthetic equipment
Medrad Inc. USA www.medrad.com

Invivo Research Inc. USA www.invivoresearch.com
Datex-Ohmeda, Finland www.datex-ohmeda.com
North American Drager, USA www.nad.com
Sims Pneupac, USA www.pneupac.com
Mammendorfer Institut fur Physik und Medizin, www.mimpm.com
Germany
Interference with ECG tracing during magnetic

resonance imaging following induction of currents
in leads by radiofrequency and gradient fields
a
ab
c

Anaesthesia and sedation
General issues common to most neuroradiological settings include:

isolated unfamiliar environment
hard narrow scanning table that will not tilt rapidly
potential for disconnection of equipment during movement within the scanner
rapid heat loss in the air-conditioned environment.
The choice of sedation or anaesthesia for patients undergoing imaging should be
discussed by the anaesthetist and neuroradiologist. High-dose sedation may be
inappropriate in patients with potential respiratory problems and raised intracranial
pressure. General anaesthesia and airway protection is required for prolonged and
uncomfortable procedures, extreme cases of anxiety and claustrophobia, failed
sedation and for critically ill patients requiring intermittent positive-pressure ventilation.
The anaesthetic technique should aim to maintain stable cerebral perfusion pressure
and minimize cerebral oedema. Both volatile and intravenous anaesthesia can be used;
the choice depends on clinical circumstances.
INR: patient immobility is crucial to ensure success and prevent complications such as
rupture or intimal tearing of small vessels. Patient management may need to allow for
the following.
Rapid titration of sedation or anaesthetic depth. Rapid neurological assessment may
be required. Problems include patient anxiety, comfort on prolonged immobility, and
discomfort following contrast injection.
Haemodynamic manipulation. To aid therapy, assess vascular reserve and treat
ischaemic episodes. This may have adverse effects in unstable patients with
neurological disease and should be used with caution.
Management of complications. These include vessel rupture and haemorrhage,
ischaemic episodes (following thromboembolism, vasospasm, hypoperfusion, vessel
dissection, stenosis or venous outflow obstruction), neurological complications, radio-
contrast reactions and pulmonary embolization of particles.
Anticoagulation. Heparin is commonly given to achieve an activated clotting time two
to three times baseline and prevent thrombosis.
CT: most procedures involve little stimulation and anaesthesia is required only for
unstable patients in intensive care and for children. Propofol is commonly used for
fast titration of levels of sedation and rapid return of consciousness. Small infants
tolerate scanning procedures without sedation if fed, wrapped well and placed prone.
Supplemental oxygen can improve the safety margin of sedation in children.
MRI requires an immobile patient to be placed in a noisy, dark, cold and uncomfortable
space that is isolated from radiology and anaesthetic staff. Induction and recovery
of anaesthesia should ideally take place with dedicated equipment incorporating
commercially constructed MR-compatible anaesthetic machines, ventilators and
infusion devices. Sedation techniques in children include ketamine, barbiturates,
benzodiazepines, high-dose chloral hydrate (50150 mg/kg) and low-dose propofol
infusions.
FURTHER READING
Burnstein R M, Menon D K. Anaesthesia for Neuroimaging. In: Matta
B F, Menon D K, Turner J T, eds. Textbook of Neuroanaesthesia and Critical Care,
London: Greenwich Medical Media, 2000; 399427.
Peden C J, Menon D K, Hall A S, Sargentoni J, Whitwam J G. Magnetic Resonance
for the Anaesthetist. Part 2: Anaesthesia and Monitoring in MR Units. Anaesthesia
1992; 47: 50817.
Summers A C, Menon D K. Neurological Imaging and Interventional Neuroradiology. In:
Van Aken H, ed. Clinical Anaesthesiology. London: Baillire Tindall, 1999; 60528.
Turner J M. Anaesthesia for Neuroradiology. In: Matta B F, Menon D K, Turner J T,
Textbook of Neuroanaesthesia and Critical Care. London: Greenwich Medical Media,
2000; 399427.

Applied Cerebrovascular
Physiology
David K Menon
Stuart A Booth is Specialist Registrar in Anaesthesia at Addenbrookes Hospital,

Cambridge, UK. After qualifying from Birmingham University, he trained in medicine
at the Derbyshire Royal Infirmary and in anaesthesia and intensive care at Bury St
Edmunds and Cambridge.

He trained at the Jawaharlal Institute, India, Leeds General Infirmary, The Royal
Free Hospital and Addenbrookes Hospital. His research interests include mechanisms
of secondary neuronal injury, metabolic imaging of acute brain injury and imaging
anaesthetic action in the brain.
Understanding the principles of the physiology of the brain, and the effects of drugs
and pathological processes on it, is of fundamental importance for anaesthetists in
the management of patients with brain injury, and for the provision of anaesthesia in
neurosurgical patients.
Cerebral metabolism and blood flow
The ability of the brain to maintain membrane ionic gradients and transmit electrical
impulses depends on a continuous supply of metabolic substrates. Glucose is the
primary energy source of the brain and is actively transported across the bloodbrain
barrier. The cerebral metabolic rate of glucose utilization is about 5 mg/100 g brain/
minute, with 90% taken up in aerobic metabolism. During starvation, however, the brain
is able to adapt and use different substances for metabolism (e.g. ketones, lactate,
amino acids: see PHYSIOLOGY). In normal circumstances, oxygen consumption
closely parallels glucose consumption (3.5 ml/100 g brain/minute or 50 ml/minute). In
adults, stores of glycogen are exhausted in less than 3 minutes in the face of normal
brain activity and there are no significant stores of oxygen. Owing to the high brain
oxygen consumption, cessation of cerebral blood flow results in unconsciousness
within 10 seconds.
The brain accounts for 20% of basal oxygen consumption and 25% of basal glucose
consumption, which under normal circumstances is more than adequately met by the
15% of cardiac output that the brain receives (750 ml/minute in adults). The mean
resting cerebral blood flow in young adults is about 50 ml/100 g brain/minute. There
are, however, regional differences in blood flow, with mean values for grey and white
matter being 80 and 20 ml/100 g brain/minute, respectively. Blood flow also parallels
metabolic activity, varying between 10 and 300 ml/100 g brain/minute. Functional
impairment results from reductions in cerebral blood flow; the EEG slows at flow rates
below 2025 ml/100 g brain/minute, it is flat at a rate of 1520 ml/100 g brain/minute,
and irreversible brain damage occurs at rates below 10 ml/100 g brain/minute.
The bloodbrain barrier
Endothelial cells in cerebral capillaries contain few pinocytic vesicles and are sealed
by tight junctions (zona occludens), with no anatomical gap. Consequently, unlike other
capillary beds, the endothelial barrier of cerebral capillaries presents a high electrical
resistance and is remarkably non-leaky. This property of the cerebral vasculature
is termed the bloodbrain barrier, and comprises three cellular components (i.e.
endothelial cell, astrocyte and pericyte), and one non-cellular structure (endothelial
basement membrane). The bloodbrain barrier is a function of the cerebral
microenvironment rather than an intrinsic property of the vessels themselves. Passage
of substances through the bloodbrain barrier is directly proportional to lipid solubility
and the presence of active transport mechanisms, but indirectly proportional to
molecular weight, ionic charge and the degree of plasma protein binding. Thus lipophilic
substances, such as carbon dioxide, oxygen and anaesthetic agents, freely enter the
brain, whereas ions, proteins and large molecules penetrate the bloodbrain barrier
poorly. Water moves freely by bulk flow, whereas there is some impedance to small ions
such as sodium. Acute changes in plasma electrolyte concentrations (and osmolality)
produce changes in the osmotic gradient between plasma and brain interstitial fluid.
Although these changes are transient, they result in rapid fluid shifts in the brain,
leading to altered neurological function. Thus, marked abnormalities in serum sodium or
glucose should be corrected slowly. Disease processes, such as severe hypertension,
stroke, infection, tumours, trauma, sustained seizure activity, marked hypercapnia and
hypoxia, can cause disruption of the bloodbrain barrier. If this occurs, fluid movements
across the barrier become dependent on hydrostatic gradients rather than osmotic
gradients.
CSF
The main function of CSF is to protect the brain from trauma. It also recirculates
interstitial proteins back to plasma (there are no brain lymphatics). The volume of
CSF in an adult is about 150 ml (with a turnover of 21 ml/hour) with roughly equal
proportions in the cranial and spinal compartments. Most CSF is formed (secretion
and ultrafiltration) in the choroid plexus of the cerebral ventricles (mainly lateral). It is
iso-osmolar compared with plasma, but has a lower concentration of K+, Ca2+, HCO3 ,
H+ (pH 7.33), protein and glucose, and a higher concentration of Na+, Cl, Mg2+ and
carbon dioxide. CSF flows from the lateral ventricles, through the foramen of Monro,
to the third ventricle and then the fourth ventricle (via the aqueduct of Sylvius). It then
passes through the foramen of Magendie (medial) and foramina of Luschka (lateral)
into the cisterna magna to continue into the subarachnoid spaces around the brain and
spinal cord. Reabsorption of CSF occurs at the arachnoid granulations.
Intracranial pressure and volume relationships
In adults, the skull is a rigid structure, which forms an almost completely closed
box. It contains four components: brain parenchyma and interstitial fluid (80%), blood
which is mainly venous (12%) and CSF (8%). Each fluid component is essentially
incompressible, and any increase in the volume of one component if unaccompanied by
a compensatory decrease in the volume of another, will result in a rise in intracranial
pressure (ICP), as the intracranial volume is fixed (MonroKellie doctrine). The normal
ICP is less than 15 mm Hg, but varies with arterial pulsations, respiration, coughing
and straining (venous pressure). Blood flow to the brain is governed by cerebral venous
pressure only when it exceeds ICP; in such situations, cerebral blood flow is dependent
on arteriovenous pressure differences. In most instances, however, cerebral blood flow
is dependent on the pressure difference between the mean arterial pressure (MAP)
measured at the level of the brain and ICP. This is the cerebral perfusion pressure
(CPP):
CPP = MAP ICP (or cerebral venous pressure)
A sufficiently large rise in blood, brain tissue or CSF volume, or the presence
of a space-occupying pathological process
(e.g. haemorrhage, tumour, abscess), will result in an increase in ICP. However,
compensatory mechanisms can initially prevent rises in ICP. These include:
displacement of CSF from the cranial to spinal compartment
increased CSF absorption
decreased CSF production
decreased cerebral blood volume.
Intracranial compliance is initially high due to these processes. However, as intracranial
space occupation continues (by physiological or pathological means), the limits of these
mechanisms are exceeded. Intracranial compliance falls and ICP rises dramatically
with small increases in intracranial volume, such as 510 ml of blood (Figure
1). Therefore, although the cerebral blood volume forms only a small part of the
intracranial volume, inappropriate anaesthetic management may cause it to increase as
a result of coughing, positive end-expiratory pressure (PEEP), or severe hypertension.
Conversely, physiological and pharmacological interventions by the anaesthetist may
result in marked reductions in ICP in the presence of intracranial hypertension.
Although the absolute magnitude of such a decrease in volume may be small, it may
result in a marked fall in ICP.
1
Physiological determinants of cerebral blood flow and volume
Regional metabolism
Increases in local neuronal activity are accompanied by increases in regional cerebral
metabolic rate. This is termed flowmetabolism coupling. It has now been shown that
increases in regional cerebral blood flow during functional activation tend to track
glucose utilization, but may be far in excess of an increase in oxygen consumption.
This results in regional anaerobic glucose utilization, and a consequent decrease in
the local oxygen extraction ratio and increase in local oxyhaemoglobin saturation. The
cellular mechanisms underlying these observations have highlighted the role played by
astrocytes in the regulation of cerebral metabolism. These data suggest that astrocytes
utilize glucose glycolytically and produce lactate, which is transferred to neurons where
it serves as a fuel in the citric acid cycle. Astrocytic glucose utilization and lactate
production appear to be, in large part, coupled to the astrocytic reuptake of glutamate
released at excitatory synapses.
The regulatory changes involved in flowmetabolism coupling have a short latency
(about 1 second) and may be mediated by metabolic or neurogenic pathways.
The metabolic pathways include the increases in perivascular K+ or adenosine
concentrations that follow neuronal depolarization. Dopamine, acetylcholine, nitric
oxide and, possibly, 5-hydroxytryptamine, substance P and neuropeptide Y, released
by nerves that supply cerebral vessels, may mediate neurogenic flowmetabolism
coupling.
Cerebral perfusion pressure

The ability of the cerebral circulation to maintain cerebral blood flow at a
relatively constant level, in the face of changes in cerebral perfusion pressure, by
altering cerebrovascular resistance is termed autoregulation (Figure 2). In normal
circumstances, as both ICP and cerebral venous pressure are low, systemic arterial
perfusion pressure (i.e. mean arterial pressure) becomes the primary determinant of
cerebral perfusion pressure. However, in pathological states, ICP becomes a significant
factor for cerebral perfusion pressure. Autoregulation has limits above and below which
cerebral blood flow is directly related to perfusion pressure. Above the higher limit of
autoregulation, increases in mean arterial pressure lead to forced dilatation of cerebral
arterioles, disruption of the bloodbrain barrier and formation of cerebral oedema with
a resultant increase in cerebral blood volume and ICP. Below the lower autoregulatory
limit, cerebral blood flow falls linearly with decreasing perfusion pressure.
Unlike flowmetabolism coupling, autoregulatory responses are not immediate;
estimates of the latency for compensatory changes in regional cerebrovascular
resistance range from 10 to 60 seconds. Changes in cerebrovascular resistance
probably arise as a result of myogenic reflexes in the resistance vessels, but these
may be modulated by sympathetic nervous system activity or the presence of chronic
systemic hypertension. Thus, sympathetic blockade or cervical sympathectomy shifts
the autoregulatory curve to the left, while chronic hypertension or sympathetic activation
shifts it to the right. These modulatory effects may arise from angiotensin-mediated
mechanisms. Primate studies suggest that nitric oxide is unlikely to be important in
pressure autoregulation.
In reality, the clear-cut autoregulatory thresholds with varying cerebral perfusion
pressure shown in Figure 2 are not observed; the autregulatory knees tend to be
more gradual, and there may be wide variations in regional cerebral blood flow
for a given value of cerebral perfusion pressure. Symptoms of cerebral ischaemia
have been shown to appear when the mean arterial pressure falls below 60% of an
individuals lower autoregulatory threshold. However, generalized extrapolation from
such individualized research data to the production of safe lower limits of mean arterial
pressure for general clinical practice is hazardous for several reasons. These include
the wide individual scatter in regional cerebral blood flow autoregulatory efficiency and
the coexistence of local fixed vascular obstruction (e.g. carotid atheroma or vascular
spasm).

Partial pressure of carbon dioxide in arterial blood (PaCO2)

Cerebral blood flow is proportional to PaCO2, subject to a lower limit, below which
vasoconstriction results in tissue hypoxia and reflex vasodilatation, and an upper limit
of maximal vasodilatation (Figure 3). On average, in the middle of the physiological
range, each kPa change in PaCO2 produces a change of about 15% in cerebral blood
volume and 20% in cerebral blood flow. In patients with low intracranial compliance, this
decrease in cerebral blood volume can result in dramatic reductions in ICP. However,
moderate hypocapnia (PaCO2 of about 3.5 kPa) is no longer recommended to reduce
cerebral blood volume in intracranial hypertension because these levels of hypocapnia
in head-injured patients can result in dangerously low regional cerebral blood flow
levels. Prostaglandins and nitric oxide mediate the vasodilatation produced by carbon
dioxide.
Arterial oxygen content

Classical teaching is that cerebral blood flow is unchanged until the partial pressure of
oxygen in arterial blood (PaO2) falls below about 7 kPa, but rises sharply with further
reductions (Figure 3). However, recent transcranial Doppler data suggest cerebral
thresholds for cerebral vasodilatation as high as 8.5 kPa (about 8990% oxygen
saturation). This nonlinear behaviour is because tissue oxygen delivery governs
cerebral blood flow, and arterial oxygen content is related primarily to haemoglobin
oxygen carriage (and thus oxygen saturation) rather than PaO2. The vasodilator
responses to hypoxaemia show little adaptation with time, but may be substantially
modulated by PaCO2 levels. Nitric oxide does not play a role in the vasodilatory
response to hypoxia. Blood haematocrit (and hence viscosity) was also thought to
play a role in determining cerebral blood flow. However, it is more likely that changes
in cerebral blood flow caused by alterations in haematocrit are the consequence of
changes in arterial oxygen content, rather than in blood viscosity.
Temperature
Cerebral blood flow changes by about 57%/oC. Hypothermia decreases both cerebral
metabolic rate and cerebral blood flow so that, at 27oC, metabolic utilization of
oxygen is 50% of normal. These reductions in cerebral metabolic rate allow safe
circulatory standstill for up to 40 minutes in patients maintained at temperatures of 18oC.
In healthy brains at this temperature, autoregulation, flowmetabolism coupling and
carbon dioxide reactivity remain intact. An increase in temperature to 42oC leads to an
increase in the utilization of oxygen and cerebral blood flow. Temperatures exceeding
42oC appear to cause neuronal damage and reduced oxygen uptake.
Autonomic nervous system

The autonomic nervous system mainly affects the larger cerebral vessels, up to and
including the proximal parts of the anterior, middle and posterior cerebral arteries.
1-adrenergic stimulation results in vasodilatation while 2 -adrenergic stimulation leads
to vasoconstriction. The effects of systemically administered - or -agonists are less
significant. However, significant vasoconstriction can be produced by extremely high
concentrations of catecholamines (e.g. in haemorrhage) or centrally acting 2 -agonists
(e.g. dexmedetomidine). The autonomic nervous system may be involved in cerebral
vasospasm after brain injury (e.g. subarachnoid haemorrhage).
Cerebral venous pressure

Venous obstruction can be caused by supine or head-down positioning, coughing,
straining, incomplete muscle relaxation, or tight tracheal tube ties in ventilated patients.
While PEEP levels that result in cerebral venous pressures greater than ICP can
exacerbate intracranial hypertension, in most instances moderate applications of PEEP
will improve arterial oxygenation and potentially result in reductions in ICP. Obstruction
of cerebral venous drainage increases ICP by increasing cerebral blood volume and
by promoting cerebral oedema formation due to hydrostatic pressure changes. Such
oedema can produce microcirculatory disturbances that add to the detrimental effects
of intracranial hypertension on cerebral blood flow via cerebral perfusion pressure
changes.
Mechanisms in regional cerebral blood flow control
Some of the mechanisms involved in cerebrovascular control are shown in Figure

4, several of which have been referred to earlier. In addition, the level of free Ca2+ is
important in determining vascular tone, and arachidonate metabolism can produce
prostanoids that are either vasodilators (e.g. prostacyclin) or vasoconstrictors (e.g.
thromboxane A 2). Endothelin (ET), produced by endothelin-converting enzyme in
endothelial cells, balances the vasodilator effects of nitric oxide in a tonic manner by
exerting its influences at ETA receptors in the vascular smooth muscle.
Nitric oxide in the regulation of cerebral haemodynamics

Recent interest has focused on the role of nitric oxide (NO) in the control of cerebral
haemodynamics. NO is synthesized in the brain from the amino acid L-arginine by
the constitutive form of the enzyme NO synthetase. This form of the enzyme is
calmodulin dependent and requires Ca2+ and tetrahydrobiopterin for its activity. Under
basal conditions, endothelial cells synthesize NO, which diffuses into the muscular
layer and, via a mechanism mediated by cyclic guanosine monophosphate (cGMP),
produces relaxation of vessels. There is strong evidence to suggest that NO exerts a
tonic dilatory influence on cerebral vessels. Some of the endothelium-derived relaxant
factor (EDRF) activity in cerebral vessels may be due to compounds other than NO.
For example, carbon monoxide produced by heme-oxygenase may be responsible for
significant cerebral vasodilatation, especially when NO production is reduced.
NO plays an important role in cerebrovascular responses to functional activation,
excitatory amino acids, hypercapnia, ischaemia and subarachnoid haemorrhage.
Furthermore, NO may also play an important part in mediating the vasodilatation
produced by volatile anaesthetic agents, although other mechanisms, including a direct
effect on the vessel wall, cannot be excluded.
Neurogenic flowmetabolism coupling

In the last 10 years, focus has been placed on flowmetabolism coupling being effected
by a diffusible extracellular mediator. However, there is now accumulating evidence
to suggest that dopaminergic neurons may play a major part in such events and, in
addition, may control bloodbrain barrier permeability.
Measurement of cerebral blood flow and oxygenation
All clinical and many laboratory methods of measuring global or regional cerebral
blood flow are indirect and may not produce directly comparable measurements. It is
also important to treat results from any one method with caution, and attribute any
observed phenomena to physiological effects only when demonstrated by two or more
independent techniques. Methods that provide absolute estimates of regional cerebral
blood flow use one of two principles: they either measure the distribution of a tracer,
or estimate blood flow from the wash-in or washout curve of an indicator. Other
techniques do not directly estimate regional cerebral blood flow, but can be used either
to measure a related flow variable (such as arterial flow velocity) or to infer changes
in flow from changes in metabolic parameters. Some techniques that have been used
for the measurement of cerebral blood flow and oxygenation are described briefly in
Figure 5.
Techniques for measuring cerebral blood flow and oxygenation
Technique Global/regional Features

KetySchmidt Global Invasive (requires jugular bulb and arterial catheters). Time consuming (1020
minute data collection). Repeated measures possible. Can be performed in ICU
Intracarotid 133Xe Regional Invasive. One hemisphere only. Primarily looks at superficial cortex. Washout or
dynamic CT method. Repeated measures possible
Inhaled 133Xe Regional Non-invasive. Primarily looks at superficial cortex. Washout or dynamic CT method.
Repeated measures possible but not at rapid intervals. Extracranial tissue
contamination
SPECT Regional Distribution of photon-emitting tracer estimates rCBF. Cheaper than PET, but
poorer resolution. Difficult to repeat measurements. Not bedside test
PET Regional Distribution of positron-emitting tracer estimates rCBF. Good resolution. Expensive
and complex. Repeated measures possible. Not bedside test
Functional MRI Regional Intravenous contrast label used or utilizes change in regional oxygenation during
functional activation. Excellent resolution. Repeated measures easy with non-
contrast method. Not bedside test. Non quantitative in most settings
TCD ultrasound Regional Measures flow velocity and therefore CBF indirectly. Measures relative, not
absolute CBF. Non-invasive bedside measurement for continuous monitoring.
Repeatable but needs same probe angle and vessel diameter to compare values
SjvO2 Regional Permits continuous monitoring of jugular venous bulb oxygen saturation. Fibre-
optic catheter commonly used. Invasive bedside measurement. Indicates balance
between oxygen supply and demand
NIROS Regional Spectroscopic measurement of regional haemoglobin oxygenation and
cytochrome redox state in restricted and poorly defined volume (transcranial
cerebral oximetry).Non-invasive bedside measurement for continuous monitoring
Abbreviations: rCBF, regional cerebral blood flow; SPECT, single photon emission tomography; PET, positron emission tomography; TCD,
transcranial Doppler; SjvO2, jugular venous oxygen saturation; NIROS, near infrared optical spectroscopy.
5
The KetySchmidt technique
The KetySchmidt technique involves the insertion of catheters into a peripheral artery
and the jugular bulb. An inert, freely diffusible tracer, such as 1015% inhaled nitrous
oxide, is administered, and paired arterial and jugular venous samples of blood are
obtained at rapid intervals for measurement of nitrous oxide levels. The resultant plot
of concentration versus time produces an arterial and a venous curve (Figure 6). The
jugular venous level of nitrous oxide rises more slowly than the arterial levels because
delivered nitrous oxide is taken up by the brain. The rate of equilibration of the two
curves measures the rate at which nitrous oxide is delivered to the brain, and thus
provides a means of measuring global cerebral blood flow.
Xenon-133 washout
An array of collimated scintillation counters positioned over the head can be used
to measure the regional decay in radioactivity after the intracarotid or intra-aortic
injection of 133Xe. The slope of the washout curve for radioactivity is proportional to
regional cerebral blood flow. This washout curve is bi-exponential (Figure 7) and
may be resolved into two mono-exponential components, which represent fast and
slow washout components. Although these are often referred to as grey matter and
white matter components, there is no basis to support such an anatomical distinction
because the two curves represent pharmacokinetic compartments, rather than specific
neuroanatomical structures. The technique provides two-dimensional information
regarding regional cerebral blood flow, but is invasive and primarily evaluates superficial
cortical blood flow. Furthermore, intra-carotid injection permits the assessment of only
a single cerebral hemisphere at a time. One modification involves the inhalational or
intravenous administration of 133Xe; although this makes the technique less invasive,
problems arise because of recirculation and contamination by extracranial tissues. The
simultaneous presence of activity in both cerebral hemispheres also leads to the look-
through phenomenon, where regional cerebral blood flow reductions on one side may
be missed because of activity sensed in deeper areas of contralateral brain tissue.
Tomographic regional cerebral blood flow measurement

Tomographic information regarding regional cerebral blood flow may be obtained
by quantitative studies of the washout of a radiodense contrast agent, using rapid
sequential X-ray CT imaging (dynamic CT scanning). Inhaled stable xenon has been
used most often as the contrast agent. Xenon-enhanced CT gained popularity owing
to its high spatial resolution and the availability of the equipment. In addition, it can be
performed in neurological emergencies because of the short examination time. Recent
studies have been performed using standard radioiodinated intravenous contrast
agents.
Single photon emission tomography (SPECT) and positron emission tomography
(PET) use -emitting (e.g. 99Tc) and positron-emitting isotopes (e.g. 15O, 18F, 11C, 13N),
respectively, to produce tomographic images of regional cerebral blood flow. PET,
in addition to imaging cerebral blood flow, can provide information about cerebral
blood volume, oxygen metabolism, and the oxygen extraction fraction. Functional
MRI (fMRI) produces tomographic images of regional cerebral blood flow in one of
two ways. One technique uses an intravenous contrast agent in the same way as the
techniques previously mentioned use other agents. MRI can also produce, without the
use of external contrast agents, tomographic images of changes in regional cerebral
blood flow. The technique maps the increases in magnetic resonance signal intensity
produced by the decreases in regional deoxyhaemoglobin levels that occur during
regional activation.
In general, continuous clinical monitoring of the adequacy of cerebral perfusion
tends to use techniques other than those outlined above. The parameter most
commonly monitored in head-injured patients is cerebral perfusion pressure, though
many centres are increasingly using fibre-optic jugular venous oximetry and
transcranial Doppler measurement of middle cerebral artery flow velocity. Monitoring
of the processed EEG or evoked potentials provides information regarding the
consequences of reduced cerebral blood flow, and this technique has been used in the
context of cardiopulmonary bypass and carotid endarterectomy. Near-infrared optical
spectroscopy and laser Doppler flowmetry are investigational techniques the roles of
which have not been clearly defined.
Transcranial Doppler (TCD) ultrasonography

TCD measures the velocity of RBCs flowing through the large vessels at the base of
the brain using the Doppler shift principle. Since the diameter of these basal vessels
is unaffected by common physiological variables, such as mean arterial pressure and
PaCO2, flow velocity in these vessels provides an index of flow. Although many of
the intracranial arteries may be studied, the middle cerebral artery is most commonly
insonated because it is easy to detect, receives a substantial proportion of the blood
flow from the internal carotid artery and allows easy probe fixation. Provided the
angle of insonation and the diameter of the vessel insonated remain constant, relative
changes in cerebral blood flow velocity correlate closely with changes in cerebral
blood flow. Changes in TCD velocities and waveform patterns can be used to detect
cerebral ischaemia, hyperaemia and vasospasm. In addition, the characteristics of the
TCD waveform may be used to provide a non-invasive estimate of cerebral perfusion
pressure.
Jugular venous oximetry

Cerebral oxygenation has conventionally been assessed by jugular bulb oximetry.
Traditionally, the superior sagittal sinus is thought to drain primarily into the right internal
jugular vein, and it is common practice to place jugular bulb catheters on this side in
order to monitor the oxygenation in the supratentorial compartment. More recent data
suggest that supratentorial venous drainage is less lateralized, and a case has been
made for bilateral jugular bulb catheterization. Normal jugular bulb oxygen saturations
tend to be 6570%. Reductions in the jugular bulb oxygen saturation or increases in
arterio-jugular difference in oxygen content of more than 9 ml/dl provide useful markers
of inadequate cerebral blood flow and can guide therapy. Values of jugular bulb oxygen
saturation below 50% have been shown to be associated with a worse outcome in head
injury. Conversely, marked elevations in jugular bulb oxygen saturation may provide
evidence of cerebral hyperaemia.
FURTHER READING
Fitch W. Physiology of the Cerebral Circulation. In: Moss E, Ellis F R, eds. Baillieres
Clinical Anaesthesiology. Vol. 13 (4). London: Baillire Tindall, 1999; 48798.
Matta B F, Menon D K, Turner J M, eds. Textbook of Neuroanaesthesia and Critical
Care. London: Greenwich Medical Media, 2000.
Menon D K. Cerebral Circulation. In: Priebe H-J, Skarvan K, eds. Cardiovascular
Physiology. 2nd ed. London: BMJ Publishing Group, 2000; 24077.

Clinical Neuroprotection
David K Menon
Elisabetta Bandera

Elisabetta Bandera is Specialist Registrar at the Istituto di Anestesia e Rianimazione,

Ospedali Civili di Brescia, Italy. She qualified from Universit degli Studi di Brescia. She
trained and worked for 6 months as specialist registrar at the Neurocritical Care Unit at
Addenbrookes Hospital, Cambridge, UK.
Neuroprotection begins with basic resuscitation comprising airway, respiratory and

cardiovascular support. Unless normoxia and normotension are maintained, the
application of drugs is ineffective. While this article focuses on agents that achieve
neuroprotection by reversing one or more of the secondary injury processes, other
therapeutic interventions can reduce neuronal injury by optimizing cerebrovascular
physiology. Drugs such as mannitol and dexamethasone, can reduce post-traumatic
and peritumoral oedema, respectively, and thus augment cerebral perfusion pressure
and oxygen delivery. Similarly, haemodynamic augmentation for hypervolaemia and
hypertension can enhance cerebral blood flow in the setting of intracranial hypertension
or cerebral vasospasm. Agents that antagonize most recognized injury mechanisms
have been shown to be neuroprotective in animal models. This contrasts with the
clinical setting, where one of the major disappointments in recent years has been the
repeated failure of neuroprotective agents.
Neuroprotective interventions
Categories of drugs that have been evaluated in animal models of CNS ischaemia and
trauma are outlined below. Specific issues that need to be considered when evaluating
the clinical relevance of experimental studies are listed in Figure 1.
Critical issues in assessing preclinical neuroprotective studies
Species in which studies are performed (effectiveness in more than one species
is reassuring; primate models are increasingly seen as relevant)
Is the model well characterized? (especially problematic in traumatic brain injury)
Is intervention at a relevant time point? (pre-ischaemic interventions may be

irrelevant to clinical stroke therapy)
Duration of follow-up (increasing evidence supports a need to follow up animals

for several days to weeks, because neuronal loss may be delayed)
Does the study address outcome or only modification of mechanistic changes?
Have age and gender of the experimental animals been specified and/or
controlled? (older animals may show less benefit, there may be gender
variations)
1
Excitatory amino acid antagonists (EAAs): raised levels of glutamate in the

extracellular fluid (ECF) have been demonstrated following ischaemia and trauma,
and neuroprotective interventions have been targeted at all three glutamate receptor
subtypes (N-methyl-D-aspartate (NMDA), -amino-3-hydroxy-5-methyl-4-
isoxazolepropionate (AMPA/kainite) and metabotropic) and at various regulatory sites
on the NMDA receptor (e.g. the glycine site). The reference compound in this category
is dizocilpine (MK-801), a non-competitive antagonist at the NMDA receptor, which had
significant CNS side-effects and never reached clinical trials. Newer compounds and
regulatory site agents (e.g. glycine and polyamine antagonists) may be better. NMDA
receptor antagonists may provide additional neuroprotection when used in combination
with antioxidants or thrombolysis, suggesting a possible role for multidrug combinations
in neuroprotection.
Experimental data attest to the efficacy of EAAs in animal models. However, a variety
of EAAs, including cerestat (a non-competitive NMDA blocker), selfotel (a competitive
NMDA blocker) and eliprodil (a polyamine regulatory site antagonist), have proved
disappointing in stroke and head injury.
Sodium channel blockers: the neuroprotective potential of drugs such as phenytoin

(and its prodrug fosphenytoin), lamotrigine, lubeluzole and riluzole has been shown
experimentally. They block sodium channels and attenuate glutamate release. No
clinical successes have been reported.
Antioxidants and free radical scavengers: several antioxidants have been

effective in animal models, including superoxide dismutase and catalase, the spin-
trap phenyl-t-butyl nitrone (PBN), iron chelators (e.g. desferroxamine) and the
aminosteroid tirilazad. They all exhibit neuroprotective efficacy in animal models but
there have been no successful clinical trials. Initial optimism regarding pegorgotein
(PEG conjugated superoxide dismutase) and tirilazad mesylate has been unfounded.
One of the few exceptions to the list of failures is the use in acute spinal cord injury of
methylprednisolone at high doses (3035 mg/kg, followed by 5.4 mg/kg/hour for 24
hours) which may provide part of its benefit through antioxidant effects.
Inflammation and corticosteroids: inhibition of tumour necrosis factor (TNF),

interleukin-1 (IL-1), and IL-8 release or activity improves outcome in focal cerebral
ischaemia and trauma models. Inhibition of leukocyte-endothelial interactions is also
neuroprotective, and antagonism of adhesion molecules such as ICAM-1, E-selectin
and P-selectin reduces neuronal injury.
Despite experimental success with anti-inflammatory therapy, a recently reported trial

of anti-ICAM-1 antibody (Enlimomab) in acute stroke showed increased morbidity
and mortality in treated patients, and recent guidelines covering the intensive care
management of patients with head injury have emphasized the lack of objective benefit
from corticosteroids. Animal data provide evidence of both harm and benefit from
corticosteroid therapy. However, a recent meta-analysis of corticosteroid therapy in
head injury concluded that available clinical evidence cannot exclude a benefit from
corticosteroid therapy. These conclusions have been widely discussed and have
triggered a large (10,000 patients) MRC-sponsored randomized trial of corticosteroid
therapy in head injury (the CRASH trial; http://www.crash.lshtm.ac.uk).
Anaesthetic neuroprotection does not depend exclusively on the extent of metabolic

suppression and may involve several mechanisms (Figure 2). There is increasing
interest in the neuroprotective effects of non-barbiturate anaesthetics. Barbiturates,
propofol and isoflurane provide neuroprotection. Ketamine, in addition to its anaesthetic
effects, may provide neuroprotection by acting as an NMDA receptor antagonist.
Recent clinical studies of anaesthetic neuroprotection are inconclusive. One study
addressing the relative merits of intravenous anaesthetic agents and isoflurane in the
clinical setting of temporary clip application during aneurysm surgery showed that pre-
treatment with intravenous anaesthetics improved tolerance to ischaemia, but patient
numbers were small and it is not clear whether comparable metabolic suppression was
achieved. In another study, while barbiturate coma was effective in treating refractory
intracranial hypertension following stroke, it produced no improvement in outcome.
Mechanisms by which anaesthetic agents may exert their

neuroprotective effects
Reduction in synaptic transmission

Reduction in calcium influx
Ability to block sodium channels
Membrane stabilization
Improvement in distribution of regional cerebral blood flow
Suppression of cortical EEG activity
Reduction in cerebral oedema
Free radical scavenging
Potentiate -aminobutyric acid (GABA)-ergic activity
Alteration of fatty acid metabolism
Suppression of catecholamine-induced hyperactivity
Reduction in CSF secretion
Anaesthesia, de-afferentation and immobilization
Facilitates uptake of glutamate in synapses
Nitric oxide and the endothelin system: the vasoconstrictor effects of endothelin are
normally balanced by vasodilatation produced by endothelial nitric oxide. Overactivity
of the endothelin system represents a potential therapeutic target in stroke and
subarachnoid haemorrhage. However, neuronal nitric oxide can worsen secondary
injury, and nitric oxide synthase inhibition in experimental animals has variable effects,
depending on the selectivity of the inhibitor, the model and the systemic haemodynamic
perturbations that are produced. Reduced nitric oxide production may be one of the
mechanisms by which hypothermia (see below) effects neuroprotection; no clinical
studies are available.
Calcium channel blockade: studies continue to show neuro-protection by calcium

blockers active at several calcium channel subtypes. Failures in other studies may
be explained by the relative importance of the N, Q and P subtypes of voltage-gated
calcium channels in neuronal injury, because they may be relatively resistant to block
by common calcium-blocking agents. The use of prophylactic nimodipine in aneurysmal
sub-arachnoid haemorrhage is one of the few clinically neuroprotective interventions
that has been successful, with reductions in morbidity and improvements in outcome.
Hypothermia: several reports document continued experimental success with mild

hypothermic neuroprotection. It causes metabolic suppression above 30oC, but other
mechanisms are also important. Mild-to-moderate hypothermia (> 28oC) can reduce
excitatory amino acid release, nitric oxide production, cytokine responses, adhesion
molecule expression, neutrophil infiltration, arachidonate release and production of free
radicals. The effects of hypothermia result in better preservation of the bloodbrain
barrier, reduced intracranial hypertension, preservation of cytoskeletal integrity, a lower
frequency of spreading depolarization and modulation of gene expression.
Clinical hypothermia the ischaemic brain tends to be warmer than systemic

temperature, and this finding has been confirmed in clinical head injury and stroke. Use
of an extracorporeal heat exchanger has been described for rapid cooling following
brain trauma, but forced convective cooling seems to be the best means of inducing
hypothermia in patients. Pharmacological methods of temperature reduction have
non-sustained effects. Selective cooling of the brain during retrograde perfusion in
hypothermic circulatory arrest for major cardiovascular surgery may enhance cerebral
hypothermia and give added protection while reducing systemic risks.
A series of pilot studies in 1993 suggested significant benefit from induced hypothermia
in patients with closed head injury, and formed the basis of an NIH multicentre trial of
nearly 400 patients using mild hypothermia (33oC for 48 hours) following head trauma.
The initial results were encouraging, but the final results suggest that hypothermia is
ineffective in this setting. This is disappointing because many of the expected
mechanistic effects of mild hypothermia have been documented in clinical disease.
One explanation for this discordance is that hypothermia worsens outcome in patients
with head injuries without intracranial hypertension, suggesting that the risk to benefit
ratio from hypothermia is maximal in patients with refractory intracranial hypertension
in whom the benefits are maximal. A more recent case-controlled pilot study suggests
that mild hypothermia (33oC for 12 hours) may improve outcome in patients who
experienced cardiac arrest out of hospital.
Miscellaneous and emerging neuroprotective targets

Calpain is a protease implicated in several events in the injury cascade. The potent
calpain inhibitor MDL 28,170, rapidly penetrates the brain, prevents cleavage of
structural and regulatory proteins and produces significant neuroprotection with therapy
initiated up to 6 hours after the onset of ischaemia.
Immunophilins the immunosuppressant drugs cyclo-sporin A and FK506 bind to

specific receptors in the brain and inhibit calcineurin and nitric oxide synthase, modulate
neurotransmitter release and cytosolic calcium increases, and mediate nerve growth
and regeneration following ischaemia. They are beneficial in ischaemia models.
Caspases are a family of cysteine aspartate proteases (including interleukin converting

enzyme (ICE) and CPP32 or caspase 3) involved in apoptotic neuronal death. Their
inhibition has been associated with neuroprotection in transient focal ischaemia.
Poly (ADP-ribose) polymerase (PARP) is an abundant nuclear enzyme activated

as a DNA repair mechanism by DNA nicks that are typically mediated by oxidant or
nitric oxide. PARP transfers ADP monomers from NAD + and depletes cellular adenine
nucleotide and hence ATP stores when the demand and supply balance of cellular
energy is critical. Inhibition or genetic inactivation of the enzyme is neuroprotective.
Matrix metalloproteases are upregulated in a variety of experimental brain injury

models, and result in damage to the extracellular matrix with disruption of the blood
brain barrier following ischaemia. Matrix metalloprotease inhibitors can reduce peri-
haemorrhagic oedema formation and neuronal injury in ischaemia models.
Adenosine may have neuroprotective effects at A1 receptors by modulating glutamate-
induced rises in cytosolic calcium. Adenosine may also improve microvascular flow,
inhibit platelet aggregation, reduce inflammatory responses, and at low concentrations
may protect against apoptosis. Adenosine is thought to play a role in ischaemic
preconditioning, and exogenous adenosine agonists may potentiate the neuroprotective
effects of transient brief ischaemia. The synergistic effects of aspirin and dipyridamole
in stroke prevention may be at least partly due to dipyridamole acting as an adenosine
reuptake inhibitor.
Neural repair, regeneration and gene therapy neurotrophins and neural

transplantation have been used extensively in neuronal culture preparations, in animal
models of ischaemia, Parkinsons and Huntingdons disease, and these interventions
are now being clinically tested for Parkinsons and Huntingdons disease. Epidermal
growth factor, brain-derived neurotrophic factor, nerve growth factor and hepatocyte
growth factor all improve neuronal survival or behavioural outcome following
experimental ischaemia or trauma. Published clinical trials of neurotrophic therapy
have been disappointing, and there are no clinical data addressing the use of these
substances in acute neuro-protection. Grafting neural cell lines into ischaemia lesioned
brains has improved behavioural outcome, and temporar gene transfer for therapy may
be feasible in acute brain injury.
Failure of clinical neuroprotection

For most neuroprotective agents, the translation of experimental success into clinical
benefit has been disappointing. Clinical trials that have recently been halted or shown
no benefit are listed in Figure 3. Figure 4 lists possible reasons for the failures.
Results from clinical outcome studies of neuroprotective agents
Mechanism of action Agent Outcome data

Non-competitive NMDA blocker Aptiganel Studies in stroke and acute head injury terminated
at interim analysis due to lack of benefit
Magnesium No benefit in in-hospital cardiac arrest
Competitive NMDA blocker Selfotel Stroke study halted by steering group due to lack
of benefit
NMDA polyamine site antagonist Eliprodil Stroke study halted by pharmaceutical sponsor
GABA agonist Chlormethiazole No benefit in acute stroke within 12 hours in study

population
Possible benefit in large strokes
Anti-ICAM-1 antibody Enlimomab No benefit in acute stroke
Antioxidants Ebselen No benefit in stroke on intention-to-treat basis

Possible subgroup efficacy
High-dose Stroke study stopped after 126 patients: no
tirilazad significant benefit
Poorly defined Lubeluzole Multinational study showed no benefit in acute

stroke within 6 hours
Piracetam No benefit with therapy within 12 hours
Post hoc analysis suggests benefit with early
treatment
Possible neuroprotective benefit in
cardiopulmonary bypass
Citicholine No benefit on intention-to-treat basis
Possible subgroup efficacy
GABA, -aminobutyric acid; ICAM-1, intercellular adhesion molecule; NMDA, N-methyl-D-aspartate.
Possible causes of failure of clinical neuroprotection trials
Experimental demonstration of neuroprotection incomplete (functional

end-points?)
Inappropriate agent: mechanism of action not relevant in humans
Inappropriate dose of agent (plasma levels suboptimal either globally

or in subgroups)
Poor brain penetration by agent
Efficacy limited by side-effects that worsen outcome (e.g.
hypotension)
Inappropriate timing: mechanism of action not active at time of
administration
Inappropriate or inadequate duration of therapy
Study population too sick to benefit
Study population too heterogeneous: efficacy only in an unidentifiable
subgroup1
Study cohort too small to remove effect of confounding factors
Failure of randomization to distribute confounding factors equally1
Insensitive, inadequate or poorly implemented outcome measures1
1
May benefit from small mechanistic studies in homogeneous, well
characterized, clinical subgroups.
4
The future
The success of experimental neuroprotection is undeniable and several publications
have explored exciting new therapeutic targets. However, the challenge facing clinical
neuroscientists is the failure to translate these successes into positive results from
outcome trials. Two approaches have been suggested for overcoming the problems
of patient heterogeneity and lack of sensitivity of outcome measures. The first is
to accept that these problems are unavoidable and mount larger outcome trials of
10,00020,000 patients which will address benefits of a magnitude less than the 10%
improvement in outcome that most drug trials are designed to detect. The alternative is
to mount smaller, more detailed, studies in homogeneous subgroups of patients whose
physiology is characterized by modern monitoring and imaging techniques. Repeated
application of these techniques during the course of a trial can provide evidence of
reversal of pathophysiology and hence mechanistic efficacy. Such surrogate end-points
could be used to select drugs or combinations of drugs for larger outcome trials. u
FURTHER READING
Cheng M A, Theard M A, Tempelhoff R. Intravenous Agents and Intraoperative
Neuroprotection Beyond Barbiturates. Crit Care Clin 1997; 13:18599.
Doppenberg E M R, Bullock R. Clinical Neuroprotection Trials in Severe Traumatic

Brain Injury: Lessons from Previous Studies. J Neurotrauma 1997; 14: 7180.
Lees K R. Neuroprotection. Br Med Bull 2000; 56(2): 40112.
Menon D K, Summors A J. Neuroprotection. Curr Opin Anaesthesiol 1998; 11: 48596.
MRC Field Review. Neuroprotection in Acute Brain Injury after Trauma and Stroke.
From Preclinical Research to Clinical Trials. London: Medical Research Council, 1998.
(http://www.mrc.ac.uk/).

Critical Care Management of
Head Injury
C A Eynon
David K Menon
C A Eynon is Clinical Fellow in Neurocritical Care at Addenbrookes Hospital

Cambridge, UK. He qualified from St Georges Hospital, London, and trained in
general medicine, intensive care and emergency medicine in Oxford, Cambridge and
Philadelphia, USA.

Cambridge. He trained at the Jawaharlal Institute, India; Leeds General Infirmary, The
Royal Free Hospital and Addenbrookes Hospital.
Head injuries account for up to half of all trauma-related deaths and often cause
severe functional impairment in survivors. The in-patient case fatality rate varies widely
between centres with mortality ranging from 15 to over 50%. Good outcome, defined
as a Glasgow outcome scale (Figure 1) of 1 or 2, varies from less than 50% to nearly
70%. Few of the interventions used by specialist centres in severe head injury have
been subject to prospective, randomized clinical trials. Recommendations for their use
are based largely on clinical experience.
Glasgow outcome scale
1 Good recovery
Resumption of normal life
Minor neurological or psychological deficits may persist
2 Moderate disability
Able to travel independently, work in sheltered environment or at
reduced level to that before injury
May have deficits in speech and memory and personality change
3 Severe disability
Usually dependent in activities of daily living and institutionalized
May live at home with large amount of support
Unable to work even in sheltered environment
4 Persistent vegetative state

Eyes open, sleepwake cycles
No speech, communication or response to external stimuli
5 Death
Timing of assessment should be stated.

1
Determinants of outcome: cerebral injury from trauma can be divided into primary
and secondary types. Primary injuries result from mechanical disruption of brain
tissue occurring at the time of the initial trauma. Secondary insults occur in the period
following the initial injury and can be related to outcome (Figure 2). The severity of
secondary insults has an additive effect on outcome. Management of head injury in
the critical care unit aims to avoid, detect and treat secondary injuries. It is important to
emphasize the role of rapid resuscitation and appropriate transfer of such patients to
neurological critical care units.
Effects of physiological insults following head injury on mortality and neurological outcome
Insult Mortality Grades within Glasgow

outcome score
Duration of hypotension (systolic blood pressure 90 mm Hg) Yes Yes
Duration of hypoxia (SaO2 90%) Yes No
Duration of pyrexia (core temperature > 38C) Yes No
Intracranial hypertension (intracranial pressure > 30 mm Hg) Yes No
Cerebral perfusion pressure (< 50 mm Hg) Yes No
Pathophysiology of acute head injury

Macroscopic and microscopic changes: the severity and type of impact affects
the structural changes that occur following head injury (Figure 3). Acceleration and
deceleration forces can produce axonal injury, brain contusions and intracranial
haematomas. Microscopic injury includes ischaemia, astrocyte swelling with
microvascular compromise, disruption of the bloodbrain barrier and recruitment of
inflammatory cells.
Cerebral haemodynamics and intracranial pressure: cerebral blood flow (CBF)

shows a triphasic response following head injury (Figure 4). In the first 12 hours, global
blood flow is reduced, the magnitude being directly related to the severity of the injury.
Between 12 and 24 hours, CBF increases and the brain may exhibit supranormal CBF,
which is often described as hyperaemia, but may be coupled to hypermetabolism in
many patients. CBF begins to fall again several days after injury. In some patients, the
fall in CBF may be associated with significant increases in large vessel flow velocity
suggesting vasospasm.
Apart from intracranial haematomas, elevation of intracranial pressure (ICP) in the

early phase following head injury is usually a result of cytotoxic oedema. From the
second day, elevations of CBF and cerebral blood volume make vascular engorgement
an important contributor to raised ICP. The bloodbrain barrier becomes leaky between
days 25 post injury and vasogenic oedema then contributes to raised ICP (Figure 4).
Secondary neuronal injury: several mechanisms have been implicated in secondary

neuronal injury including excitatory amino acid release, intracellular calcium overload,
free-radical mediated injury and activation of inflammatory processes. Production of
pro-inflammatory cytokines with upregulation of adhesion molecules leads to early
neutrophil influx and later recruitment of lymphocytes and macrophages. Mononuclear
cells may contribute to a prolonged inflammatory response associated with amyloid
deposition. Head injury is a risk factor for the deposition of amyloid in the brain and for
Alzheimers disease.
Genetic influences: polymorphism of the apolipoprotein-E (ApoE) genotype directly

affects outcome from severe head injury. Possession of the ApoE4 genotype confers
an increased risk of poor outcome. Identification of further genetic markers of outcome
may allow targeted neuroprotection strategies.
Management of severe head injury

There is no universally accepted treatment algorithm for patients with severe brain
injury but that used at the authors hospital is given in Figure 5. Widespread variations
in practice have led to the recent production of two sets of guidelines from the
European Brain Injury Consortium, and a collaboration of the Brain Trauma Foundation,
the American Association of Neurological Surgeons and the Congress of Neurological
Surgeons. Basic physiology supports the benefits of maintaining CBF and oxygenation.
Hypotension (systolic blood pressure < 90 mm Hg) and hypoxia (partial pressure of
oxygen in arterial blood (PaO2) < 60 mm Hg (8 kPa)) worsen outcome.
Cerebrovascular autoregulation may be impaired in patients with severe head injuries.

CBF is maintained at a cerebral perfusion pressure (CPP = mean arterial pressure
ICP) above 6070 mm Hg, a figure higher than in healthy subjects. Although there
is controversy over appropriate therapeutic targets, most centres aim for a CPP above
70 mm Hg and an ICP less than 20 mm Hg. A CPP below 50 mm Hg is significantly
related to increased mortality. ICP is an independent, albeit weaker, determinant of
outcome. Elevations in blood glucose and body temperature may also worsen outcome
in acute brain injury.
Systemic monitoring: invasive monitoring of arterial blood pressure, continuous pulse

oximetry, core temperature monitoring and regular analyses of arterial blood gases
and blood glucose are required to optimize physiology. Manipulation of mean arterial
pressure may require the placement of central venous or pulmonary artery catheters.
Intracranial pressure monitoring: the need to optimize CPP mandates the need for
ICP monitoring. ICP monitoring allows early detection of mass lesions or increasing
cerebral oedema in sedated and paralysed patients. The most accurate monitoring
method is an intraventricular catheter, but intraparenchymal micromanometers
(Codman, USA) or fibre-optic probes (Camino, USA) are increasingly used owing
to ease of insertion and lower infection rates. Intraventricular catheters offer the
advantage of being able to drain CSF to control ICP. The choice of monitoring
technique depends on local preference and expertise.
Other monitoring techniques

Jugular venous oximetry placement of a catheter high in the jugular bulb allows
continuous recording of jugular venous oxygen saturation (SjO2). SjO2 varies with the
ratio of cerebral oxygen consumption to CBF. Reductions in SjO2 (< 50%) and increases
in SjO2 (> 75%) may be associated with worse outcomes. The technique averages SjO2
from the whole brain and may be normal when ischaemia and hyperaemia coexist. SjO2
monitoring is technically difficult and up to half the episodes of cerebral desaturation
may be false-positive results.

Transcranial Doppler (TCD) ultrasound can be used to measure blood flow velocity
in major cerebral arteries. The most commonly imaged artery is the middle cerebral
artery. Reductions in flow velocity are a useful indicator of reduced intracranial
perfusion if ICP is raised. Increased flow velocities may result from either hyperaemia
or arterial vasospasm. Vaso-spasm can occur in patients suffering traumatic
subarachnoid haemorrhage and increases the incidence of poor neurological outcome.
Hyperaemia and vasospasm may be distinguished by relating intracranial velocities to
those in the carotid artery in the neck.
Newer techniques near infra-red spectroscopy, direct tissue oximetry, cerebral

microdialysis, xenon-enhanced CT scanning and PET imaging are being investigated in
acute head injury.
Basic intensive care

Exclusion of surgically treatable lesions
CT scanning should be used routinely for all patients with severe head injury to exclude
any surgically treatable mass lesions. CT scans should be repeated for any new
episode of unexpected intracranial hypertension.
Ventilatory support
Patients with a Glasgow Coma Score (GCS) less than 8 require intubation for airway
protection. Mechanical ventilation ensures that oxygenation is adequate and that the
partial pressure of carbon dioxide (pCO2) is controlled in the low normal range. The use
of hyperventilation to reduce cerebral blood volume and hence ICP is controversial.
Even moderate hyperventilation may reduce CBF to ischaemic levels and patients
without intracranial hypertension are managed at near-normal partial pressures of
carbon dioxide in arterial blood (PaCO2 4.55.0 kPa). Controlled hypocapnia can be
used to reduce an elevated ICP, but PaCO2 levels are generally maintained above 4.0
kPa, and cerebral oxygenation monitored using jugular bulb oximetry.
Sedation: intravenous anaesthetic agents decrease CBF, cerebral metabolism and

ICP. Autoregulation and the cerebrovascular response to carbon dioxide are preserved.
Continuous infusions of propofol or midazolam have largely replaced barbiturates
because of their better pharmacokinetic profiles. The lipid load resulting from
continuous infusion of propofol should be taken into account when calculating daily
calorific intake. The routine use of neuromuscular blockers varies between centres,
but they may be useful in preventing the rises in ICP associated with coughing or
patientventilator asynchrony. Long-term use of neuromuscular blockers (especially
the corticosteroid-based agents) has been associated with the development of acute
neuromyopathy and prolonged neuromuscular blockade.
Fluid management: fluid replacement in the patient with head injuries should be
guided by repeated measurement of volume status. Fluid movement across the intact
bloodbrain barrier is governed by osmolarity rather than oncotic pressure. As such,
hypotonic fluids such as dextrose-containing solutions should be avoided. Residual free
water after dextrose metabolism can worsen cerebral oedema and elevated plasma
glucose levels are associated with worse outcomes.
Osmotherapy: mannitol, 0.251 g/kg, may be used to elevate plasma osmolality and
reduce brain oedema when ICP is elevated. Volume status must be measured and
plasma osmolality should not be allowed to exceed 320 mosm/litre. Hypertonic saline
(525%) has also been used to treat intracranial hypertension, and may produce
ICP reductions without the large volume shifts that are triggered by mannitol-induced
diuresis.
Feeding and stress ulcer prophylaxis: enteral feeding should be established early.
Patients with head injuries have high nutritional requirements and the aim should be
to replace 140% of resting metabolic expenditure by the seventh day following trauma.
Parenteral nutrition should be considered for patients who cannot be fed enterally, but
it is associated with a higher incidence of hyperglycaemia. Patients in whom enteral
feeding has not or cannot be established should receive stress ulcer prophylaxis with
sucralfate or H2-blockers.
Anti-epileptic therapy: the incidence of post-traumatic seizures is highest in patients

with a GCS less than 10 and in those in whom an intracranial haematoma, contusion,
penetrating injury or depressed skull fracture is present. Seizure prophylaxis with
phenytoin or carbamazepine can reduce the incidence of early post-traumatic epilepsy
but has little effect on late seizures, neurological outcome or mortality.
Second-line therapy
Induced hypertension: the rationale for maintaining CPP stems from the finding that
CBF is commonly reduced following traumatic brain injury, and that cerebral ischaemia
is consistently found on post-mortem examination of fatal head injury. Inadequate
CPP may result in ischaemia-induced secondary brain injury. Cerebral vasodilatory
responses to CPP reductions increase cerebral blood volume and further increase ICP.
The optimum target for CPP is unclear and may vary between patients and in the same
patient at different times following injury. Most centres agree on the range 6070 mm
Hg for maintaining CPP. If ICP is increased, mean arterial pressure may be elevated
using volume expansion, inotropes and vasopressors. The relative efficiency and safety
of these interventions has not been studied.
Therapeutic hypothermia is widely used in cardiac and neurological surgery to

protect the brain during cardiac standstill, and reduces elevated ICP. In animal studies,
mild- to-moderate hypothermia (3336C) has been shown to be neuroprotective
in cerebral ischaemia, but the clinical benefit remains unproven in patients who do
not have refractory intracranial hypertension. Although early studies of moderate
hypothermia in head injury suggested benefit, recent publication of the largest study to
date has shown a lack of effect. Mortality and poor neurological outcomes were similar
in the hypothermia and the normothermia groups, with patients in the hypothermia
group having more hospital days with complications.
Barbiturate coma: intravenous barbiturates have been used to reduce ICP in acute
head injury for many years. Although their use may improve ICP when other measures
have failed, the effects on outcome are unclear. Barbiturates are administered as a
continuous infusion; titrated to produce burst suppression on the EEG. This achieves
near-maximal suppression of cerebral metabolism and blood flow. Further increasing
the dose of barbiturates may increase complications without therapeutic benefit. The
most common side-effect is cardiovascular depression and hypotension. Barbiturates
should be used only with appropriate cardiovascular support. The prolonged period
required for recovery after barbiturates is another drawback to their use.
Decompressive surgery: drainage of CSF via a ventriculostomy is effective in

reducing ICP especially (but not exclusively) in patients with hydrocephalus. Two other
surgical options are available for the management of resistant intracranial hypertension,
craniectomy and lobectomy. Removing part of the skull allows room for the brain to
swell. Although ICP usually falls acutely, the pressure may rise over time as swelling
continues. Lobectomy of either the non-dominant temporal or frontal lobe also
reduces ICP. These techniques have not been subject to a prospective, randomized,
controlled study. The decision to perform decompressive surgery lies with the individual
neurosurgeon.
Brain volume regulation (Lund therapy) is based on concepts that are contrary to
many conventional beliefs regarding the management of intracranial hypertension,
and focuses on the prevention and control of cerebral oedema rather than CPP.
Transcapillary filtration is controlled by using clonidine and metoprolol to reduce mean
arterial pressure. Cerebral blood volume is reduced using a combination of low-
dose thiopental (thiopentone) as a sedative, and dihydroergotamine to constrict large
veins. Normal colloid oncotic pressure is maintained by infusion of albumin or plasma.
Neurological outcome is favourable, but a randomized, controlled trial is awaited.
Investigational neuroprotective agents

Calcium channel blockers nimodipine has been used successfully for the treatment
of vasospasm associated with primary subarachnoid haemorrhage. Trials in traumatic
subarachnoid haemorrhage are inconclusive.
Corticosteroids although the use of early high-dose methylprednisolone is of

benefit in traumatic spinal cord injury, the use of corticosteroids in acute head injury is
controversial. The use of high-dose, short-duration methylprednisolone therapy is the
subject of an ultra-large, randomized, controlled trial, the Corticosteroid Randomization
After Significant Head injury (CRASH) trial.
Excitatory amino acid antagonists have a role in experimental head injury and
antagonists of their action can afford neuroprotection. However, they have not been
effective in outcome trials.
Antioxidants animal studies suggest that free radicals play a prominent role in head
injury and that this may be ameliorated by the use of antioxidants. Two antioxidants
(pergorgotein and tirilazad) have been studied in large scale, human trials but have
demonstrated no improvement in clinical outcome. u
FURTHER READING
Brain Trauma Foundation. Management and Prognosis of Severe Traumatic Brain
Injury.
www.braintrauma.org/index.nsf/pages/guidelines-main.
Doppenberg E M R, Bullock R. Clinical Neuroprotection Trials in Severe Traumatic

Brain Injury: Lessons from Previous Studies. J Neurotrauma 1997; 14: 7180.
Jones P A, Andrews P J D, Midgley S et al. Measuring the Burden of Secondary Insults

in Head Injured Patients during Intensive Care. J Neurosurg Anesthesiol 1994; 6: 414.
Maas A I R, Dearden M, Teasdale G M et al. EBIC Guidelines for Management of

Severe Head Injury in Adults. Acta Neurochir 1997; 139: 28694.
Menon D K. Cerebral Protection in Severe Brain Injury: Physiological Determinants of

Outcome and their Optimisation. Br Med Bull 1999; 55: 22658.

General Principles of
Neurosurgical Postoperative
Care

The postoperative period can be critical for neurosurgical patients, who may present
with intracranial hypertension, altered sensorium and/or depressed airway reflexes.
The deterioration in physiological homeostasis produced by anaesthesia and surgery
poses additional risks. Failure to detect and correct alterations in systemic and
cerebral physiology rapidly can result in irretrievable neurological damage. The main
groups of neurosurgical patients requiring intensive or high dependency care following
neurosurgery are listed in Figure 1.
Neurosurgical patients requiring postoperative intensive or high

dependency care
Patients with preoperative cardiorespiratory illness
Long surgery, large blood loss, coagulopathy, incidental hypothermia,

unstable haemodynamics
Patients at risk of, or documented to have, intracranial hypertension
Patients requiring ventilation to provide stability for venous haemostasis
Patients requiring or recovering from a period of hypothermia induced for

cerebral protection
Patients requiring postoperative intracranial pressure monitoring
Requirement for blood pressure manipulation as a part of induced

hypertension for cerebral perfusion pressure maintenance or as a part of
triple-H therapy
Induced hypotension for treatment of hyperaemia following carotid

surgery or surgery for arteriovenous malformations
Monitoring
Clinical assessment is the primary form of monitoring. Other basic monitoring includes
blood pressure, ECG monitoring, pulse oximetery and careful recording of fluid balance.
Arterial blood gases and invasive blood pressure

Arterial access is required in all ventilated patients for the measurement of arterial
blood gases. Direct arterial pressure measurement is indicated following neurovascular
procedures (clipping of ruptured aneurysms, resection of arteriovenous malformations,
and the early postoperative period following carotid endarterectomy) in patients with
haemodynamic instability, intracranial hypertension, and those requiring vasoactive
agents for blood pressure control.
Central venous pressure (CVP) monitoring and pulmonary artery catheterization

CVP monitoring is needed for patients with large volume losses, cardiac disease,
vasoactive infusions, and hypotension or oliguria not readily responsive to fluid
challenge. CVP monitoring may also be essential in the patient with pathological
polyuria due to diabetes insipidus or the condition of cerebral salt wasting that occurs
following subarachnoid haemorrhage. However, the CVP is an indirect measure of
intravascular volume status, which is influenced by right heart compliance, pulmonary
or right heart disease, intrathoracic pressure and posture. Measurement of pulmonary
artery wedge pressure provides a more reliable index of intravascular volume status in
the critically ill patient, and the use of thermodilution catheters allows the monitoring of
cardiac output and systemic vascular resistance. These data are of particular benefit in
patients with concurrent severe cardiorespiratory disease or sepsis. Pulmonary artery
catheters are also valuable to guide the use of complex vasoactive interventions as a
part of cerebral perfusion pressure augmentation in intracranial hypertension or triple-
H therapy (see Anaesthesia and Intensive Care Medicine 3:4: 143) for vasospasm
following subarachnoid haemorrhage.
Neurological examination
Changes in conscious level or new focal deficits may provide the first evidence of
postoperative intracranial bleeding or cerebral oedema. Neurology should be reviewed
with particular regard to the operation performed and preoperative neurological status.
Regular observations should include the measurement of pupillary size and reaction,
limb power and the Glasgow Coma Score (GCS; see Anaesthesia and Intensive Care
Medicine 3:4: 132). Although originally designed to quantify the severity of head injury,
the GCS allows wider quantification of neurological dysfunction and facilitates the
detection of trends in neurological status. One crucial decision is whether to undertake
CT in a patient whose GCS is substantially worse than in the preoperative period. While
many decisions are clear-cut, a short period of observation may help in others. Gradual
improvement in GCS, absence of new focal neurology and the presence of normally
reacting pupils and acceptable haemodynamics suggest residual anaesthetic effects.
However, clinical signs of intracranial events may be nonspecific, and it is better to err
on the side of over-investigation rather than to miss an early intracranial event.
Intracranial pressure (ICP) monitoring

ICP monitoring should be considered in all patients who have intracranial hypertension
or are at risk of developing it. It is particularly indicated in patients who remain sedated
and cannot be assessed by regular neurological examination. It is essential to relate
ICP measurements to mean arterial pressure (MAP), and to monitor cerebral perfusion
pressure (CPP; where CPP = MAPICP) continuously, because many therapies to
treat neurosurgical patients target ICP or CPP. They include a reduction in cerebral
oedema by cerebral dehydration, administration of corticosteroids, hyperventilation,
blood pressure control, reduction of CPP, surgical decompression, CSF drainage and
hypothermia.
Other monitoring modalities

Transcranial Doppler ultrasound, jugular venous saturation monitoring, and EEG and
evoked potential monitoring may be useful in individual patients. Their use is discussed
in Anaesthesia and Intensive Care Medicine 3:4: 127.
Investigations
Routine postoperative tests including a full blood count, clotting screen, urea and
electrolytes are required after most major neurosurgical procedures, along with
arterial blood gases if the patient is ventilated or has a low oxygen saturation. A chest
radiograph is indicated if the patient is ventilated, a central line has been inserted
or gas exchange is abnormal. Imaging of the CNS should be undertaken if there is
deterioration in the patients neurological state or a rise in ICP.
ICU management
Airway and ventilation
Inability to protect or maintain the airway or maintain acceptable blood gases mandates
intubation and ventilation. Airway protection should also be considered in patients with
a GCS of 8 or less, haemodynamic instability, inadvertent post-operative hypothermia,
sepsis or those who require controlled hyperventilation in order to reduce ICP.
While conventional ventilation strategies are generally applicable to neurosurgical

patients, some specific issues need attention. It is important to maintain partial
pressure of carbon dioxide in arterial blood (PaCO2) within tight limits (the author uses
an initial target value of 4.55 kPa), because even mild hypercapnia can result in
cerebral vasodilatation and a rise in ICP. Conversely, profound hypocapnia may result
in dangerous cerebral vasoconstriction and ischaemia. Central ventilatory drive may
be compromised by drugs or disease, therefore the use of ventilatory modes that do
not assure a near constant minute volume (e.g. pure pressure support ventilation) may
be inappropriate. Similarly, while mild arterial desaturation (SaO2 < 90%) is often well
tolerated by non-neurosurgical patients, the resulting hypoxic cerebral vasodilatation
can markedly increase ICP in a non-compliant brain.
Haemodynamic management
Intraoperative blood loss can be difficult to estimate, and the pulse rate, blood pressure,
urine output and CVP provide a guide to the patients haemodynamic state. Blood
or colloid replacement should be guided by these modalities in conjunction with the
haematocrit. Fluid and electrolyte balance must be monitored closely with regular
assessment of blood gases, urea and electrolytes. Glucose-containing solutions
should be withheld from neurosurgical patients at risk of cerebral oedema or ischaemia,
because the residual free water after glucose is metabolized reduces plasma osmolality
and accelerates cerebral oedema formation; also, increases in blood sugar can worsen
outcome in the ischaemic brain. Prompt normalization of coagulation and platelet levels
is essential in patients who have undergone intracranial procedures.
Analgesia, sedation and muscle relaxation

Postoperative pain after brain surgery is an important clinical problem. Pain most
often occurs within the first 48 hours after surgery but a significant number of patients
endure pain for longer. The subtemporal and suboccipital surgical routes result in
the highest incidence of postoperative pain. Appropriate analgesia for spontaneously
breathing patients includes codeine phosphate, 3060 mg up to 6 hourly i.m./p.o./n.g.,
paracetamol, 1 g 6 hourly p.o./n.g./p.r., and/or diclofenac, up to 150 mg/day (if the
patient has no bleeding problem or renal insufficiency). Traditionally, powerful opiates
have not been used in patients undergoing cranial surgery, but there is increasing
recognition that some of these patients may be in significant pain, and many centres
are now beginning to use small doses of intravenous opiates in selected patients
with careful monitoring of CNS state. Parenteral opiates, preferably using a patient-
controlled analgesia system, are widely used following spinal surgery where changes
in the level of sedation are not a critical part of postoperative monitoring. Patients
undergoing simple discetomies often do not require strong opiates for postoperative
analgesia.
Sedatives are used to decrease anxiety and diminish awareness of noxious stimuli
in ventilated patients. Propofol, 15 mg/kg/hour, is appropriate for short periods of
sedation, while longer periods of ventilation may be facilitated by midazolam. Prolonged
or high-dose propofol use presents problems of cost, cardiovascular depression and
lipid loading. Low-dose fentanyl, 12 g/kg/hour, is commonly used, but there may
be a role for shorter acting opioids (e.g. alfentanil, remifentanil) which facilitate rapid
recovery and weaning from ventilatory support.
Neuromuscular blockade is sometimes required to facilitate ventilation and prevent

increases in ICP. Prolonged neuromuscular blockade and myoneuropathy are most
commonly reported with the long-acting or steroid-based neuromuscular blockers,
therefore atracurium is commonly used if paralysis is indicated.
Complications specific to neurosurgical operations

Management of raised ICP
Intracranial hypertension is multifactorial and may result from hydrocephalus, vascular
congestion and/or cerebral oedema. A patent airway, adequate oxygenation and mild
hyperventilation, along with maintenance of an adequate CPP, provide the foundation
of care in such patients. There is no role for fluid restriction in patients with raised ICP,
because cerebral hypoperfusion will worsen cerebral ischaemia and cause further
increases in ICP by promoting cerebral vasodilatation. Reduction in vasogenic oedema
can be achieved using osmotic agents. Both 20% mannitol, 5 ml/kg, and 5% hypertonic
saline, 2 ml/kg, are effective, and may improve cerebral perfusion via micro-circulatory
and rheological effects. Furosemide (frusemide) can be used as an adjunct.
Corticosteroids are effective in reducing vasogenic oedema associated with mass

lesions (e.g. intracerebral tumour or haematoma). The ICP effects of corticosteroids
require many hours to become apparent and they are ineffective (and possibly
detrimental) in brain trauma and ischaemic stroke.
Hypocapnia causes cerebral vasoconstriction and reduces cerebral blood volume,

thereby reducing brain bulk and ICP. Aggressive hyperventilation should be avoided,
because there is a danger of severe vasoconstriction with resultant ischaemia. Mild-
to-moderate hyperventilation (PaCO2 of about 4.5 kPa) may be relatively safe, but is
best used with the safeguard of jugular bulb oximetry, which provides a warning against
cerebral ischaemia.
Changes in CVP can have a marked influence on ICP. Flexion or torsion of the neck can
obstruct cerebral venous outflow and increase brain bulk and ICP. Application of positive
end-expiratory pressure (PEEP) or other ventilatory patterns that increase intrathoracic
pressure can theoretically increase ICP, but seldom do so in practice, because CVP
dictates ICP only when ICP is less than CVP. There is no reason to withhold PEEP if it is
required to optimize gas exchange. Muscle relaxation and sedation can indirectly reduce
elevated ICP by decreasing mean intrathoracic pressure and spikes in pressure caused by
coughing.
It is generally accepted that reducing brain temperature lowers metabolism, cerebral

blood flow, cerebral blood volume and CSF secretion with resultant reductions in
ICP. However, there is debate as to whether hypothermia may be neuroprotective in
the absence of intracranial hypertension. There is no doubt that elevations in body
temperature are injurious to the ischaemic or traumatized brain, and aggressive
treatment of pyrexia is essential in neurosurgical patients.
In the event of intractable intracranial hypertension with preserved electrical activity on
EEG, the use of high-dose intravenous anaesthetics such as thiopental (thiopentone),
titrated to burst suppression, may reduce metabolic needs and result in cerebral
vasoconstriction and ICP reduction.
Intracranial hypertension can be reduced by CSF drainage, especially (but not

exclusively) in the presence of hydrocephalus. External ventriculostomy allows
controlled drainage of CSF and permits catheter flushing in the event of blockage, but
it is associated with a significant risk of infection, and microbiological surveillance is
mandatory. Surgical removal of intracranial tissue or masses reduces ICP, and can
reduce shifts in brain tissue that are associated with herniation and/or focal neurological
dysfunction. Intractable intracranial hypertension may respond to decompressive
craniectomy.
Intracranial bleeding
Awake patients may suffer reductions in GCS and/or focal neurological deficits related
to the site of bleeding. In sedated patients, ICP monitoring may provide an early
indication of postoperative intracranial haemorrhage, which should prompt early CT
scanning for confirmation.
Seizures
Prolonged seizure activity produces irreversible cerebral damage, independent of any
accompanying hypoxia and acidosis, as a result of the excessive metabolic demands
and energy depletion in continuously firing neurons. Cerebral oedema and lactic
acid accumulation ensue. Intravenous benzodiazepines are commonly used as initial
treatment for seizure control, followed by phenytoin (intravenous loading dose 15 mg/kg
over 1 hour, with maintenance at 34 mg/kg/day) because it does not cause significant
depression of the conscious level.
Fluid and electrolyte imbalance in neurosurgical patients

Hypokalaemia and hypomagnesaemia are common in neurosurgical patients who have
received mannitol, and aggressive correction is advised because they may predispose
to cardiac arrhythmias.
Hyponatraemia may be caused by the syndrome of inappropriate antidiuretic hormone

(SIADH) secretion, which may accompany hypothalamic and cerebral lesions, including
cerebral infarction, tumour, abscess, trauma or subarachnoid haemorrhage. Such
patients present with a low plasma sodium and osmolality, preserved or expanded
intravascular volume and a high urinary osmolality. Headache, nausea, confusion,
disorientation, coma and seizures are often observed when the plasma sodium falls
below 120 mmol/litre. Treatment depends on the presence or absence of clinical
manifestations, which may also relate to the speed of onset of hyponatraemia. While
such patients are usually treated with fluid restriction, this approach is inappropriate in
many critically ill patients in whom maintenance of intravascular volume and cerebral
perfusion are paramount. Hyponatraemia may worsen cerebral oedema, therefore the
author has a low threshold for treating SIADH with demeclocycline, 3001200 mg/day,
when fluid therapy with normal saline does not restore plasma sodium to the normal
range. Occasional patients who present with severe acute hyponatraemia, coma and
fits may require hypertonic saline therapy. It is important not to elevate plasma sodium
levels too rapidly in patients who have been chronically hyponatraemic, because this
may predispose to the development of central pontine myelinolysis. In such patients,
plasma sodium should not be raised at a rate greater than 1 mmol/hour or 12 mmol in
24 hours.
Hyponatraemia in other neurosurgical patients, especially following subarachnoid

haemorrhage, may be the consequence of cerebral salt wasting. Such patients
present with a low plasma sodium and high urinary sodium output, and are usually
fluid depleted. This syndrome may be the consequence of excessive secretion of brain
natriuretic peptide, and is treated with aggressive volume expansion with sodium-
containing crystalloid or colloid.
Many neurosurgical conditions including trauma, intracranial hypertension, tumours,

subarachnoid haemorrhage and brainstem death can lead to diabetes insipidus. The
relative lack or absence of antidiuretic hormone in these patients
results in the passage of large volumes of dilute urine (up to 0.51 litre/hour) with the
rapid development of hypovolaemia, plasma hyperosmolality and hypernatraemia.
Diagnosis is made by detecting high plasma osmolality coupled with low urinary
osmolality. Treatment is with deamino-D-arginine vasopressin (DDAVP, 18 g
boluses, repeated as required) and hypotonic fluids. Mild elevations in plasma sodium
should be left untreated, because they may help to minimize vasogenic oedema. Also,
the aggressive and rapid reduction of plasma sodium and osmolality in patients who
have been chronically hypernatraemic may result in cerebral oedema. Diagnosis of
changes in plasma osmolality in neurosurgical patients is facilitated by reference to
nomograms that relate plasma and urine osmolality (Figure 2).

Fluid Electrolyte and
Acid-Base Disorders.

Intrahospital transfers
Tomographic imaging is commonly needed in the postoperative neurosurgical patient,
and for some patients this may involve multiple journeys. Such transfers expose
the sick brain to the risk of physiological insults, and careful planning, appropriate
monitoring, and the presence of an anaesthetist is essential for patients who are
ventilated or haemodynamically compromised. Communication with the imaging
department is a priority to prevent delays. Monitoring levels should be similar to those
used in the ICU, and should include pulse oximetry, ECG, blood pressure (invasive
if arterial line in situ), ICP monitoring and capnography. Infusions required on the
ICU should continue, including appropriate doses of sedation, analgesia and muscle
relaxant. Haemodynamic control in a ventilated patient can be difficult during transfer
with periods of hyper- or hypotension. Gentle movement, with carefully timed boluses of
sedation can help to minimize this problem. Resuscitative drugs should be carried with
the patient. During the time spent in the scanner careful attention must be paid to the
patients physiological state with particular regard to airway, breathing and circulation.
Ideally, the scanning room should have its own piped oxygen and compatible mains
electricity supply to avoid the hazards of running out of oxygen or battery power. Any
intervention to stabilize the patient must take priority over the scanning procedure. u
FURTHER READING
Andrews P J D, Piper I R, Dearden N M, Miller J D. Secondary Insults during
Intrahospital Transport of Head-injured Patients. Lancet 1990; 335: 32730.
De Benedittis G, Lorenzetti A, Migliore M et al. Postoperative Pain in Neurosurgery: a

Pilot Study in Brain Surgery. Neurosurgery 1996; 38: 4669.
Harrigan M R. Cerebral Salt Wasting Syndrome: a Review. Neurosurgery 1996; 38:

15260.
Quiney N, Cooper R, Stoneham M, Walters F. Pain after Craniotomy. A Time for

Reappraisal? Br J Neurosurg 1996; 10: 2959.

Neuromonitoring
Luzius A Steiner
David K Menon
Luzius A Steiner is Clinical Research Fellow in Anaesthesia and Neurosurgery at

Addenbrookes Hospital, Cambridge, UK. He qualified from the University of Basel,
Switzerland, and trained in anaesthetics and intensive care medicine in Switzerland.
His current research is on cerebrovascular autoregulation in patients with head injuries.

Neuromonitoring has become an important aspect of neuro-anaesthesia and intensive

care because it is assumed that the early detection of insults to the brain is possible
and can reduce injury. Various monitoring technologies are available, but there is little
evidence that their use improves outcome. Although most clinical monitoring is based
on sound physiological premises, the absence of such evidence makes the objective
choice of best monitoring technique for a particular patient or procedure difficult.
Monitoring cerebral function

EEG
The EEG signal is predominantly generated by postsynaptic potentials of cortical
pyramidal neurons. When neighbouring cells have synchronous changes of these
potentials, their current loops are summed in the extracellular fluid, which creates
a regional current flow that is large enough to be detected by scalp electrodes
(the normal range of EEG amplitude in adults is 10100 V). The EEG is therefore
predominantly a cortical phenomenon. Magnitude and frequency of the EEG signal
are determined by the synchronicity of postsynaptic potentials. Synchronicity is
strongly influenced by neuronal circuits connecting the cortex with the thalamus and
the brainstem. Higher cortical function is associated typically with desynchronization
while anaesthesia and other factors that depress cortical function are associated with
increasing synchronicity.
Indications for EEG monitoring in neuroanaesthesia and intensive care include

diagnosis and management of seizures, assessment of drug effects (e.g. dose
control for EEG burst suppression), making specific diagnoses (e.g. certain types of
encephalitis), monitoring for ischaemia during carotid surgery and monitoring depth of
anaesthesia.
Processed EEG: a standard EEG consists of an 832 channel trace printed on paper
at 30 mm/second (or 300 pages/hour) and provides an enormous amount of data,
which requires interpretation by a specialist who assesses frequency, amplitude and
specific waveform patterns. The standard EEG is not well suited for intraoperative use.
Various approaches have been used to summarize such information in a format that
can be rapidly understood and allows recognition of trends. The number of tracings
is reduced (typically one per hemisphere) and after artefact detection the signal is
further processed. The technique most commonly used calculates a spectral array. This
calculation results in a set of frequency bins, with the power in each bin representing
the magnitude of the signal. Two display methods are popular. The Compressed
Spectral Array (CSA) displays a temporal series of frequency versus power histograms
in a three-dimensional manner, while the Density Spectral Array (DSA) transforms
the power of each frequency bin into a grey-scale intensity and plots this versus time
(Figure 1). Both techniques allow display of up to 1 hour of data on a single screen.
Two common methods for transforming EEG data
Bispectral index (BIS): bispectral analysis provides a new approach to computerized

EEG analysis. It analyses the frequency and phase angles of the components of a
signal and takes into account the interactions of some waves with others. It calculates
new summary measures of EEG activity. The BIS, as calculated by a commercially
available device (Aspect Medical Systems, Natick, MA, USA), makes use of this
approach. Its calculation involves the determination of several ECG descriptors,
including information from bispectral analysis. Each of these descriptors performs
best in a specific range of anaesthetic effects. The displayed BIS value is the result
of a proprietary combination of these descriptors, which has been selected using
a database incorporating EEG recordings from thousands of patients undergoing
anaesthesia with different anaesthetic regimens and clinical information relating to
anaesthetic depth.
The BIS is a dimensionless number ranging from 0 to 100 that gives information on
depth of anaesthesia. Using propofol, midazolam or isoflurane, 95% of patients are
unconscious at a BIS of 50. However, caution must be used when choosing a single
value as a threshold for non-responsiveness or awareness. Many questions remain
concerning the effects of various classes of drugs (e.g. anticonvulsants, anxiolytics) or
effects of temperature on the BIS. The BIS has not been validated for titrating sedation
in the ICU, and its utility in patients with organic CNS disease is unknown.
Evoked potentials
In contrast to the EEG, which measures spontaneous electrical activity of the cortex,
evoked potentials are a measurement of potentials that are produced in response to a
stimulus. They allow assessment of defined neural tracts including peripheral nerves
and subcortical regions. The evoked potentials most often used in anaesthesia are
somatosensory evoked potentials. A peripheral nerve is stimulated, and the response
at various predefined anatomical sites is measured (e.g. Erbs point, cervical spine,
sensory cortex after stimulation of the median nerve at the wrist). Typically, the
amplitude of the evoked response and the latency between stimulus application and
cortical response are used as indices of well-being of the monitored neural pathways.
Motor evoked potentials provide corresponding information regarding the integrity of
motor tracts. A transcranial electrical or magnetic stimulus is used to activate cortical
pyramidal neurons, and the resulting peripheral motor nerve response or muscle
activity is recorded. Evoked potentials generate very small signals (< 10 V) and signal
averaging is used to separate the response from the much stronger EEG and ECG
signals.
Evoked potentials can be used to assess patients with head injury. Somatosensory
evoked potentials from stimulation of the median nerve can predict unfavourable
outcome fairly accurately. Intraoperative somatosensory evoked potentials and motor-
evoked potentials are used mainly in spinal surgery, typically during procedures for
correction of scoliosis. Inhalational anaesthetics generally increase the latency and
decrease the amplitude of somatosensory evoked potentials. Opioids and intravenous
anaesthetics (especially propofol) have a much smaller influence on the signals and are
the preferred agents for procedures in which evoked potentials are monitored.
Monitoring intracranial pressure and compliance

Monitoring intracranial pressure (ICP) is widely used in patients with severe head
injuries (Glasgow Coma Score 38) and is recommended even when the CT scan
is normal. ICP is used to calculate cerebral perfusion pressure (CPP = mean arterial
pressure ICP) and many units use a management strategy based on CPP. The
placement of pressure transducers is important for obtaining a correct value of CPP,
particularly when patients are not nursed flat. The foramen of Monroe (or for clinical
purposes the external auditory meatus) is the reference point for zeroing transducers.
The relationship between intracranial volume and ICP is not linear. Initial increases
in intracranial volume can be compensated for by reductions in intracranial blood
volume and CSF and result in small changes in ICP, however, with rising ICP these
mechanisms are exhausted and small increases in intracerebral volume lead to large
rises in ICP (Figure 2a). This is illustrated by the fact that the amplitude of the ICP
curve, which is brought about by the small increase in cerebral blood volume that every
cardiac contraction causes, is normally in the range of a few mm Hg, but is much larger
when the intracranial compliance is reduced. In the presence of reduced intracranial
compliance, changes in cerebral blood volume caused by changes in CPP are reflected
in ICP (Figure 2b).
The gold standard in ICP monitoring is the direct measurement of intraventricular

fluid pressure via a catheter inserted into one of the lateral ventricles. In addition to
monitoring pressure, these catheters allow withdrawal of CSF to treat raised ICP,
however, the infection rate is up to 10%. The best alternatives to the ventricular catheter
are probes that use a miniature strain gauge pressure sensor mounted at the tip of a
thin catheter (change of ICP results in a change in resistance) or a fibre-optic catheter
(change of ICP results in a change of reflection of the light beam). These catheters are
inserted into the brain parenchyma and have a low infection rate. Their main problem
is a small drift of the zero line. It is important to realize that an intraparenchymal
reading probe reflects a local value and that ICP is not necessarily uniform within the
skull; significant pressure gradients may exist in patients with intracranial hypertension
(e.g. supratentorial measurements do not necessarily reflect infratentorial pressure).
When it is impossible to insert an ICP monitoring device (e.g. because of severe
coagulopathy) it is possible to estimate CPP from a transcranial Doppler examination.
Pressure measured in the lumbar CSF space is not a reliable estimate of ICP, and such
measurements may be dangerous in patients with space-occupying lesions.
A recent development is the Spiegelberg Compliance Monitor. It uses an intraventricular

catheter with an air-filled pouch at its tip. By repetitively injecting small volumes of air
into this pouch and measuring the pressure response, the cranio-spinal compliance can
be calculated. Whether this information improves the management of patients with head
injuries is unknown.
Monitoring cerebral blood flow and metabolism

Inadequately low cerebral blood flow (CBF) significantly contributes to the occurrence
of (secondary) brain insults. This suggests that monitoring CBF would detect and
prevent such insults and thus improve treatment and outcome in neurosurgical patients.
There is no ideal method of monitoring CBF; most methods produce non-quantitative
measurements of physiological variables, which are assumed to be proportional to CBF.
Many methods to measure CBF are available, but in most centres they are not routine
procedures in patients with brain injuries. The most common approach is to assess the
adequacy of CBF using jugular bulb oximetry.
Jugular bulb oximetry
Jugular bulb oximetry provides information about the adequacy of global CBF in relation
to metabolic demands. A catheter is inserted into one of the internal jugular veins and
advanced upwards into the jugular bulb where blood draining from the hemispheres can
be sampled. All methods that rely on blood sampling from one of the jugular bulbs are
prone to the influence of asymmetry of cerebral venous drainage. This may introduce
an unquantifiable risk of acquiring misleading data and there is no consensus on
which side should be cannulated. Generally, the right internal jugular vein is preferred
because it is often the dominant vessel. The position of the catheter should be checked
radiologically. A catheter tip at the level of the first or second cervical vertebral body
lies above the point at which the jugular vein receives its first extracranial tributary
(the common facial vein), and samples intracranial venous drainage. Blood can be
sampled intermittently or a fibre-optic catheter can be used to determine jugular venous
oxygen saturation (SjO2) continuously. Intermittent sampling can give erroneous results
because a certain amount of extracranial blood can be aspirated, especially if the
sample is withdrawn too quickly. The fibre-optic technique needs regular recalibration
of the sensor to deliver accurate readings and is susceptible to artefact because of
suboptimal catheter position inside the vessel. Normal values for SjO2 are thought to be
5585%. Low CBF (ischaemia) raises oxygen extraction, increases the arterio-jugular
oxygen content difference and leads to lower values for SjO2, whereas hyperaemia
leads to a decrease in arterio-jugular oxygen content difference and high values for
SjO2 (Figure 3). Some centres use SjO2 to optimize hyperventilation in patients with
head injuries, but it has not been demonstrated convincingly that this approach is
superior to CPP oriented management, one reason being the low sensitivity of SjO2 to
detect ischaemia.
Recently, two techniques for quantitative determination of global CBF at the bedside
using jugular bulb catheters have been proposed. One uses continuous jugular
thermodilution the other a double-indicator (dye and iced water) method providing
non-continuous measurements. The usefulness of both methods is currently being
evaluated.
Transcranial Doppler (TCD) ultrasonography

TCD ultrasonography makes use of the fact that the temporal bone can be penetrated
by ultrasound and uses the Doppler shift principle to measure blood flow velocity in
the basal cerebral arteries (Figure 4). It is easy to use and non-invasive. However,
the assumed linear relationship between flow velocity and CBF (CBF ~ FV x area
of the insonated vessel x angle of insonation) is present only if the diameter of the
insonated vessel does not change during the examination. This assumption is fulfilled
for most clinical situations because changes in common physiological variables (e.g.
blood pressure, partial pressure of carbon dioxide in arterial blood) do not change
the diameter of the investigated vessels significantly. The main disadvantage of
TCD is that although continuous measurements are possible they are prone to
artefact. TCD is a valuable tool for rapid estimation of CBF and can differentiate
vasospasm from hyperaemia, which influences the treatment of patients after
subarachnoid haemorrhage or head injury. TCD can be used to assess cerebrovascular
autoregulation and vasoreactivity to carbon dioxide, which can give prognostic
information about patients with head injuries. Mean flow velocity (the time averaged
mean of the signal) is mainly used for interpretation. Further pulsatility of the Doppler
wave form is often reported and mainly graded by the (Gosling) pulsatility index, which
is calculated as the signal amplitude divided by mean flow velocity. The pulsatility index
is not a reliable estimator of cerebrovascular resistance and should be interpreted with
caution because it is influenced by many uncontrollable variables (Figure 5).
Interpretation of transcranial Doppler results
Diagnosis FVm MCA FVm ICA MCA:ICA ratio Pulsatility

Normal 6070 cm/s 4050 cm/s 1.76 0.1 0.7 0.1
Hyperaemia
Vasospasm
ICP
FVm, mean flow velocity; ICP, intracranial pressure; MCA, middle cerebral artery. Normal values for
FVm MCA are reported over a wide range and influenced by age, gender, haematocrit and metabolic
factors. ICA, internal carotid artery. An MCA:ICA ratio (or Lindegaard ratio) > 3 in combination with
FVm MCA > 120 cm/second indicates MCA spasm. This ratio has not been validated for vasospasm
of the anterior or posterior cerebral artery.
Near infrared spectroscopy (NIRS)

NIRS measures changes in the chromophore levels of oxygenated and deoxygenated
haemoglobin (i.e. cerebral haemoglobin saturation). It is a non-invasive monitor
that is placed on the forehead and allows estimation of relative changes in cerebral
oxygenation and blood flow. The main limitation of NIRS is the inability to discriminate
between extracranial and intracranial blood flow changes. NIRS is the most
controversial method for monitoring the brain. This is reflected in the conflicting results
correlating NIRS measurements with other modalities to monitor CBF and cerebral
oxygenation.
Thermal diffusion and laser Doppler flowmetry

Measuring microcirculatory blood flow to estimate CBF is an alternative to monitoring
CBF. The thermal diffusion probe is inserted through a burr hole and placed on a
cortical region of interest. The probe consists of two small metal plates, one of which
is heated. Blood flow is calculated from the temperature difference between the plates.
Recently an intraparenchymal thermal diffusion probe has been evaluated. Its values
of CBF are in good agreement with values obtained by stable xenon CT for a volume
of about 5 cm3 around the probe. Laser Doppler flowmetry allows continuous real-time
measurements of local microcirculatory blood flow. However, the sample volume is
small (12 mm3) and only relative changes in flow can be assessed.
Partial pressure of oxygen (pO2) in brain tissue

Recently, intraparenchymal catheters that measure tissue pO2 and in the case of the
Neurotrend TM monitor pCO2, pH and temperature have been introduced. Two methods
of measurement are available, one uses a miniature Clark-type electrode, the other
uses fibre-optic technology. Normal brain tissue pO2 is in the range 3.54.0 kPa. The
role of brain tissue pO2 monitoring has yet to be defined.
Microdialysis
Microdialysis samples extracellular brain fluid. It is based on the transfer of molecules
(520 kD) over a semipermeable membrane. A thin catheter lined with a dialysis
membrane is placed in the brain parenchyma and perfused continuously at a slow
rate (0.32.0 l/minute) with a physiological solution. The concentration of glucose,
lactate, glutamate, aspartate and other neurotransmitters, drugs and cytokines can be
determined in the dialysate. Studies to determine the value of cerebral microdialysis in
clinical decision-making are under way.
Multimodality monitoring
Secondary ischaemic insults can be short-lived and may be missed because of
limited temporal and spatial resolution as well as the limited sensitivity of monitoring
devices. This led to the concept of multimodality monitoring. The combination of several
monitors can improve understanding of the continuing pathophysiology and also
increases the likelihood of detecting relevant insults (Figure 6). u
FURTHER READING
Czosnyka M. Monitoring Intracranial Pressure. In: Matta B F, Menon D K, Turner M,
eds. Textbook of Neuroanaesthesia and Critical Care. London: Greenwich Medical
Media, 2000; 99111.
Peerdeman S M, Girbes A R J, Vandertop W P. Cerebral Microdialysis as a New Tool

for Neurometabolic Monitoring. Intens Care Med 2000; 26: 6629.
Rampil I J. A Primer for EEG Signal Processing in Anesthesia. Anesthesiology 1998;

89: 9801002.
Sloan T B. Evoked Potentials. In: Albin M S, ed. Textbook of Neuroanesthesia with

Neurosurgical and Neuroscience Perspectives. New York: McGraw-Hill, 1997; 22176.

Neuromuscular Disorders:
Relevance to Anaesthesia and
Intensive Care
Jonathan G Hudsmith
David K Menon
Jonathan G Hudsmith is Specialist Registrar at Addenbrookes Hospital, Cambridge,

UK. He qualified from Southampton University, and trained in anaesthesia in
Canterbury and Lewisham. His interests include postgraduate anaesthetic teaching,
undergraduate teaching and obstetric anaesthesia.

Guillain-Barr syndrome
Guillain-Barr syndrome is an acute inflammatory poly-neuropathy characterized by
a progressive neuropathic weakness and areflexia. The incidence is 12/100,000 and
affects all age groups. Up to 75% of patients have preceding infection, usually of the
upper respiratory tract or gastrointestinal tract. Various bacterial and viral organisms
have been implicated, including Campylobacter jejuni and Mycoplasma pneumoniae.
The mechanism of the disease is unclear, but the association with preceding infection
suggests an immune mechanism for the demyelination of peripheral nerves. The
presence of circulating antibodies against neural gangliosides supports this view. It is
possible that the immune response to the infection generates self-reactive antibodies
that mediate the inflammatory demyelination.
Diagnosis
Guillain-Barr syndrome is diagnosed by the presence of:
progressive weakness of more than one limb (due to neuropathy)
areflexia
duration of progression of less than 4 weeks.
Laboratory features include an increase in CSF protein (in 90%) a normal white cell
count (in 90%), and an electromyograph suggestive of demyelination and axonal
damage. Other supportive diagnostic criteria are presented in the clinical features
below. Figure 1 lists the differential diagnoses.
Differential diagnosis of Guillain-Barr syndrome
Acute myasthenia gravis

Diabetes mellitus
Poliomyelitis
Botulism
Acute intermittent porphyria
Polymyositis
Lead poisoning
Organophosphate poisoning
Shellfish poisoning
Transverse myelitis
1
Clinical features
Guillain-Barr syndrome can present with symmetrical weakness, pain and sensory
impairment. The weakness commonly ascends from the legs, with 90% of patients
affected maximally at 34 weeks. Proximal limb weakness is usually the earliest motor
sign. Paraesthesia occurs in 50% of patients, and is often in a glove and stocking
distribution. Neuropathic pain (which may be severe) commonly occurs in the back,
sides and between the scapulae. The Miller-Fisher syndrome is an atypical variant of
the condition characterized by a classical triad of areflexia, ataxia and ophthalmoplegia.
About one-third of patients have respiratory muscle weakness requiring positive
pressure ventilation. Bulbar weakness often occurs in association with respiratory
muscle weakness and predisposes to pulmonary aspiration, which necessitates
adequate airway protection.
Autonomic dysfunction occurs in 65% of patients. Sinus tachycardia is the most

common manifestation and requires treatment only if severe. Vagal stimulation may
precipitate dangerous bradyarrhythmias. Other autonomic features include urinary
retention, postural hypotension, sweating and ileus.
Management
The management of patients in ICU involves supportive therapy and specific
treatments. Vigilant nursing is essential. Careful, regular turning prevents pressure
sores. Passive physiotherapy (and use of limb splints) reduces the risk of tendon
contractures. Patients often require long-term ventilation. Tracheostomy should be
performed early if prolonged ventilation is likely.
Deep vein thrombosis prophylaxis is mandatory, because thromboembolic

complications remain a major cause of morbidity and mortality. All patients should
receive prophylactic subcutaneous low molecular weight heparin, and wear
thromboembolic disease prevention stockings. Adequate nutritional support can be
provided via enteral feeding. If ileus is severe and unresponsive to prokinetic agents
such as metoclopramide, parenteral nutrition may be required. Autonomic disturbances
such as persistent tachycardia and hypertension should be treated appropriately,
usually with -blockers. Temporary or permanent cardiac pacing may occasionally be
indicated for severe episodes of bradycardia. Infection, particularly of the respiratory
tract is common, and should be treated promptly and effectively.
Pain is common, and can be particularly distressing at night. Despite sometimes being
responsive to simple analgesics, stronger pain relief is often indicated. The constipating
effects of opioids should be avoided if possible. Neuropathic pain can be relieved by
carbamazepine or amitriptyline.
Specific therapy includes two immunomodulatory interventions: plasma exchange

and intravenous immunoglobulin. Plasma exchange is most beneficial if given within
2 weeks of diagnosis and instituted before positive pressure ventilation is required.
Typically 200250 ml/kg of the patients plasma is exchanged with 4.5% human
albumin solution. This exchange is repeated up to five times.
Intravenous immunoglobulin (IvIg) is easier to administer than plasma exchange but

is expensive. Patients with autonomic dysfunction or cardiovascular disease may
tolerate IvIg better, but it also has adverse effects. Anaphylaxis, aseptic meningitis
and renal failure have been reported, and the risks of transfusing a blood product
are also present. A recent study has suggested that the combination of IvIg and
methylprednisolone may be more effective than IvIg alone. However, despite the clear
therapeutic benefit of immunotherapies on reducing length of hospital stay and residual
disability, there appears to be no reduction in mortality rate compared with that of
untreated patients. Typical mortality for patients with Guillain-Barr syndrome is 5%,
and 25% are left with a degree of disability 1 year after the onset of symptoms.
Myasthenia gravis
Myasthenia gravis is a rare disease of the neuromuscular junction, with an incidence of
1/20,000. It is an autoimmune disease characterized by fatiguable muscle weakness
resulting from failure of neuromuscular transmission. This is a result of production of
IgG antibodies to the postsynaptic membrane (anti-acetylcholine receptor antibodies),
which reduce receptor density at the neuromuscular junction. It may be congenital or
acquired later in life. It is more common in females, and has a peak incidence in the
third decade of life. 34% of patients with myasthenia gravis have other autoimmune
disease (e.g. thyrotoxicosis, pernicious anaemia, rheumatoid arthritis, systemic lupus
erythematosus). Myasthenia gravis is characterized by fluctuating weakness of the
muscles of the head, face and neck. Classic presentation is with diplopia and ptosis
due to weakness of the ocular muscles. Bulbar weakness may present as dysarthria
and dysphagia. Moderate proximal muscle weakness may occur, as may respiratory
muscle weakness, especially during exacerbations. Weakness increases with exercise
and improves with rest.
Diagnosis is from the history and confirmed by a high titre of receptor antibodies on
immunoassay. Diagnosis can also be confirmed clinically by a positive Tensilon (an
anticholinesterase) test. Edrophonium (Tensilon) is administered and improved muscle
function is observed when compared with administration of placebo. Electromyography
studies show decreased amplitude following a single twitch, fade on tetanic stimulation
and post-tetanic facilitation.
Management: patients may present to the ICU during a myasthenic crisis,

often precipitated by infection, or as a consequence of over-treatment with
anticholinesterases, causing a cholinergic crisis. Treatment for myasthenia gravis
includes anticholinesterases (pyridostigmine), immunosuppression (corticosteroids,
azathioprine, cyclosporin (ciclosporin)), removal of antibodies (plasma exchange) or
thymectomy. Thymectomy is indicated in patients with a thymoma, younger patients
(< 50 years), and women of child-bearing age (in whom immunosuppressants may be
inappropriate).
Preoperatively, the ability to swallow should be assessed. Respiratory function should
be optimal before surgery, and adequacy of ventilation checked with an arterial
blood sample. Plasma exchange may be necessary. A chest radiograph may reveal
signs of aspiration, a thymoma with upper mediastinal widening or an anterior mass
(lateral film). Anticholinesterase therapy should be reduced by 20% preoperatively,
and withdrawn on the day of surgery. Patients are better slightly myasthenic than
cholinergic.
Patients with myasthenia gravis are relatively resistant to small doses of

suxamethonium, and tend to get a dual (phase II) block with high doses. Conversely,
they are extremely sensitive to non-depolarizing neuromuscular blocking drugs, and
these should be avoided if possible. Drugs such as atracurium should be administered
at one-tenth the normal dose. Spontaneous return of neuromuscular function should be
allowed, to avoid clinical confusion caused by the administration of anticholinesterase
agents. It is also essential not to exacerbate muscle weakness by avoiding
hypokalaemia, aminoglycosides, quinine and ciprofloxacin.
Regional anaesthesia should be used if possible to avoid the use of neuromuscular

blocking drugs. Additionally, intubation may also be achieved via deep inhalational
anaesthesia and local anaesthetic spray to the vocal cords.
During anaesthesia for thymectomy, it is essential to place intravenous access in a

lower limb vein, because there is a risk of damage to the superior vena cava during
surgery.
Postoperatively, patients may require ventilation. Anticholinesterases should be

restarted, but the initial dose required may be less than the preoperative dose.
LambertEaton myasthenic syndrome

LambertEaton myasthenic syndrome is characterized by severe muscle weakness.
It occurs in 1% of patients with bronchial carcinoma. It is also associated with thyroid
disease and connective tissue disease, and is mediated by decreased release of
acetylcholine from the presynaptic membrane. It can be distinguished from myasthenia
gravis because:
it causes proximal rather than bulbar/ocular weakness
muscle power increases with exercise
tendon reflexes are diminished
there is no fade on tetanic stimulation
tetanic stimulation increases muscle strength
the Tensilon test is negative
muscle pains are common.
Treatment is by removal of the bronchial tumour, or admin-istration of 3,4-

diaminopyridine. Patients are sensitive to both depolarizing and non-depolarizing
neuromuscular blocking drugs.
Myotonic syndromes
Myotonic syndromes are a group of hereditary diseases characterized by delayed
muscle relaxation following contraction. Myotonic dystrophy is the most common,
with an incidence of 1/25,000. Inheritance is autosomal dominant with anticipation
(increasing severity in successive generations). Males and females are equally
affected. Patients typically present between 20 and 40 years with a reduced life
expectancy. A characteristic facies is present, with frontal balding, an expressionless
face, smooth forehead, ptosis, presenile cataracts and a lateral (or inverted) smile.
Masseter and sternocleidomastoid muscle wasting occurs, and bulbar weakness can
predispose to aspiration and chest infections. Once muscle wasting develops, tone
and reflexes are reduced and foot drop is common. Myotonia is secondary to abnormal
closure of sodium/chloride channels following depolarization, leading to repetitive
discharge and contraction. It is precipitated by:
cold
exercise
shivering
pregnancy
hyperkalaemia
suxamethonium
neostigmine.
Associations include a low IQ, gonadal atrophy, diabetes mellitus, dysphagia,

constipation, delayed gastric emptying, respiratory muscle failure, obstructive sleep
apnoea and thyroid adenoma. Cardiac involvement includes conduction defects, valve
defects and cardiomyopathy. There is a progressive worsening of cardiac conduction,
with an increasing risk of tachyarrhythmia and sudden death.
Cardiorespiratory function must be thoroughly investigated preoperatively, because
cardiac pacing may be necessary. Invasive cardiac monitoring may be indicated.
Monitoring of body temperature and neuromuscular blockade is essential. Patients
are sensitive to all depressant drugs, therefore sedative premedication is avoided.
There is also increased sensitivity to induction agents, opioids and non-depolarizing
neuromuscular blocking drugs. Suxamethonium may produce a generalized myotonic
response rendering laryngoscopy, tracheal intubation and ventilation difficult or
impossible. This may not be reduced by subsequent administration of non-depolarizing
neuromuscular blocking drugs. If neuromuscular blockade is required, atracurium is
the agent of choice, with spontaneous reversal (because neostigmine may precipitate
myotonia). Myotonic contraction may also occur with surgical diathermy. Regional
anaesthesia can be useful, although the myotonic reflex is not blocked.
Admission to intensive care may be required if there is cardiovascular instability, or

if the patient is slow to regain consciousness or adequate neuromuscular function.
Swallowing and gastric emptying are often impaired, therefore asymptomatic aspiration
is common, necessitating a delay in feeding postoperatively.
Myotonia congenita
Myotonia congenita is less prevalent than myotonic dystrophy, with little systemic
involvement and a normal life expectancy. There is generalized muscular hypertrophy
and stiffness on initiating movement, which is relieved by exercise. There is no muscle
weakness, although the myotonia may be severe. Anaesthetic problems are the same
as for myotonic dystrophy, although there is an important association with malignant
hyperthermia.
Muscular dystrophies are a hereditary group of conditions of unknown aetiology,
characterized by atrophy of some muscle groups and pseudohypertrophy of others.
The most common is Duchenne muscular dystrophy (transmitted as an X-linked
recessive condition, occurring in 1/3500 live male births). Symmetrical weakness of
the proximal and pelvic muscles is evident from 2 years of age, which progressively
worsens, with patients becoming wheelchair bound due to contractures and scoliosis.
Cardiorespiratory problems and mental retardation are common. Serum creatine kinase
is often elevated from birth and can be 30300 times the normal value. Death usually
occurs before 30 years of age as a result of cardiorespiratory failure.
Preoperatively, assessment of cardiorespiratory function by exertion is problematic
because effort is limited by the muscular disease and most patients are extremely
immobile. Echocardiography is essential and often reveals chamber hypertrophy
and mitral valve prolapse (25%). If respiratory function is severely compromised
(vital capacity < 20 ml/kg), the risk of death is high. During the perioperative period,
physiotherapy is essential and antibiotics are often indicated. There is an increased
risk of malignant hyperthermia in these patients, and suitable precautions, including
the availability of dantrolene, are recommended. Suxamethonium is additionally
contraindicated because of the risks of hyperkalaemia and cardiac arrest. Volatile
anaesthetic agents and suxamethonium have both been implicated in precipitating
rhabdomyolysis and cardiac arrest. Intravenous anaesthetic agents and opioids appear
to be safe. Patients are sensitive to non-depolarizing neuromuscular blocking drugs
and they should be used incrementally with appropriate monitoring. There is still a risk
of delayed recovery associated with skeletal muscle weakness. Regional anaesthesia
should be used if possible, avoiding many of the above complications and providing
good postoperative analgesia. High dependency postoperative care is essential,
with aggressive physiotherapy and clearance of secretions. Despite all the above
precautions, cardiac arrest resistant to resuscitation may occur.
Neuromuscular complications of intensive care

Muscle weakness in critically ill patients is not a result of inactivity, as previously
thought, but caused by neuromuscular disorders arising during the ICU stay. It usually
presents as a failure to wean patients from the ventilator. Three causes are recognized:
critical illness polyneuropathy
prolonged neuromuscular blockade
necrotizing myopathy.
Motor neuron disease

Motor neuron disease is a group of disorders characterized by a progressive
degeneration in motor function, while sensory and higher function remain normal.
Males are affected more commonly than females. The diagnosis is made clinically and
using EMG studies. No treatment is of any proven benefit. Patients typically present
with weakness and wasting of muscle groups with fasciculation. The disease affects
smooth, striated and cardiac muscle. Death occurs within 35 years of diagnosis.
Anaesthetic problems relate to the increased sensitivity to intravenous induction

agents and both depolarizing and non-depolarizing neuromuscular blocking agents.
Respiratory muscle involvement is commonplace and must be managed appropriately
in the perioperative period. If the brainstem is involved, there is a significant risk of
aspiration due to bulbar weakness. u
FURTHER READING
Birnkrant D J, Pope J F, Eiben R M. Management of the Respiratory Complications of
Neuromuscular Diseases in the Pediatric Intensive Care Unit. J Child Neurol 1999; 14:
13943.
Coles A J. Neuromuscular Diseases in the Neurological Intensive Care Unit. In: Matta
B F, Menon D K, Turner J M, eds. Textbook of Neuroanaesthesia and Critical Care.
London: Greenwich Medical Media, 2000; 37180.
Martz D G, Schreibman D L, Matjasko M J. Neurological Diseases. In: Katz J, Benumof

J L, Kadis L B, eds. Anaesthesia and Uncommon Diseases. 3rd ed. Philadelphia: WB
Saunders, 1990; 56089.
Provencio J J, Bleck T P, Connors A F Jr. Critical Care Neurology.

Neurovascular Anaesthesia and
the Management of Ischaemic
Stroke
Jonathan G Hudsmith
David K Menon
Jonathan G Hudsmith is Specialist Registrar at Addenbrookes Hospital, Cambridge,

UK. He qualified from Southampton University, and trained in anaesthesia in
Canterbury and Lewisham. His interests include postgraduate anaesthetic teaching,
undergraduate teaching and obstetric anaesthesia.

the Royal Free Hospital and Addenbrookes Hospital. His research interests include
Neurovascular anaesthesia covers the preoperative resuscitation and optimization,

intraoperative management and postoperative neurointensive care of patients with
intracranial vascular lesions. This article deals mainly with subarachnoid haemorrhage
(SAH) and arteriovenous malformations (AVM) and briefly describes the management
of ischaemic stroke.
Regardless of the cause of intracranial haemorrhage, many pathological mechanisms

operate to precipitate cerebral ischaemia. Management of intracranial haemorrhage
centres around adequate neuroprotection, via maintenance of adequate cerebral blood
flow (CBF) and prevention of secondary cerebral ischaemia.
Subarachnoid haemorrhage (SAH)

Cerebral aneurysms account for 7580% of SAH, cerebral AVM for 45%, and in the
remaining 1520%, no source of haemorrhage can be found.
Cerebral aneurysms
Aneurysms arise from vessels of the circle of Willis, usually at a bifurcation. They occur
in 25% of the population, and are three times more common in women than in men.
90% of aneurysms involve the anterior circulation and 10% the posterior circulation.
20% of patients have multiple aneurysms. SAH accounts for 10% of cerebrovascular
disease and has an annual incidence of 15/100,000. It can occur at any age, with a
peak incidence between 55 and 60 years of age. Aneurysm formation is more likely in
those with hypertension, some genetic and collagen abnormalities and in those who
smoke or are pregnant.
Risk of rupture is 0.056%. Rupture is often, but not always, related to hypertensive
episodes. One-third of patients die before reaching hospital, one-third have a poor
outcome and one-third are functional survivors. The main risks facing patients who
reach hospital include recurrent haemorrhage, development of delayed ischaemic
neurological deficits (vasospasm) and hydrocephalus. For those who survive the initial
haemorrhage, the peak risk of re-bleed occurs in the first 48 hours. On the first day of
SAH, there is a 4% risk of re-bleeding, which decreases to 1.5% by the third day. By
day 14, the cumulative re-bleeding incidence is 19%. Six months after SAH, 50% of
patients have re-bled, and the long-term risk stabilizes at 3% per year.
Presentation of SAH
Headache is the presenting symptom in 8595% of patients. Classically, it is severe
and of sudden onset. Other symptoms include loss of consciousness, photophobia,
nausea, vomiting, lethargy and neurological deficits. Signs of meningism are also
common. Bleeding increases intracranial pressure (ICP), leading to a reduced cerebral
perfusion pressure (CPP). A sudden rise in ICP prevents continuing bleeding from
the aneurysm site. If ICP subsequently decreases, CBF recovers, allowing function to
improve. Non-survivors show no recovery of CBF.
Grading SAH
The severity of SAH is assessed and graded according to the Hunt and Hess
classification (Figure 1), or the World Federation of Neurological Surgeons (WFNS)
SAH Scale (Figure 2), which uses the Glasgow Coma Scale (GCS). A higher WFNS
grade results in worse outcome as a result of increased initial damage, an increased
risk of developing intracranial hypertension, reduced CBF autoregulation (Figure 3) and
reduced carbon dioxide vasoreactivity (Figure 4). These physiological abnormalities
expose the injured brain to ischaemic insults and reduce its ability to cope with them.
Management
Hunt and Hess classification of intracranial aneurysms
Category Criteria
0 Unruptured aneurysm
I Asymptomatic or minimal headache and

slight nuchal rigidity
II Moderate to severe headache, nuchal

rigidity cranial nerve palsy
III Drowsiness, confusion or mild focal deficit
IV Stupor, moderate-to-severe hemiparesis,

possibly early decerebrate rigidity and
vegetative disturbances
V Deep coma, decerebrate rigidity, moribund

appearance
1
World Federation of Neurological Surgeons (WFNS) SAH Scale
WFNS grade GCS score Motor deficit
I 15 Absent
II 1314 Absent
III 1314 Present
IV 712 Present or absent
V 36 Present or absent
Conservative non-surgical management of SAH is associated with a higher mortality

than surgical management (40% versus < 10%). Reasons include reduction in the risk
of re-bleeding, removal of the blood clot, irrigation and toilet of the operative site, and
improved acute functional outcomes, which improve long-term survival.
Timing of surgery: surgery can be early (13 days post SAH) or late (1014 days post
SAH). Early surgery, soon after aneurysm rupture, reduces the risk of re-bleeding (and
subsequent morbidity and mortality). Early surgery is technically more difficult because
of oedema and inflammation. However, because the risk of vasospasm relates to the
presence and extent of cisternal blood, some studies suggest that early removal of
clot may reduce the risk of developing a delayed ischaemic deficit. Surgery typically
involves ablation of the aneurysm with specialized clips (clipping). In some cases,
operative access may make this impossible, and the aneurysm is wrapped in muslin
to induce fibrosis (wrapping). While this does not ablate the aneurysm immediately it
does secure it over time. Increasingly, interventional neuroradiology is being used as an
alternative to surgery, usually by placing thrombogenic coils in the aneurysm (coiling).
Early clipping or coiling facilitates the medical and neuroradiological treatment of
vasospasm.
Cardiovascular dysfunction: ECG changes following SAH are common, and occur
more often in those with severe neurological impairment. The degree of myocardial
dysfunction does not correlate with the SAH-induced ECG changes, however, the
greatest degree of myocardial dysfunction occurs in patients with worse WFNS
grades. Pathological Q waves can develop after an SAH, and can be misinterpreted
as evidence of a recent myocardial infarction. Diffuse myocardial ischaemia occurs
in 50% of patients, with widespread ST segment and T wave changes. Mechanisms
for this cardiovascular dysfunction include catecholamine release triggered by SAH,
direct trauma to cerebral autonomic control centres, and a hypothalamic neurogenic
mechanism. It is difficult to differentiate between SAH-associated ECG changes
and actual myocardial ischaemia. Most patients with ECG changes have acceptable
perioperative cardiovascular risk, but further investigation (with echo-cardiography) may
be needed in some patients, and delayed surgery may be justified in patients with major
left ventricular dysfunction, or in those with new Q waves or bundle branch block, who
are at high risk of malignant dysrhythmias.
Blood pressure commonly rises after SAH, and is often a normal compensatory
response to maintain CPP, in response to a rising ICP. Hypertension in this setting
should only be treated if it is severe. Systolic pressures above 160 mm Hg may
increase the risk of re-bleeding and rupture, and antihypertensive treatment may
be indicated, preferably using drugs that do not produce cerebral vasodilatation
(e.g. labetalol). It is also important to avoid hypotension, and the pressure at which
neurological deterioration occurs should be recorded so it can be used to guide blood
pressure goals intraoperatively.
Volume status and electrolyte imbalance: hypovolaemia and intravascular volume

depletion are common and fluid resuscitation is essential. Volume depletion may
be the result of poor intake, autonomic hyperactivity, bed-rest or increased urinary
volume loss. Inappropriate diuresis may be the consequence of diuretics, diabetes
insipidus or the syndrome of cerebral salt wasting, which result in increased urinary
losses of sodium ions and water. Hyponatraemia occurs in up to 40% of patients and,
when severe, is associated with an impaired level of consciousness, cerebral oedema
and vasospasm. This may be due to cerebral salt wasting, inappropriate secretion
of antidiuretic hormone or administration of hypotonic maintenance fluids. Invasive
monitoring may be required to guide fluid management. Normoglycaemia should be
maintained, to prevent the poor outcome associated with hyperglycaemia after brain
injury.
Premedication: the use of sedative premedication is controversial and probably best
avoided. Grade IIIV patients seldom require premedication, and it is best reserved for
particularly anxious grade III patients. Antacid prophylaxis is mandatory for those at
risk of aspiration.
Monitoring should include ECG, pulse oximetry, end-tidal capnography, urinary output
and temperature. Invasive arterial blood pressure measurement should be established
before induction, allowing accurate observation of blood pressure as well as allowing
sampling for blood gas and haemoglobin measurements. Central venous catheters are
inserted after induction, to guide fluid management when using diuretics and mannitol.
Pulmonary arterial pressure monitoring should be used if impaired myocardial function
is present. Such monitoring is also useful in elderly patients, and those with poor grade
SAH, because hypertensive, hypervolaemic and haemodilutional therapy is often
used in these patients. More specialized intraoperative monitoring may include jugular
bulb oximetry, transcranial Doppler, electroencephalography (EEG), intraparenchymal
probes and cerebral function monitors.
Induction of anaesthesia involves titration of the depth of anaesthesia and the blood
pressure to match surgical need. The ICP must be controlled and cerebral metabolic
demands minimized to prevent cerebral ischaemia and provide good operating
conditions. Aneurysmal rupture is related to transmural pressure across the wall of the
aneurysm. Abrupt increases in arterial pressure or sudden decreases in ICP may cause
a re-bleed. Aggressive hyperventilation and hypocapnia can also predispose to rupture.
The incidence of rupture at induction is 12%, and is associated with high mortality
and postoperative morbidity. Rupture should be suspected when a sustained rise in
blood pressure occurs on, or shortly after, induction or intubation. Intubation is ideally
preceded by a short trial of laryngoscopy with careful monitoring of blood pressure; a
significant hypertensive response should trigger administration of a supplemental dose
of induction agent before intubation is attempted. Supplemental doses of induction
agent or high dose opiates may also be required to avoid the pressor responses
associated with the placement of surgical pins. If an aneurysm re-bleeds at induction,
surgery should be deferred to allow detailed assessment of the patient. Management of
intraoperative rupture is discussed below.
Maintenance: the ideal technique produces a slack brain (to minimize retraction
pressure), while ensuring maximal cerebral protection by keeping cerebral metabolic
requirements to a minimum. No evidence favours one particular technique. Total
intravenous anaesthesia, using propofol and an opioid (e.g. remifentanil), is increasingly
used for maintenance of anaesthesia during aneurysm surgery. Propofol allows rapid
adjustment of anaesthetic depth and has better recovery characteristics than other
agents.
Brain relaxation: several methods are used to reduce the brain bulk, CSF volume
and cerebral blood volume (CBV), including a 1530 head-up tilt, mild hypocarbia,
mannitol and furosemide (frusemide). A head-up tilt facilitates venous return and
reduces ICP. Mild hypocarbia (about 4.5 kPa) can be used, however the potential
ischaemic effects of hyperventilation must be balanced against the benefits of reducing
CBV. Hyperventilation is a quick method of reducing CBV, but its application is best
guided by a monitor of the adequacy of cerebral oxygenation, such as a jugular bulb
saturation (SjO2) monitor. Hyperventilation should be titrated to keep the SjO2 above
55%.
Mannitol is an osmotic diuretic administered as a 20% solution at a dose of 0.51.0

g/kg. Brain bulk is reduced by osmotic dehydration and a transient increase occurs in
intravascular volume and CBF. CBV is reduced as a consequence of these changes,
and by improved rheology of red blood cells, and CSF production is reduced. These
effects result in a decrease in ICP, which peaks at 4560 minutes. Furosemide
(frusemide) is often used in conjunction with mannitol or alone in patients whose
cardiovascular system may be compromised by mannitol. Bolus administration of
propofol, thiopental (thiopentone) or lidocaine (lignocaine) also reduces CBV by
reducing cerebral metabolism and thus CBF.
Hypothermia: most drugs reduce only the active component of cerebral metabolism.
However, hypothermia reduces the active and basal components, which increases the
time of ischaemia tolerated. Cerebral metabolism is 15% of normal at 20C
(Figure 5). Other mechanisms (e.g. suppression of cytokine, free radical and glutamate
release) are thought to contribute to the neuroprotection offered by hypothermia
in addition to the reduction in cerebral metabolism. Prophylactic hypothermia
during aneurysm clipping is the focus of a multicentre Phase III trial (Intraoperative
Hypothermia during Aneurysm Surgery Trial 2; IHAST 2). Deep hypothermia is not
without risks. Problems include the accuracy of temperature measurement, optimal
temperature used, method of rewarming, delayed awakening, postoperative shivering,
coagulation disorders and aggravation of cardiovascular disease.
Temporary clipping/induced hypotension: intraoperative rupture of an aneurysm

is an emergency. Management should include administration of 100% oxygen and
prompt volume replacement, with blood if necessary. Other measures that may be used
include the application of temporary vascular clips on the feeding artery, controlled
hypotension, anaesthetic neuroprotection (usually with barbiturates) or the prophylactic
use of hypothermia in high-risk cases.
Temporary clips applied to the feeding vessel are used to reduce the risks of
intraoperative rupture, or the risk of bleeding from a ruptured aneurysm. This results
in focal ischaemia in the vessel territory, which may be worsened by systemic
hypotension. Brisk haemorrhage from a ruptured aneurysm may obscure the surgical
field and make clipping of the aneurysm or application of a temporary clip impossible.
Under these circumstances, the induction of systemic hypotension using potent
anaesthetic agents, short-acting vasodilators or -blockers may allow visualization
of the surgical field and stop haemorrhage. The minimum mean arterial pressure
required to prevent ischaemia is unknown. Temporary clipping is becoming more
popular and induced hypotension is practised less. This distinction is crucial, because
induced hypertension during temporary clipping may permit improved collateral flow
and reduce the risk of infarction. The risk of infarction is high if clipping is prolonged
beyond 15 minutes. Bolus doses of intravenous anaesthetic agents or the application
of hypothermia may be neuroprotective in this setting, but strong evidence is lacking.
While many intravenous agents are used in this setting, what little evidence there is
supports the use of barbiturates (typically thiopental (thiopentone), 2501000 mg),
which may be effective even when administered after the application of the temporary
clip.
Recovery: a rapid return to consciousness allows early neurological assessment. It

is important to normalize mean arterial pressure and the partial pressure of carbon
dioxide in arterial blood (PaCO2) before closure, to reveal any bleeding points and
ensure that intraoperative brain swelling does not increase the likelihood of intracranial
hypertension in a normocapnic patient. Obvious brain swelling may prompt a
decision to leave the bone flap out, institute ICP monitoring, and/or opt for a period
of postoperative sedation and ventilatory support. Assuming a smooth intraoperative
course, grade III patients are extubated. Grade IIIV patients often require a period
of postoperative ventilation, unless their preoperative conscious level permits more
rapid recovery. Blood pressure must be closely monitored in recovery. Hypertension
is often seen as a response to restore CPP and CBF. Uncontrolled hypertension in
the immediate postoperative period can precipitate intracerebral haemorrhage and/or
vasogenic oedema. Boluses of short-acting opioids, propofol or lidocaine (lignocaine)
can facilitate blood pressure control at extubation. More prolonged hypertension,
despite adequate analgesia, needs prompt treatment with nifedipine, labetalol or
esmolol.
Failure to recover to an expected GCS level is usually related to anaesthetic factors,

though this must not be assumed to be the case. Factors that need to be considered
include:
partial neuromuscular blockade
residual opioid and sedative drugs
hypoxia and hypercarbia
metabolic factors (e.g. hyponatraemia)
postictal state
brain swelling
hydrocephalus
postoperative haemorrhage
ischaemia (surgical/vasospasm).
The time-course of recovery or deterioration may suggest surgical causes of poor

recovery. Once drug-related effects have been excluded and/or treated, a CT scan
is performed to exclude hydrocephalus, cerebral oedema, intracranial haemorrhage,
haematoma or a re-bleed. A negative CT may prompt a cerebral angiogram to exclude
vascular occlusion or vasospasm.
Management of delayed ischaemic neurological damage

Delayed ischaemic neurological damage classically presents as a focal deficit in the
second week after SAH, and has been attributed to reductions in large vessel calibre
(vasospasm). However, the presentation and presumed cause may be different.
Reductions in large vessel calibre may be observed at presentation and deficits may
persist into the fourth week post-bleed. There is also increasing evidence that while
large vessel vasospasm may contribute to ischaemic deficit, microcirculatory and
autoregulatory abnormalities are also important.
The differential diagnosis includes aneurysmal re-bleed, postoperative haemorrhage,

retraction injury (which follows long periods of intraoperative brain retraction), epilepsy
with postictal Todds paralysis, hydrocephalus and electrolyte abnormalities. The
history, radiographs, CT and routine biochemistry help to exclude these diagnoses and
an EEG is occasionally required to exclude non-convulsive seizures. A clear history of
deficit modulated by blood pressure alterations strongly supports a diagnosis of delayed
ischaemic neurological damage.
Confirmation of the diagnosis requires angiography, but strong supportive evidence is

provided by transcranial Doppler ultrasound, with perfusion imaging that demonstrates
reductions in regional CBF. Patients with significant deficits that constitute a
neurological emergency must be treated within hours. Prompt and effective therapy
can reverse ischaemia and substantially improve outcome. Management includes the
following three therapies.
Prophylactic therapy with calcium channel blockers nimodipine therapy over the
first 3 weeks after aneurysmal SAH has been shown significantly to reduce incidence
of vasospasm and improve outcome. Both enteral, and more commonly, intravenous
nimodipine may result in significant hypotension requiring haemodynamic support.
Triple H therapy includes the induction of controlled hypervolaemia (with monitoring

of CVP or PA pressures), haemodilution (to a haematocrit of 3033%, ostensibly to
improve flow characteristics through the narrowed vessel) and hypertension to improve
flow through narrowed arteries. Mean arterial pressure tends to be maintained below
110 mm Hg in patients with unclipped aneurysms, but levels of 130140 mm Hg
are occasionally required (and achieved) in some patients with clipped aneurysms.
Interventional neuroradiology selective intra-arterial vasodilator infusions or

angioplasty may be beneficial in resistant vasospasm or in patients who develop
cardiovascular complications of triple H therapy.
Arteriovenous malformations (AVMs)

AVMs are congenital abnormalities of the cerebrovascular bed. Most are supratentorial
and superficial, the remainder are infratentorial or dural. They usually present at 2040
years of age. The risk of bleeding is 2% per year and the annual rate of death and
disability is 4%. 510% are associated with cerebral aneurysms (most of which resolve
following AVM resection).
Most patients present with an intracranial haemorrhage. Presenting symptoms

include seizures, headache and signs of intracranial hypertension. A steal syndrome
manifesting as a progressive neurological deficit may also occur. In contrast to cerebral
aneurysms, haemorrhage is unrelated to blood pressure and is usually venous in origin.
Most AVMs are treated by embolization particularly if the surgical risk is high. Surgical
risk depends on size, anatomy of feeding arteries and venous drainage, and location
and eloquence of adjacent brain areas. Surgical resection tends to be reserved for
small, superficial AVMs.
Perioperative management: blood products should be readily available because

bleeding from AVMs can be torrential. Increases in jugular venous pressure can be
transmitted to the cerebral circulation and further enhance bleeding from the AVM.
Care must be taken with head-down positioning, tracheal tube tapes, central lines and
the application of positive end-expiratory pressure. Induced hypotension may promote
visualization of the surgical field, but at the risk of inducing venous thrombosis or
ischaemia in non-autoregulating adjacent brain. Blood pressure management should be
discussed with the surgical team.
Postoperative haemorrhage may occur from a residual AVM. In addition, hyperaemia

is a major source of postoperative morbidity and mortality, producing oedema or
haemorrhage and intracranial hypertension, which may be caused by two factors.
Normal perfusion pressure breakthrough occurs when the brain bordering the
lesion is subjected to steal from the low resistance circuit of the AVM and adapts
by lowering its autoregulatory thresholds. Resection of the AVM exposes this brain
to the normal CPP, which may exceed its upper limit of autoregulation. Hyperaemia,
microhaemorrhages and vasogenic oedema may result. Staged removal by excision or
embolization may allow the brain to regain autoregulatory mechanisms.
Occlusive hyperaemia. Venous outflow obstruction may cause haemorrhage if
arterial feeders are not occluded completely. Venous obstruction may also result in
hypoperfusion, owing to stagnation of CBF.
The risk of seizures following AVM resection is about 50%. Blood pressure control is
of paramount importance in the postoperative period. Hypertension must be avoided
to prevent hyperaemia. -blockers can be used to control blood pressure, without
delaying emergence. Blood pressure should be maintained in the low to normal range.
Postoperative ventilation is indicated for patients who suffer excessive bleeding, or have
brain swelling. ICP monitoring may be needed.
Management of ischaemic stroke

The annual incidence of stroke is 12/1000 population. 80% are caused by ischaemic
cerebral infarction, 10% by SAH and 10% by primary intracerebral haemorrhage.
The publication of the National Institute of Neurological Disorders and Stroke (NINDS)
trial of alteplase (rtPa) for acute stroke patients in 1995, and its subsequent approval
by the US Food and Drug Administration, has increased interest in acute stroke
treatment. If given within 3 hours of onset of stroke, rtPa resulted in a trend towards
neurological recovery at 24 hours, and at 3 months 50% of survivors had no or minimal
disability compared with 38% in the control group. Mortality at 3 months was the same
in both groups, despite the rate of symptomatic brain haemorrhage increasing tenfold.
There is controversy about its safety, its wider applicability outside clinical trials and
its availability. Furthermore, recent studies from Europe do not confirm the positive
results of the NINDS study. At present, only 612% of stroke patients are likely to be
eligible for thrombolysis. Advancements in investigating acute stroke, particularly MRI,
may improve the targeting of thrombolysis to those patients most likely to benefit. Any
increasing use of thrombolysis will have major implications on stroke services in the
future.
There is increasing interest in using intensive care in patients with ischaemic stroke in
specific settings. The first of these is to provide physiological optimization in patients in
whom cardiorespiratory dysfunction exposes the ischaemic brain to risks of secondary
insults. Specific issues include airway and blood gas maintenance in patients with low
GCS levels, and thresholds for intervention to treat hypertension in the early stroke
period. In general, it is important to maintain near-normal arterial blood gas levels and
to avoid treating mild-to-moderate hypertension in the acute period. Sustained blood
pressure elevation above 200/120 mm Hg may provide a reasonable threshold for
considering antihypertensive therapy.
A second indication is the care of patients who have undergone thrombolysis and
require careful monitoring, either because of comorbidities, or complications of the
procedure. Finally, there is increasing interest in the use of ICP and CPP oriented
therapies (including decompressive craniectomy) in patients with massive non-
dominant hemisphere infarctions. u
FURTHER READING
Godsiff L S, Matta B F. Anaesthesia for Intracranial Vascular Surgery. In: Matta B F,
Menon D K, Turner J M, eds. Textbook of Neuroanaesthesia and Critical Care. London:
Greenwich Medical Media, 2000; 191208.
Guy J, McGrath B J, Borel C O, Friedman A H, Warner D S. Perioperative Management

of Aneurysmal Subarachnoid Hemorrhage: Part 1. Operative Management. Anesth
Analg 1995; 81: 106072.
McGrath B J, Guy J, Borel C O, Friedman A H, Warner D S. Perioperative Management

of Aneurysmal Subarachnoid Hemorrhage: Part 2. Postoperative Management. Anesth
Analg 1995; 81: 1295302.
Ogilvy C S, Stieg P E, Awad I et al. Recommendations for the Management of

Intracranial Arteriovenous Malformations: A Statement for Healthcare Professionals
from a Special Writing Group of the Stroke Council, American Stroke Association.
Circulation 2001; 103: 264457. Web access at: http://circ.ahajournals.org/cgi/reprint/
103/21/2644.
Treib J, Grauer M T, Woessner R, Morgenthaler M. Treatment of Stroke on an Intensive

Stroke Unit: A Novel Concept. Intens Care Med 2000; 26: 1598611.

Pharmacological and
Pathological Modulation of
Cerebrovascular Physiology
Stuart A Booth
David K Menon
Stuart A Booth is Specialist Registrar in Anaesthesia at Addenbrookes Hospital,

Cambridge, UK. After qualifying from Birmingham University, he trained in medicine
at the Derbyshire Royal Infirmary and in anaesthesia and intensive care at Bury St
Edmunds and Cambridge.

His research interests include mechanisms of secondary neuronal injury, metabolic
imaging of acute brain injury and imaging anaesthetic action in the brain.
Pharmacological modulation of cerebral physiology
The importance of understanding the effects of drugs used in anaesthetic practice on

cerebral physiology cannot be overemphasized. Drugs can exert changes in cerebral
blood flow, cerebral metabolic rate and cerebral perfusion pressure, and on cerebral
blood volume and intracranial pressure (ICP). These effects may be desirable, for
example by reducing intracranial volume and ICP, and thereby improving neurosurgical
conditions, or undesirable, for example increasing intracranial volume and ICP, and
thereby predisposing to brain herniation in patients with intracranial hypertension
(Figure 1).
Effect of drugs used in anaesthetic practice and hypocapnia on cerebral metabolic rate and cerebral blood flow
1
Fluorinated volatile anaesthetic agents
Fluorinated volatile anaesthetic agents have previously been thought to cause a
disturbance in flowmetabolism coupling and attenuate or abolish autoregulation with
increasing concentrations, leading to an increase in cerebral blood volume, and thus
ICP, despite a reduction in cerebral metabolic rate. However, it is now appreciated
that commonly used agents (e.g. isoflurane) preserve flowmetabolism coupling
and autoregulation at clinically useful concentrations. There is a dose-dependent
decrease in cerebral metabolic rate (to a lower limit), which predisposes to cerebral
vasoconstriction as flowmetabolism coupling is preserved. Superimposed on this
is the dose-dependent vasodilatory effect of these agents. The effect on cerebral
blood volume is a balance between these two antagonistic processes. For example,
isoflurane, although a more potent vasodilator of cerebral vessels than halothane,
causes more of a reduction in cerebral metabolic rate at equipotent doses. This
leads to greater vasoconstriction (secondary to flowmetabolism coupling), which
antagonizes the greater dilating effect of isoflurane. Carbon dioxide reactivity of the
cerebral circulation is preserved in a normal brain despite the use of these agents, and
hypocapnia can further reduce their vasodilatory effect.
The initial popularity of halothane as a neurosurgical anaesthetic agent was reversed
by the discovery that it was a potent cerebral vasodilator and could result in clinically
significant elevations in ICP in patients with intracranial space-occupying lesions.
Enflurane was shown to produce epileptogenic activity, causing an increase in cerebral
metabolic rate, cerebral blood flow and thus cerebral blood volume and ICP. As a result,
its use in the context of neuroanaesthesia also declined. Halothane reduces cerebral
metabolic rate to a lower level than isoflurane. It also has the greatest attenuating
effects on autoregulation compared with the other volatile agents. Halothane at 1 MAC
(minimum alveolar concentration) almost completely abolishes autoregulation, whereas
isoflurane significantly impairs it only above 1 MAC. There is little difference between
the two agents in the reduction in global cerebral blood flow at levels of about 1
MAC. Halothane selectively increases cortical blood flow while markedly decreasing
subcortical blood flow, whereas isoflurane produces a more generalized reduction in
cerebral blood flow. As with all volatile agents, cerebral blood flow increases with
increasing concentrations of isoflurane (> 1 MAC) towards the levels in awake patients.
Isoflurane has been shown to have a beneficial effect on CSF dynamics by increasing
reabsorption.
Initial studies suggested that desflurane and sevoflurane have effects on the
cerebral vasculature very similar to isoflurane (e.g. similar reductions in cerebral
metabolic rate). However, more recent studies have shown distinct differences between
these agents. Desflurane, like isoflurane, can produce EEG burst suppression, but this
effect may be attenuated over time. Initial clinical reports suggest that desflurane may
cause a clinically significant rise in ICP in patients with supratentorial lesions, despite its
proven ability to reduce cerebral metabolic rate. These increases in ICP may be related
to cerebral vasodilatation and/or changes in CSF production and reabsorption.
Sevoflurane is non-irritant and has desirable pharmaco-kinetics for
neuroanaesthesia. Unlike other volatile agents, sevoflurane up to 1.5 MAC preserves
autoregulation. Although reductions in cerebral metabolic rate are similar with both
agents, the vasodilatory effect of sevoflurane is about one-third of that seen with
isoflurane.
Nitrous oxide
In equi-MAC doses, nitrous oxide is a more powerful vasodilator than any of the
fluorinated volatile anaesthetic agents. It also leads to an increase in cerebral metabolic
rate, which results in increases in cerebral blood flow and volume, producing a
particularly unfavourable pharmacodynamic profile in patients with raised ICP (Figure
1). Furthermore, the vasodilatation produced by nitrous oxide is not decreased by
hypocapnia. The effects of nitrous oxide in neuroanaesthesia need to be considered
in relation to the effects of the other anaesthetic agents used. Sevoflurane (like all the
volatile agents) reduces cerebral blood flow compared with the awake state, but the
addition of nitrous oxide can increase cerebral blood flow to a level greater than that
in the awake state. Conversely, when propofol is used to maintain anaesthesia, the
addition of nitrous oxide has no effect on cerebral blood flow or cerebral metabolic
rate, which is an effect that is also seen when barbiturates are used in combination
with nitrous oxide.
Intravenous anaesthetics
Intravenous anaesthetic agents, with the exception of ketamine, all reduce global
cerebral metabolic rate to a minimum of about 50% of baseline (which corresponds
to an isoelectric EEG), coupled with similar reductions in cerebral blood flow
(Figure 1). As flowmetabolism coupling is unaffected, these agents have an indirect
vasoconstrictive effect, thereby reducing cerebral blood volume and ICP. Autoregulation
and carbon dioxide responsiveness are unaffected.
Propofol has a favourable pharmacokinetic profile for neuroanaesthesia and is the
only agent that can provide a realistic alternative to volatile agents for maintenance of
anaesthesia. As a result, it is being used increasingly in neuroanaesthesia and critical
care. However, it is a potent cardiodepressant and systemic vasodilator, and can cause
significant reductions in mean arterial pressure. Consequently, it is important to be
aware of its potential for causing a fall in cerebral perfusion pressure.
Experimental studies have indicated that intravenous anaesthetic agents may have a
neuroprotective role in patients with intracranial disease. Both thiopental (thiopentone)
and propofol have significant anticonvulsant activity, reduce intracellular calcium influx,
scavenge free radicals and inhibit N-methyl-D-aspartate (NMDA) responses in vitro.
However, direct evidence of clinical benefit from these agents is scanty.
Ketamine dilates cerebral vessels and increases global cerebral blood flow and ICP.
Total cerebral metabolic rate is unchanged, but regional increases occur particularly in
limbic structures. Seizure activity is also a concern and CSF absorption is impaired.
These changes may be partially attenuated by hypocapnia, propofol, benzodiazepines
and halothane. Recently, there has been renewed interest in the use of ketamine, an
NMDA antagonist, for its neuroprotective properties. The results of further studies are
awaited.
Opioids
If ventilation is not controlled, increases in cerebral blood flow, volume and ICP,
secondary to respiratory depression and hypercapnia, can occur after opioid use.
During controlled ventilation, however, the administration of small-to-moderate doses
of opioids does not adversely affect cerebral blood flow and cerebral metabolic rate.
Autoregulation and carbon dioxide reactivity are also maintained. Nevertheless, high
doses of fentanyl and sufentanil have been shown to depress cerebral metabolic
rate and cerebral blood flow. Chest wall rigidity, causing a rise in central venous
pressure, may also occur. Bolus administration of fentanyl, sufentanil or alfentanil may
be associated with increases in ICP in patients with intracranial hypertension. This is
probably due to autoregulatory vasodilatation of cerebral vessels that follows an initial
decrease in cerebral blood flow (due to reductions in mean arterial pressure and thus
cerebral perfusion pressure), which leads to an increase in cerebral blood volume.
These effects are unlikely to be clinically significant if detrimental haemodynamic and
blood gas changes can be avoided. Remifentanil, like alfentanil, has similar minimal
effects on cerebral haemodynamics when given as an infusion.
Muscle relaxants
Most nondepolarizing neuromuscular blockers have little effect on cerebral blood
flow or cerebral metabolic rate, although atracurium, mivacurium and D-tubocurarine
may increase cerebral blood volume and ICP secondary to histamine release and
vasodilatation. Succinylcholine can produce increases in ICP, probably secondary to
increases in cerebral blood flow mediated via muscle spindle activation. However, these
effects are transient and mild and can be blocked by prior precurarization if necessary;
they provide no basis for avoiding succinylcholine in patients with raised ICP when its
rapid onset of action is desirable for clinical reasons.
Other drugs
Benzodiazepines tend to produce small decreases in cerebral metabolic rate and
cerebral blood flow, but there is a ceiling on this effect whereby increasing doses
produce no further reductions in these variables. Droperidol has no effect on cerebral
metabolic rate and minimally reduces cerebral blood flow. 2-agonists, such as
clonidine, dexmedetomidine and xylazine, reduce cerebral blood flow if there is no
significant reduction in mean arterial pressure. Vasodilators, such as nitrates and
sodium nitroprusside, increase cerebral blood flow and volume in the absence of
hypotension, so predisposing to raised ICP. Vasopressors increase cerebral perfusion
pressure, cerebral blood flow and volume when autoregulation is impaired (with disease
processes or outside the autoregulatory pressure limits). However, increases in CPP
in the presence of intact autoregulation result in reductions in CBV and hence ICP.
Mannitol is an osmotically active diuretic that does not normally cross the bloodbrain
barrier. It decreases ICP in two ways. First, it has an almost immediate effect by
improving microcirculatory flow and oxygen delivery; reflex vasoconstriction reduces
cerebral blood volume. Secondly, it causes a reduction in brain water thereby reducing
intracranial volume.
Pathological modulation of cerebral physiology
Ischaemia
Graded reductions in cerebral blood flow are associated with specific
electrophysiological and metabolic consequences (Figure 2). Ischaemia is thus a
continuum between normal cellular function and cell death; cell death, however, is not
merely a function of the severity of ischaemia, but is also dependent on its duration
and several other circumstances that modify its effects. Thus, the effects of ischaemia
may be ameliorated by the cerebral metabolic depression produced by hypothermia
or drugs, exacerbated by increased metabolic demand associated with excitatory
neurotransmitter release, or compounded by other mechanisms of secondary neuronal
injury (such as cellular calcium overload or reperfusion injury).
Electrophysiological and metabolic consequences of graded reductions in cerebral blood flow
Cerebral blood flow Electrophysiological/metabolic

(ml/100 g brain/minute) consequence
> 50 Normal neuronal function
? Immediate early gene activation
? Cessation of protein synthesis
? Cellular acidosis
2023 Reduction in electrical activity
1218 Cessation of electrical activity
810 ATP rundown, loss of ionic homeostasis
<8 Cell death (also depends on other modifiers, such as duration and metabolic rate)
2
Head injury
Severe head injury is accompanied by both direct and indirect effects on cerebral blood
flow and metabolism. Cerebral blood flow may be high or normal but is more usually
low soon after the ictus. Studies have shown that 30% of patients have significant
cerebral ischaemia within 68 hours of a head injury. Global hypoperfusion in these
studies was associated with 100% mortality at 48 hours, and regional ischaemia with
significant deficits. Patterns of cerebral blood flow also vary in relation to the time
after injury. Initial reductions are replaced, especially in patients who achieve good
outcomes, by a period of relative increase in cerebral blood flow. Towards the end of
the first week after injury, this may be replaced by reductions in cerebral blood flow
resulting from vasospasm associated with traumatic subarachnoid haemorrhage.
Changes in cerebral blood flow are non-uniform in the injured brain. Blood flow tends
to be reduced in the immediate vicinity of intracranial contusions, and so cerebral
ischaemia associated with hyperventilation may be extremely regional and not reflected
in global monitors of cerebrovascular adequacy.
Elevations in ICP result in reductions in cerebral perfusion pressure and cerebral
ischaemia, which lead to secondary neuronal injury (Figure 3). There is strong
evidence that maintenance of a perfusion pressure above 60 mm Hg improves outcome
in patients with head injury and raised ICP. Traditionally, patients with intracranial
hypertension have been nursed head-up in an effort to reduce ICP. It is important to
realize, however, that such manoeuvres will also reduce the effective mean arterial
pressure at the level of the head, and run the risk of reducing cerebral perfusion
pressure. A 30o head-up elevation may provide the optimal balance by reducing ICP
without decreasing cerebral perfusion pressure.
Hypertensive encephalopathy
Current concepts of the causation of hypertensive encephalopathy are based on the
forced vasodilatation hypothesis. Severe acute or sustained elevations in mean arterial
pressure overcome autoregulatory vasoconstriction in the resistance vessels and
result in forced vasodilatation. These vasodilated vessels, exposed to high intraluminal
pressures, leak fluid and protein and result in cerebral oedema, which is multifocal and
later diffuse. In the absence of actual encephalopathy, it is important to recognize that
untreated hypertension results in a shift of the autoregulatory curve to the right, with
elevation of cut-off points for loss of autoregulation.
Subarachnoid haemorrhage
Cerebral autoregulation and carbon dioxide responsiveness are grossly distorted
after subarachnoid haemorrhage, more so in patients with worse clinical grades.
Such patients may be unable to compensate for reductions in mean arterial
pressure produced by anaesthetic agents and develop clinically significant deficits.
Significant vasospasm after subarachnoid haemorrhage occurs in up to 3040% of
patients, typically several days after the initial bleed, and may be due to one or more
mechanisms. Nitric oxide may be taken up by haemoglobin in the extravasated blood
or be converted to peroxynitrite (a highly reactive free radical species) by superoxide
radicals produced during ischaemia and reperfusion. Alternatively, spasm may be
secondary to lipid peroxidation of the vessel wall by various oxidant species, including
superoxide and peroxynitrite. Other authors have proposed a role for endothelin.
Vasospasm tends to be worst in patients with the largest amounts of subarachnoid
blood, suggesting that the blood contributes to the phenomenon. Vaso-spasm is
associated with parallel reductions in regional cerebral blood flow and cerebral
metabolic rate in the regions affected.
The clinical impact of late vasospasm has been substantially modified by the
routine use of calcium channel antagonists, such as nimodipine, and by the routine
use of hypertensive hypervolaemic haemodilution (triple H therapy). Triple H therapy
involves the use of colloid administration (with venesection if needed) to increase
filling pressures and reduce haematocrit to 3035%. If moderate hypertension is not
achieved with volume loading, vasopressors and inotropes are used to maintain mean
blood pressures as high as 120140 mm Hg. The hypertensive element of this therapy
protects non-autoregulating portions of the cerebral vasculature from hypoperfusion,
while the haemodilution improves flow and oxygen delivery through vessels, the
calibre of which is reduced by spasm. Such interventions produce clinically useful
improvements in cerebral blood flow in regions of ischaemia.

Preoperative Assessment of
the Patient with Neurological
Disease
Catherine Duffy
Catherine Duffy is Consultant Neuroanaesthetist at Addenbrooke's Hospital,

Cambridge, UK. She graduated from the University of Queensland, Australia. She
trained in anaesthesia in Queensland and did a fellowship in neuroanaesthesia in
Toronto, Canada.
The role of the anaesthetist in neurosurgery is to provide the safest possible operating
conditions for the surgeon and the patient. To achieve this, a comprehensive knowledge
of CNS physiology and the effects of drugs on the brain are required. The anaesthetist
must assess the patients presenting neurological condition and any underlying medical
disease that may affect neurosurgery (Figure 1). The urgency of surgery tends to be
determined by the patients presenting neurology. The Glasgow Coma Score (GCS)
(Figure 2) provides a useful and easily communicated means of rapidly assessing
neurological status.
Glasgow Coma Score
Eye opening
spontaneous 4
to speech 3
to pain 2
none 1
Best verbal response
orientated 5
confused 4
inappropriate words 3
incomprehensible sounds 2
none 1
Best motor response
obeys commands 6
localizes pain 5
withdraws to pain 4
abnormal flexion to pain 3
extension to pain 2
none 1
Total 315
Airway and ventilation: patients with a GCS less than 9 are at risk of developing
hypoxia and hypercarbia, which exacerbate intracranial hypertension. To control
intracranial pressure and protect the airway, tracheal intubation and ventilation should
be instituted at the earliest opportunity in neurologically obtunded patients.
Fluid and electrolyte balance should be optimized before surgery. To maintain

adequate cerebral perfusion, it is important to correct dehydration, which occurs as
a result of reduced intake or use of diuretics (including mannitol) in the preoperative
period. An attempt should be made to correct electrolyte abnormalities that may occur
as a result of syndrome of in-appropriate antidiuretic hormone secretion (SIADH) or
diabetes insipidus. Corticosteroids are used preoperatively to control tumour-related
cerebral oedema. They cause hyperglycaemia, which has to be controlled, often
using an insulin sliding scale regimen. This may have to be continued intraoperatively
because hyperglycaemia worsens neurological outcome in the event of an ischaemic
injury.
Cardiovascular disease: patients with ischaemic heart disease should be assessed

and optimized before neurosurgery. Chronic hypertension causes rightward shift of the
cerebral blood flow autoregulation curve such that hypotensive episodes are more likely
to cause cerebral hypoperfusion. It is therefore important that blood pressure is well
controlled preoperatively.
Preoperative investigations: the anaesthetist should ensure that appropriate

preoperative investigations have been performed and the results are available. In
particular, it is vital that clotting abnormalities are assessed and corrected before
surgery. Depending on the anticipated blood loss, blood should be grouped and saved
or cross-matched.
Concurrent medication: the patients usual medications, including corticosteroids,

anticonvulsants, antihypertensives, antacids and antibiotics should be continued
throughout the perioperative period. Sedative premedication is best avoided in
neurologically compromised patients. In anxious patients with a GCS of 15, oral
benzodiazepines are useful. In patients with a history of postoperative nausea and
in those undergoing posterior fossa surgery, which predisposes to nausea and
vomiting, an oral anti-emetic should be included in the premedication. In patients
undergoing spinal surgery, and in whom there is no contraindication, a non-steroidal
anti-inflammatory drug (NSAID) premedication is effective in reducing postoperative
analgesic requirements. An antisialagogue may be used in patients in whom awake
fibre-optic bronchoscopic intubation is planned.
Planning perioperative care: for major neurosurgical procedures, appropriate

provision should be made for intensive care or high-dependency nursing in the
postoperative period. Some factors specific to the site and nature of neurosurgery
warrant special consideration; this article is restricted to the neurological diseases
encountered by the neurosurgical anaesthetist.
Craniotomy for supratentorial masses
Masses in the supratentorial compartment fall into three groups.
Tumours primary lesions range from benign meningiomas to highly malignant

glioblastomas. Secondary tumours are the most common intracranial neoplasm; 50% of
secondaries originate in the lung. The patient should have been investigated for primary
disease and a thorough assessment of the primary site should be made.
Haematomas traumatic acute extradural and subdural haematomas are often
associated with other injuries, which must be prioritized. Major chest or abdominal
injuries cause cerebral hypoperfusion as a result of hypotension and necessitate
urgent surgery to stop blood loss. In trauma patients, the cervical spine should be
treated as unstable until radiographs or CT scans prove otherwise. To achieve optimal
neurological results, acute haematomas must be evacuated within 46 hours of onset.
Abscesses patients with an abscess may be immuno-compromised and are often
systemically unwell due to infection. Surgery should not be delayed. Antibiotics must
be continued perioperatively.
CT scans should be reviewed by the anaesthetist for evidence of raised
intracranial pressure, looking in particular for oedema, hydrocephalus and midline shift.
Proximity to venous sinuses should be noted, because of the high risk of severe
intraoperative haemorrhage. Preoperative angiography provides useful information
about the vascularity of tumours. Occasionally, large vascular meningiomas can be
embolized in the neuroradiology suite before surgery. This can limit intra-operative
blood loss but successful embolization requires that surgical removal take place within
48 hours because the process of necrosis can trigger marked cerebral oedema.
Posterior fossa surgery

The posterior fossa is a small rigid compartment that contains vital structures and
through which there is a narrow outflow of CSF. Patients with posterior fossa lesions
can present as life-threatening emergencies. Expansion of a posterior fossa lesion can
cause acute intracranial hypertension due to hydrocephalus which must be drained
urgently (Figure 3).
As with the supratentorial compartment, posterior fossa tumours, haematomas and
abscesses may require surgical removal. Posterior fossa surgery is also undertaken to
decompress cranial nerves and to correct craniocervical abnormalities.
To allow surgical access, the patient may have to be placed in the prone, lateral,
'park bench' or sitting position. Preoperatively, the patients suitability for the proposed
surgical position must be assessed. For example, obese patients are not suited to
lying prone for a prolonged period. Because of its significant risk of morbidity and
mortality, the sitting position is reserved for patients in whom it provides the only means
of accessing the surgical lesion. Patients with cervical spine disease are unsuitable
for this position because neck flexion stretches the spinal cord causing hypoperfusion
and potential quadriplegia. The sitting position is contraindicated in patients
with known right-to-left shunts because of the risk of paradoxical air embolism
following entrainment of venous air. Exclusion of a right-to-left heart defect on
preoperative echocardiography does not rule out the risk of paradoxical air embolism.
Transpulmonary passage of air can probably still occur in the absence of a right-to-left
shunt.
Large posterior fossa masses compress the brainstem resulting in lower cranial
nerve palsies. Patients should be examined for impaired gag reflex and evidence of
chronic aspiration. If it is anticipated that the patient will be unable to maintain airway
protection after surgery, appropriate support in intensive care should be arranged at the
time of preoperative evaluation.
a Patient with hydrocephalus b complicating posterior fossa haematoma (arrow).

3
Neurovascular surgery
Cerebral aneurysms
Cerebral aneurysms are present in 25% of the population. Rupture occurs at a
rate of 0.056% per year and is related to hypertensive episodes. In the event of
a subarachnoid haemorrhage, one-third of patients do not reach hospital, one-third
have a poor outcome and one-third are functional survivors. Outcome correlates with
neurological condition at presentation which is graded according to Hunt and Hess
(Figure 4) or World Federation of Neurological Surgeons (Figure 5) scales. Early
surgery (within 48 hours of subarachnoid haemorrhage) reduces the risk of rebleeding
but does not change the incidence of vasospasm, which typically occurs 49 days after
the haemorrhage. Nimodipine improves outcome following subarachnoid haemorrhage
and should be started on admission and continued throughout the perioperative period.
Of major concern to the anaesthetist is the cardiac dysfunction that is often
associated with patients with a poor grade. This manifests as arrhythmias and
depression of ventricular wall function secondary to diffuse myocardial ischaemia. The
underlying mechanism is thought to be massive catecholamine release triggered by
subarachnoid haemorrhage. These patients are usually in an ICU or high-dependency
environment in the preoperative phase. Cardiac function should be assessed and
optimized before surgery.
Hunt and Hess classification of patients with intracranial aneurysms
Category Criteria
0 Unruptured aneurysm
I Asymptomatic or minimal headache and slight nuchal rigidity
II Moderate to severe headache, nuchal rigidity, no neurological
deficit other than cranial nerve palsy
III Drowsiness, confusion or mild focal deficit
IV Stupor, moderate to severe hemiparesis, possibly early
decerebrate rigidity and vegetative disturbances
V Deep coma, decerebrate rigidity, moribund appearance
World Federation of Neurological Surgeons (WFNS) Subarachnoid

Haemorrhage Scale
WFNS Grade Glasgow Coma Score Motor deficit

I 15 Absent
II 1413 Absent
III 1413 Present
IV 127 Present or absent
V 63 Present or absent
Carotid artery surgery

Multi-centre trials in Europe and North America have shown carotid endarterectomy to
be worthwhile in symptomatic high-grade (> 70%) carotid artery stenosis. The place
of surgery in low-grade and intermediate stenosis is not established. Patients with
vascular disease are often elderly and have coexisting medical conditions that must be
optimized before surgery.
55% of patients presenting for carotid artery surgery have evidence of ischaemic
heart disease. The risk of postoperative myocardial infarction is ten times greater in
these patients than in those without coronary artery disease. Given that myocardial
infarction accounts for 4060% of postoperative mortality, it is essential that ischaemic
heart disease is optimized preoperatively using medical therapy.
70% of patients with carotid endarterectomy have a history of hypertension.
Poorly controlled blood pressure increases myocardial oxygen demands, thereby
increasing the risk of myocardial ischaemia. Postoperative hypertension is associated
with hyperperfusion syndrome in which an area of brain that has lost the ability
to autoregulate owing to chronic underperfusion is suddenly reperfused following
endarterectomy. Hyperperfusion can lead to cerebral oedema and intracerebral
haemorrhage. To minimize the risk of surgery, blood pressure must be controlled.
Smoking is a risk factor for vascular disease and many patients presenting
for carotid endarterectomy have chronic obstructive pulmonary disease. Some
improvement in lung function may be achieved with preoperative bronchodilator
and corticosteroid therapy. To benefit from surgery, patients should stop smoking
permanently.
20% of carotid endarterectomy patients have diabetes mellitus, which is associated
with renal impairment, ischaemic heart disease and autonomic neuropathy. Diabetic
patients should be assessed for evidence of end-organ disease. A sliding scale may be
needed to achieve tight control of blood glucose in the perioperative period.
The patients preoperative neurological condition should be carefully documented.
Progressive neurological deficits are associated with an increased risk of postoperative
deficit.
Spinal surgery
Spinal injuries
In patients with spinal injuries, care must be taken to minimize the risk of secondary
spinal cord damage. Hypoxia, hypercarbia and hypovolaemia should be treated
aggressively and a neutral position should be maintained whenever the patient is
moved.
The anaesthetist is often involved in the airway management of patients with
cervical spine injuries. To minimize the risk of neurological injury in a patient with
an unstable cervical spine, patients should be intubated using manual in-line traction
and stabilization. The neck is immobilized using a hard collar or sand bags, while an
assistant applies gentle traction to the mastoid processes. Fibre-optic intubation may
provide the best alternative for securing the airway in some patients.
If the patient deteriorates neurologically, early surgery may be required to stabilize
the spine. The anaesthetist needs to be aware of the systemic effects of spinal injury
and make a thorough preoperative assessment.
Within the first 35 days of injury, these patients present a picture of spinal shock.
Patients with high spinal injuries are bradycardic due to the loss of T14 sympathetic
cardiac innervation. In subsequent months, they develop autonomic hyperreflexia and,
in the chronic phase, postural hypotension.
Patients with spinal injuries at or above C5 need ventilatory support and are at
risk of chest infections. Below C6, there may be some respiratory impairment due
to paralysis of intercostal muscles. Provision for appropriate postoperative respiratory
support should be made at the time of preoperative assessment. Patients with chronic
spinal damage may have renal failure with electrolyte abnormalities secondary to long-
term bladder dysfunction.
Chronic spinal disease

Of particular concern to the anaesthetist is the patient with ankylosis of the cervical
spine in whom intubation can be difficult, especially when temporomandibular joint
movement is restricted, as in rheumatoid cervical joint disease, or when dentition
is abnormal. When difficulty is anticipated, preparation should be made for awake
fibre-optic intubation. This must be discussed in advance with the patient. The
anaesthetist should ensure the anaesthetic room is equipped for providing topical
airway anaesthesia and fibre-optic intubation. Sedation and an antisialagogue can be
administered intravenously on arrival in the anaesthetic room.
Patients with connective tissue disorders must be assessed for cardiac, respiratory,
renal and haematological manifestations of their disease. These patients are often
taking long-term corticosteroid or other immunosuppressive therapy. The side-effects
of such medication must be considered and care paid to the sterility of technical
procedures.
Pituitary surgery
Pituitary lesions present as a mass effect or as endocrine changes. 30% of tumours

are hormonally inactive and present with headaches or visual field defects due to
compression of the optic chiasm. The remainder present with a range of symptoms
due to hyper- or hypo-secretion of one or more hormones. Expansion of one cell-type
adenoma can compress surrounding normal areas resulting in undersecretion of
other cell types. Large pituitary lesions compress the hypothalamo-pituitary stalk,
reducing the effect of hypothalamic neuroregulatory hormones. Because of the complex
nature of pituitary lesions, these patients are assessed by the endocrinology team in
conjuction with the neurosurgeon.
The usual surgical approach is trans-sphenoidal; the nasal mucosa is
vasoconstricted using intranasal cocaine post-induction. The anaesthetist should
ensure that the patient does not have any conditions (e.g. ischaemic heart disease)
that contraindicate the use of cocaine. Patients should be warned that they will have
nasal packs at the end of the procedure and will have to breathe orally. A transcranial
approach is preferred for tumours that have spread extensively beyond the pituitary
fossa but it is associated with a higher rate of morbidity.
Patients undergoing pituitary surgery receive perioperative corticosteroid therapy.
An appropriate dosage regimen is usually prescribed by the endocrinology team.
Posterior pituitary damage is rare when the trans-sphenoidal approach is used so
vasopressin replacement therapy is seldom required.
Acromegaly
Enlargement of soft tissues and cartilage makes patients with acromegaly difficult to
intubate. A history of hoarseness and stridor should alert the anaesthetist to airway
problems. Indirect laryngoscopy may be helpful in the preoperative work-up. If difficulty
is anticipated, plans should be made for awake fibre-optic intubation.
A history of sleep apnoea should be sought. This is usually peripheral in
origin owing to airway changes but there may also be a central component as
a result of elevated levels of growth hormone. 30% of patients with acromegaly
have hypertension. Occasionally they may have cardiomyopathy, in which case a
preoperative echocardiogram to assess left ventricular function is useful. Appropriate
intraoperative invasive monitoring should be planned in advance. 25% of patients
develop diabetes, which should be controlled preoperatively.
Cushings disease
The classic features of Cushing's disease (central obesity with a short thick neck) can
make patients with this disease difficult to intubate. There may be an associated history
of sleep apnoea. If there is a history of gastro-oesophageal reflux or peptic ulcer
disease, preoperative antacid therapy should be prescribed and plans made for rapid
sequence induction. 85% of patients with Cushings disease have hypertension, which
can be refractory to treatment. Left ventricular hypertrophy and congestive cardiac
failure are not uncommon. Appropriate cardiac investigations should be available
preoperatively. 60% of patients with Cushings disease have diabetes mellitus. Due to
osteoporosis and a tendency to bruising, care should be taken when transferring and
positioning these patients. Vascular access may be trouble-some due to fragile skin
and loss of connective tissue.
FURTHER READING
Cottrell J E, Smith D S. Anaesthesia and Neurosurgery. St Louis: Mosby, 1994.
Gupta A K, Summors A. Notes in Anaesthesia and Critical Care. London: Greenwich
Medical Media, 2001.
Guy J, McGrath B J, Borel C O, Friedman A H, Warner D S.Perioperative Management
of Aneurysmal Subarachnoid Hemorrhage: Part 1. Operative Management. Anesth
Analg 1995; 81: 106072.
Matta B F, Menon D K, Turner J M. Textbook of Neuroanaesthesia and Critical Care.
London: Greenwich Medical Media, 2000.

Secondary Neuronal Injury
Mechanisms
Dan W Wheeler
David K Menon
Dan W Wheeler is Clinical Lecturer in Anaesthesia at the University of Cambridge, UK.

He qualified from Oxford University. His research interests include modelling human
gas exchange and delivering genes to neurons.

Cambridge. His research interests include mechanisms of secondary neuronal injury,
metabolic imaging of acute brain injury and imaging anaesthetic action in the brain.
Cerebral injury is common and results in substantial morbidity and mortality. Neuronal
systems are fragile owing to structural and functional complexity, the post-mitotic status
of neurons and their specialized metabolic requirements.
Primary neuronal injury occurs when there is trauma causing physical disruption of
neurons, or when the oxygen supply is deficient owing to inadequate oxygenation of
blood or perfusion of brain tissue. It is common to cite cerebral blood flow thresholds
at which several physiological or pathophysiological processes occur, but little is known
about what triggers these important biological processes (e.g. immediate early gene
expression)(Figure 1).
Secondary neuronal injury is caused by damaged and dying neurons releasing

factors that have a detrimental effect on other cells, especially neighbouring cells in
the CNS. Increasing knowledge of secondary injury mechanisms may provide further
useful treatments. The mechanisms may be directly cytotoxic or may compound the
imbalance between oxygen supply and demand by:
further reducing cerebral perfusion through pathological vasoconstriction
(vasospasm), autoregulatory dysfunction or microcirculatory occlusion
increasing neuronal oxygen requirements by inducing ionic shifts, inducing
epileptiform activity or precipitating slow waves of depolarization (spreading depression)
compromising systemic cardiorespiratory physiology.
Reducing secondary injury simple measures are important. Rapid correction of

cerebral hypoperfusion and hypoxia reduce secondary injury. A fuller understanding
of the molecular mechanisms of secondary neuronal injury may allow neurons to
be protected from secondary injury by other means. However, current application of
such knowledge is limited, and clinical trials of drugs inhibiting some secondary injury
mechanisms have proved disappointing.
Most knowledge about secondary neuronal injury mechanisms comes from

experiments in cell cultures or animal models, some of which produce contradictory
results. The importance and timing of many of these mechanisms remains speculative
in humans (Figure 2) and direct observation of human pathophysiology may be required
to understand clinical disease.
Neuronal death is complex. Cells may die by necrosis when cell membrane pumps fail
and cells burst, or death may be triggered by an active process (programmed suicide)
called apoptosis. Necrosis and apoptosis can both occur in the same cell, and dying or
struggling cells can switch between them as their environment and metabolic demands
change. Cellular damage eventually leads to an inflammatory response, which may
contribute to late CNS damage. This article concentrates on what kills neurons rather
than the means by which they die.
Pathways that damage neurons

Figure 3 shows the main pathways that damage and kill neurons. They are interlinked
and can form positive feedback systems.
Processes in secondary neuronal injury

Glutamate-mediated neurotoxicity and calcium homeostasis

Glutamate is an essential amino acid. In the 1950s, monosodium glutamate was
thought to be beneficial in the treatment of mental retardation and seizures. While
evaluating this treatment, glutamate was found to induce rather than alleviate retinal
neurodegeneration in rats. Later, glutamate was found to be toxic to neurons in the
arcuate nucleus and hypothalamus and produce a characteristic syndrome of vomiting
and seizures.
Other excitatory amino acids (EAAs) and neurotransmitters (e.g. aspartate) were
found to have similar effects and introduced the concept of excitotoxicity. When a
neuron is injured or is depleted of energy stores, its cell membrane depolarizes and
large amounts of glutamate are released. More glutamate leaks out of damaged cell
membranes. Glutamate reuptake systems also fail, and extracellular glutamate levels
rise precipitously. Neighbouring cells are depolarized by the excessive glutamate
and release more glutamate causing positive feedback, resulting in a vicious spiral
of increasing extracellular glutamate concentration. Glutamate damages neurons by
depolarizing their membranes, allowing a huge influx of sodium and calcium. The
swollen neuron can survive if it has sufficient ATP to power its Na+/K+ -ATPase pumps
and handle the osmotic load, but exhibits cytotoxic oedema following metabolic failure,
with eventual loss of viability. Human intracerebral glutamate levels are markedly
elevated in brain injury, but there is doubt as to whether synaptic levels are truly toxic. In
experimental models, inhibition of glutamate-induced depolarization and cytosolic Ca2+
overload improves neuronal survival.
Receptors: the fact that glutamate can damage discrete areas of brain and leave
others untouched implied the effect was receptor-mediated. Two classes of glutamate
receptor have been identified: ionotropic and metabotropic.
Ionotropic receptors are coupled directly to ion channels and their activation causes
sodium and calcium influx. Depending on their subunit assembly and specific agonist
sensitivity, ionotropic receptors are either classified as N-methyl-D-aspartate (NMDA)
receptors, or -amino-3-hydroxy-5-methyl-4-isoxazole propionate/kainic acid binding
(AMPA/kainite) receptors.
There are eight subtypes of metabotropic receptor expressed on specific neuron
subpopulations and coupled to different secondary messenger systems. Their effects
range from excitatory to anti-excitatory. There are several regulatory sites on the NMDA
receptor complex that modulate calcium influx when the receptor is activated (Figure
4). Regulatory sites that increase calcium influx (e.g. the glycine site) provide additional
targets for neuroprotective interventions.
Calcium influx acts as an important effector of glutamate neurotoxicity. The

arrival of extracellular calcium triggers the release of intracellular calcium stores
from the endoplasmic reticulum. The cytosolic calcium concentration rises to such
an extent that protein kinase C, nitric oxide synthase (NOS) and a cascade of
phospholipases, endonucleases and proteases are activated, which destroy the cell
and its contents. The process has been described as an osmotic explosion. It is
possible to block calcium channels and spare the cell. The main calcium channels
responsible for extracellular influx are the N, P and Q channels. There are no selective
pharmacological blockers for these channels, but nimodipine improves outcome
in spontaneous and traumatic subarachnoid haemorrhage. Whether this is due
to prevention of catastrophic calcium influx into struggling neurons or its effect on
vasospasm is unknown.
Increases in cytosolic calcium concentrations are partly buffered by mitochondrial

calcium uptake. However, mitochondrial calcium overload can change the permeability
of the inner mitochondrial membrane to macromolecules (a change in the properties
of the mitochondrial permeability transition pore). The subsequent leak of cytochrome
C is one trigger for apoptosis via the caspase pathway (see below). Drugs such as
cyclosporin and tacrolimus can inhibit this process, and may be useful neuroprotective
agents.
Glutamate, nitric oxide synthase and free radicals
When NMDA receptors are activated, nitric oxide (NO) is generated in the presence of
calcium. NO is mildly cytotoxic. It is synthesized from L-arginine by the three isoforms
of nitric oxide synthase (NOS). NO and O2~ react to form peroxynitrite (ONOO ~). With
a relatively long half-life of about 1 second, this highly reactive free radical can diffuse
over several cell diameters and breaks down into the damaging hydroxide radical
(OH~).
It would be reasonable to expect that high glutamate levels would cause secondary
neuronal injury via these pathways too. The corollary of this is that inhibiting NOS might
limit injury. Surprisingly, NOS inhibition has been found to reduce, to not affect, or even
to increase secondary neuronal injury. These contradictory results may result from the
specific isoform of NOS inhibited, the time at which NOS inhibition occurs, and the levels
of NO present in injured tissue. Soon after injury, endothelial NOS (eNOS) produces NO,
which dilates cerebral blood vessels and inhibits platelet aggregation, processes that
result in improved blood flow and oxygen delivery. Low levels of NO may also modulate
the redox regulatory site at the NMDA receptor to prevent calcium influx. Later, neuronal
NOS (nNOS) and inducible NOS (iNOS) in inflammatory cells become the dominant
source of NO production. The high levels of NO produced by these routes in the brain
parenchyma overwhelm the beneficial effects of eNOS and NO becomes predominantly
neurotoxic.
Cells generate free radicals as byproducts of normal and aberrant activity. In health,
free radicals are scavenged and inactivated by a number of enzymes (superoxide
dismutase, catalase, glutathione peroxidase) and chelators (ferritin, transferrin, vitamin
E, uric acid). If oxygen and ATP are scarce, these energy-requiring safety mechanisms
are compromised. An excess of free radicals breaks DNA strands, modifies DNA
bases, alters protein structure and function and damages lipid bilayers. Free radical
production and protection by free radical antagonists is well established in experimental
CNS injury.
Immediate early genes and transcription factors

Acute insults to the brain trigger the expression of immediate early genes (IEGs) via a
highly complex alteration in the balance of secondary messenger enzyme activity. IEGs
most commonly expressed in CNS injury include c-jun, c-fos, jun-B and jun-D. The
gene products are transcription factors, which activate another cascade of proteins via
activator protein-1 (AP-1). AP-1 alters the expression of genes involved in the cell cycle,
cell survival and regeneration. Several key genes also have a role in preventing (bcl-2,
bclx) or producing (bad, bax) apoptosis.
Nuclear factor-B (NF-B) is another transcription factor independent of the AP-1

family. It can transduce a signal directly from the cell membrane to the nucleus without
the need for enzyme cascades, implying a rapid response time. NF-B release results
in upregulation of a variety of proinflammatory mediators including cytokines and
adhesion molecules, and may injure neurons through non-inflammatory mechanisms.
Paradoxically, NF-B expression may be neuroprotective in some settings.
Proteases: caspases and calpains

Caspases (cysteinyl aspartate-specific proteases) are a family of proteases
fundamental to apoptosis. Their role was first elucidated in the nematode
Caenorhabditis elegans. Three genes (ced genes) were found to regulate cell death as
the worm developed, two causing cell death and one preventing it. Humans probably
have 14 such genes, divided into the ICE (interleukin-1 converting enzyme) and CED-
3 subfamilies. In vivo studies have shown that caspases are important in effecting
neuronal apoptosis after cerebral injury.
Calpains are calcium-activated proteases belonging to a papain family of cysteine

proteases. They are the enzymes that break down the cells cytoskeleton, digest signal
transduction enzymes and second messenger systems, and digest cell membrane
receptors. They are the end-point of apoptosis, destroying its machinery and packaging
it so that it can be phagocytosed. They may also be important in neuronal differentiation
and long-term potentiation. As the end-point of apoptosis, they may be useful targets
for future interventions.
The inflammatory response

The bloodbrain barrier isolates the CNS from systemic inflammatory processes in
health, but an inflammatory response is observed following acute CNS insults. The
temporal pattern of inflammatory cell recruitment is modified in the CNS, but cytokine
production, chemokine release, inflammatory adhesion molecule upregulation, and
neutrophil recruitment are all observed in cerebral ischaemia and trauma (Figure 5).
Neutrophils can be found at injury sites within hours, and remain for 2448 hours.
Macrophages arrive later, either recruited from the circulating monocyte population,
or derived from the resident CNS macrophage population called microglia. Microglia
behave differently from peripheral macrophages. In their resting state they have few
of the features of macrophages and express few of the same genes. When activated
they become phagocytic and secrete the inflammatory factors TNF and TGF. The
population of microglia in the CNS is small so the debris of a dead neuron is removed
more slowly than in the peripheral nervous system. When the debris is cleared,
astrocytes grow where the neuron once was, in response to IL-6 and TGF. This
astrocytic scar forms a barrier to re-innervation.
Inflammatory responses following acute brain injury

Intervening to prevent scar tissue formation and possibly to encourage re-

innervation is attractive. However, the molecular relationship between neurons,
microglia and astrocytes is poorly understood and likely to be highly complex. Many
trophic factors are yet to be identified, but transplanting primary neurons and stem cells
into injured areas is a mode of delivery that is generating much interest. u
FURTHER READING
Dirnagl U, Iadecola C, Moskowitz M A. Pathobiology of Ischaemic Stroke: An Integrated
View. Trends Neurosci 1999; 22: 3917.
Graham S H, Chen J. Programmed Cell Death in Cerebral Ischemia. J Cereb Blood

Flow Metab 2001; 21: 99109.
Kermer P, Klcker N, Bhr M. Neuronal Death after Brain Injury. Cell Tissue Res 1999;
298: 38395. (Web access on: http://link.springer-ny.com/link/service/journals/00441/
papers/9298003/92980383.pdf)
Mattson M P, Camandola S. NF-kappaB in Neuronal Plasticity and Neurodegenerative

Disorders. J Clin Invest. 2001; 107: 24754. (Web access on http://www.jci.org/cgi/
reprint/107/3/247)
Menon D K, Summors A C. Neuroprotection (including Hypothermia). Curr Opin

Anaesthesiol 1998; 11: 48596.

Obstetrics
Anaesthesia
on CD-ROM
Anaesthesia for Operative
Obstetrics
Andrew McLeod
Roshan Fernando
Andrew McLeod is Specialist Registrar in Anaesthetics at the Middlesex/UCL/Royal

Free School of Anaesthesia, London. He began his training and interest in obstetric
anaesthesia at St Thomas Hospital, London.
Roshan Fernando is Consultant Anaesthetist at the Royal Free Hospital, London,

where he also heads the Obstetric Anaesthesia Services. His research interests
include balance function after combined spinal-epidural analgesia in labour and platelet
function during pregnancy.
Anaesthesia for obstetric operations must accommodate the physiological changes

of pregnancy, and preserve maternal and fetal well-being. Delivery may be required
rapidly when the fetus is at risk. Emergency procedures often occur outside working
hours and in remote facilities. Obstetric surgery is associated with comparatively high
mortality, and increasing medico-legal involvement.
Caesarean section
Elective lower segment caesarean section is performed for cephalopelvic disproportion,

malpresentation, multiple pregnancies, placental insufficiency, and at maternal request
following previous caesarean section. Emergency caesarean section is required when
fetal or maternal well-being is acutely threatened.
Assessment: patients at high risk of operative delivery should be made known to the
anaesthetic team and assessed. Women presenting for caesarean section are often
well informed, and many have experienced it before. It is important to establish the
womans preference for anaesthesia and elicit information about any:
obstetric history and previous caesarean sections
previous anaesthetics used (or family history of suxamethonium apnoea or
malignant hyperthermia)
problems in this pregnancy (e.g. hypertension, diabetes, coagulation disorders)
medications and allergies (e.g. latex, skin preparations, antibiotics).
Regional anaesthesia should be encouraged, and anxieties allayed, though potential
complications must be discussed honestly. The presence of painful labour contractions
may limit the extent of any discussion, but not its legal validity. An assessment of
intubation difficulty must always be made and recorded. A simple bedside test such as
Mallampatis classification is useful, but lacks a high positive predictive value. Difficult
intubation (see page 218) should always be anticipated. Early insertion of an epidural
catheter (for analgesia) is highly desirable when operative delivery is likely, particularly
if general anaesthesia involves an added risk (e.g. known difficult intubation).
Emergency caesarean section: fetal distress is diagnosed from continuous fetal heart
rate monitoring and fetal blood gas analysis, but remains an unreliable predictor of
condition at birth. A briefer decision-to-incision and incision-to-delivery interval is
associated with better initial fetal outcomes. Infants delivered by emergency caesarean
section under general anaesthesia have been shown to have lower Apgar and
other neurobehavioural scores compared with those under regional techniques. Both
anaesthetist and obstetrician should decide which anaesthetic to use depending on the
speed and safety required. All methods aim to prevent fetal acidosis by:
ensuring adequate maternal oxygenation
avoiding hypotension
minimizing aortocaval compression
preventing excessive maternal hypocapnia.
The left lateral position minimizes aortocaval compression (and improves uterine
perfusion). Supplementary oxygen for the mother also improves fetal oxygenation.
Maternal blood pressure should be maintained with non-glucose-containing
crystalloid solutions and intravenous ephedrine. Discontinuing oxytocin infusions, and
administering tocolytic agents (e.g. magnesium or -agonists) reduces uterine activity
and can improve acidosis. Fetal monitoring should be continued, because lasting
improvement may allow time to convert to regional anaesthesia.
Regional techniques avoid many of the life-threatening complications of general
anaesthesia. An increasing use of regional anaesthesia, has paralleled a fall
in anaesthetic-related maternal mortality, though the absolute number of general
anaesthetics has fallen only marginally. Apart from safety, regional anaesthesia has
four other advantages.
Fetal exposure to depressant drugs is minimized.
Maternal participation at delivery is made possible, and the mother can bond with,
and care for, her baby sooner.
Blood loss is reduced.
Postoperative analgesia is improved using spinal or epidural opioids.
Regional anaesthesia should be performed in a fully equipped operating theatre or
anaesthetic room. Adequate resuscitation facilities must be available, together with the
necessary drugs and equipment in case conversion to general anaesthesia is required.
Reliable, large-bore (14 G or 16 G) venous access must be established before any
regional procedure, and pulse oximetry and ECG monitoring established with frequent
measurements of arterial blood pressure. Fluid pre-load of 10001500 ml of crystalloid
solution is normally given. Correct aseptic technique includes wearing a gown, mask
and gloves. Skin preparation with chlorhexidine in alcohol solution is effective, provided
it is allowed to dry. Skin and deeper tissues are infiltrated with local anaesthetic (e.g.
2% lidocaine (lignocaine)) at the intended site.
Spinal anaesthesia is the quickest and simplest technique. It produces a superior

quality of anaesthetic block, and requires anaesthetic doses that cause minimal
toxicity to mother or fetus. However, there is no opportunity to provide intraoperative
supplementation via the same route in the event of inadequate anaesthesia, or
prolonged surgery.
Spinal injection can be performed in the lateral position, but in the obese patient the
sitting position helps to identify the midline, and assists the mother to flex her back.
The L3/4 or L4/5 interspaces are chosen to avoid direct trauma to the spinal cord. A
25 G or preferably 27 G pencil-point (Whitacre or Sprotte) needle causes a low rate
of post-dural puncture headache (PDPH). These small-gauge needles often require an
introducer needle. Commonly used regimens are listed in Figure 1.
Commonly used regimens for regional anaesthesia
Caesarean section
Spinal
Bupivacaine (hyperbaric usually 0.5% bupivacaine in 8% glucose), 1012
mg, fentanyl, 25 g, or diamorphine, 200300 g
Epidural
Test dose: 0.5% bupivacaine, 3 ml ( adrenaline (epinephrine), 5 g/ml)
Loading dose: 0.5% bupivacaine, 20 ml ( adrenaline (epinephrine), 5 g/ml)
+ fentanyl, 50100 g, or diamorphine, 25 mg (in saline, 10 ml)
0.5% levobupivacaine, 20 ml, + opioid
0.75% ropivacaine, 20 ml, + opioid
Extension of in situ epidural

2% lidocaine (lignocaine), 1520 ml, + adrenaline (epinephrine), 5 g/ml,
opioid
0.5% bupivacaine, 1520 ml, ( adrenaline (epinephrine), 5 g/ml) opioid
50:50 mixture 0.5% bupivacaine and 2% lidocaine (lignocaine), 1520 ml, (
adrenaline (epinephrine), 5 g/ml, 8.4% sodium bicarbonate, 2 ml) opioid
0.5% levobupivacaine, 1520 ml, opioid
0.75% ropivacaine, 1520 ml, opioid
Operative vaginal delivery (forceps, ventouse)
In situ epidural catheter

0.250.5% bupivacaine, 1015 ml, + fentanyl, 2550 g
Spinal or combined spinal-epidural

0.5% bupivacaine (hyperbaric), 1.52 ml, fentanyl, 25 g
Epidural anaesthesia: insertion of an epidural catheter is technically more difficult

than spinal injection, and more time is required to produce an effective block. However,
the block can be established incrementally if needed, and supplemented during
surgery. Preparation, precautions and position are the same as for spinal anaesthesia.
The two approaches to the epidural space are the midline and the paramedian; the
former is most commonly used.
For the midline approach, the epidural needle is inserted into the interspinous
ligament, normally below the L2/3 interspace, and the epidural inner stylet withdrawn.
The epidural space is identified by loss of resistance to injection of saline. The saline
technique reduces the incidence of dural puncture with the epidural needle. The
epidural catheter is passed through the needle, which is itself removed, leaving only the
epidural catheter in situ. The epidural catheter is then withdrawn leaving 45 cm in the
epidural space, and finally taped to the skin and a bacterial filter attached to the distal
end. A test dose of local anaesthetic should be administered to exclude subarachnoid
or intravascular placement (Figure 1). If dural puncture has occurred, the catheter can
be resited in an adjacent space, but the response to the test dose must be monitored
carefully. Alternatively, the catheter can be advanced into the subarachnoid space, and
used as a spinal catheter.
In situ epidural catheter: an epidural catheter, that has been used for labour analgesia
and is functioning correctly, can be used to extend the existing block for emergency
caesarean section. No optimum solution has been found to do this rapidly and
effectively, but choices are shown in Figure 1.
Combined spinal-epidural anaesthesia combines the speed of onset and quality of

spinal anaesthesia, with the flexibility of an epidural catheter, though it is technically
more difficult to perform. Concerns have been raised that drug flux may occur from the
epidural space once a hole has been made in the dura. This has been reported, but the
risk is thought to be significant only if large-gauge spinal needles are used, and high
local anaesthetic concentrations are subsequently injected epidurally.
This combined technique is most commonly performed as a needle through needle
technique, in which a long spinal needle such as a 119 mm, 27 G Whitacre spinal
needle is advanced (once the epidural needle has been correctly located in the epidural
space) through the dura mater into the subarachnoid space. The spinal injection
provides rapid anaesthesia for surgery and the epidural catheter is used for intra-
operative supplementation or for postoperative analgesia.
Infiltration and field block: direct infiltration of the anterior abdominal wall with local
anaesthetic, layer by layer, can make surgery possible. Alternatively, intercostal and
iliohypogastric blocks and/or rectus sheath block combined with direct infiltration of the
incision line have been used. Visceral reflexes can also be obtunded to some degree by
injection of local anaesthetic around the uterovesico fold and paracervical area. Up to
100 ml of 0.5% lidocaine (lignocaine) with 1:200,000 adrenaline (epinephrine) may be
used. Most obstetricians have limited experience with this technique.
Intraoperative care of the patient: the patient should be placed in the full lateral
position while the block develops, and supplementary oxygen given. Complaints of
nausea normally indicate hypotension and require prompt treatment with ephedrine.
Ethyl chloride spray or needle-prick testing will establish the extent of sensory blockade,
which should reach an upper level of the T4 dermatome (See Anaesthesia and
Intensive Care Medicine 1:1: 42). Surgery should not proceed until this sensory level
is achieved. Patients should be warned that some discomfort may be encountered
at delivery, or if the uterus is brought out during closure. Continued reassurance is
important. Oxytocin, 10 i.u., is routinely given after delivery and at the end of surgery,
rectal analgesics (e.g. diclofenac sodium, 100 mg) can be administered.
Problems
Hypotension (defined as a 20% or greater fall in systolic blood pressure) is more
common during spinal than epidural anaesthesia, and also in non-labouring women.
Sympathetic blockade causes reduced venous tone, pooling of blood in the lower body,
and decreased systemic vascular resistance. Hypotension adversely affects uterine
perfusion and fetal acidosis, and precipitates maternal nausea and vomiting. It requires
prompt treatment, including the adoption of the lateral position, intravenous fluids and
vasoconstrictors. Ephedrine is the vasoconstrictor of choice, owing to its sparing effect
on uterine vasculature.
Nausea and vomiting are common. They may potentially lead to the aspiration
of gastric contents. Hypotension is the most common precipitant, though prior opioid
administration contributes.
Inadequate block results from failure of technique, or allowing insufficient time for
the block to develop. It is more common with epidural than with spinal anaesthesia, due
partly to inadequate spread within the epidural space, and also catheter migration into
paravertebral spaces. Poor block is the most common reason for conversion to general
anaesthesia, and also a potential source of litigation.
Dural puncture has a theoretical frequency of 0.3% or 1/200 (to which units
should aspire), but is often more common. The symptoms of PDPH can be severe
and disabling in post-partum patients, and are also associated with significant
sequelae (see page 222). Symptoms should be actively sought at follow-up, and
established headaches treated actively with epidural blood patching. Many units treat
milder headaches with conservative treatment including bed rest, oral analgesics,
intramuscular ACTH, subcutaneous sumatriptan and oral or intravenous caffeine.
Total spinal blockade occurs when an epidural dose of local anaesthetic is
inadvertently given intrathecally, causing complete motor and sensory blockade,
profound hypotension, loss of consciousness and airway reflexes.
Side-effects of local anaesthetic drugs manifest as toxicity when upper safe
limits are exceeded, or accidental intravenous injection occurs. Spinal or epidural
opioids can cause pruritus and respiratory depression. Delayed respiratory depression
with opioids is uncommon in obstetric patients and less likely to occur with more lipid-
soluble compounds (e.g. fentanyl, diamorphine). Intrathecal or epidural diamorphine is
probably the most common opioid used in the UK to provide postoperative analgesia
after caesarean section under regional block.
Neurological complications are four times more likely to be caused by the fetus
passing through the pelvis, or by iatrogenic injury. In contrast, complications from
regional anaesthetic techniques occur in about 1/13,000 deliveries.
Paraplegia and cauda equina syndrome result from spinal cord compression
by epidural haematoma, or abscess. Haematoma is extremely rare, but classically
presents with sharp irradiating back pain and sensorimotor deficit. Early symptoms
of epidural abscess include headache and backache, which may be most severe at
the epidural site. Later signs of bladder and bowel disturbance may occur with or
without signs in the lower limbs. Once symptoms have developed, urgent surgical
decompression is required within 8 hours, to prevent permanent neurological damage.
Nerve injury can be caused by epidural or spinal needles. Direct contact with a
nerve root for example, may produce transient paraesthesia, while nerve root trauma
usually causes severe lancinating pain radiating to the dermatome it supplies. Patients
may be left with areas of paraesthesia, hypoanalgesia or weakness, which take variable
lengths of time to resolve. Adequate follow-up and reassurance are important, ideally
involving a neurologist experienced in this area.
Meningitis is a rare but recognized complication of regional anaesthesia. Bacterial
meningitis is usually caused by species of Streptococcus or Staphylococcus, resulting
from direct haematological spread or poor aseptic technique on insertion. Aseptic
meningitis may be caused by viral infection, equipment contamination, or in association
with certain drugs.
Contraindications may be absolute or relative (Figure 2). The need for extremely
urgent delivery may allow insufficient time for regional methods to be performed. Spinal
deformities (e.g. scoliosis) make regional anaesthesia technically more difficult and less
reliable. Neurological diseases (e.g. multiple sclerosis) are not a contraindication to
epidural anaesthesia, though data on intrathecal injections are lacking.
Coagulopathy can place patients at risk of epidural haematoma, though most
women are prothrombotic in late pregnancy. Adequate haemostasis depends on platelet
numbers and function. Most UK centres agree that a count of over 100 x 109 /litre is safe
for performing neuraxial blockade, and the range 80100 x 109 /litre remains acceptable
if coagulation tests are normal. Counts below 50 x 109 /litre represent an absolute
contraindication. Pre-eclamptic patients may present with falling platelet counts, or
impaired coagulation, and recent values are essential. Prophylactic administration of
heparin, particularly low molecular weight heparin (LMWH), is increasingly common.
For unfractionated heparin, present guidelines state that neuraxial blocks can be
performed 4 hours after the last dose, and the catheter removed 4 hours following a
subsequent one. For LMWH, 12 hours should elapse. Recent consensus is that aspirin
and other antiplatelet drugs when used alone are not a contraindication to regional
block. In less clear-cut cases, point of care monitors such as the thromboelastogram
may have a role, and advice from a haematologist should be sought.
Anticipation of significant haemorrhage placenta praevia occurs where the
placenta implants ahead of the presenting fetal part (in about 1/200 pregnancies). It
remains a principal cause of massive obstetric haemorrhage, but is now better detected
and managed by caesarean section. The exact grading depends on the extent to which
the placenta covers the lower segment and os, but this does not dictate the choice
of anaesthesia. There is no consensus, though modern practice is increasingly using
regional techniques, except where urgent delivery is essential, or significant maternal
hypovolaemia has occurred. In all cases, potential haemorrhage must be anticipated.
It results from incision of the placenta (particularly when anterior), uterine atony,
or the occurrence of placenta accreta. Reliable, large-bore venous access must be
established before surgery, cross-matched blood should be available, and measures to
promote uterine contraction may be needed.
Systemic sepsis maternal pyrexia is common in labour, but does not generally
indicate sepsis. Prolonged rupture of membranes (defined as over 24 hours) is the
most important cause, and may be associated with chorioamnionitis in which 8% of
women will be bacteraemic. Regional techniques may incur the risk of meningitis or
epidural abscess, though a causal relationship is unproven, and the incidence of these
complications remains low, even in febrile patients. Most authorities conclude that
epidural catheters can be safely sited in patients with chorioamnionitis once antibiotic
treatment has commenced, but should be avoided if there are signs of untreated sepsis.
Contraindications to the use of regional anaesthesia
Absolute
Maternal refusal
Coagulopathy
Local sepsis
Severe uncorrected hypovolaemia
Known allergy to local anaesthetic agent
Relative
Urgent delivery
Spinal deformities
Anticipation of significant haemorrhage
Systemic sepsis
General anaesthesia
Large-bore venous access must be established (minimum calibre 16 G). The patient
should be prepared on the operating table, in a left tilted position or with a left uterine
wedge. Pulse oximetry, automated blood pressure cuff, and ECG are the minimum
levels of monitoring required. Capnometry is also considered essential to confirm
tracheal intubation, and satisfactory ventilation. A source of suction, gum elastic
bougies, and smaller sized tracheal tubes (e.g. 57 mm internal diameter) must be
available, together with short-handled laryngoscopes and alternative designs of blade
(e.g. the McCoy laryngoscope). Equipment to assist with oxygenation in the event of
failed intubation should be immediately accessible, and includes simple oral airways,
laryngeal mask airways, and a cricothyroid puncture set.
The surgical team routinely prepare and drape the skin before induction, to minimize
subsequent delay. Preoxygenation of the lungs is achieved by 3 minutes' breathing (or
four vital capacity breaths) 100% oxygen through a close-fitting mask. Anaesthesia is
induced intravenously as a rapid sequence with thiopental (thiopentone), 67 mg/kg,
and suxamethonium, 1.5 mg/kg. Cricoid pressure is applied by an assistant. Tracheal
intubation must be confirmed by observing the chest for equal expansion, auscultating
the chest at both axillae and over the stomach, and by the presence of a regular
capnograph waveform. Preparations for a potential failed intubation (see page 218)
must be made beforehand, and a drill followed.
Anaesthesia should be ensured by administering adequate concentrations of a
volatile agent (e.g. 1% isoflurane with oxygen:nitrous oxide 50:50), and a non-
depolarizing muscle relaxant (e.g. atracurium). After delivery and clamping of the
umbilical cord, the nitrous oxide concentration can be increased, and opioid analgesia
given (e.g. morphine, 10 mg i.v.), together with prophylactic antibiotics. Oxytocin, 10
i.u., is routinely given once the fetus has been delivered, and may be followed by an
infusion (e.g. 2040 units over 24 hours). At the end of surgery, rectal analgesics
(e.g. diclofenac sodium, 100 mg) can be administered, and patients recovered in the left
lateral position and extubated when awake.
Problems
Failure of oxygenation is the most serious and life-threatening complication of
general anaesthesia. Functional residual capacity is reduced in pregnancy, causing
rapid desaturation in the apnoeic patient. Hypoxia results from an inability to manage
a difficult airway, though this has usually followed unsuccessful tracheal intubation.
Failed intubation in obstetric patients (see page 218) is eight times more common than
in the general surgical population. Full dentition and enlarged breasts make insertion
of the laryngoscope more difficult, while obesity and upper airway oedema impede
direct laryngoscopy, and make the airway more difficult to manage. Additionally, cricoid
pressure applied in the wedged position can displace the glottis laterally, and intubation
attempted before suxamethonium is maximally effective will be more likely to fail.
Aspiration of gastric contents continues to cause maternal morbidity and
mortality. Lower oesophageal sphincter tone is reduced in pregnancy and gastric
emptying is delayed during labour, the delay being exacerbated by opioid
administration. All women must receive antacid prophylaxis before caesarean section.
Ranitidine, 150 mg, given orally at 12 and 3 hours before surgery effectively reduces
acid secretion, and metoclopramide, 10 mg, on the morning of surgery contributes
to reduced gastric volume, and increased lower oesophageal sphincter pressure. For
emergency surgery, ranitidine, 50 mg, can be given intravenously. A non-particulate
antacid (e.g. sodium citrate 0.3 M, 30 ml) should also be given within 20 minutes of
surgery.
Hypertensive response to intubation may be exaggerated in patients with pre-
eclampsia or pre-existing hypertension. It may be obtunded by -blockade, or short-
acting opioid drugs and, if hypertension poses an increased risk (e.g. cerebrovascular
disease), intra-arterial blood pressure monitoring should be instituted.
Maternal awareness represents a terrifying ordeal with potentially long-lasting
psychological consequences. In the past this has resulted from small induction doses
of thiopental (thiopentone) causing inadequate anaesthetic drug concentrations before
intubation, and from deliberate avoidance of volatile agents caused by concerns of
uterine relaxation (leading to past awareness rates of 1226%). Pregnant women may
have higher anaesthetic requirements owing to increased cardiac output, and high
catecholamine levels secondary to pain and anxiety.
Fetal depression is increased with a longer induction-to-delivery interval.
Postoperative care
patients should ideally be cared for in a designated recovery area. Blood pressure,
pulse rate, respiratory rate and arterial oxygen saturation must be monitored for at least
1 hour before return to the post-natal ward.
Postoperative analgesia after regional techniques (see page 214) can be provided
with intrathecal opioids (e.g. diamorphine, 200300 g) administered together with the
local anaesthetic at the time of spinal injection, or by subsequent top-ups of epidural
opioid (e.g. diamorphine, 2.5 mg) via an epidural catheter. Respiratory depression,
especially with less lipid-soluble opioids, is a serious complication, and if adequate
observations cannot be made, these techniques should be used with caution. Lipid-
soluble opioids (e.g. diamorphine) are seldom associated with delayed respiratory
depression in the obstetric population and are routinely used in many UK units.
Paracetamol and regular non-steroidal suppositories are highly effective (e.g. diclofenac
sodium, 150 mg/day, in divided doses for 35 days).
Monitoring for complications of regional anaesthesia (as listed above) must
include observation for signs of spinal cord compression or neurological deficit, and
also headache and backache.
Thromboprophylaxis in recent years, thromboembolism has been the leading
cause of death in pregnancy, occurring frequently after caesarean section. Important
risk factors are age over 35 years, obesity, grand multiparity, immobility, pre-eclampsia
and emergency caesarean section. Women at moderate or high risk must receive
thromboprophylaxis, for example unfractionated heparin starting at the time of surgery
and continued until discharge from hospital.
Pregnancy-related illnesses
A number of maternal medical conditions can complicate pregnancy, but pre-eclampsia

and cardiac diseases have particularly important implications for anaesthesia.
Pre-eclampsia complicates 510% of pregnancies, presenting as a syndrome of

hypertension, proteinuria and/or oedema usually after 20 weeks gestation. The only
definitive treatment is delivery for which caesarean section is commonly required.
Regional anaesthesia is strongly indicated except where coagulopathy is present.
In mild disease, most women have normal platelet counts and coagulation, though
20% may show evidence of a consumptive thrombocytopenia and platelet function
abnormalities especially in severe pre-eclampsia. In the HELLP (Haemolysis, Elevated
Liver enzymes, Low Platelets) syndrome variant, thrombocytopenia can be severe with
counts of less than 50 x 109 /litre. If a recent platelet count is above 100 x 109 /litre,
coagulation is unlikely to be abnormal. Below this level, a coagulation screen must be
performed. Spinal and epidural techniques for caesarean section in patients with pre-
eclampsia are equally acceptable, and the incidence of hypotension is equivalent. Fluid
pre-loading in women with severe pre-eclampsia should be restricted to no more than
500 ml of crystalloid or colloid solution, and hypotension corrected with ephedrine.
With general anaesthesia, the hypertensive response to intubation must be
obtunded, to reduce cerebral haemorrhage risk. Intravenous alfentanil, 1020 g/kg, or
labetalol, 1020 mg, can be used. Upper airway oedema is common, making intubation
and airway management difficult. Smaller sized tracheal tubes may be required, and
postoperative ventilation should be considered in cases of potential obstruction. Pre-
eclamptic patients are increasingly receiving magnesium therapy, which potentiates
non-depolarizing muscle relaxants, and reduced doses should be used.
Cardiac disease is causing increasing maternal mortality, as more women with
congenital defects survive to reproductive age. Patients require care in specialist
units, with individual assessment and planning, but some general points can be made.
Elective caesarean section is commonly favoured. Epidural block may be considered
if a slow incremental top-up technique with intra-arterial blood pressure monitoring is
used. Sudden cardiovascular changes are reduced, and conditions such as aortic or
mitral regurgitation may benefit from reduced systemic vascular resistance.
General anaesthesia may be unavoidable if anticoagulation is required, and in other
individual instances. Cardiac considerations should dictate the choice of anaesthesia
and, because intra-operative opioids improve haemodynamic stability, they will often
be the agents of choice. However, fetal respiratory depression can occur, requiring
ventilatory assistance or administration of naloxone.
Oxytoxic drugs can increase pulmonary vascular resistance, promote fluid retention
and lead to cardiac decompensation. Many units avoid them at delivery but because
this risks post-partum haemorrhage, it is preferable to administer dilute oxytocin over 30
minutes or administer it cautiously in incrementally diluted solutions.
Anaesthesia for other procedures
Cervical cerclage
Cervical incompetence can cause recurrent mid-trimester abortions. In most cases, the
cervix can be re-enforced by cerclage, and this is typically performed at 1218 weeks
gestation as a prophylactic procedure. It may also be attempted in an emergency
for actively bulging membranes and, in this situation, reduction of intrauterine and
intra-abdominal pressure is important. General anaesthesia has been advocated,
because volatile agents can decrease intrauterine pressure and facilitate reduction of
the membranes, but coughing and straining must be avoided. In contrast, a regional
technique reduces these risks, but positioning, movement and vomiting may increase
the possibility of membrane rupture. There is little definite evidence to support either
approach. The procedure is performed transvaginally and, if a regional technique is
chosen, blockade to T8/10 level is required for which epidural and spinal anaesthesia
are both suitable.
Manual removal of retained placenta

The placenta must be manually removed if normal separation does not occur or
fragments remain within the uterus. Post-partum haemorrhage may occur in both
instances, and patients must be adequately resuscitated first. The choice of anaesthetic
technique depends on the degree of haemorrhage and the presence of an in situ
epidural catheter. Manual removal requires anaesthetic block to a sensory level of
T6. If an epidural catheter is in place, incremental boluses of 0.5% bupivacaine or
2% lidocaine (lignocaine) with adrenaline (epinephrine) 1:200,000 up to a total volume
of 20 ml may be used to provide anaesthesia. Alternatively, a spinal technique as
outlined above can be used, using bupivacaine, 10 mg.
General anaesthesia is required if regional methods are contraindicated or at
maternal request. Conduct is the same as for caesarean section, though opioids can
be used at induction because fetal depression is not a consideration. Intraoperative
uterine relaxation can be provided with transiently high concentrations of volatile
agent. Alternatively, nitroglycerine, 50500 g i.v., has been used to relax the uterus.
Haemorrhage and uterine inversion are potential complications.
Operative vaginal delivery

Additional analgesia or anaesthesia is often needed for ventouse or forceps delivery.
The choice of technique is influenced by the presence of an existing epidural catheter,
the degree of pain that the mother is likely to experience (e.g. forceps delivery
compared with ventouse), the urgency of delivery and the likelihood of success;
failed vaginal delivery usually necessitates immediate caesarean section. The following
options can be considered.
An existing epidural catheter can be used to augment the block (Figure 1).
An epidural, spinal or combination catheter can also be inserted.
The obstetrician can perform a pudendal nerve block to provide analgesia for a
low forceps or ventouse delivery, or infiltrate local anaesthetic into the perineum before
episiotomy. Entonox (oxygen: nitrous oxide) can be given to supplement the block.
FURTHER READING
Chestnut D H, ed. Obstetric Anesthesia: Principles and Practice. 2nd ed. St Louis:
Mosby, 1999.
Department of Health, Welsh Office, Scottish Office Department of Health, Department
of Health and Social Services Northern Ireland. Why Mothers Die. Report on
Confidential Enquiries into Maternal Deaths in the United Kingdom 199496. London:
The Stationery Office, 1998.
Yentis S M, Brighouse D, May A, Bogod D, Elton C. Analgesia and Anaesthesia in
Pregnancy: A Practical Guide. Philadelphia: W B Saunders, 2000.

Anaesthetic Management of
Labour (Induction and
Augmentation)
Andrew H Shennan
Andrew H Shennan is Senior Lecturer in the Maternal and Fetal Research Unit at St
Thomas Hospital, London. He qualified from St Marys Hospital, London. He trained in
London, Newcastle and South Africa in obstetrics and gynaecology.
Labour management aims to ensure a safe delivery for both mother and baby. This
is achieved through close monitoring of labour progress, together with assessment of
maternal and fetal well-being. When problems arise, the options are to instigate more
intensive surveillance, introduce therapeutic measures to correct pathology, or to deliver
the baby. This article defines labour and its different stages and describes the methods
for detecting problems and how to deal with them.
Diagnosis of labour
The correct diagnosis of labour is essential and can be difficult. Incorrect diagnosis
leads to high rates of intervention. Labour is characterized by regular uterine
contractions, dilatation of the cervix and descent of the presenting part. The key
to diagnosing labour is observing a change in cervical state on consecutive vaginal
examinations.
Partogram
The partogram is a graphical record of the progress of labour (Figure 1). The cervical
dilatation is plotted against time, along with the descent of the presenting part (usually
cephalic). Adequate and progressive descent of the fetal head is a good sign of
labour progress. Descent should always be sought in addition to cervical dilatation,
because the latter can occur in an obstructed labour. Abdominal assessment of descent
is necessary because vaginal assessment can falsely suggest progress when there
is increasing swelling on the head (caput). Lines are often drawn to indicate when
progress (as judged by cervical dilatation) is slow; this indicates the need for action.
The strength and frequency of the contractions are noted,
but they are not reliable signs of an adequate labour.
The state of the liquor is documented. Staining with meconium or blood indicates
possible fetal compromise and warrants close fetal monitoring. No liquor with ruptured
membranes may be a sign of fetal compromise.
Maternal temperature, pulse and blood pressure are recorded regularly. The fetal
heart rate is also noted, primarily to identify a rise in baseline. Tachycardia may indicate
fetal distress or infection, and the need for continuous monitoring by cardiotocogram.
Section of the labour partograph

C CC C CC C
The alert and action lines are printed on the partograph
1
Assessing risk
The onset of labour: a spontaneous onset of labour is associated with the best
chance of a normal delivery. Induction of labour is achieved by ripening the cervix (if
necessary) usually with vaginal prostaglandins (PGE2), repeated as necessary. This
is followed by an artifical rupture of the membranes when possible, which releases
endogenous prostaglandins. Stimulation with oxytocin is used if labour does not
become established, usually within a couple of hours. The indication for induction and
the induction itself significantly increase the need for intervention in labour, including
operative deliveries.
Parity: compared with a multiparous woman, a woman in her first labour (primiparous)
is much more likely to require intervention, the progress of labour is slower, and
oxytocin is needed more often. Caesarean section and operative vaginal delivery rates
are higher in primiparous women (about tenfold). The same partogram is used for all
women. A delayed labour in a multiparous woman is more likely to be a result of a
serious cause, and is therefore more urgent.
Maternal and fetal disease: risk in labour is dependent on maternal and fetal
well-being. A growth-restricted fetus, or a poorly functioning placenta (e.g. in pre-
eclampsia) increases the risk of fetal distress. These types of labour are often induced,
confounding the problems. Pregnancies of more than 42 weeks gestation are prone to
increased rates of fetal distress and intervention.
Regional analgesia: women having difficult labours often request epidural analgesia.
A significant proportion of these women do not achieve a spontaneous vaginal delivery
because a regional block increases the need for oxytocin stimulation and assisted
vaginal delivery. However, it is unlikely to increase the need for caesarean section.
Support in labour: emotional and physical support in labour has been shown to
improve outcome. Having a birthing partner or one-to-one midwifery care is probably
the best way to avoid problems.
Stages of labour
Intervention in labour is aimed at preventing a long labour associated with fetal distress
and infection.
First stage
The first stage occurs from the onset of cervical change to 10 cm dilatation. The first
stage of labour can be divided into latent and accelerative phases (Figure 1). The
latent phase can last up to 8 hours, without the need for intervention. A prolonged
latent phase should be managed by artificial rupture of the membranes, followed by an
oxytocin infusion if progress remains slow. At about 3 cm, the rate of cervical change
increases. In about 75% of women in labour in their first pregnancy, the cervix will
dilate at least 1 cm/hour during this later accelerative phase. Rates less than this may
be abnormal, and indicate a dysfunctional labour or secondary arrest. A dysfunctional
labour is usually caused by inadequate uterine activity and is common in primiparous
women. It can be corrected using an oxytocin infusion. However, secondary arrest
must be excluded. This can result from malposition (e.g. occipitoposterior position)
or malpresentation (e.g. brow, which usually requires delivery by caesarean section).
Whatever the cause of delay (as assessed on cervical dilatation and head descent),
the degree and severity of obstruction can be assessed by the caput and moulding on
the head, and the adequacy of the pelvis, during vaginal examination. This determines
whether oxytocin can be used to augment the labour and if there is a need for
caesarean section. Inefficient uterine action is uncommon in a multiparous women, and
oxytocin must be used cautiously even when there are no other signs of obstruction,
or the uterus may rupture. True cephalicpelvic disproportion, a possible cause of
secondary arrest (i.e. normal presentation with adequate uterine activity and delay) is
rare. Women with a previous caesarean section also have the risk of scar rupture and
should be assessed closely, but over 70% achieve vaginal delivery.
Vaginal examinations are performed every 4 hours in normal labour, but can be
performed more often if delay develops (usually 2 hourly). If an intravenous infusion
of oxytocin is used, it is titrated to contraction frequency so that there are no more
than five contractions in 10 minutes. Increased frequency above this may not allow the
uterus to relax and increases the risk of fetal distress. Women with prolonged labour
should be adequately hydrated, and often require intravenous fluid. The fetus should
be continuously monitored with an electronic fetal heart rate monitor. Slow progress
between 7 and 10 cm has been associated with higher rates of instrumental vaginal
delivery.
Second stage
The second stage occurs from full dilatation (10 cm) to delivery of the baby. A prolonged
second stage may increase the risk of fetal distress and pelvic floor damage. The
diagnosis depends on the time of the vaginal examination and, in practice, it is the
length of pushing that equates best to risk and should be limited. If women do not
have the desire to push, and the head still has room to descend, then a delay before
pushing is often advised. This is often necessary with an epidural, when oxytocin is also
more commonly used. It is unusual to wait for more than 2 hours before commencing
pushing, but if delivery has not occurred after 1 hour of pushing, the need for assistance
should be considered urgently. Maternal exhaustion usually requires intervention at this
time. A ventouse is generally safer, particularly from the maternal viewpoint, and can
be performed without an episiotomy in some cases. Forceps are more often used in
difficult cases. Rotational forceps, although not widely used, can be employed when the
presenting part is malpositioned, but their use requires more skill.
Third stage
The third stage occurs from delivery of the baby to delivery of the placenta.
Syntometrine (a combination of oxytocin, 5 IU, and ergometrine, 0.5 mg) is given
intramuscularly with the delivery of the anterior shoulder. This reduces the incidence
of post-partum haemorrhage. Ergometrine can cause nausea and sickness. The
placenta is delivered by cord traction, once the uterus has contracted and the placenta
separated.
FURTHER READING
Gibb D M F, Arulkumaran S. Uterine Contractions and the Fetus. In: Progress in
Obstetrics and Gynaecology. Vol 6. Edinburgh: Churchill Livingstone, 1987.
Malvern J. The Clinical Management of Labour. In: Obstetrics. Edinburgh: Churchill
Livingstone, 1989.
ODonnell E. Abnormal Patterns of Labour. In: Managing Obstetric Emergencies.
Oxford: Bios, 1999.
ODriscoll K, Foley M, MacDonald D. Active Management of Labour as an Alternative to
Caesarean Section for Dystocia. Obstet Gynaecol 1984; 63: 48590.

Anatomy of the Uterus
Hazel Adams
Hazel Adams is Consultant Anaesthetist at the Princess Royal and Hurstwood Park
Neurological Hospitals, Haywards Heath, UK. Her interests include obstetric and
neurosurgical anaesthesia.
The uterus is a muscular tube, widest at the top and flattened anteroposteriorly (Figure
1). It lies between the bladder and the rectum and is separated from them by a layer
of peritoneum. The uterine tubes are embedded in its upper lateral edges and extend
laterally to the ovaries. The fundus is the domed area above the insertion of the tubes.
The body is mainly smooth muscle (the myometrium) arranged in three ill-defined
layers. The outer fibres tend towards longitudinal and the inner layers are more circular,
acting like sphincters around the blood vessels. The lowest 3 cm of the uterus is the
cervix and the part of the body adjacent to the cervix is the isthmus. During pregnancy,
the isthmus forms the lower uterine segment, which is where the uterine incision is
usually made during a caesarean section.
Small bowel loop

Pouch of Douglas
Uterus
Fundus
Myometrium
Endometrium
Rectum
Isthmus
Cervix Bladder (empty)
Symphysis pubis
1 MRI of the female pelvis
The cervix protrudes into the anterior wall of the vagina. The ureters pass forwards
to the bladder in the parametrium (the connective tissue surrounding the cervix). The
ureters are closely related to the uterine arteries.
The vagina is a fibromuscular tube at 60 to the horizontal. The space between the
cervix and vagina is the fornix. Anteriorly the vagina is in contact with the base of the
bladder. The urethra is adherent to the anterior wall of the vagina.
The ovaries are attached to the posterior border of the broad ligament by a double fold
of peritoneum. The obturator nerve (anterior primary rami of L2, 3, 4) and vessels lie
laterally. Pain from the ovary may be referred to the inner thigh. During pregnancy the
ovaries are pulled upwards.
Peritoneum: the uterus is enclosed by peritoneum, a double fold of which extends

laterally to the walls of the pelvis as the broad ligament. Posteriorly, the peritoneum
extends beyond the cervix to the wall of the vagina. It forms the recto-uterine pouch of
Douglas, which contains small and large bowel. Anteriorly, the peritoneum is reflected
on to the bladder at the level of the isthmus. During a lower segment caesarean section
it must be divided in order to avoid damaging the bladder.
Blood supply
The uterus is supplied by the uterine arteries, which usually branch from the internal
iliac artery. They pass medially across the pelvic floor in the broad ligament to reach the
cervix and give branches to the cervix and vagina. There are anastomoses between
both uterine arteries and the ovarian arteries, which increase during pregnancy.
Venous drainage is through the several pelvic plexuses to the internal iliac veins. These
plexuses are the cause of the severe haemorrhage associated with a fractured pelvis.
There are no valves in the pelvic veins. Raised intra-abdominal pressure may cause
back flow through the sacral veins into the venous plexuses within the vertebral column.
From there, blood drains into the superior vena cava via the posterior intercostal and
the azygos veins.
The ovaries the ovarian arteries are branches of the aorta below the renal arteries.
They are retroperitoneal and enter the broad ligament each giving off a tubal branch.
Nerve supply
The sympathetic supply
Fibres from cell bodies at T11L2 pass to plexuses continuing downwards in front of
the aorta. They form the superior hypogastric plexus at the level of L5 along with fibres
from L3 and L4. This plexus divides into right and left hypogastric nerves, which run into
the pelvis to form the inferior hypogastric plexus. Each inferior hypogastric plexus lies
lateral to the rectum on the side walls of the pelvis. They receive contributions from the
sacral sympathetic ganglia.
The uterus is supplied by the superior and inferior hypogastric plexuses. The cell
bodies of the sympathetic motor supply to the uterus are mainly at T11 or T12.
The ovaries are supplied by the aortic and coeliac plexuses.
The parasympathetic supply comes from S2, 3, 4. Sacral nerves join the inferior
hypogastric plexuses. They continue to the lexuses surrounding the cervix where they
synapse.
Function of the autonomic supply: the sympathetic supply is vasoconstrictor and

facilitates muscular contraction, especially of fibres near the cervix.
Uterine muscle is mainly responsive to hormonal changes. Some authorities describe

motor nerves from T6 and T7 accompanying the sympathetic nerves to the uterus.
There is little evidence of parasympathetic innervation of muscle.
The sensory supply

Stretch, contraction, infection and possibly ischaemia all cause pain (Figures 2 and 3).
Pain from the body of the uterus is transmitted by sympathetic sensory fibres that enter
the sympathetic chain at L5 and ascend. They enter the cord between T10 and L1 and
pain can be referred to the corresponding dermatomes. Early labour pain is often felt in
the T1112 dermatomes. As the pain becomes more severe it spreads to T10 and L1.
Other fibres travel with the aortic, superior and inferior hypogastric plexuses (i.e. there
are alternative pathways entering the spinal cord at different levels).
Pain pathways of relevance to the obstetric anaesthetist
Sympathetic afferents T10L1

Parasympathetic afferents S2, 3, 4
The rectal, perineal and pudendal branches of the sacral plexus (S2, 3, 4)
transmit the pain of perineal stretching
The iIioinguinal nerve (L1) supplies the root of the clitoris, the labia, the
mons pubis and the upper and medial part of the groin
The genitofemoral nerve (mainly L2) supplies the labia majora
The posterior femoral cutaneous nerve (S1, 2, 3) supplies the posterolateral
labia majora
A pudendal nerve block will not anaesthetize the whole vulva
2
Important points for the obstetric anaesthetist
The inferior hypogastric plexus receives fibres from the superior hypogastric
plexus, which receives fibres from the coeliac plexus supplied by the
splanchnic nerves from T5T12
Nerve fibres may enter the spinal cord higher than expected
Synapses may occur several segments higher
The peritoneum is supplied segmentally by the spinal nerves that innervate

the overlying muscles. Without a block to T4, traction on the peritoneum can
cause pain
The diaphragm is supplied predominantly by C4 (via the phrenic nerve).

About one-third of the fibres in the phrenic nerve are sensory and pain is
referred to the shoulder tip. The periphery of the diaphragm has a sensory
supply from the lower intercostal nerves
A block from T4S4 is required for a caesarean section even though the
principal nerve supply to the uterus is from T10T12. Even then sensation
from the diaphragm is not completely blocked
3
Pain from the cervix is classically considered to be carried by the pelvic splanchnic
nerves (S2, 3, 4). It may be referred to the area supplied by the sacral plexus extending
from the lower back to the buttocks, thighs and the mid-calf.
Pain from the isthmus may also be carried via the same pathways as pain from the
body of the uterus and be referred to the T12 and L1 dermatomes.
Somatic pain is also perceived during labour. A and C fibres supply the uterus and
cervix and accompany the sympathetic nerves. These nociceptive fibres enter the roots
between T10 and L1 and synapse at the interneurons in the dorsal horn.
The ovaries: sympathetic vasoconstrictor fibres, with their cell bodies at T10 and T11,
reach the ovaries from the aortic plexus. Sensory fibres travel with the sympathetic
nerves. Pain from the ovary may be referred to the peri-umbilical area (as well as the
inner thigh, see above).
The vagina: sympathetic fibres from the inferior hypogastric plexus and the
paracervical plexus supply the blood vessels and smooth muscle. Sensory fibres travel
via the pudendal nerve (anterior divisions of S2, 3, 4) to supply the lower vagina. u
FURTHER READING
Lee R. The Anatomy of the Nerves of the Uterus. Am J Obstet Gynecol 1996; 174(3):
10756 (A reprint of Lee R. The Anatomy of the Nerves of the Uterus. London:
Hippolyte Baillire, 1841).
Stables D. Physiology in Childbearing with Anatomy and Related Biosciences.

London: Baillire Tindall, 1999.

Antenatal Assessment of the
Pregnant Mother
Anne May
Anne May is Consultant Anaesthetist with a special interest in obstetric anaesthesia at

the Leicester Royal Infirmary. She is actively involved in research and teaching obstetric
anaesthesia and is President of the Obstetric Anaesthetists' Association. She has been
running an obstetric anaesthetic assessment clinic since 1991.
Preoperative assessment is a well-recognized part of the anaesthetists clinical practice

and many hospitals have preoperative assessment clinics run by anaesthetists or
nursing staff. It is often assumed that pregnancy is a normal physiological condition
without risk, but an anaesthetist will be involved with the care of over 50% of women at
some time during their delivery. In the UK, the caesarean section rate is over 20% in
many units and there are parts of the world where the rates are much higher. In the UK,
epidural analgesia rates vary from 5% to 80%.
The need for anaesthetic assessment of the pregnant mother has been
highlighted by successive reports on the Confidential Enquiries into Maternal Deaths
(CEMD) 198184, 198587, 198890, 199193 and 199496. Antenatal anaesthetic
assessment of pregnant women with cardiac disease was recommended in the
198587 CEMD report.
Though maternal mortality has fallen in the last 50 years, as reported in the triennial
reports into maternal death, pregnancy still carries a significant risk, which is greatest
for women with coexisting medical diseases. An increasing number of women who
become pregnant have significant concomitant disease. Some years ago, many of
these women would not have contemplated pregnancy, but advances in management
and treatment of many diseases mean that such woman can now expect normal fertility.
A good example is the excellent control that many women with insulin-dependent
diabetes achieve. However, it is important to remember that the underlying condition
is still present and may be influenced by the physiological changes of pregnancy and
delivery.
Other women who may benefit from antenatal assessment by an anaesthetist
include those who may present an anaesthetic problem and those who need to have
their anxieties and fears about analgesia and anaesthesia allayed. It could be argued
that all women should be seen by an anaesthetist in the antenatal period because
they are all potentially in need of obstetric anaesthetic intervention. If a woman has
had an antenatal consultation with an anaesthetist, the problems of assessment and
consent are less than when the woman presents in a distressed state for anaesthetic
intervention. Explanation and assessment are easier in the antenatal period when the
woman is calm and pain free.
Women with coexisting medical problems
It is important for the practitioner to consider the effects of the physiological changes
at each stage of pregnancy on the disease. The stress of labour and delivery (including
pain), and the potential effects of any anaesthetic intervention should also be taken
into account.
Cardiac disease
In the Western world, there has been a change in the pattern of cardiac disease, which
is illustrated in the most recent CEMD. It is now less common to see women with
rheumatic heart disease, while the number with congenital heart disease and ischaemic
heart disease has increased. A number of physiological changes of pregnancy affect
the cardiovascular system.
Cardiac output increases to a maximum of 40% at 2028 weeks gestation.
Stroke volume increases and heart rate increases by 1020 beats/minute.
Blood pressure decreases in the first and second trimesters and increases in the
third trimester.
Systemic and pulmonary vascular resistance decrease by 2530%.
Plasma oncotic pressure decreases by 1015%, therefore the patient will be prone
to pulmonary oedema.
In labour, the cardiac output increases by 2550%; mainly mediated through the
sympathetic nervous system.
Autotransfusion of blood from the placenta occurs.
Supine hypotension may cause a reduction in cardiac output of up to 20%. This
occurs when the weight of the gravid uterus reduces blood flow through the large
vessels (inferior vena cava and aorta) in the supine position.
All pregnant women with cardiac disease should have a full history and examination
taken early in pregnancy. Where appropriate, ECG, echocardiography and chest
radiography assessments should be undertaken. The team caring for the woman in
pregnancy should plan her management in detail and liaise with the cardiologist. It
is useful to classify the severity of the cardiac disease using the New York Heart
Association (NYHA) classification (Figure 1).
Women with NYHA class 1 or 2 heart disease usually present little problem in
pregnancy or labour. Those with more severe cardiac disease may not tolerate
the physiological changes of pregnancy, especially as they approach 2028 weeks
gestation, and will need to be managed by a multidisciplinary team. Caesarean section
is required only for obstetric reasons.
In women with severe cardiac disease, epidural analgesia removes the stress
response to the pain of labour. Modern low-dose epidural techniques cause little
sympathetic block and therefore are safe for most women with cardiac disease.
Epidurals are beneficial to women with left heart failure. However, in women with
heart disease in whom a drop in systemic vascular resistance would be deleterious,
epidural analgesia is not advised. Patients with hypertrophic cardiomyopathy and
primary pulmonary hypertension are particularly at risk. Epidural analgesia may be
considered in some cases of aortic stenosis where the gradient across the valve is not
too great. It is essential to remember the autotransfusion that occurs in the third stage
of labour as well as the effect of oxytocin.
Women with cardiac disease need careful monitoring and management throughout
labour and the puerperium. Antibiotic cover is important as the CEMD has shown a
continuing problem with endocarditis. Clear management plans should be written and
agreed by all members of the multidisciplinary team in the antenatal period.
New York Heart Association (NYHA) Classification
NYHA 1
Known cardiac disease with no limitation of physical activity and no objective
evidence of cardiovascular disease
NYHA 2
Slight limitation of normal physical activity and objective evidence of minimal disease
NYHA 3
Marked limitation of physical activity and objective evidence of moderate disease
NYHA 4
Severe limitation of activity including symptoms at rest and objective evidence of
severe disease
Respiratory disease
The most common respiratory problems seen in pregnant women are asthma and
cystic fibrosis. The lung disease may be primarily obstructive or restrictive.
Obstructive conditions (e.g. asthma, bronchiectasis, cystic fibrosis) may improve
after treatment with bronchodilators.
Restrictive conditions include granulomatous (sarcoid) and fibrotic (postradiation
fibrosis, fibrosing alveolitis) disease; they are characterized by fibrotic changes in the
lungs, and may be progressive or stable.
Respiratory disease may be exacerbated by the increased respiratory demands of
pregnancy. If the disease is severe, pre-pregnancy counselling is advisable. A number
of important physiological changes need to be considered.
Oxygen consumption increases by 20% and metabolic rate by 15%.
The resting minute ventilation increases by 4050% with the tidal volume increasing
and the respiratory rate remaining unchanged.
The functional residual capacity (FRC) is decreased in the third trimester, though the
vital capacity remains unchanged.
Forced expiratory volume in 1 second, peak expiratory flow rate and the partial
pressure of oxygen in arterial blood remain unchanged while the partial pressure of
carbon dioxide in arterial blood decreases to 4.0 kPa.
Arterial pH is 7.44.
The respiratory centre is reset early in pregnancy as a result of progesterone
enhanced by oestrogen, which increases the sensitivity of the chemoreceptors to
carbon dioxide. Patients with respiratory disease, in particular those with asthma, are
aware of the hyperventilation early in pregnancy and may need reassurance. Towards
the end of pregnancy, the enlarging uterus displaces the diaphragm and reduces
FRC. FRC remains greater than closing pressure in the upright posture though in the
recumbent posture it falls. In the second trimester, airway closure falls within the normal
tidal ventilation in a significant number of women.
The effects of these physiological changes may severely compromise the woman
with respiratory disease. Pulmonary function tests carried out in the first trimester give a
baseline value and these should be repeated in the third trimester or earlier if clinically
indicated. Regular peak flow monitoring is a useful assessment in those with obstructive
lung disease and may be used as a guide to therapy. Many women avoid taking
medication when pregnant and it is important that they are encouraged to continue their
maintenance medication.
Women who have treated malignancies may have restrictive lung function and
cardiac damage, and require echocardiographic examination of the heart.
In general, women with significant respiratory disease should be encouraged to
have a stress-free labour and delivery, minimizing pain and hyperventilation. Epidural
analgesia is an integral part of the pain management of these women. If an operative
delivery is required, regional anaesthesia is the anaesthetic of choice because general
anaesthesia is poorly tolerated.
Haematological disease
In many parts of the world, including the UK, antenatal screening for anaemia,
thalassaemia and sickle cell disease is routine. Women with haematological disease
may have:
reduced oxygen carrying capacity (e.g. sickle cell trait)
increased risk of clotting (e.g. thrombophilia)
increased risk of bleeding (e.g. idiopathic thrombocytopenia, von Willebrands
disease).
Antenatal assessment is best undertaken by a multidisciplinary team including a
haematologist, ideally at a combined clinic. Detailed plans for the management of
labour and delivery should include the risks and benefits of regional analgesia and
anaesthesia. If regional analgesia is contraindicated, the woman should be told what
options are available to her for pain relief including the use of patient-controlled opiate
analgesia.
Musculoskeletal disease
Musculoskeletal diseases seen in pregnant women range from physical disability
resulting from nonspecific back problems to those who are severely disabled and
wheelchair bound. Assessment includes respiratory and cardiac function for those with
severe disease (e.g. severe kyphoscoliosis).
The effect of each stage of the pregnancy on the disease needs to be assessed and
this must include the possibility of vaginal delivery. The musculoskeletal abnormality
should be assessed by an obstetric anaesthetist to balance the risks and benefits
of a regional block; it is helpful if previous records of surgery and radiographs are
available. Antenatal consultation is important so that informed consent is obtained for
any anaesthetic intervention.
Endocrine disease
The most common endocrine diseases that present in the childbearing population are
diabetes and thyrotoxicosis. These women are best managed in a combined clinic,
where the obstetrician and endocrinologist manage the pregnancy and plan for delivery.
For most of these women a stress-free delivery is advised and epidural analgesia is
an integral part of management.
Neurological disease
Antenatal assessment is advisable for women with, or with a history of, neurological
disease. Patients with a history of trauma, tumours, infection or cerebrovascular
accidents need to be assessed to determine whether there is any residual problem that
will be affected by the pregnancy or labour. Consultation with the obstetric anaesthetist
is advisable because many of these women are frightened by the thought of a needle
in their back or any sensation of numbness. They may have had a bad experience with
a lumbar puncture or paralysis, for example in acute post-infective neuropathy. Careful
explanation and reassurance about regional analgesia and anaesthesia is important.
Women with established neurological disease include those with spina bifida,
myasthenia gravis, epilepsy, or multiple sclerosis. In all these conditions, the
assessment should take account of the effect of the pregnancy and labour on the
disease. Many women who cope with crutches will need a wheelchair in the later
stages of pregnancy. Women with spina bifida may have other risk factors (e.g.
associated kyphoscoliosis, tethered spinal cord). Early consultation allows time for
full investigations including MRI, and to obtain records of previous investigations and
surgery.
Traditionally, regional analgesia and anaesthesia have been avoided in patients
with neurological conditions because of the fear of making the condition worse or
being blamed if worsening should occur. Although randomized controlled trials are
unavailable, there is increasing clinical experience of regional blocks being safely
and successfully carried out in these women. Antenatal consultation with an obstetric
anaesthetist is important so that the risks and benefits may be explained and a plan
made for analgesia and anaesthesia during delivery.
Women with potential anaesthetic problems
General anaesthesia is associated with maternal mortality, although the incidence

of death as a direct cause of general anaesthesia has fallen in recent years as
demonstrated by successive CEMD reports. The increased risks of general anaesthesia
in pregnancy are mainly a result of the physiological changes of pregnancy, in particular
the cardiovascular and respiratory changes. These changes are compounded by the
physiological changes of pain, the work of the contracting uterus, and the oxygen
demands and stress response of labour. Weight gain, oedema, large breasts and
swollen mucosa all increase the difficulty in visualizing the larynx at laryngoscopy. The
physiological and anatomical changes of pregnancy make airway management and
hypoxia more of a problem than in the nonpregnant state. Failed intubation associated
with acid aspiration (Mendelsons syndrome) is still a major anxiety for anaesthetists in
obstetrics. Failure to intubate the trachea occurs in about 1/300 pregnant women and is
ten times more common than in nonpregnant women.
Women who have a potential anaesthetic problem include those with:
coexisting disease
obesity
difficult intubation (known or potential)
previous anaesthetic problems
genetic conditions associated with general anaesthetic problems.
Obese women
Obese women have several potential anaesthetic problems. These range from difficulty
in finding intravenous access and placing regional blocks to major difficulties in
intubation and ventilation if general anaesthesia is required.
Difficult intubation
In women who have had a previous difficult or impossible intubation, the difficulty must
be clearly stated in the medical record and clear guidelines for the labour and delivery
set out. These women need to be told that regional anaesthesia is the anaesthetic
of choice and this may indicate epidural analgesia in labour. If regional anaesthesia
is not an option then these women may have to be delivered by caesarean section
as an elective procedure using fibre-optic intubation techniques. Antenatal planning is
essential for these women.
Genetic diseases
Genetic diseases associated with potential anaesthetic problems are malignant
hyperpyrexia and suxamethonium sensitivity. Women with malignant hyperpyrexia are
usually aware of the hazards of general anaesthesia and the safety of regional
analgesia and anaesthesia for them. It is essential that a clear plan for their delivery is
made in the medical record so that all carers are aware of the problem. Women who
are suxamethonium sensitive usually have a reasonable knowledge of the problem of
prolonged apnoea, though they may not be aware that suxa-methonium is a standard
drug used in emergency anaesthesia in obstetrics. They should be encouraged to have
regional anaesthesia but told that there are alternative drugs if they need a general
anaesthetic. Antenatal assessment is important for these women.
Women with adverse drug reactions
Many women have drug allergies. The antenatal period allows time for records to
be found and the advice of an immunologist and pharmacist to be sought where
appropriate. Some women need reassurance because their reaction was a side-effect
of a drug rather than an allergic reaction. The anaesthetist should ensure that there is
clear documentation of true allergies that may be life threatening and that guidelines
for suitable pain relief in labour are drawn up taking account of relevant drug allergies
and sensitivities.
Women with specific anxieties about their delivery
Elective caesarean section

Women scheduled to have an elective caesarean section are usually admitted on the
day of surgery and this makes it difficult to discuss the risks and benefits of regional
anaesthesia with them. Many units have introduced leaflets to explain the basics of their
anaesthetic. This is helpful, but there are still some women for whom this information
is inadequate and who need an antenatal consultation with the anaesthetist. Ideally,
this should be available to all women who are to be delivered by planned caesarean
section.
Planned pain relief in labour

Information on pain relief in labour is available to all women but some may have
particular anxieties and benefit from detailed discussion on epidurals. Women for whom
an epidural has been suggested as a planned part of their labour management (e.g.
for twins, breech or hypertensive disease of pregnancy) may also benefit from a more
detailed discussion.
Previous anaesthetic or analgesic problems

Previous anaesthetic or analgesic problems include a previous bad obstetric experience
or, for example:
dural puncture
difficult or failed epidural
pain at caesarean section
epidural did not extend for caesarean section
bad experience of general anaesthesia
bad opiate experience.
These women benefit from antenatal assessment so that plans for their labour and
delivery can be made and recorded in their notes.
FURTHER READING
Chamberlain G, Wraight A, Steer P, eds. Pain and its Relief in Childbirth. The Results
of a National Survey Conducted by the National Childbirth Trust. Edinburgh: Churchill
Livingstone,1993.
Gambling D R, Douglas M J. Obstetric Anesthesia and Uncommon Disorders.
Philadelphia: Saunders, 1998.
HMSO. Report on Confidential Enquiries into Maternal Deaths in the United Kingdom
198587. London: The Stationery Office, 1991.
HMSO. Why Mothers Die. Report on Confidential Enquiries into Maternal Death in the
United Kingdom 199496. London:
The Stationery Office, 1998.
Yentis S M, Brighouse D, May A, Bogod D, Elton C. Analgesia and Anaesthesia and
Pregnancy: A Practical Guide. London: Saunders, 2000.

Assessing the Fetus
Kate Langford
Andrew H Shennan
Kate Langford is a Subspecialty Trainee in Maternal-Fetal Medicine at Guy's and St

Thomas' Hospital, London. She qualified from Cambridge University and King's College
Hospital, London. Her research interests include monitoring of fetal health and in utero
programming of patterns of adult disease.
Andrew H Shennan is Senior Lecturer in the Maternal and Fetal Research Unit at St
Thomas Hospital, London. He qualified from St Marys Hospital, London. He trained in
London, Newcastle and South Africa in obstetrics and gynaecology. His main research
interests are in the diagnosis and prevention of pre-eclampsia, intra-partum regional
analgesia, and the prevention of prematurity. He specializes in running clinical trials.
The two key assumptions underlying fetal assessment are that:

fetal compromise is progressive and can be detected at an early stage before
permanent damage has occurred to the fetus
an effective intervention can prevent or ameliorate fetal damage.
Despite widespread use of fetal assessment techniques, these underlying assumptions
are not always met. Fetal compromise has various aetiologies that progress at different
rates. It is the underlying aetiology that determines whether the assessment of
fetal well-being is successful in detecting a stage before permanent fetal damage
occurs. The only intervention that can rescue the fetus from an adverse intrauterine
environment is delivery, which may result in death or disability from prematurity. In order
to minimize the number of fetuses exposed to the risks of iatrogenic prematurity, a
judgement must be made as to when fetal compromise becomes permanent damage.
Delivery should be undertaken just before this point. Unfortunately, current assessment
techniques do not predict this point accurately, and so some fetuses will be delivered
more prematurely than necessary and others delivered after they are irreversibly
damaged.
Ante-partum assessment
There is no single agreed method of assessing fetal well-being in the ante-partum

period and in practice a variety of different parameters are used to provide an
overall impression of fetal health. Individual units have different approaches to fetal
assessment depending on the technology and expertise available. At its most simple,
fetal well-being is assessed throughout pregnancy by health professionals asking the
mother at each visit whether the baby is moving well. Ultrasound scanning is commonly
used in fetal assessment with parameters such as fetal growth, amniotic fluid volume,
placental maturity, and fetal and placental blood flow being measured.
Whatever the method used, effective assessment of fetal well-being depends on the
background risk in the pregnancy. All methods of monitoring may give false-positive
or false-negative results, the impact of which may be reduced by bearing in mind
the likelihood of fetal compromise in the pregnancy being assessed. For example, a
decline in movements may indicate a compromised fetus, but in most cases it will
not. Decreased movements are most likely to represent compromise in a pregnancy at
high risk of fetal problems, such as one complicated by fetal growth restriction, and so
should be taken most seriously in this context.
Electronic fetal heart rate (FHR) monitoring to produce a cardiotocograph (CTG)
is widely available, but research does not support its use in the ante-partum period.
CTGs have never been shown to improve fetal outcome and their use is associated
with a trend towards an increase in perinatal deaths (odds ratio 2.85, 95% confidence
interval 0.99 to 7.12).
Intra-partum assessment
Fetal heart rate monitoring

The aim of intra-partum FHR monitoring is to identify those fetuses who become
hypoxic and acidotic during labour so that delivery can be expedited before permanent
damage or death ensues. It was hoped that this would reduced the incidence of
cerebral palsy, but it has not done so. This partly reflects the limitations of the method,
but is also explained by increasing evidence that most cases of cerebral palsy follow
an insult in the antenatal period and therefore will not be prevented by changes to the
management of labour.
Intra-partum FHR monitoring may be undertaken by intermittent auscultation using
a Pinard stethoscope or hand-held Doppler monitor, or by continuous electronic fetal
monitoring to produce a CTG. This article focuses on the CTG, but this does not
mean that it is superior to intermittent auscultation for most women. Trials comparing
intermittent auscultation with continuous electronic fetal monitoring consistently show
no reduction in perinatal death with electronic fetal monitoring. Electronic fetal
monitoring is associated with a reduction in perinatal morbidity because it reduces the
incidence of early neonatal seizures, however, this is not associated with any reduction
in longer-term morbidity (e.g. cerebral palsy). An important drawback of electronic
fetal monitoring is that it increases the number of instrumental vaginal deliveries and
caesarean sections performed. This increases maternal morbidity and mortality for no
improvement in long-term neonatal outcome.
Interpretation of the CTG: the CTG consists of parallel tracings of uterine activity
and FHR. The physiological basis for monitoring FHR to detect developing acidosis is
that FHR is under the control of the autonomic nervous system. As a fetus becomes
hypoxic, and eventually acidotic, the autonomic nervous system is affected before
the CNS develops permanent injury. Changes in the FHR may therefore be seen
before permanent damage has occurred. The following elements are considered when
interpreting the CTG:
background risk to the pregnancy
presence and frequency of contractions
baseline rate (normal range 110150 beats/minute at term)
baseline variability (normal range 1025 beats/minute)
presence or absence of accelerations in the FHR
presence or absence of decelerations in the FHR.
Figure 1 shows a normal CTG from a low-risk pregnancy illustrating the signs of fetal
health. The baseline rate is 135 beats/minute and the baseline variability is 1520
beats/minute. Accelerations in the FHR are present and there are no decelerations.
Such a CTG is described as reactive or reassuring as it is a reliable indication that
the fetus is not acidotic.
CTG changes that may indicate developing acidosis include:
a rising baseline rate
decrease in baseline variability
lack of accelerations
presence of decelerations.
Decelerations are classified as early, variable or late depending on their relationship
to the timing of contractions and are of differing significance. Late decelerations start
after the contractions begin, reach their nadir after the contraction peaks and recover
after the contraction has finished. This type of deceleration is most strongly associated
with fetal acidosis.
A CTG indicating possible acidosis may be described as abnormal or non-
reassuring. There is a high false-positive rate for diagnosing acidosis from the CTG
(over 50%) and the term fetal distress should be avoided because it is emotive and a
less accurate description of the information conveyed by the CTG than non-reassuring.
Fetal scalp blood sampling

The CTG should be regarded as a screening tool for fetal acidosis and a suspicious
CTG requires further investigation or delivery if this is impossible. Once the cervix has
dilated beyond 3 cm it is usually possible to obtain a sample of blood from the fetal
scalp, which can be analysed for pH and base deficit. In the UK, a scalp pH less than
7.2 is an indication for delivery, though this is arbitrary. There is no significant increase
in risk of neurological deficit in the neonate until the pH falls below 7.0 and the base
deficit is above 16 mmol/litre, which indicates a metabolic acidaemia. The use of fetal
scalp blood sampling has not been shown to improve fetal outcome but rather to reduce
the rate of operative delivery and thus maternal morbidity by allowing identification of
the numerous cases where the CTG is non-reassuring but the fetus is not acidotic.
Umbilical cord gases

After birth, blood can be taken from the arteries and vein of the umbilical cord and
analysed for pH, base deficit and partial pressure of carbon dioxide, providing an
indication of whether the fetus was acidotic in utero and, if so, whether this was
respiratory or metabolic in origin. This is unnecessary if the neonate is vigorous and
obviously healthy at birth but may provide useful information if the neonate shows signs
of compromise. Good recovery from a respiratory acidosis is the rule but the risk of
neurological deficit is raised in significant metabolic acidosis as described above.
FURTHER READING
Enkin M, Keirse M J N C, Neilson J, Crowther C, Duley L, Hodnett E, Hofmeyr J.
Effective Care in Pregnancy and Childbirth. Oxford: Oxford University Press, 2000.
Gibb D, Arulkumaran S. Fetal Monitoring in Practice. Oxford: Butterworth-Heinemann,
1997.
MacLennan A. A Template for Defining a Causal Relation between Acute Intrapartum
Events and Cerebral Palsy: International Consensus Statement. BMJ 1999; 319: 1054
9.

Ethical Issues in Obstetric
Analgesia
Cleave W Gass
Cleave W Gass is Consultant Obstetric Anaesthetist at St Georges Hospital, London.

After completing undergraduate medical education at the University of Cape Town,
South Africa, he trained in anaesthetics at the St Georges School of Anaesthesia,
There has been a shift away from the paternalistic attitude that doctor knows best to
a more patient-focused view, respecting the patients autonomy to make choices about
the treatments they receive. This requires doctors to explain the various treatment
options to patients as well as the risks involved, so that patients may make an informed
choice. In obstetrics particularly, documents such as Changing Childbirth have stated
that women should be encouraged to express their views and expectations regarding
labour and treatments they would prefer in labour, and these should be met in most
cases.
The obstetric anaesthetist is likely to be faced with numerous ethical dilemmas,

revolving around the ability of a woman to give truly informed consent in labour, which
is a period of intense discomfort and anxiety for some women. Additionally, women
may have received opiates (e.g. pethidine) before having to make a choice, which could
limit their ability to give truly informed consent to anaesthetic interventions in labour. A
further ethical complication is the presence of the fetus, especially if there is conflict
between the womans wishes and the optimal outcome for her child. There are also
ethical concerns about research on pregnant women. Nationally, anaesthetists may
be involved in resource allocation and setting standards of care for women in labour,
as well as being required to participate in the National Enquiries into Maternal Death,
which may involve issues of confidentiality.
Consent issues in labour

Undertaking a procedure without consent constitutes battery under English law. It is
difficult to obtain informed consent for epidural analgesia from the labouring parturient.
Ideally, information about proposed anaesthetic interventions in labour should be given
before labour begins, but this is not common practice in the UK. A recent study showed
that recall of the risks of epidural analgesia was better in women who had attended
antenatal education classes than in those who received the information in labour,
though the overall recall of information was poor.
Birth plans
Difficulties may arise if a woman has made a birth plan before labour refusing epidural
anaesthesia, particularly if there are disagreements between previously expressed
wishes and currently expressed desires. Scott maintains that it would be unethical
not to provide epidural anaesthesia in these circumstances. However, she cites a
case in which an anaesthetist was threatened with physical violence by a woman's
partner should an epidural be performed contrary to her prior expressed wishes. Some
commentators have compared birth plans with advance directives made by patients
in other circumstances (e.g. not to undergo cardiopulmonary resuscitation in certain
circumstances). Legally, this situation has not been tested in the UK in pregnancy. In
the USA, pregnant women are specifically excluded from the effectiveness of any such
declarations while they are pregnant. Therefore, while a birth plan may be taken into
account when deciding on epidural anaesthesia, a woman has the right to deviate from
this plan at any stage of her labour and the prudent anaesthetist should obtain as valid
a consent as applicable in the particular circumstances at that time.
Human Rights Act 1998

The introduction of the Human Rights Act may result in the definitions of informed
consent and negligence being challenged. Obstetric anaesthetists should be familiar
with the provisions of the Act. Informed consent will probably change to the model used
in the USA in which patients are informed of every risk, no matter how minuscule.
Forced obstetric intervention

The way English Courts have regarded enforced caesarean section cases has
developed from the highly paternalistic view taken in Rochdale Healthcare (NHS)
Trust v C in which the judge held that a woman who was in labour was incompetent to
make a decision if she was prepared to accept death rather than undergo a caesarean
section. It is now recognized that a woman carrying a fetus is entitled to the same
respect as any other woman and that refusal of medical treatment can be for any
reason, rational or irrational, or for no reason at all.
Under English law, a fetus has no legal status and this concept has been re-affirmed
many times in various cases. There is no justification therefore in acting on behalf of
the unborn child in these decisions. It is important that anaesthetists recognize that
stringent conditions must be satisfied in order that an enforced caesarean section be
undertaken, and that if they provide anaesthesia to a competent woman who is refusing
an obstetric intervention, they may be accused of battery. An excellent summary of
the law and ethics of enforced caesarean sections in the UK can be obtained from
the Royal College of Obstetricians and Gynaecologists website at www.rcog.org.uk/
guidelines/ethics/ethics.htm.
Research on pregnant women

Anaesthetists involved in research on pregnant women must ensure that there are no
unnecessary risks to the woman or the fetus. Some commentators have suggested that
the standards for obtaining ethical committee approval for research involving pregnant
women should be more stringent. A full explanation of the research aims should be
provided and informed consent obtained from the women involved. Failure to do so may
leave the anaesthetist open to charges of trespass and battery.
Analgesia for pregnant women

Resource allocation: anaesthetists should ensure that all women have equal access
to the provision of safe analgesia and anaesthesia during labour. In the UK, the
Obstetric Anaesthetists Association and other national bodies have responsibility to
ensure that training and anaesthetic service in labour wards are of a uniformly high
standard. Some anaesthetists may be involved in resource allocation for their hospital
or at a national level. Most healthcare service resource allocation is still provided by
the medical profession, which is considered to have a largely male perspective in its
approach to womens health issues. Resources should be distributed fairly, in a non-
discriminatory manner.
Confidentiality must be maintained at all times. Anaesthetists may be required to

submit data to various bodies, such as the National Enquiries into Maternal Death.
The duty of confidentiality must be maintained after death and the anaesthetist should
ensure that no aspects of the case could identify the woman or the hospital involved.
Analgesia for abortion: anaesthetists may be asked to provide analgesic services

for women undergoing third-trimester abortions. Scott argues that it would be morally
wrong to accept a post knowing that one could not possibly undertake all the duties
implied in the job description. The present author does not think that doctors should be
compelled to provide services that go against their own beliefs. Senior anaesthetists
involved in the provision of labour ward analgesia services should ensure that no
anaesthetist is forced into a situation in which their own moral code may be violated.
Alternative anaesthetists should be sought at an early stage to ensure that women
receive analgesia without compromising any individuals beliefs. u
FURTHER READING
Expert Maternity Group Department of Health. Changing Childbirth. London: HMSO,
1993.
Mason J K, McCall Smith R A, Laurie G T. Law and Medical Ethics.

5th ed. London: Butterworths, 1999.
Scott W E. Ethics in Obstetric Anaesthesia. Anaesthesia 1996; 51: 71718.
Scott W E. Anaesthesia and Pregnancy. In: Scott W E, Vickers M D, Draper H, eds.

Ethical Issues in Anaesthesia. Oxford: Butterworth-Heinemann, 1994.
Swan H B, Borshoff D C. Informed Consent Recall of Risk Information Following

Epidural Analgesia in Labour. Anaesth Intens Care 1994; 22: 13941.

Failed Intubation in Obstetrics
Samyuktha K Backe
Gordon R Lyons
Samyuktha K Backe is Senior Registrar training in the Northern Ireland Deanery and
is currently on a years sabbatical as a Research Fellow in Obstetric Anaesthesia at
St James University Hospital, Leeds. She qualified from Madras University, India, and
trained in anaesthesia in the UK.
Gordon R Lyons is Consultant Obstetric Anaesthetist at St James University Hospital,

Leeds, UK. He qualified from the University of Leeds. His research interests are
clinical obstetric anaesthesia,epidural local anaesthetics and thromboelastography in
the obstetric setting.
In the UK, between 1979 and 1987, failed intubation was a common cause of direct
anaesthetic maternal deaths (Figure 1). In the past 20 years, anaesthetic practice has
seen a rise in the use of regional anaesthesia, an increased number of caesarean
sections, the routine use of pulse oximetry and capnography and the appointment of
anaesthetists with a commitment to obstetrics. Parallel to these changes, anaesthetic
maternal mortality has declined sharply.
In practice, the relative impact of the changes on the decrease in maternal deaths
is speculative. An audit in the authors teaching hospital from 1981 to 1999 showed
that caesarean deliveries increased from about 400 to 900 per year. Over the same
period, the number of general anaesthetics fell from 300 to 20 per year. In the UK, a
survey of 31 obstetric units showed a doubling of emergency caesarean section rate
since 1982, but the absolute number of general anaesthetics remained about the same.
Increasingly, a general anaesthetic is chosen only for women at high risk and only if
urgent anaesthesia is required. This suggests that the decrease in maternal deaths
related to general anaesthesia is probably due to improved standards of practice rather
than simply the increased use of regional techniques.
The incidence of failed intubation in obstetrics is about 1/130300, which is eight
times the rate reported for the general patient population. The obstetric population
differs from the surgical population in that it includes young women, mostly with a full
set of teeth. Pregnancy is accompanied by changes in physiology that can promote
difficulties with intubation, increase the risk of aspiration and accelerate desaturation.
Oedema of the larynx due to capillary engorgement and increased total body water
in pregnancy is compounded by the venous distension of the head and neck that
accompanies the strenuous effort of labour. Pethidine delays gastric emptying and
mothers who have had opioids in labour are more likely to present with a full
stomach in theatre. Many of these factors coincide, resulting in an urgent general
anaesthetic occurring out of hours when organizational weaknesses will be exposed.
A full list of contributory factors is given in Figure 2.
The way in which these factors come together can be seen in an imaginary
scenario in which an anaesthetic trainee with 18 months experience is asked to do an
emergency caesarean section at night at short notice. The mother is distressed and
communication is difficult because she speaks little English. To circumvent problems
with communication the trainee elects to give a general anaesthetic. The theatre
technician is unfamiliar to the anaesthetist and with the set-up in the obstetric
theatre. Overconcern for fetal transmission of the drug leads to the administration
of an inadequate dose of thiopental (thiopentone). Cricoid pressure is applied with
enthusiasm resulting in a Cormack grade 4 view on laryngoscopy. Multiple attempts at
intubation with intermittent pauses to oxygenate follow until more senior help arrives.
Further attempts at laryngoscopy coincide with the lightening of anaesthesia and return
of muscle tone and regurgitation occurs.
Factors leading to failed intubation in pregnancy
Causes of increased difficulties of intubation

Full dentition
Large breasts due to engorgement and increased body fat
Increased total body water causing pharyngeal and laryngeal oedema
especially in women with pre-eclampsia
Engorgement of capillary mucosa
Left lateral tilt, or presence of badly placed wedge
Poorly applied cricoid pressure
Causes of increased risk of aspiration

Reduced oesophageal barrier pressure promoting reflux of oesophageal
contents
Opioid administration in labour leading to delayed gastric emptying
Factors leading to accelerated desaturation

Reduced functional residual capacity which is compounded in the supine
position
Increased maternal oxygen consumption
Organizational issues
Greater use of general anaesthesia out of hours and for sicker patients
24-hour service dependent on less experienced non-consultant staff
It is important to learn to recognize failure, so that a failed intubation drill can be

initiated. By starting the failed intubation drill promptly, hypoxia and aspiration may
be averted. Preoxygenation can assure survival for only 35 minutes and ventilation
has proved difficult in one of ten failed intubations. One working definition, intended to
avoid surgical intervention in the cant intubate cant ventilate situation is the inability to
intubate after a single dose of suxamethonium.
The American Society of Anesthesiologists (ASA) task force defined difficult tracheal
intubation as occurring when proper insertion of the tracheal tube with conventional
laryngoscopy requires more than three attempts or more than 10 minutes. While this
definition may assist audit, it does not help management. The Cormack and Lehane
classification of laryngoscopy (Figure 3) provides an immediate grading of difficulty that
can be used in a management plan.
Unanticipated difficult intubation is commonly associated with a Cormack grade
3 view, for which a gum elastic bougie is recommended, while with a grade 4
view, intubation is often impossible. The routine use of capnography should prevent
unrecognized oesophageal intubation, which can occur especially when intubation has
been blind. The two most likely causes for a grade 4 view are an obvious gross
anatomical abnormality or poorly applied cricoid pressure. In an otherwise healthy
pregnant woman, a grade 4 view is likely to be caused by the latter. Unanticipated
difficult intubation might be reduced by good preoperative assessment.
Airway assessment
Tests to assess the airway must be easy, rapid, accurate and performable at the
bedside. As no test is 100% accurate, higher sensitivity and specificity can be achieved
by combining several.
The three most commonly used predictors for difficult intubation are:
inability to view the posterior pharyngeal wall when mouth is opened wide and
tongue protruded
a thyromental distance less than 7 cm when head is fully extended
inability to protrude the jaw such that the lower incisors lie in front of the upper
incisors.
Frerk predicted difficulty in 14 out of 244 patients in a non-pregnant population using
the first two tests. At intubation, 11 proved difficult, of which 9 had been predicted,
giving a sensitivity of 81% and specificity of 98%.
Mallampatis original three-tier grading of oropharyngeal view was modified to four
by Samsoon and Young with grade 4 representing the most difficult. A significant
correlation exists between the Mallampati score and the Cormack and Lehane
laryngoscopy view. In 99% of the cases, grade 1 and grade 34 laryngoscopic views
were associated with class 1 and class 4 airways, respectively. Inter-observer variability
can be high, due to phonation, arching of the tongue, and performing the test in the
supine position. Wilsons five factors take into consideration the patients body weight,
inter-incisor gap, buck teeth, neck movement and receding mandible. Similar to
Mallampatis modified score, it showed a 50% chance of predicting difficult intubation
but the inter-observer variability was lower. Other potential risk factors such as short
neck and, missing, protruding or single maxillary incisors, have been reported to be
significantly associated with difficult intubation.
An assessment that summates anatomical characteristics is more likely to predict
problems accurately. If one test is abnormal it cautions the anaesthetist but if two
or more are abnormal then appropriate preparation should be made and an awake
intubation considered. The high false-positive values of these tests mean that the
anaesthetist is often faced with an anticlimax. This is a benign consequence and should
not deter clinicians from airway evaluation.
There is no preoperative test with 100% accuracy and the anaesthetist must be
prepared for unanticipated difficult intubation. A range of intubation aids should be
available. Particularly useful are a short-handled laryngoscope, McCoy laryngoscope
and tracheal bougie.
Technique
Tunstall described the first failed intubation drill in 1976. He proposed that if delivery
was not urgent, then general anaesthesia should be abandoned, the woman placed
in the head-down, left lateral position, and allowed to wake up before proceeding to
a regional technique. Urgent delivery proceeded only after stomach emptying with
general anaesthesia, using trilene and face mask. Personal experience has taught
us that stomach emptying in this situation is not easy and trilene has been replaced
by more acceptable and more rapid agents. There are as many expert opinions in
management as there are anaesthetists and many modifications of the drill now exist.
A general principle of any drill is that the time of greatest risk is not the time
to perform previously unattempted practical procedures. The drill should consist of
manoeuvres that are daily events for clinical anaesthetists. Management principles
should be based on common sense with the aim of maintaining maternal oxygenation
and survival.
Cricoid pressure: general anaesthesia should not be initiated without an anaesthetic

assistant who is trained to apply cricoid pressure. Before induction, cricoid pressure
is started and is increased firmly to a maximum of 30 Newtons or 3 kg force, which
should be sufficient to prevent regurgitation even from a gastric pressure of 40 mm Hg.
Forces greater than 40 Newtons, which can be easily misjudged even in trained hands,
can lead to airway obstruction, a poor view at laryngoscopy, and difficulty in passing
the tracheal tube. Before abandoning intubation it is worth releasing cricoid pressure
momentarily to assess if visualization of the airway improves.
Left lateral position: the original drill advocated the left lateral position. When
combined with the head-down position, the mouth is lower than the larynx and
pharyngeal pooling will spill out of the mouth before aspiration can occur. If it does
occur it is most likely that only one lung will be affected. Cricoid pressure is therefore
unnecessary. Also the tongue falls forward resulting in a better airway. However, there
are arguments against using the left lateral position.
Hand ventilation of the patient is more difficult because the counter pressure at the
occiput is lost.
Cricoid pressure cannot be given adequately.
Surgery or cricothyrotomy is impossible in this position.
Moving a heavy patient can be difficult.
A balanced practice would be to use the left lateral position if the airway is controlled
and a decision has been made to abandon general anaesthesia.
Laryngeal mask airway (LMA): though easy and atraumatic to insert, a LMA does
not protect against aspiration, and continuous cricoid pressure interferes with insertion
and placement. Without cricoid pressure, the LMA has been used routinely for elective
and emergency caesarean section in 224 women with a success rate of 99%. There
are reports of successful use of the LMA for failed intubation in caesarean section. On
balance, it seems that the LMA should have a place in the drill. Much of the debate
is based on arguments that are largely untested and founded either on opinion or
anecdote. The only outcome study of failed intubation in relation to caesarean section
used cricoid pressure and turned women on their side and head down, in the main
without the LMA. All women made a complete recovery. It seems that the measures
discussed above are unlikely to make a noticeable change to outcome, and use of any
drill is more important than the constituent parts. One example of a failed intubation drill
Cricothyrotomy: in a cant ventilate cant intubate situation, cricothyrotomy

is sometimes used. Surgical intervention, which includes cricothyrotomy and
tracheostomy, performed in haste, and by inexperienced personnel, has led to fatal
results. A cricothyrotomy kit should be simple, obvious, and should not require any
unfamiliar skills. The basic requirement of such a kit might be a large-gauge cannula,
which can be attached to the fresh gas outlet of the anaesthetic machine. Ventilation
is achieved by intermittently using the emergency oxygen flush of the anaesthetic
machine. In order to prevent barotrauma, every inflation should be followed by deflation
as oxygen escapes through the glottis. To maximize expiratory flow, an oral airway or
elevation of the mandible can be used.
Post-natal counselling
During follow-up, a detailed explanation is given, bearing in mind that failed intubation
in the obstetric setting does not guarantee that every subsequent intubation will fail. If
anaesthesia has been neglected in the heat of the moment, awareness is possible, and
specific questions should be directed to detect this.
Training issues
The decline in the use of general anaesthesia in obstetrics has reduced training
opportunities. One report shows that individual trainee exposure to general anaesthesia
for caesarean section has decreased from 23/year in 1983 to 5/year in 1998. There is
no evidence that this has affected standards, but complacency would be misplaced.
FURTHER READING
Cooper S D, Benumof J L, Reisner L S. The Difficult Airway: Risk, Prophylaxis and
Management in Obstetric Anesthesia. In: Chestnut D H, ed. Obstetric Anaesthesia:
Principles and Practice. St Louis: Mosby, 1994; 577605.
Cormack R S, Lehane J. Difficult Tracheal Intubation in Obstetrics. Anaesthesia 1984;

39: 110511.
Hawthorne L, Wilson R, Lyons G R, Dresner M. Failed Intubation Revisited: 17 year

Experience in a Maternity Unit. Br J Anaesth 1996; 76: 6804.
King T A, Adams A P. Failed Tracheal Intubation. Br J Anaesth 1990; 65: 40014.
McGrady E. Problems with Intubation. In: Lyons G R, Russell I F, eds. Clinical Problems
in Obstetric Anaesthesia. London: Chapman & Hall Medical, 1997; 13348.

Maternal Analgesia,
Anaesthesia and the Fetus
Felicity Reynolds
Felicity Reynolds is Emeritus Professor of Obstetric Anaesthesia at St Thomas

Hospital, London. She has published four books and over 200 articles on obstetric
analgesia, placental drug transfer and related topics. She was awarded the FRCOG in
1995. Since retirement she has continued with writing, editing and clinical research.
Although natural labour is painful, such pain has little value and is potentially detrimental
to the fetus. Some mechanisms for this detriment are outlined in Figure 1. Reducing
labour pain is therefore of potential benefit to the baby.
Drugs given to a parturient may have a direct effect on the baby after crossing the
placenta, and an indirect effect via changes in maternal physiology and biochemistry.
Systemic analgesia depends on an effective concentration of drug in the maternal
blood. Since any compound that crosses the bloodbrain barrier also crosses the
placenta, such an approach is likely, given time, to affect the fetus as well as the
parturient. Regional analgesia does not depend for its effect on the presence of
analgesic drug in the maternal circulation, therefore a direct drug effect on the baby is
less likely. However, regional analgesia may produce changes in maternal physiology or
biochemistry that can affect the baby indirectly. It is seldom appreciated that regional
analgesia, properly handled, is not only more effective than systemic analgesia, but
also safer for the baby.
Potential adverse effects of maternal labour pain on

the fetus

Placental drug transfer
Drugs used for anaesthesia and analgesia cross the placenta by passive diffusion.
In this respect the placenta behaves like other lipid membranes, allowing lipophilic
particles up to a molecular weight of 6001000 (encompassing most drugs but not
plasma proteins) and polar substances up to 60100 to cross readily. Therefore, drugs
used to provide systemic and regional analgesia cross the placenta readily in the
unbound and non-ionized state, while hydrophilic substances such as neuromuscular
blocking drugs, diffuse slowly and are unlikely to attain effective concentration in the
fetus.
The transplacental distribution of lipophilic substances, whose unbound and non-
ionized moiety equilibrates readily across the placental membrane, is influenced by
the trans-placental gradient for pH and binding protein (Figure 2). As fetal plasma pH
is lower than maternal, free base tends to concentrate on the fetal side due to ion
trapping, the reverse being true for weak acids. This increases the exposure of the
acidotic fetus to basic drugs such as opioid analgesics and local anaesthetics.
Acidic drugs are bound mainly to albumin, which shows little transplacental gradient.
While a few basic drugs are also bound to albumin, the principal binding protein is
1-acid glycoprotein, the concentration of which is variable, but always much lower
in fetal than in maternal plasma. Figure 3 shows the physicochemical properties and
characteristic equilibrium fetal:maternal ratios of some basic drugs, with antipyrine,
which is neither ionized nor protein-bound, for comparison. For drugs mainly bound
to 1-acid glycoprotein, equilibrium fetal:maternal ratio is inversely related to binding.
Figure 2 illustrates how such a ratio may be predicted. Although diffusion is no bar to
the transfer of lipophilic drugs, the fetal compartment is deep, and equilibration takes
longer in fetal than in maternal tissues. Fetal exposure is therefore dependent on blood
flow on either side of the placenta (so-called flow-dependent transfer), equilibrium
ratios and duration of maternal exposure.
Although the immediate effect of the drug is related to the concentration of
the free moiety, a large albumin-bound component represents a storehouse for the
newborn. Albumin binding, moreover, tends to decline in the first postnatal days,
thereby exacerbating the many adverse effects of a drug such as diazepam.
Placental transfer of hydrophilic substances is slower, permeability-dependent and
inversely related to molecular size. Thus, if given in normal doses during general
anaesthesia for caesarean section, neuromuscular blocking drugs do not achieve
effective concentrations in fetal plasma. Even if polar compounds are given to a mother
over a long period, they never reach high concentration in fetal plasma because they
are rapidly excreted by the kidney and accumulate instead in amniotic fluid.
Physicochemical and pharmacokinetic characteristics of some basic drugs

Molecular pKa1 Partition Adult protein Fetal:maternal
weight coefficient2 binding (%) ratio
Antipyrine 188 1.5 1.7 0 1.0
Pethidine 251 8.5 20 604 13
Lidocaine (lignocaine) 234 7.9 39 754 0.55
Alfentanil 416 6.5 70 914 0.3
Bupivacaine 288 8.1 250 944 0.3
Diazepam 285 3.4 310 955 2.0
Fentanyl 336 8.4 550 885 1
1
The higher the pKa the stronger the base.
2
Approximate oleyl alcohol/buffer partition coefficient.
3
The fetal:maternal plasma ratio for pethidine rises with time to exceed unity in 3 hours or more.
4
Principally bound to 1-acid glycoprotein.
5
Diazepam is bound principally to albumin and fentanyl to a mixture of plasma proteins.
Systemic opioid analgesia
Most studies of the fetal and neonatal effects of maternal systemic opioid analgesia
relate to pethidine, which is the most widely used agent. It may cause loss of short-term
variability in the fetal heart trace, and reduced muscular activity, aortic blood flow
and oxygen saturation, largely via a direct effect. Pethidine exacerbates the episodes
of maternal haemoglobin desaturation that normally occur during labour, which may
contribute indirectly to its detrimental fetal effects.
Large doses of pethidine are associated with low Apgar scores, while minor
degrees of neonatal depression from smaller doses may be undetected by this
method of assessment. Nevertheless, even small doses depress neonatal respiration.
Neurobehavioural scores are usually reduced while all neonatal effects are reversed by
giving naloxone to the baby. Detrimental effects may last for 72 hours or more after
delivery and are attributed principally to accumulation of norpethidine. Fetal:maternal
ratios of pethidine rise with time after intra-muscular administration (Figure 3), and
maximal fetal exposure occurs if pethidine is given to the mother 34 hours before
delivery, while effects are barely discernible if it is given only within 1 hour of birth.
There are few important differences between pethidine and other opioid analgesics,
though it has been claimed that meptazinol produces less neonatal depression.
Morphine and diamorphine may not be as dangerous for the baby as was once
supposed. Fentanyl, and more recently remifentanil, have been used systemically in
labour with less neonatal detriment than is seen with pethidine.
It is probably logical to administer naloxone to every baby whose mother has
received opioid analgesics during labour.
Nitrous oxide
Nitrous oxide is not only a slightly less ineffective analgesic in labour than pethidine, it is
also less cumulative and less harmful to the baby, who can excrete it via the lungs once
born. Nevertheless, in an attempt to obtain maximum analgesia from it, a parturients
natural tendency to hyperventilate during contractions may be encouraged, resulting
in hypoventilation and consequent desaturation between contractions, thus potentially
exacerbating the detrimental fetal effects outlined in Figure 1. When nitrous oxide
is combined with 50% oxygen as Entonox, the oxygen may partly offset this effect,
though if supplementary oxygen is needed to treat a distressed fetus, administration
should be continuous rather than intermittent. Prolonged administration of nitrous oxide
is associated with inhibition of the enzyme methionine synthase, a theoretical risk for
the fetus.
Despite these theoretical disadvantages, maternal analgesia using 50:50 nitrous
oxide and oxygen during labour has not been shown to produce any obvious neonatal
detriment.
Adjuncts to nitrous oxide analgesia: to improve analgesia during labour,

subanaesthetic concentrations of various volatile inhalational agents (trichloroethylene,
methoxyflurane, enflurane and currently isoflurane) have been tried, alone or in
conjunction with nitrous oxide. There is some gain in analgesic efficacy, with little
obvious neonatal detriment, though higher concentrations have caused neonatal
sedation.
Regional analgesia
Direct effects
Adverse direct drug effects on a baby are likely to be observed only if maternal systemic
effects reach a detectable threshold. Thus, when lidocaine (lignocaine) was used to
provide continuous epidural analgesia, toxic effects were observed in both mother and
baby. The longer action of correctly sited bupivacaine denotes slow absorption and thus
favours a local over a systemic effect; the latter is usually observed only after accidental
intravenous administration. Although opioids are well recognized to produce direct fetal
and neonatal depression when used systemically, their potential to do so when used for
regional analgesia is more debatable.
Indirect effects
Following regional analgesia, indirect effects are more likely to be clinically important.
Regional blockade, as the only reliable form of labour analgesia, can block the
detrimental fetal effects of pain shown in Figure 1. It does, however, have circulatory
effects that may be beneficial or otherwise and are summarized in Figure 4. Provided
maternal aortocaval compression and hypotension are avoided, the occurrence of a
significant increase in maternal placental flow following epidural local anaesthetic is
well documented, and is particularly consistent in the presence of pre-eclampsia. With
correct management of the mother, adverse fetal effects are unlikely. Although regional
analgesia may prolong labour, there is no evidence that this is harmful to the fetus.
Fetal heart rate

The value of continuous fetal heart rate monitoring in labour is often questioned,
but cardiotocography is usually considered mandatory for mothers receiving regional
analgesia. As a consequence, numerous fetal heart changes have been observed
after the institution of epidural and intrathecal analgesia. Recently, loss of short-term
variability, decelerations and major bradycardias have been reported following opioids,
particularly given intrathecally. In randomized studies, however, such changes are no
more common than after epidural bupivacaine, while meta-analysis of controlled trials
shows that fetal heart abnormalities are no more common after epidural than after
systemic opioid analgesia.
Fetal bradycardia has been associated with the rapid onset of analgesia, and various
mechanisms have been considered to explain this, even though a causal relationship
has not been established. Maternal placental flow ceases during a uterine contraction.
At least some of the bradycardias in question are associated with uterine hypertonus,
which is thought to result from a decline in the circulating adrenaline (epinephrine)
concentration, itself a myometrial inhibitor (Figure 4). Direct fetal effects from the
opioids (unlikely with intrathecal doses), plus maternal hypotension and hypoventilation
are possible factors, though unlikely to be unnoticed.
Several points should be borne in mind.
If local anaesthetic is omitted in the loading dose, and intrathecal opioid given alone,
then there will be no sympathetic blockade to cause uterine vasodilatation (Figure 4).
Fluid infusion before inducing regional analgesia has become less fashionable. A
fluid preload has been shown to inhibit uterine contractions and to reduce the incidence
of fetal heart decelerations. Uterine hypertonus is, therefore, theoretically more likely to
occur in the absence of preload.
Although a good midwife will continue to monitor the fetal heart, the external
tocodynamometer belt is commonly removed before siting an epidural needle. Unless
the belt is replaced quickly after the procedure, with the onset of analgesia uterine
contractions will be undetected.
There are occasions when the obstetrician is keen to continue the administration of
oxytocin without a break. This should be resisted during epidural insertion in order to
avoid the adverse situation outlined in Figure 5.
Whether such cardiotocographic changes are associated with adverse neonatal
outcome is unsure, but at times decelerations have been so prolonged as to prompt
caesarean section. Provided the changes are brief and do not reflect poor placental
perfusion resulting from uterine hypertonus, maternal hypotension or aortocaval
compression, their presence is probably irrelevant to fetal outcome.
Administration of oxytocin
Fetal and neonatal acidbase status

Cord blood gas and acidbase balance reflect in utero status but give little indication
of a newborns ability to sustain adequate respiration and circulation. Umbilical vein
values reflect placental exchange, while umbilical artery values indicate the status of
fetal tissue more accurately, though the two are closely related.
Normal labour, associated as it is with maternal pain, stress and tension, may cause
progressive maternal respiratory alkalosis and metabolic acidosis (Figure 1). These
changes tend to be mirrored in the fetus, while any reduction in placental exchange may
increase the transplacental gradient for oxygen, [H +] and fixed acids. This gradient is
also increased during the second stage, particularly with expulsive efforts. Alleviating
pain, therefore, has a variable effect on fetal pH, but base excess is more consistently
improved. This is confirmed by meta-analysis of trials comparing epidural with systemic
opioid analgesia (Figure 6), which also suggest a protective effect of epidural analgesia
in long labour.
Apgar score
Apgar score is strongly influenced by the intrauterine environment and can be used only
during the first 10 minutes of life, which is a highly stimulating time for the newborn, so
subtle degrees of neonatal depression may be undetected. Nevertheless, meta-analysis
of controlled trials showed that there were significantly fewer low Apgar scores at both 1
and 5 minutes with epidural than with systemic opioid analgesia.
Neurobehavioural assessments
Over the years, various tests have been developed to assess the newborn further
into the postnatal period. The most popular with anaesthetists the neurological
and adaptive capacity score (NACS) may not be the most sensitive or reliable.
Studies have shown epidural local anaesthetic to be associated with neurobehavioural
scores that are variously lower, similar or higher than systemic or no analgesia, while
meta-analysis of randomized trials revealed no significant difference in NACS scores
between epidural bupivacaine and systemic opioid analgesia, though slightly favouring
babies in the epidural group.
Similarly variable results are seen when plain bupivacaine is compared with low-
dose combinations of local anaesthetic and opioid. Dose-related effects have been
demonstrated for epidural sufentanil and alfentanil, but not for fentanyl, though its use
has been occasionally associated with slightly reduced NACS.
Neonatal respiration
Epidural analgesia using bupivacaine, unlike systemic pethidine, is not associated
with any depression of neonatal respiration, but the question arises whether neuraxial
opioids might reintroduce this danger. Painstaking studies of neonatal respiration
have not revealed any obvious detriment from epidural fentanyl infusion, although
unnecessarily large doses of neuraxial opioid by bolus or infusion should probably
prompt neonatal naloxone administration.
Maternal anaesthesia
It is generally agreed that regional anaesthesia is not only safer than general
anaesthesia for the mother but also preferable for the sake of the baby. This is largely
true, although with carefully conducted anaesthesia there may be little to choose
between them.
General anaesthesia
All general anaesthetic drugs, whether used for induction or maintenance, will
accumulate in fetal tissues for about 2040 minutes, thus if surgery is delayed or
prolonged, the baby may be born sedated. This is of little importance, however,
compared with asphyxia. It is therefore more important for the baby that the mother
receiving general anaesthesia should be induced in a calm stress-free environment,
with adequate doses of all agents. Awareness represents a further major stress
potentially far more damaging to the fetus than a little fully reversible anaesthesia.
Propofol is unsuitable for induction of anaesthesia before operative delivery. Too
small a dose risks maternal awareness with all its attendant dangers, too big a dose
depresses the fetus more than thiopental (thiopentone), and an intermediate dose risks
both maternal awareness and neonatal depression.
Regional anaesthesia has been associated with higher Apgar scores and less neonatal
acidosis than general anaesthesia after both elective and emergency caesarean
section, but nowadays the difference may be slight. Interestingly, in most comparative
studies, neonatal acidosis is more severe with spinal than with epidural anaesthesia.
For epidural use, bupivacaine is likely to be safer for the baby than lidocaine
(lignocaine), but details of anaesthetic technique may be of less importance to neonatal
welfare than other factors.
Other factors in neonatal well-being

Other factors to be considered in neonatal well-being are:
aortocaval compression to avoid this a wedge may be better able to
produce something approaching the prescribed 15 left tilt than tilting the table
(most tables only reach 10 tilt)
maternal circulatory status prolonged maternal hypotension may result in fetal
acidosis
maternal oxygen and carbon dioxide tension
maternal stress
slow surgery particularly uterine incision to delivery interval
fetal status before starting the procedure.
FURTHER READING
Halpern S H, Leighton B L, Ohlsson A, Barrett J F R, Rice A. Effect of Epidural vs
Parenteral Opioid Analgesia on the Progress of Labor. JAMA 1998; 280: 210510.
Consider all these factors before allowing anaesthesia to be blamed for neonatal
depression. A baby depressed by drugs is easily resuscitated.

Medical Diseases
Complicating Pregnancy
Hassan A Shehata
Catherine Nelson-Piercy
Hassan A Shehata is Consultant and Senior Lecturer in Obstetric Medicine at Epsom

and St Helier Hospital, Surrey. He qualified from Khartoum University, Sudan, and
trained in general obstetrics and gynaecology in the South West Thames Region based
mainly at St Georges Hospital, London. He trained in obstetric medicine at St Thomas
Hospital. His research interest is in haematological problems in pregnancy and he
is currently involved in a study of carbohydrate metabolism in pregnant women with
obstetric cholestasis.
Catherine Nelson-Piercy is Consultant Obstetric Physician at Guys and St Thomas

Hospitals and Whipps Cross Hospital, London. She qualified from Cambridge University
and St Bartholomews Hospital, London, and trained in obstetric medicine at Queen
Charlottes and University College Hospitals, London. Her research interests include
obstetric cholestasis, thromboembolism and hyperemesis.
In the most recent Report on Confidential Enquiries into Maternal Deaths in the UK
covering 19941996, the leading causes of direct maternal deaths are thromboembolic
disease (46 patients), hypertension (20), early pregnancy loss (14), haemorrhage (12),
amniotic fluid embolism (17), genital tract sepsis (14) and death from anaesthesia (1).
This pattern shows little change from the previous triennium. Heart disease (28) is
a major cause of indirect death. Other causes of indirect death include epilepsy (19)
and asthma (3).
Thromboembolic disease
In the UK, thromboembolic disease remains the leading cause of maternal mortality,
accounting for 36% of direct deaths. The rate was 2.1 deaths per 100,000 maternities
in 19941996 and is increasing. Thromboembolic disease may occur at any gestation,
and healthcare professionals should have a low threshold for investigating leg or chest
symptoms in pregnant women.
A thromboembolic event occurs in 1/1500 pregnancies. Antenatal deep vein thrombosis
(DVT) occurs in 0.060.09% of pregnancies, being twice as common in women over
35 years. In the puerperium DVT is also related to maternal age and mode of delivery.
Pulmonary emboli are more common in the puerperium, especially following caesarean
section.
Physiological changes of the coagulation system in pregnancy: the risk of

thromboembolic disease is increased six-fold in pregnancy. There is an increase in
coagulation factors I (fibrinogen), V, VII, VIII, IX, X, XII, von Willebrand factor antigen
and ristocetin cofactor activity and a decrease in some endogenous anticoagulants
(antithrombin, protein S and activated protein C ratio) which is most marked near term
and following delivery. Fibrinolysis is impaired during pregnancy.
Peripheral vasodilatation occurs in normal pregnancy, resulting in a marked fall in
velocity of blood flow. This fall is most marked in women undergoing caesarean section.
It also occurs to a greater extent in the left femoral vein compared with the right.
This is secondary to compression of the left iliac vein by the right iliac artery and the
ovarian artery, which cross the vein only on the left side, leading to the predominance of
left-sided (85%) DVTs in pregnancy.
Management
Ante-partum: every pregnant womans risk of thromboembolic disease should be
assessed at booking, by establishing whether she has a personal or family history.
In addition, every pregnant woman who enters a high-risk situation should have
her risk re-evaluated. Prophylactic treatment for thromboembolic disease should be
offered to women at high risk. Women who have experienced a thrombosis during
pregnancy should be closely followed up, preferably by a doctor with an interest in the
management of thrombosis in pregnancy.
Previous thromboembolic event women who have had a single previous
thromboembolic event, have no family history and a negative thrombophilia screen
should take aspirin, 75 mg/day, throughout pregnancy and low molecular weight
heparin (LMWH) at a thromboprophylactic dose (e.g. dalteparin sodium, 5000 U/day
subcutaneously) from the onset of labour until 6 weeks post-partum. Women who have
had more than one thromboembolic event or who have had a single event but have
a positive family history or thrombophilia screen should take prophylactic LMWH from
early pregnancy until 6 weeks after delivery.
Positive thrombophilia screen increasingly, women discover they have a
thrombophilia when a family member is screened. The risk of thrombosis in the
presence of thrombophilia is lower in those with a family rather than a personal history
of thromboembolic disease. It may be appropriate to give low dose aspirin antenatally.
Thromboprophylaxis should be determined on an individual basis, but these women
require LMWH if they undergo caesarean section.
High-risk obstetric guidelines in 1995, the Royal College of Obstetricians
and Gynaecologists issued guidelines relating to thromboprophylaxis in pregnancy,
including treatment following caesarean section (Figure 1). Each unit should have a
locally agreed policy, based on these guidelines, which is strictly adhered to. Many
hospitals give thromboprophylaxis to most, if not all, women undergoing caesarean
section.
Acute episodes it is essential to confirm or exclude a diagnosis of thrombosis
with objective testing. Data from non-pregnant individuals suggest that 16% of patients
with untreated DVT develop pulmonary embolus, and 13% of these die, though
anticoagulation reduces the risk. Thus, a positive diagnosis of thrombosis requires
immediate management, but because the treatment is not without risk, it is vital that
the diagnosis is confirmed.
Chest radiography seldom diagnoses pulmonary embolism but may reveal other
causes of dyspnoea or chest pain. It should not be withheld solely because of the
pregnancy, and can be performed with the knowledge that the amount of radiation is
negligible (Figure 2).
Arterial blood gas analysis should be performed in the sitting or left lateral position
because in the supine position, inferior vena caval compression by the gravid
uterus and functional reduction in pulmonary residual capacity and closing
volume may give a false impression of hypoxia. In uncomplicated pregnancy,
the partial pressure of oxygen is unchanged or increased, compared with the
non-pregnant situation, but falls by about 2 kPa (17 mm Hg) when lying
supine. The partial pressure of carbon dioxide in normal pregnancy falls from
5 kPa (3540 mm Hg) to 4 kPa (30 mm Hg).
ECG lacks specificity, but shows a sinus tachycardia if pulmonary embolism is
present. D dimers may be elevated in pregnancy as a result of the prothrombotic
changes that occur and are therefore unreliable. There should be a low threshold for
performing Doppler ultrasound of the femoral veins or lung ventilation and perfusion
scanning (Figure 2).
If a DVT or pulmonary embolus is diagnosed (or strongly suspected),
anticoagulation with heparin should be commenced. Warfarin should not be used in the
first-line management of thromboembolic disease in pregnant women: it is teratogenic
in the first trimester, increases the risk of miscarriage and stillbirth, anticoagulates the
fetus and increases the risk of spontaneous haemorrhage (especially intracerebral) in
utero. Both, heparin and warfarin are safe during lactation.
When an intravenous infusion of unfractionated heparin is used for acute treatment,
chronic-phase treatment is commenced after 57 days. This is given traditionally
as unfractionated heparin 10,000 U b.d. subcutaneously, because the standard non-
pregnant dose of 5000 b.d. is insufficient. LMWH is effective and safe in pregnancy,
and it is used for treatment and prophylaxis. If used for treatment, it is continued
in therapeutic doses to complete 612 weeks of therapy depending on individual
circumstances and local policy. It is then replaced by a once daily prophylactic dose of
LMWH (e.g. enoxaparin, 40 mg, dalteparin sodium, 5000 U, tinzaparin, 50 U/kg) which
is continued until 6 weeks postnatally. For pulmonary embolism or extensive iliofemoral
DVT, intravenous unfractionated heparin may be used as first-line treatment in the acute
phase until there is enough evidence for the efficacy of LMWH in pregnancy in these
circumstances.
Thromboprophylaxis at caesarean section
Definition Management
Low risk
Elective caesarean section Early mobilization
Uncomplicated pregnancy Good hydration
No other risk factors
Moderate risk
Emergency caesarean section in labour Prophylactic stockings for
Age (> 35 years) thromboembolic disease
Obese ( > 80 kg) or subcutaneous heparin
Gross varicose veins
Current infection
Pre-eclampsia
Immobilization before caesarean section for more than 4 days
Major current illness (e.g. heart or lung disease, inflammatory
bowel disease, nephrotic syndrome, diabetes)
High risk
Three or more moderate risk factors Prophylactic stockings for thromboembolic disease
Extended abdominal or pelvic surgery plus subcutaneous heparin (commencing during
(e.g. caesarean hysterectomy) caesarean section and continuing for 5 days)
Personal or family history of thromboembolic disease
Positive thrombophilia
Paralysis of lower limbs
Source: Royal College of Obstetricians and Gynaecologists. Report of the RCOG Working Party on Prophylaxis against Thromboembolism in Gynaecology
and Obstetrics. London: Chameleon Press, 1995.
Estimated radiation to the fetus and increased risk of childhood cancer following common diagnostic
procedures1
Investigation Estimated radiation Probability of fatal cancer

to the fetus (mGy) to age 15 years
Conventional radiograph
Chest 0.01 < 1/1,000,000
Pelvis 1.1 1/300,000
Skull 0.01 < 1/1,000,000
Spine 1.7 1/20,000
CT
Chest (including spiral CT) 0.06 1/560,000
Pelvimetry 0.2 1/170,000
Nuclear medicine
Lung perfusion (technetium 99m) 0.2 1/170,000
Lung ventilation (technetium 99m) 0.3 1/110,000
1
The baseline UK national risk for cancer in the first 15 years of life is about 1/650, of which 50% is fatal.
Intra-partum: it is important to have a clear delivery plan including every possible

emergency situation. The plan should be clearly documented in the patients notes and
agreed by the woman, obstetrician, anaesthetist and haematologist/obstetric physician.
Most obstetric anaesthetists are willing to perform a regional blockade 12 hours
following the last LMWH dose. It is important to remember that removal of the epidural
catheter has a higher incidence of LMWH-related complications than insertion and
this should be delayed until at least 12 hours post LMWH dose. For women with
antithrombin deficiency, depending on the titre in the weeks leading up to delivery, an
antithrombin infusion may be required before and/or during labour.
Thrombolysis in non-pregnant patients, there is no clear evidence that
thrombolysis improves the clinical outcome of thromboembolic disease, and most
physicians reserve its use for critically ill patients. Experience of thrombolytic treatment
in pregnancy is even more limited. There is a significant risk of bleeding and it is
recommended for use only in life-threatening circumstances.
Post-partum: for women who had thromboembolic disease during pregnancy, a

thrombophilia screen should be performed after discontinuation of anticoagulation
treatment at least 6 weeks postnatally to assess the risk of recurrence, and to plan
management during future pregnancies. Warfarin does not pass into breast milk,
therefore women injecting heparin may wish to change to warfarin after delivery, once
the risk of post-partum haemorrhage has passed (up to day 5). However, they will
have to attend regularly for measurement of their prothrombin time. Contraception
should also be discussed. The oestrogen-containing combined oral contraceptive pill is
contraindicated in women who have had a thrombosis, but other forms of contraception
(hormonal and non-hormonal) are permissible.
Cardiac disease
In the UK, cardiac disease is the second most common cause of maternal death. The
physiological haemodynamic adaptation to pregnancy and delivery may place the
woman with cardiac disease at serious risk. In the most recent Report on Confidential
Enquiries into Maternal Deaths, 29% of the indirect deaths were a result of cardiac
disease, of which 26% were congenital, 21% ischaemic and 53% acquired. The
incidence of congenital heart disease in pregnancy is increasing, reflecting advances
in corrective surgery for severe defects. It is important to consider the womans risk of
ventricular failure (particularly when the right ventricle is acting as the systemic pumping
chamber) and any residual pulmonary hypertension. Paradoxical embolism through a
right-to-left shunt may cause cerebrovascular accidents in uncorrected Fallots tetralogy
and atrial septal defects. The incidence of rheumatic fever has declined, but rheumatic
heart disease, most commonly mitral stenosis, may present for the first time in pregnancy,
especially in immigrants.
Whatever the underlying cardiac problem, the ability to tolerate pregnancy and
delivery is related to the presence of cyanosis and pulmonary hypertension, the
haemodynamic significance of any lesion and the functional state (Figure 3). Cyanosis
alone may not be as important in predicting poor outcome as the association of
cyanosis with Eisenmengers syndrome, poor functional class, or both. Poor pregnancy
outcome is more likely if the woman is in a poor functional status (NYHA class III or
IV) regardless of the specific lesion. Conversely, those in functional classes I or II are
likely to do well in pregnancy. Each case must be assessed individually, but women
with certain conditions must always be treated as high risk. These include pulmonary
hypertension and Eisenmengers syndrome, severe aortic or mitral stenosis, Marfans
syndrome or cyanotic congenital heart disease.
New York Heart Association (NYHA) functional

classification
Grade I No breathlessness
Grade II Breathlessness on severe exertion
Grade III Breathlessness on mild exertion
Grade IV Breathlessness at rest
Cardiac disease
In the UK, cardiac disease is the second most common cause of maternal death. The
physiological haemodynamic adaptation to pregnancy and delivery may place the
woman with cardiac disease at serious risk. In the most recent Report on Confidential
Enquiries into Maternal Deaths, 29% of the indirect deaths were a result of cardiac
disease, of which 26% were congenital, 21% ischaemic and 53% acquired. The
incidence of congenital heart disease in pregnancy is increasing, reflecting advances
in corrective surgery for severe defects. It is important to consider the womans risk of
ventricular failure (particularly when the right ventricle is acting as the systemic pumping
chamber) and any residual pulmonary hypertension. Paradoxical embolism through a
right-to-left shunt may cause cerebrovascular accidents in uncorrected Fallots tetralogy
and atrial septal defects. The incidence of rheumatic fever has declined, but rheumatic
heart disease, most commonly mitral stenosis, may present for the first time in pregnancy,
especially in immigrants.
Whatever the underlying cardiac problem, the ability to tolerate pregnancy and
delivery is related to the presence of cyanosis and pulmonary hypertension, the
haemodynamic significance of any lesion and the functional state (Figure 3). Cyanosis
alone may not be as important in predicting poor outcome as the association of
cyanosis with Eisenmengers syndrome, poor functional class, or both. Poor pregnancy
outcome is more likely if the woman is in a poor functional status (NYHA class III or
IV) regardless of the specific lesion. Conversely, those in functional classes I or II are
likely to do well in pregnancy. Each case must be assessed individually, but women
with certain conditions must always be treated as high risk. These include pulmonary
hypertension and Eisenmengers syndrome, severe aortic or mitral stenosis, Marfans
syndrome or cyanotic congenital heart disease.
Management
Ante-partum: women with cardiac disease should be assessed before pregnancy.
Counselling regarding possible fetal and maternal risks and, in some women, the need
to avoid pregnancy, may be appropriate. Detailed assessment by an obstetrician,
cardiologist and obstetric anaesthetist with an agreed plan for delivery is crucial.
Women with congenital heart disease should be referred for a detailed fetal cardiac
ultrasound scan because the risk of a congenital heart defect (25%) is more than double
that of the general population. Some women require elective admission for bed rest to
maximize oxygen saturation. Maternal cyanosis and hypoxaemia may adversely affect the
fetus increasing the risks of intrauterine growth restriction, miscarriage and spontaneous
and iatrogenic prematurity. Serial assessment of fetal growth and well-being is appropriate.
If antidysrhythmics are required there is most experience in pregnancy with digoxin and
-blockers. Verapamil, adenosine and DC cardioversion are safe, and flecainide is safe in
the second and third trimesters.
Intra-partum: antibiotic prophylaxis to cover delivery is advocated for women with

structural heart defects. The exceptions are those with a repaired patent ductus arteriosus,
those with an isolated ostium secundum atrial septal defect, and those with mitral valve
prolapse without regurgitation. Prophylaxis is mandatory for women with artificial heart
valves and those who have had endocarditis.
Women should be nursed in the left or right lateral position. The supine and
lithotomy positions should be avoided to minimize the risk of pulmonary oedema. If
the mother has to be kept on her back, the pelvis should be rotated so that the
uterus drops forward, and cardiac output as well as uteroplacental blood flow are
optimized. Continuous ECG and oxygen saturation monitoring, and for certain patients,
more invasive monitoring with central venous and arterial cannulation, is required. Full
resuscitation facilities must be available.
Epidural anaesthesia and analgesia using incremental doses and with judicious
pre-loading are well tolerated in most conditions. Nevertheless, extreme caution is
needed in cases of limited stroke volume and left ventricular outflow tract obstruction
(e.g. aortic stenosis, hypertrophic cardiomyopathy). If a pudendal block is required
lidocaine (lignocaine) without adrenaline (epinephrine) should be used. Oxytocin
without ergometrine is recommended for management of the third stage. If there are
concerns regarding the need to avoid vasodilatation, this can be administered by small
increments of a dilute solution. Women should sit up as soon as possible after delivery.
Close and regular observation is required for at least 24 hours after delivery, and
transfer to a high-dependency or intensive care ward may be appropriate.
Post-partum: if the mother is well, breast-feeding is not contraindicated. Contraception

should be discussed together with the safety of future pregnancies.
Pulmonary hypertension
Pulmonary hypertension may be the result of lung disease (e.g. cystic fibrosis),
primary pulmonary hypertension, pulmonary veno-occlusive disease, or Eisenmengers
syndrome. The fall in systemic vascular resistance in pregnancy combined with the
fixed pulmonary vascular resistance (which usually falls in pregnancy) means that there
is an increase in right-to-left shunting and these women cannot increase pulmonary
blood flow to match the increased cardiac output.
Maternal mortality is 3050% in Eisenmengers syndrome, and pregnancy is
contraindicated. If a woman with significant pulmonary hypertension becomes
pregnant, termination should be offered. If this is declined, prophylactic heparin should
be given and bed rest and oxygen therapy instituted if hypoxia develops. Any systemic
hypotension or vasodilatation (such as intra-partum or post-partum haemorrhage or related
to anaesthesia) may lead to shunt reversal or increased right-to-left shunting, and should
be avoided by immediate volume replacement. Opinion varies as to whether these patients
should be delivered by elective caesarean section and whether regional anaesthesia is
safe. They should be managed in an ICU by anaesthetists, cardiologists and obstetricians
with expertise in the care of complicated heart disease. Any drug given to reduce
pulmonary artery pressure (other than inhaled nitric oxide) will also reduce systemic
pressures and the temptation to manipulate pulmonary artery pressure with vasodilators
should be resisted. For this reason, monitoring with arterial and central venous lines with
attention to adequate filling is recommended in preference to SwanGanz catheterization.
Most women with Eisenmengers syndrome who die as a result of their pregnancy, do
so after delivery.
Aortic stenosis
Aortic stenosis is unlikely to cause problems unless the gradient is severe (over 100
mm Hg in the non-pregnant state). The risks are angina, hypertension, heart failure and
sudden death. Symptoms (e.g. angina, dyspnoea, syncope) as well as hypertension
may be controlled with -blockers, provided left ventricular function is good. The
development of resting tachycardia may indicate a failing left ventricle, unable to
maintain the increased stroke volume of pregnancy. Balloon valvotomy may allow relief
of severe stenosis and continuation of the pregnancy in severe cases. During delivery,
the main complications are pulmonary oedema secondary to left ventricular failure
and low cardiac output from decreased venous return. Venocaval compression and
hypovolaemia must therefore be avoided.
Mitral stenosis
The increased blood volume, heart rate, and cardiac output accompanying normal
pregnancy increase left atrial pressure and may cause pulmonary congestion and
pulmonary oedema. Tachycardia is particularly dangerous in mitral stenosis, because
diastolic filling of the left ventricle (which is slowed in mitral stenosis) is further
decreased, and there is a consequent fall in stroke volume and a rise in left atrial
pressure, precipitating pulmonary oedema. Even if a woman is asymptomatic at the
beginning of pregnancy, she may deteriorate rapidly and develop exertional dyspnoea,
orthopnoea and paroxysmal nocturnal dyspnoea due to pulmonary oedema later in
gestation. This may be precipitated by a rise in the resting heart rate as a result of a
failure to increase stroke volume adequately. If tachycardia develops, -blockers should
be given to slow the heart rate and allow time for left atrial emptying. If atrial fibrillation
occurs, this should be converted to sinus rhythm with digitalization, or DC cardioversion.
The risk of pulmonary oedema is greatest immediately after delivery, owing to the
increase in wedge pressure accompanying the rise in blood volume. For this reason,
cautious reduction in pre-load is desirable before delivery. Generally, fluid restriction
and the fluid losses accompanying labour are adequate to produce a wedge of 14 mm
Hg or less. If the pre-load is decreased too much, cardiac output will fall. Decreases
in systemic vascular resistance lead to tachycardia and should be avoided. Epidural
anaesthesia is desirable for vaginal and abdominal delivery. Pulmonary oedema should
be treated promptly if it occurs.
Marfans syndrome
The cardiovascular features of Marfans syndrome include mitral valve prolapse,
mitral regurgitation, aortic root dilation and aortic incompetence. Marfans syndrome is
inherited as an autosomal dominant condition and those with cardiac lesions tend to
have offspring with cardiac abnormalities. Women should be advised that pregnancy
carries a significant risk if the aortic root diameter is greater than 44.5 cm, or if
there has been a steady increase in the aortic root dimension over preceding visits.
Pregnancy increases the risk of aortic dissection and aortic rupture, particularly in
those with pre-existing aortic dilatation. This risk is related to the family history, and
is increased if relatives with the syndrome have suffered aortic rupture. There is a
significant risk even in the absence of preconceptual cardiovascular abnormality and
though aortic root dilatation may be a predictor of risk, dissection may occur without
significant dilatation or hypertension.
Regular echocardiography assessments should be performed throughout
pregnancy. -blockers have been shown to reduce the rate of aortic dilatation and the
risk of complications. They should be continued or started in pregnant patients with
aortic dilatation or hypertension. For women with stable aortic measurements less
than 4 cm, a vaginal delivery under epidural anaesthesia is recommended, unless
there are obstetric indications for caesarean section. Epidural anaesthesia helps
to limit the rise in systolic and diastolic blood pressure occurring with the pain and
anxiety accompanying uterine contraction. Elective caesarean section with regional
anaesthesia is recommended for those with aortic root dimensions greater than 4 cm or
with increases in aortic root diameter during pregnancy, in order to avoid the rise in
cardiac output associated with labour.
Peri-partum cardiomyopathy
Peri-partum cardiomyopathy is a rare condition specific to pregnancy that usually
presents peri-partum or in the first month after delivery. There is a dilated
cardiomyopathy and congestive cardiac failure with markedly reduced left ventricular
function. There is a significant risk of pulmonary, cerebral and systemic embolization.
Peri-partum cardiomyopathy is more common in multiple pregnancy, pregnancy
complicated by hypertension, and in multiparous and older women. Management
includes anticoagulants and conventional treatment for heart failure including bed
rest, diuretics, digoxin, after-load reduction and inotropes. Elective delivery should
be undertaken if the condition presents antenatally. Thromboprophylaxis should be
continued intra-partum and post-partum. Angiotensin-converting inhibitors may be used
to treat cardiac failure after delivery. About 50% of patients make a spontaneous and
full recovery. Women should be counselled regarding the high risk of recurrence in
future pregnancies especially if cardiac size does not return to normal.

The incidence of myocardial infarction in pregnancy is increasing as older women
who smoke are becoming pregnant. The risk is highest in the third trimester and
overall maternal mortality is about 20%. Myocardial infarction in pregnancy has been
successfully managed with thrombolysis, balloon angioplasty and coronary artery
bypass grafting. Low-dose aspirin, 75150 mg/day, is safe in pregnancy and should
be continued or commenced for primary and secondary prophylaxis or in the acute
management of myocardial infarction. Anti-anginal medication including nitrates and
heparin may also be used safely.
Asthma
The prevalence of asthma in women of childbearing age is increasing. Asthma is the

most common pre-existing medical disorder encountered in pregnancy. Management
during pregnancy should include reassurance regarding the safety of medications used
to control asthma. The biggest danger to the mother and fetus comes from poorly
controlled or undertreated disease.
Changes in respiratory function during pregnancy: normal pregnancy is associated

with a 20% increase in oxygen consumption and a 15% increase in the maternal
metabolic rate. This extra demand is achieved by a 4050% increase in resting minute
ventilation, resulting mainly from a rise in tidal volume rather than respiratory rate.
This hyperventilation causes the partial pressure of oxygen in the arteries to increase
and that of carbon dioxide to fall, with a compensatory fall in serum bicarbonate to
1822 mmol/litre. A mild respiratory alkalosis is normal in pregnancy (arterial pH
7.44). Up to 75% of women experience a subjective feeling of breathlessness at some
time during pregnancy, possibly because of an increased awareness of physiological
hyperventilation. This is most common in the third trimester and may lead to diagnostic
confusion. In late pregnancy, the diaphragmatic elevation caused by the enlarging
uterus leads to a decrease in functional residual capacity (FRC), but diaphragm
excursion is unaffected and therefore vital capacity is unchanged. There is no change
in peak expiratory flow rate or forced expiratory volume in 1 second in pregnancy.
However, the fall in FRC may exacerbate hypoxaemia because of premature airway
closure when acute asthma complicates pregnancy.
The effect of pregnancy on asthma in an individual woman is unpredictable. Women
with mild disease are unlikely to experience problems, whereas those with severe
asthma are at greater risk of deterioration, particularly late in pregnancy. Physiological
changes during pregnancy that may improve asthma include progesterone-mediated
bronchodilation and increased serum free cortisol. Those that may explain deterioration
include increased stress and increased gastro-oesophageal reflux. Many asthmatics
experience worsening of their symptoms during pregnancy because they stop or reduce
medication, due to unfounded fears (either their own or their medical advisers) about
its safety.
The effect of asthma on pregnancy in most women is negligible. However, severe,

poorly controlled asthma may have an adverse effect on fetal outcome as a result of
chronic or intermittent maternal hypoxaemia. Some studies have suggested an increase
in the risk of premature labour and low birth weight, though two prospective case-
control studies have not confirmed these findings. Similarly, higher rates of pregnancy-
induced hypertension or pre-eclampsia, and caesarean section have been reported, but
this may be a consequence of increased surveillance of asthmatic pregnancies, rather
than a result of maternal asthma. Corticosteroid use may act as a confounder. The
magnitude of any adverse effect on perinatal outcome is small and related to the degree
of control of the asthma.
Management
Management of asthma in pregnancy does not differ from management outside
pregnancy. The priority should be effective control of the disease process, with the
aim being total freedom from symptoms both day and night. The medications used to
treat asthma are safe in pregnancy. Great attention must be given to reassuring women
about the safety of the drugs used to treat asthma in pregnancy and during lactation.
Asthma should be treated as aggressively in pregnant women as in non-pregnant
women. Pregnancy, because of the increased contact with healthcare professionals,
provides an ideal opportunity to optimize asthma management. The drug treatment of
asthma requires a short-acting symptom reliever and a long-term daily medication to
address the underlying inflammation. All the drugs commonly used to treat asthma,
including short- and long-acting 2-agonists, inhaled corticosteroids, and methyl
xanthines are safe in pregnancy. Fluticasone may be used for those requiring high
doses of inhaled corticosteroids.
Acute severe asthma is dangerous and should be vigorously managed in hospital.

Treatment is no different from the emergency management of acute severe asthma
outside pregnancy. Oxygen, nebulized 2-agonists, nebulized ipratropium, oral
or intravenous corticosteroids, and in severe cases intravenous aminophylline or
intravenous 2-agonists should be used as indicated. Provided abdominal shielding is
used, a chest radiograph results in minimal exposure of the fetus to ionizing radiation,
and if clinically indicated this investigation must never be withheld because the patient
is pregnant.
Labour and delivery: acute attacks of asthma during labour and delivery are rare,
and women should be reassured. Women may continue to use their regular inhalers
throughout labour. Those taking oral corticosteroids (prednisolone, over 7.5 mg/day
for more than 2 weeks) at the onset of labour or delivery should receive parenteral
corticosteroids (hydrocortisone, 100 mg 68 hourly) during labour, and until they are
able to restart their oral medication. Prostaglandin E2 used to induce labour, to ripen
the cervix, or for early termination of pregnancy is a bronchodilator and is safe.
Prostaglandin F20, indicated for severe post-partum haemorrhage should be used with
caution because it may cause bronchospasm.
Asthmatic women may safely use all forms of pain relief in labour, including epidural
analgesia and Entonox. In the unlikely event of an acute asthma attack, opiates
should be avoided. If anaesthesia is required, women should be encouraged to
have epidural rather than general anaesthesia because of the increased risk of
chest infection and associated atelectasis. Ergometrine has been reported to cause
bronchospasm, particularly in association with general anaesthesia, but this does not
seem to be a practical problem when it is combined with oxytocin to prevent post-
partum haemorrhage. Non-steroidal anti-inflammatory drugs (NSAIDs) are commonly
used for pain relief following caesarean section. Women with asthma should be asked
about any known aspirin or NSAID sensitivity before the use of these drugs.
Epilepsy
Epilepsy is the most common chronic neurological disorder to complicate pregnancy,

affecting about 0.5% of pregnancies. Epilepsy is classified according to the clinical type
of seizure, of which the most common are grand mal (tonic-clonic seizure), petit mal
(absence seizure), and temporal lobe seizures (complex partial seizure). The term petit
mal should be reserved for typical absences occurring almost exclusively in children
and associated with 3 Hz spike and wave discharge on the EEG. Absence attacks
occur in adulthood as a feature of partial seizures.
Most cases of epilepsy are idiopathic. Secondary epilepsy may be encountered
in pregnancy in patients who have previously undergone surgery to the cerebral
hemispheres or who have intracranial mass lesions. This should always be considered
if the first fit occurs in pregnancy. Epilepsy may be a feature of antiphospholipid
syndrome. Other causes of seizures in pregnancy include eclampsia, cerebral vein
thrombosis, thrombotic thrombocytopenic purpura, cerebral infarction, drug and alcohol
withdrawal and hypoglycaemia (complicating insulin-treated diabetes). Most women
with epilepsy in pregnancy have already been diagnosed, but when a first fit occurs
in pregnancy, having excluded pre-eclampsia, imaging with CT or MRI of the brain is
appropriate.
Effect of pregnancy on epilepsy: in general, pregnancy does not affect the frequency
of seizures. About 25% of women report improvement, and 1030% experience an
increased seizure frequency in pregnancy. Poorly controlled epileptics, especially those
who fit more than once a month, are more likely to deteriorate in pregnancy. There is
no relation to the seizure type or the course of epilepsy during previous pregnancies.
Reasons for deterioration in seizure control during pregnancy are shown in Figure 4.
There is no difference in the change of seizure frequency between trimesters, though
the risk of seizures is greatest peri-partum (see below).
Ante-partum: folic acid should be continued throughout pregnancy because there is a

small risk of folate deficiency anaemia. There is no need to change the anticonvulsant
used in pregnancy if the woman is well controlled. Prenatal screening for congenital
abnormalities with maternal serum screening or nuchal translucency and detailed
ultrasound at 1820 weeks should be offered. A repeat scan at 22 weeks is advisable
if cardiac defects are suspected.
The altered pharmacokinetics (Figure 4) in pregnancy mean that drug levels are
likely to change, and for most drugs, concentration of the free drug falls. This is
because of the increased plasma volume and the enhanced renal and hepatic drug
clearance. These effects are partially offset by decreased protein binding. In practice it
is useful to have a baseline blood level early in pregnancy to confirm compliance, and
to guide any necessary increases. If a woman is fit free there is no need to measure
serial drug levels or adjust the dose. In women who have regular seizures, and who
are dependent on critical drug levels, it is worth monitoring drug levels (preferably of
the free drug) because they are likely to fall, and increasing doses of anticonvulsants
should be guided by serum concentrations. The dose of anticonvulsant should be
altered only on clinical grounds. Vitamin K, 1020 mg orally, should be prescribed from
36 weeks gestation because, in women taking hepatic enzyme-inducing drugs, vitamin
K-dependent clotting factors in the fetus may be reduced, thus increasing the risk of
haemorrhagic disease of the newborn.
Intra-partum: the risk of seizures increases around the time of delivery. 12% of
women with epilepsy will have a seizure during labour, and 12% will fit in the first
24 hours post-partum. Caesarean section is required only for obstetric indications or if
there are recurrent generalized seizures in labour.
Reasons for increase in seizures in pregnancy

Poor drug compliance
Nausea and vomiting
Increased blood volume
Changes in protein binding
Increased drug clearance
Lack of sleep
Reduction of absorption of anticonvulsant drugs from the
gastrointestinal tract during labour
Hyperventilation during labour
4
Post-partum: epileptic patients require particular care in the immediate puerperium
because of the increased risk of seizures. They should be supervised in the bath.
Mothers with major seizures require advice regarding precautions such as bathing
infants with somebody else around and changing nappies on the floor. The neonate
should also receive vitamin K. All women with epilepsy should be encouraged to breast-
feed.
Amniotic fluid embolism
Amniotic fluid embolism is rare but it is associated with a mortality rate of about 80%.
Despite a low incidence of 1/80,000 deliveries, amniotic fluid embolism was responsible
for 17 confirmed and suspected cases of maternal death in the 19941996 UK triennial
report. The anaphylactic-like reaction occurs as a result of passage of amniotic fluid
and particulate debris into the maternal circulation. Associated maternal factors include
multiparity, caesarean section, uterine stimulation, uterine manipulation and increased
age. Fetal factors include large baby, polyhydramnios, intrauterine death, placental
abruption and rupture of membranes. All but one case in the triennial report had one
or more of these complications.
There is a national register for suspected amniotic fluid embolism set up in the UK
and the USA. The criteria for entry are detailed in Figure 5.
Management: death usually occurs as a result of cardio-respiratory collapse or

disseminated intravascular coagulation. The treatment of amniotic fluid embolism
remains supportive and includes adequate oxygenation and ventilation, maintenance
of cardiac output and correction of coagulopathy. Current studies are focused on the
possible role of leukotrienes, histamine, bradykinin, cytokines, prostaglandins and
thromboxane.
Entry criteria for the amniotic fluid embolism register
Acute hypotension or cardiac arrest

Acute hypoxia (dyspnoea, cyanosis or respiratory arrest)
Coagulopathy, disseminated intravascular coagulation or unexplained
haemorrhage
Onset during labour, caesarean section, uterine evacuation or within 30
minutes post-partum
Absence of any other potential explanation of above symptoms and signs
FURTHER READING
Greer I A, ed. Thromboembolic Disease in Obstetrics and Gynaecology. Baillires Clin
Obstet Gynaecol 1997; 11: 43145.
James D K, Steer P J, Weiner C P, Gonik B, eds. High Risk Pregnancy: Management
Options. London: W B Saunders, 1999.
National Radiological Protection Board. Advice on Exposure to Ionising Radiation
during Pregnancy. Chilton: NRPB, 1998.
Nelson-Piercy C, ed. Handbook of Obstetric Medicine. Oxford: Isis Medical Media,
1997.
Oakley C, ed. Heart Disease in Pregnancy. London: BMJ Publishing, 1997.
Report on Confidential Enquiry into Maternal Deaths in the United Kingdom 199496.
London: HMSO, 1998.
Royal College of Obstetricians and Gynaecologists. Report of the RCOG Working Party
on Prophylaxis against Thromboembolism in Gynaecology and Obstetrics. London:
Chameleon Press, 1995.
Royal College of Obstetricians and Gynaecologists. Thromboembolic Disease in
Pregnancy and the Puerperium: Acute Management. Guideline No. 28. London. April
2001.

Medico-legal Aspects of
Obstetric Anaesthesia
David G Bogod
David G Bogod is Consultant Anaesthetist with a special interest in obstetrics at City

Hospital, Nottingham, UK. He has an extensive medico-legal practice and is a member
of the Doctors Group advising the Association for Victims of Medical Accidents. He is
currently reading for a masters degree in health law.
This article is based on British law, but the principles can be extrapolated to most
legislatures based on the British or North American legal systems.
The concept of negligence

In order for a patient to bring a successful case of negligence against a practitioner, she
must be able to demonstrate that, on the balance of probabilities:
there was a breach of duty of care
damage arose as a direct result of that breach.
How good does the care provided by the anaesthetist have to be for him not to be in
breach of duty? It is reassuring to know that the necessary standard is not particularly
high. The anaesthetist does not have to achieve the level of care that is represented by
the brightest and best in his specialty, but only to act in accordance with the practice
accepted as proper by a reasonable body of medical men skilled in that particular
art (Bolam v Friern Hospital Management Committee (1957) 2 ALLER 118). This
standard, known widely as the Bolam principle, implies that, as long as there is support
for the individuals practice among his peers, then he has fulfilled his duty of care to
the patient, even if another body of opinion would disagree. The Bolam principle has
been clarified (some would say diluted) recently by a case in which the judge ruled
that the final decision on whether a standard of care was acceptable was the Courts
prerogative, and that the expert medical evidence was to be considered only as a guide
(Bolitho v City and Hackney Health Authority (1993) 4 Med LR 117 (CA)).
The patient who has not suffered damage does not have a claim in negligence against
her doctor, however poorly he may have performed in caring for her. Indeed, to be
successful in proving negligence, the claimant must demonstrate not only that damage
occurred, but that it was directly caused by the failure of duty of care.
Common features relating to negligence claims
Consent
Patients in the UK do not have to be given a full explanation of all the risks involved in a
procedure, but it is important to provide them with enough facts to enable them to make
an informed decision. There are no rules about how common an adverse event has to
be before it should be mentioned to a patient, and the widely quoted cut-off point of 1%
has no basis in UK law. The practitioner should bear in mind not only the probability
but also the severity of an adverse event in deciding whether to mention it, and his
explanation should relate to his own practice rather than that of the institution or the
country as a whole. If in doubt, it is better to inform the patient.
Having told the patient of the risks, benefits and alternatives to what you intend to do, it
is good practice to record a brief summary of the explanation.
Taking consent for obstetric analgesia may be difficult if the patient is in severe pain
and under the influence of powerful drugs such as nitrous oxide and pethidine. A brief
explanation may be the best that can be done in the circumstances, but the reasons for
this should be recorded. Consent to continue a procedure should be sought regularly if
it is proving difficult or if the patient is distressed.
Record-keeping
Poor record-keeping often makes negligence suits impossible to defend. A
contemporaneous record of the level of block and the modality used to test it is
essential if a defence is to be successful against a patient who claims to have felt pain
during caesarean section. The key points of good record-keeping are detailed in Figure
1. A summary of good practice points is shown in Figure 2.
Good record-keeping
Note details of risks and benefits explained when taking

consent
Record evidence of the success and extent of regional

blockade
Record reasons for deviating from standard or

accepted practice
Write legibly in black ink
Always put the date and time
Sign notes and print your name if your signature is

illegible
Put your specialty and status
Avoid writing too close to the edges of the paper

words are often missed in photocopying
It is acceptable to make notes when a crisis is over

or to add corrections later, but they must be dated
and timed and the previous notes must not be made
illegible
Ensure that all records are properly bound in the

patients folder this particularly applies to operating or
labour analgesia records, which are often loose
1
Avoiding negligence litigation
Keep good records
Note details of consent, including the risks and benefits

discussed with the patient
Be honest with the patient at all times
Prepare good local guidelines and stick to them
Establish an early referral system for potential problems
Maintain close communication with other staff involved

in the care of your patients
Do not get overly focused on the technical aspects

maintain perspective
Do not be reluctant to seek help or a second opinion
If things go wrong, apologize do not avoid the patient
Be nice nice doctors are less likely to be sued
Negligence claims relating to regional obstetric analgesia or anaesthesia
Pain during caesarean section

Pain felt during caesarean section under epidural or spinal anaesthesia is probably the
most common successful medico-legal claim made against anaesthetists in the UK.
One reason why these claims are difficult to defend is the subjective nature of pain.
This, allied to the delay in getting these cases to court, makes it almost impossible for
the defence to counter the claimants description of what she felt at the time.
Pain-free caesarean section cannot be guaranteed, however effective the block.

Consequently, the patient who feels pain during the operation is not necessarily the
victim of negligence. However, for the anaesthetist to have a good defence, he must be
able to demonstrate that he took reasonable steps to minimize the chance of pain and
then to treat it when it occurred. These steps are summarized below.
As part of the consent process, warn the patient about the risk of pain and the
possibility of conversion to general anaesthesia. Make a record of the risks explained to
the patient in case of later dispute.
Use a technique that is recognized as acceptable.
Test the extent of block and demonstrate its effectiveness. A block to touch to T5
has been shown to minimize the risk of pain, and this represents best practice, but the
minimum acceptable standard is probably a bilateral block to pinprick to T6. A survey
carried out in 1996 showed that only 4% of practitioners regard a T8 block as adequate
for caesarean section.
Treat pain when it occurs by use of epidural top-ups, intravenous or inhalational
analgesia, or induction of general anaesthesia. Incidents of pain should be recorded, as
should the efficacy of treatment. General anaesthesia should not be withheld without
good reason if the patient is not coping with the procedure.
Provide follow-up and support to the patient who feels pain.
Neurological damage after regional blockade

Neurological symptoms in the lower limbs can arise during childbirth whether or not a
neuraxial block has been used. However, the woman who develops a persistent area
of numbness or weakness after epidural analgesia is likely to link the two events. The
key feature linking neurological damage to the regional technique is whether the patient
experienced paraesthesia during the procedure. Persistent paraesthesia should always
be a sign to withdraw and reorientate the needle. Failure to do so in a patient who
subsequently develops lower limb neurological signs strongly indicates failure of duty of
care and causation.
It is not medico-legally incumbent on the anaesthetist to warn the patient of the risk of
nerve damage before embarking on the epidural (although it may be good practice).
The rare incidence of this complication means that only 20% of anaesthetists would
mention it when explaining the risks of epidural analgesia. Practitioners should avoid
the temptation to focus on the minutiae of the technical procedure, and to lose the wider
perspective. If an epidural is proving difficult and the patient is becoming restless, it
is better to call a temporary halt to the proceedings. Consider whether the epidural is
needed and whether it would be useful to ask a colleague for help.
Post-dural puncture headache (PDPH)

PDPH is a recognized complication of epidural analgesia and is not necessarily
indicative of negligence. Some PDPH claims succeed, however, and this usually relates
to delay in treatment, specifically in performing an epidural blood patch. Conservative
measures are seldom successful, therefore a blood patch should be offered early
and carried out by a senior member of staff. Meticulous follow-up is mandatory, and
it should be remembered that PDPH can recur after the patient has returned home.
Patients should be told to contact the hospital if they have a recurrence of symptoms,
the GP should be informed and it is good practice to arrange a formal follow-up
appointment after discharge. u
FURTHER READING
Association of Anaesthetists of Great Britain and Ireland. Information and Consent for
Anaesthesia. 1999.
Bourne T M, de Melo A E, Bastianpillai B A, May A E. A Survey of how British Obstetric

Anaesthetists Test Regional Anaesthesia before Caesarean Section. Anaesthesia 1997;
52: 9013.
Bush D J. A Comparison of Informed Consent for Obstetric Anaesthesia in the USA

and UK. Int J Obstet Anaesth 1995; 4: 16.
Holdcroft A, Gibberd F B, Hargrove R L et al. Neurological Complications Associated

with Pregnancy. Br J Anaesth 1995; 75: 5226.
Russell I F. Levels of Anaesthesia and Intraoperative Pain at Caesarean Section under

Regional Block. Int J Obstet Anaesth 1995; 4: 717.

Obstetric Emergencies
Diana Brighouse
Diana Brighouse is Consultant Anaesthetist to the Southampton University Hospitals.

She qualified from Southampton University and trained in anaesthesia in Oxford and
London. She has developed a particular interest in the care of women with medical and
anaesthetic problems in pregnancy.
Amniotic fluid embolism and obstetric haemorrhage are significant causes of maternal
death. In the report on Confidential Enquiries into Maternal Deaths in the UK
(CEMD) 19941996 amniotic fluid embolism is the third cause of direct death after
thromboembolism and hypertensive disorders of pregnancy; obstetric haemorrhage
is the fourth. Of the 12 deaths resulting from haemorrhage, three were caused by
placenta praevia, four by placental abruption and five by post-partum haemorrhage.
Placental abruption
Definition and diagnosis
Placental abruption is the premature separation of the placenta after the twentieth week
of gestation. Its incidence is about 2%. It is associated with a high rate (up to 50%) of
fetal mortality. The risk factors for placental abruption are:
smoking
external cephalic version
polyhydramnios (following membrane rupture)
previous abruption
increasing multiparity
multiple pregnancy
blunt trauma
cocaine ingestion.
Placental abruption is followed by concealed (2035% cases) or revealed

haemorrhage. A grading system has been proposed ranging from grade 0 in which
retroplacental clot is found at placental examination after delivery in an asymptomatic
woman, to grade 3 in which there is maternal shock, abdominal pain, uterine tetany and
a dead fetus. Revealed haemorrhage is not invariable. A coagulopathy is present in
30% of women with grade 3 abruption.
It is important to realize that although this is the typical presentation of placental

abruption there may be neither pain nor revealed bleeding. The 19941996 CEMD
describes a woman presenting in the third trimester feeling unwell and pale and
clammy. There was no complaint of pain, and no cardiovascular compromise. The
woman died 2 hours after admission to the Accident and Emergency Department, and
at emergency caesarean section was found to have 2 litres of blood in the uterus. A
high index of suspicion is required for any pregnant woman who is inexplicably unwell,
especially if her symptoms are accompanied by any abnormal signs. The incidence of
coagulopathy increases as time elapses following abruption, and in the presence of a
dead fetus. The complications of placental abruption are:
maternal hypovolaemia
fetal distress
intrauterine fetal death
disseminated intravascular coagulation (DIC)
post-partum haemorrhage from uterine atony
acute renal failure.
Management
Venous access should be secured promptly, and an intravenous infusion of crystalloid
begun. In the presence of major haemorrhage it may be necessary to administer
group O rhesus negative blood, though group-specific blood is preferable and should
be available within 15 minutes. Surgery should not be delayed until blood is available,
because the condition of mother and fetus is increasingly jeopardized by a prolonged
decision to delivery time.
If the mother is in the third trimester of pregnancy onset of labour usually follows the
abruption. If the fetus is not compromised, vaginal delivery is possible. Vaginal delivery
is also indicated in severe cases of abruption in which the fetus has died. If labour does
not start spontaneously it is usually induced with prostaglandin pessaries.
If abruption occurs during the second trimester of pregnancy, or if there is fetal distress,
delivery by caesarean section is necessary.
Anaesthesia and analgesia

Anaesthesia for operative delivery depends on the clinical presentation. Immediate
delivery is indicated in the presence of severe fetal distress, or if the mother is
hypovolaemic. Resuscitation with intravenous fluids and blood transfusion can be
performed at the same time as preparation for operative delivery is made. In this
situation, general anaesthesia is indicated. Oral sodium citrate is given before induction
of anaesthesia, and many anaesthetists also administer intravenous ranitidine or
omeprazole. The uterus is displaced off the vena cava and aorta either by tilting the
operating table or by placing a wedge under the patients right hip.
The anaesthetist must be alert to the possibility of consumptive coagulopathy in any

patient who appears to be bleeding abnormally. If DIC occurs it should be treated with
appropriate blood products and the advice of a haematologist should be sought. The
patient is at increased risk of postoperative haemorrhage due to failure of the uterus to
contract.
In less urgent situations the mothers condition can be stabilized, and results of
haematological investigations awaited. In the absence of a platelet count below
80,000 or an abnormal coagulation screen, regional anaesthesia can be used. Spinal,
combined spinal-epidural or epidural anaesthesia are all suitable; the final choice is
made according to the anaesthetists preferred technique, though the flexibility of the
combined spinal-epidural compared with single-shot spinal anaesthesia has led some
anaesthetists to recommend it as the technique of choice.
If analgesia is required for labour the mother should be advised to accept epidural
analgesia providing that there are no contraindications. Her chances of requiring
emergency caesarean section in labour are high, and a functioning labour epidural can
readily be extended for operative delivery.
Placenta praevia
Placenta praevia accounted for 25% deaths from obstetric haemorrhage in the 1994
1996 CEMD report. Placenta praevia is the persisting implantation of the placenta in
the lower uterine segment. The placenta may partially or completely cover the cervical
os and may be positioned anteriorly or posteriorly. Placenta praevia is graded I to IV.
Grade I, the placenta encroaches on the lower uterine segment.
Grade II reaches the internal os.
Grade III asymmetrically covers the internal cervical os.
Grade IV symmetrically covers the cervical os.
The main risk factors for placenta praevia are the presence of a uterine scar, increasing
maternal age and increasing parity. Previous caesarean delivery is a major risk factor,
with the risk rising from less than 0.3% in women with no previous caesarean delivery
to over 10% in women who have had four previous caesarean sections.
There is a particularly high risk of placenta accreta placental invasion of the

myometrium in women who have had previous caesarean deliveries. 24% of women
with placenta praevia and one previous caesarean section are likely to have placenta
accreta, and as many as 67% of women with placenta praevia and at least four
previous caesarean deliveries. These women should be investigated with ultrasound
scanning during the third trimester of pregnancy to ensure that the placenta is not
adherent to the uterine scar. In severe cases of placenta accreta the placenta may
invade through the myometrium and into the bladder, bowel or major blood vessels
(placenta percreta).
A rare cause of bleeding is vasa praevia, in which an insertion of the umbilical cord
encroaches on the cervical os.
Diagnosis
Placenta praevia classically presents as painless vaginal bleeding occurring at any time
during the third trimester. It may not present before the onset of labour, when the onset
of uterine contractions together with effacement of the cervix precipitates bleeding
from the abnormally implanted placenta. Placenta praevia is differentiated from
bleeding caused by abruption by the absence of pain, and the diagnosis is confirmed
by ultrasound investigation. Placenta accreta, if not diagnosed preoperatively by
ultrasound, may present as uncontrollable haemorrhage at caesarean section.
Vasa praevia is invariably accompanied by fetal distress because the blood loss occurs
entirely from the fetus.
In the absence of fetal distress, the management of placenta praevia occurring before
37 weeks gestation is initially conservative. The diagnosis is confirmed by ultrasound
scanning and blood is taken for cross-matching. Intravenous access is secured and the
woman is admitted to the antenatal ward. Traditionally she then remains in hospital until
delivery, with cross-matched blood being kept continually available. Recently, however,
obstetricians have been prepared to allow women with lesser degrees of placenta
praevia, especially those who have had only one bleed, to go home and attend the
maternity unit regularly as outpatients. Placenta praevia may cause major antenatal
haemorrhage, and the mother may present in hypovolaemic shock. If the mother is
rhesus negative she should receive anti-D prophylaxis following a vaginal bleed.
Anaesthesia and analgesia

If the mother is bleeding heavily or is hypovolaemic she is almost certain to require
operative delivery. This should not be delayed by waiting for cross-matched blood.
Volume resuscitation should occur simultaneously with preparations for induction of
general anaesthesia. Antacid prophylaxis is given as usual, and anaesthesia is induced
with the mother in the wedged supine position to minimize aortocaval compression.
The presence of a second anaesthetist is desirable to assist with resuscitation. Early
insertion of central venous and arterial cannulas has been recommended in the
hypovolaemic woman.
If there is a high suspicion of placenta accreta preoperatively it is mandatory for a

senior anaesthetist to administer general anaesthesia, and for there to be a second
anaesthetist present to assist. Two large-bore intravenous cannulas should be inserted
before induction of anaesthesia, and cross-matched blood should be available
immediately. There is a significant risk of proceeding to caesarean hysterectomy in
cases of placenta accreta, and the mother should be warned of this (and appropriate
consent obtained) preoperatively. Use of direct right atrial and intra-arterial pressure
monitoring help to guide volume replacement. If the mother is scheduled for elective
caesarean section and is haemodynamically stable many anaesthetists would consider
using regional rather than general anaesthesia. It is important to investigate the mother
for accurate ultrasound location of the placenta before initiating regional anaesthesia.
In hospitals with the facilities to perform radiological embolization of the uterine or

iliac arteries, the possibility of performing a caesarean section in the Department of
Radiology should be considered. The appropriate pelvic vessels can be cannulated
prior to performing the caesarean section and embolization can be performed in the
event of major haemorrhage.
If regional anaesthesia is chosen, epidural, combined spinal-epidural or single-shot

spinal techniques can be used. There may be advantages in choosing an epidural or
combined spinal-epidural technique that can be extended if surgery proves difficult.
Some anaesthetists favour epidural rather than spinal anaesthesia on the assumption
that it offers greater cardiovascular stability. Whichever technique is chosen it is
advisable to secure intravenous access with two large-gauge cannulas before initiating
anaesthesia. Use of direct intra-arterial monitoring may be helpful if this facility is
readily available. Cross-matched blood should be available immediately.
A trial of vaginal delivery may be considered for women with minor degrees of placenta
praevia. These women should be offered epidural analgesia and it is prudent to
anticipate greater blood loss than usual at delivery.
In the absence of access to accurate ultrasonography the anaesthetist may be asked

to assist with examination in theatre of a mother with suspected placenta praevia. In
this situation, the woman is placed in the lithotomy position and a speculum vaginal
examination is carried out. Two large-gauge intravenous cannulas should be inserted
before the woman is examined, and if major placenta praevia is confirmed the mother
is moved into the wedged supine position and rapid-sequence induction of general
anaesthesia is performed.
An alternative technique is to induce regional anaesthesia before vaginal examination

and then to proceed to caesarean section under regional anaesthesia. The
disadvantages of this technique are that major haemorrhage may occur during surgery
and induction of labour and vaginal delivery may be attempted. These considerations
should be taken into account when deciding on a suitable anaesthetic approach. In the
UK, most obstetric units have access to high-quality ultrasonography and most UK
anaesthetists are unlikely to be faced with this dilemma.
Obstetric haemorrhage
The uterus receives 1015% maternal cardiac output by term. Major haemorrhage
can occur with frightening rapidity. The causes of obstetric haemorrhage are shown
in Figure 1. Worldwide, obstetric haemorrhage remains a major cause of maternal
death. The 19941996 CEMD report considered that the care given to eight out of
the twelve mothers who died following obstetric haemorrhage was substandard.
Failure to diagnose placenta praevia occurred in two cases. In the other six cases, the
haemorrhage was recognized but was treated inadequately.
Causes of obstetric haemorrhage
Ante-partum
Placental abruption
Placenta praevia
Intra-partum
Placental abruption
Placenta praevia
Uterine rupture
Post-partum
Uterine atony
Cervical, vaginal or perineal trauma
Uterine inversion
Retained products of conception
1
Ante-partum haemorrhage
Placental abruption and placenta praevia should be treated as discussed above.
Intra-partum haemorrhage
Placental abruption and placenta praevia may both present during labour. Management
follows the guidelines outlined above.
Uterine rupture is a rare cause of intra-partum haemorrhage but is accompanied by

high fetal mortality and potential maternal mortality. Uterine rupture is almost always
associated with labour following previous caesarean section. The causes of uterine
rupture are:
previous caesarean section (especially if classical uterine incision)
external cephalic version
previous uterine rupture
prostaglandins for mid-trimester termination of pregnancy
obstructed labour (in the developing world).
Scar dehiscence may occur gradually and relatively painlessly, causing progressive
fetal distress, and may not be diagnosed until caesarean section is performed. At the
other extreme there may be rapid uterine rupture associated with fetal death, severe
abdominal pain, maternal shock and cardiovascular collapse. Suspicion of uterine
rupture should be raised when breakthrough pain occurs in women who have epidural
analgesia for labour, when there is pain that persists between contractions or when
there is a loss of beat-to-beat variability on the cardiotocograph.
Post-partum haemorrhage
Blood loss of more than 500 ml following vaginal delivery is classified as post-partum
haemorrhage; massive obstetric haemorrhage is blood loss of at least 1500 ml. Primary
post-partum haemorrhage occurs within 24 hours of delivery; secondary haemorrhage
occurs between 24 hours and 6 weeks after delivery.
Uterine atony: failure of the uterus to contract after delivery of the placenta causes
haemorrhage. Causes of uterine atony include:
prolonged labour
precipitate labour
multiple pregnancy
grand multiparity
intrauterine infection
-sympathomimetic drugs
magnesium
volatile anaesthetic agents
retained products of conception.
Genital tract trauma: blood loss from unrecognized genital tract trauma can be
extensive and examination under general anaesthesia is often necessary once initial
resuscitation is under way.
DIC may complicate major obstetric haemorrhage of any aetiology, and may also
complicate amniotic fluid embolism. The common factor in DIC, regardless of cause,
appears to be the release of tissue thromboplastin into the circulation, resulting in
platelet aggregation, coagulation and fibrinolysis.
The platelet aggregation together with fibrin production leads to formation

of microthrombi in small vessels which stimulate the release of plasminogen
activator. Fibrinolysis releases fibrin degradation products into the circulation,
which inhibit platelet aggregation and aggravate the bleeding tendency by causing
thrombocytopenia. DIC is often diagnosed clinically, and the diagnosis is confirmed
by the presence of thrombocytopenia, hypofibrinogenaemia plus elevated fibrin
degradation products or D-dimer. Thrombin time is prolonged and antithrombin III
activity is reduced.
Management
The principles of management of obstetric haemorrhage are the same regardless
of cause (Figure 2). Previous CEMD reports have given clear guidelines for the
management of obstetric haemorrhage. The extent of haemorrhage is often
underestimated. Delay in treating obstetric haemorrhage aggressively may be fatal.
Management of obstetric haemorrhage
General principles
Resuscitate the mother

Give oxygen, intravenous fluids
Deliver fetus and placenta
Ensure uterus is empty
Achieve uterine contraction
Examine under general anaesthesia if bleeding continues
Ligate uterine/internal iliac arteries
Embolize uterine/internal iliac arteries
Consider hysterectomy
Clinical management
Call for help

obstetrician and anaesthetist
extra midwife
porters
Alert haematologist, consultant obstetrician and anaesthetist
Insert at least two large intravenous cannulas
Consider CVP line
Send blood for cross-match (minimum 6 units) and clotting screen
Give oxygen
Resuscitate with colloid/group O negative/type-specific blood until cross-
matched blood available
Use blood warmer and pressure infusion device
Monitor blood pressure, ECG, urine output, blood gases, temperature
Continue fluid resuscitation following haematological advice
Consider examination in theatre
Consider early transfer to ICU
2
Uterine rupture: treatment of uterine rupture is delivery of the fetus by caesarean

section, followed by uterine repair or hysterectomy. General anaesthesia should be
used for speed and because the mother is likely to be haemodynamically compromised.
Women with a history of uterine rupture are usually delivered at 36 weeks gestation by
elective caesarean section.
Uterine atony: initial management should follow the guidelines outlined above.
Intravenous access should be secured with two large cannulas and fluid resuscitation
should be started. Any drugs likely to be contributing to uterine atony should be
discontinued, and oxytocic drugs should be given. If a bolus of syntocinon is given this
should not exceed 10 iu, and many anaesthetists would advise a maximum of 5 iu as a
bolus, followed by an infusion of 50 iu in 500 ml saline, given over 24 hours.
Manual stimulation of uterine contraction may be successful. If haemorrhage continues

a bolus of ergometrine is given (Figure 3). Ergometrine causes an increase in systemic
arterial and intracranial pressure and provokes vomiting. It should be diluted to 10 ml
and administered slowly. Its use is contraindicated in hypertensive women and those
with intracranial pathology. If bleeding continues, prostaglandins may be administered;
in the UK prostaglandin F2 (Carboprost, Hemabate) is used in a dose of 0.25 mg i.m.
or directly into the myometrium. There is a relatively high incidence of anaphylactoid
reaction to systemic prostaglandins.
Drug treatment of uterine atony
Stop tocolytics (salbutamol, magnesium)

Stop volatile anaesthetic agents
Give syntocinon, 510 iu i.v. bolus followed by infusion
Give ergometrine, 0.25 mg i.v. slow bolus repeated once
Give Carboprost, 0.25 mg i.m. or into myometrium; repeat if
necessary at 15 minute intervals; maximum dose 2 mg
3
If bleeding continues the patient should be taken to theatre for exploration of the
uterus under general anaesthesia. It is possible that undiagnosed retained products of
conception are preventing uterine contraction.
Genital tract trauma: if post-partum blood loss continues despite the above
measures it may be necessary to tie off the uterine or internal iliac arteries. If this
fails, hysterectomy should be considered. A second anaesthetist should be present
during these procedures because coagulopathy has often developed by this stage.
Appropriate blood products including fresh frozen plasma, platelets and cryoprecipitate
should be given following the advice of a haematologist. The patient should be
transferred to the ICU postoperatively.
A small number of obstetric units have access to radiological embolization of the uterine
and internal iliac arteries, and this is an alternative to surgical ligation. Although general
anaesthesia is usually indicated for obstetric hysterectomy, there have been reported
series of obstetric hysterectomies performed under epidural anaesthesia with no
difference in complication rates. Regional anaesthesia can be considered only in the
well- resuscitated and haemodynamically stable mother, in whom there is no evidence
of coagulopathy.
DIC: primary treatment is removal of the triggering event, together with intravascular
volume replacement. Replacement of blood products should be guided by a
haematologist, and should include transfusion of blood, fresh frozen plasma and
cryoprecipitate or fibrinogen. Platelet transfusion is usually indicated if the platelet count
falls below 50 x 109 /litre. The use of heparin, antithrombin III and aprotinin have all been
reported in the treatment of DIC but their efficacy has not been evaluated.
Women who refuse blood transfusion: some women refuse blood transfusion either
on religious grounds (Jehovahs Witnesses) or because of fear of contracting blood-
borne diseases such as HIV. It is important to identify these women during the ante-
natal period and to counsel them about the risks of refusing blood transfusion. Delivery
should be arranged in a large obstetric unit that has facilities for the management of
major obstetric haemorrhage. Management of these women is described in Figure 4.
Management of obstetric haemorrhage in women who refuse

blood transfusion
Ante-natal identification and counselling
Maximize iron stores antenatally
Deliver in large obstetric unit
Secure intravenous access early
Treat haemorrhage early and aggressively with crystalloid/ colloid
Consider cell-saving techniques
Administer oxygen
Provide opportunity for the woman to change her mind (partner

does not have right to consent or withhold consent)
Consider hysterectomy early
Consider hyperbaric oxygen if available
Consider erythropoietin and parenteral iron
Transfer to ICU
Arrange counselling for staff if patient dies
4
Inversion of the uterus
Uterine inversion occurs in about 1/2000 deliveries, and is defined as complete or
incomplete depending on whether the fundus of the uterus has passed through the
cervix. Acute uterine inversion occurs within 24 hours of delivery; subacute and chronic
uterine inversion may also occur. Risk factors for uterine inversion include primiparous
labour, augmentation of labour with oxytocics, macrosomic fetus, and implantation
of the placenta at the uterine fundus. Acute uterine inversion presents with pain,
haemorrhage and shock disproportional to blood loss.
Management
Current obstetric opinion favours leaving the placenta undelivered until the uterus has
been replaced. The mother should receive fluid resuscitation and an initial attempt
at manual replacement is made under regional anaesthesia once the mother is
haemodynamically stable. If immediate attempts at replacement are unsuccessful the
mother may be given intravenous magnesium, 2 g by slow bolus injection, or a -
sympathomimetic (e.g. salbutamol) to facilitate uterine replacement. The use of volatile
anaesthetic agents such as halothane is no longer advocated because of the risk of
prolonged uterine atony and further haemorrhage.
If the mother remains haemodynamically unstable despite fluid resuscitation she should
receive a general anaesthetic to facilitate uterine replacement.
Hydrostatic pressure is used to replace the uterus if this cannot be done manually, and
if this technique fails, laparotomy and abdominal replacement of the uterus is required.
Amniotic fluid embolism

The incidence of amniotic fluid embolism is unknown; in the 19941996 CEMD report
the UK mortality rate was 7.7/1 million maternities. In Australia between 1973 and 1990,
the mortality was 65/1 million maternities. There is under-reporting of non-fatal cases,
partly because of diagnostic confusion. The pathophysiology of amniotic fluid embolism
is uncertain. Current theories favour the involvement of leukotrienes as a trigger in an
anaphylactoid cascade that precipitates a systemic inflammatory response. Most of the
traditionally cited risk factors have not been substantiated. An American review found
no correlation with duration of labour, use of oxytocics, presence of intact membranes
or hypertonic uterine activity. There may be an association with increasing maternal
age.
Diagnosis
In the USA, diagnostic criteria for amniotic fluid embolism have been established
(Figure 5). Shivering, sweating, dyspnoea or cyanosis may precede cardiovascular
collapse. The woman may have convulsions, leading to misdiagnosis of eclampsia. DIC
may be apparent soon after initial presentation. Diagnosis is supported by the finding of
fetal material in the pulmonary arterial tree.
US criteria for diagnosis of amniotic fluid embolism
Acute hypotension or cardiac arrest
Acute hypoxia
Coagulopathy or unexplained haemorrhage
Onset of symptoms during dilatation and curettage,

labour, caesarean section or within 30 minutes of delivery
No other explanation for signs and symptoms

5
Management
The management of amniotic fluid embolism is entirely supportive and includes:
tracheal intubation and ventilation with high inspired oxygen
fluid resuscitation
symptomatic treatment of coagulopathy
aggressive management of haemorrhage
delivery of fetus and placenta
supportive use of inotropes.
Maternal resuscitation
Causes of collapse in the pregnant or recently delivered woman include:
hypovolaemia
embolism (pulmonary or amniotic)
cardiac disease
drug administration
anaphylaxis
high-spinal/epidural
drug abuse (cocaine, temazepam, opioids)
drug toxicity (magnesium, opioids, local anaesthetics)
eclampsia
intracranial event
sepsis.
Initial resuscitation attempts must include displacement of the gravid uterus off the
major vessels. A purpose-made resuscitation wedge can be used (this needs to be
made of a non-compressible material, and to be of adequate length), or a second
person can kneel on the floor and use their knees as a wedge. Early tracheal intubation
reduces the chances of aspiration of gastric contents.
Use of adrenaline (epinephrine) and cardiac defibrillation should follow standard

resuscitation guidelines for the non-pregnant patient. Sodium bicarbonate can
precipitate fetal intracerebral bleeding, and reduce cerebral perfusion in the mother, and
therefore should be given only in response to proof (from arterial blood gas analysis) of
severe metabolic acidosis.
Cardiopulmonary resuscitation of the pregnant mother is unlikely to succeed while the

mother remains undelivered, because aortocaval compression prevents an adequate
cardiac output being obtained with cardiac massage. The standard ABC of resuscitation
should be supplemented with D for delivery in women of more than 24 weeks
gestation. Vaginal delivery with vacuum extractor or forceps, or peri-mortem caesarean
section should be performed if resuscitation has not been successful within 5 minutes
of cardiac arrest.
North American guidelines suggest that if resuscitation has not been successful
within 15 minutes open-chest cardiac massage should be considered. Use of
cardiopulmonary bypass has been shown to be life saving in certain clinical situations
but this is an option only in hospitals where the obstetric and cardiac units are in close
proximity.
Local anaesthetic toxicity

Bupivacaine has a narrower safety margin between therapeutic and cardiotoxic
dose than lidocaine (lignocaine). It also has a narrower margin between the dose
that is neurotoxic and that which is cardiotoxic. Bupivacaine cardiotoxicity produces
asystolic cardiac arrest, or ventricular fibrillation that is refractory to defibrillation. The
drugs of choice for treatment of bupivacaine toxicity are atropine, maximum 2 mg,
and isoprenaline. Cardiac pacing may be useful. If cardiac function is restored and is
complicated by ventricular dysrhythmias these should be treated with bretylium and
adrenaline (epinephrine). u
FURTHER READING
Thompson W, TambyRaja R L, eds. Emergencies in Obstetrics and Gynaecology.
Baillires Clinical Obstetric and Gynaecology 2000; 14 vol 1.

Pain Relief in Labour:
Alternative Techniques
(Gaseous and Parenteral)
Mark Scrutton
Mark Scrutton is Consultant Anaesthetist at St Michaels Hospital and Bristol

Royal Infirmary, UK. He qualified from St Thomas Hospital, London, and trained in
anaesthesia in the South Thames Region. His teaching and research interests are in
obstetric anaesthesia and the management of the high-risk obstetric patient.
Inhalational agents (Figure 1)
Agents of historical interest

Ether was the first inhalational agent described for analgesia in labour. Although
effective, ether was irritant to the airways, slow in onset, and caused nausea and
vomiting. Chloroform, introduced at the end of 1847 and famously administered to
Queen Victoria by John Snow for the birth of Prince Leopold on 7 April 1853,
was less irritant and quicker in onset. However, the dose administered was hard to
control and loss of consciousness often occurred. Furthermore, chloroform reduced
uterine contractility and readily crossed the placenta causing neonatal depression.
Trichloroethylene (Trilene) and methoxyflurane have been used for analgesia in labour
without any great benefit.
Inhalational agents used for pain relief in labour
Agent Amount inspired for analgesia in labour (%)
Ether Unmeasured
Chloroform 0.20.9/unmeasured
Trichloroethylene 0.350.5
Methoxyflurane 0.35
Nitrous oxide 50
Enflurane 0.251.25
Isoflurane 0.20.75
Desflurane 14.5
Sevoflurane Not reported
Nitrous oxide
Entonox, a 50:50 mixture of nitrous oxide and oxygen, is the most widely used
form of inhalational analgesia in modern obstetric practice. It has a rapid onset
in sub-anaesthetic doses and is eliminated between contractions, so that there is
minimal accumulation in mother or fetus. Despite promising early reports of analgesic
efficacy, Entonox has produced poor results in placebo-controlled trials. However,
Entonox compares favourably with other forms of non-regional analgesia, such as
transcutaneous electrical nerve stimulation and pethidine.
To optimize analgesia, Entonox inhalation must begin at the start of the contraction
in order to try to attain analgesic levels as the contraction peaks. As soon as the
contraction starts to wane, inhalation should stop to minimize hangover between
contractions. Supplementary, continuous, low-flow Entonox via nasal prongs between
contractions may improve efficacy.
Side-effects include dizziness, loss of control, nausea and vomiting, but resolve
rapidly once Entonox is withdrawn. During contractions, hyperventilation may cause
hypocapnia that can decrease oxygen transfer across the placenta by causing
vasoconstriction and increasing the affinity of maternal haemoglobin for oxygen.
Between contractions, hypocapnia combined with the residual sedative effects of
Entonox may increase the incidence of maternal hypoventilation and consequent
arterial oxygen desaturation.
Entonox has no documented effect on the progress or outcome of labour.
Comparison of Apgar scores and more complex neonatal outcome measures show no
detrimental effects on the baby. The high inspired concentration of oxygen in Entonox
may be of benefit, particularly when there is fetal distress.
Other agents
The newer volatile agents, desflurane and sevoflurane, offer rapid onset and
elimination. Desflurane provides similar analgesia to Entonox but with an increased
incidence of amnesia. However, the cost of desflurane, the complex vaporizer required
for its delivery and its lack of significant therapeutic advantage makes widespread use
unlikely. Sevoflurane has not been investigated in obstetric practice, but may become
an alternative or adjunct to Entonox.
Parenteral analgesics (Figure 2)

History
Opioids have been used for analgesia in labour for hundreds of years, often as an
incidental component of a complex potion. In twilight sleep, first described in 1902, a
single dose of morphine was followed by intermittent doses of hyoscine. Side-effects
were severe, analgesia was poor and the technique was abandoned at the end of
the 1930s.
Parenteral drugs used for pain relief in labour
Drug Dose
Pethidine 50100 mg i.m. 34 hourly;

2550 mg i.v. 34 hourly;
1025 mg i.v. PCA (lock-out 10 minutes)1
Morphine 510 mg i.m. 34 hourly
Diamorphine 2.55 mg i.m. 34 hourly
Meptazinol 100150 mg i.m. 24 hourly
Pentazocine 40 mg i.m. 24 hourly
Nalbuphine 1020 mg i.m. 24 hourly
Fentanyl 25100 g/hour i.v.;

12.525 g i.v. PCA (lock-out 5 minutes)1
Remifentanil 0.50.75 g/kg i.v. PCA (lock-out 3 minutes)1
Tramadol 50100 mg i.m. 34 hourly
1
PCA, patient-controlled analgesia.
Pethidine
Pethidine was introduced in the 1930s and has since become the most commonly used
and widely investigated systemic opioid in labour. Widespread availability and ease of
administration has resulted in the continued use of systemic pethidine in labour, despite
overwhelming evidence that it is ineffective and has detrimental effects on both mother
and baby.
Pethidine is usually given as an intramuscular injection, although intravenous
boluses and infusions have been used in an attempt to improve the quality of analgesia.
Better analgesia has been reported with intravenous boluses and infusions, but the
side-effect profile remains unchanged. Improved efficacy has also been reported with
patient-controlled analgesia (PCA), though pethidine consumption may be increased
and neonatal depression more common.
A number of attempts have been made to improve the efficacy of pethidine
by administering it in combination with other drugs. In general, such combinations
have only increased sedation, amnesia and dysphoria, while having little impact on
analgesia. When compared with epidural analgesia in randomized trials, pethidine
invariably produces clinically inferior analgesia.
Effects on the mother: pethidine causes sedation and dysphoria. Pain relief
during contractions is minimal, although some women report feeling less distressed.
Respiratory alkalosis caused by hyperventilation associated with pain continues to
occur during contractions. This causes a reduction in uterine blood flow and impairs
placental gas exchange. Hypocapnia and sedation between contractions exacerbates
maternal hypoventilation and hypoxia. Pethidine causes nausea, vomiting and delays
gastric emptying.
Effect on the progress of labour: conflicting reports have suggested that pethidine
might either slow or accelerate the progress of labour. Slowing of labour may be
caused by an effect on maternal oxytocin and acceleration of labour by a number of
mechanisms including: increasing the contractility of the body of the uterus; decreasing
the contractility of the cervix; and stimulating the production of enzymes responsible
for degrading cervical collagen and elastin. None of these changes has been shown to
correlate with the duration of the active phase of labour and there continue to be no
randomized, controlled trials to suggest that opioids in general, or pethidine in particular,
have any effect on the progress of labour.
Effects on the baby: pethidine is a highly lipophilic molecule that is able to diffuse
rapidly across the placenta. It is bound principally (3060%) to 1-acid glycoprotein. At
term, levels of this protein tend to be higher in the maternal than in the fetal circulation
and, in theory, favour distribution of pethidine into the maternal compartment. pH
gradients across the placenta may be of greater importance. In the compromised
fetus, acidosis may cause ion trapping, resulting in increased fetal pethidine levels and
concomitant side-effects.
The neonatal side-effects of pethidine are compounded by production of its active
metabolite norpethidine by both mother and fetus. Norpethidine is a considerably less
potent analgesic than pethidine, but causes more respiratory depression and has pro-
convulsant properties. The half-lives of pethidine and norpethidine in the mother are
approximately 4 hours and 20 hours, respectively, but in the neonate are 13 hours
and 62 hours, respectively. These prolonged half-lives probably explain why some of
the behavioural changes observed in exposed neonates persist for several days after
delivery.
Intrauterine effects of pethidine include changes in fetal heart rate pattern (reduced
variability), fetal breathing movements and muscular activity, fetal EEG activity and
fetal scalp oxygen tension. Though these changes may not represent fetal distress per
se, they may result in unnecessary obstetric intervention.
Early neonatal effects of pethidine include respiratory depression that is worst after
a dose delivery interval of about 3 hours, and particularly after repeated maternal
doses. This results in decreased Apgar scores, depressed oxygen saturations and
increased arterial carbon dioxide tensions. Babies are sleepy, less able to develop
suckling skills and take longer to establish breastfeeding. In large doses, pethidine can
cause impaired thermoregulation in the newborn.
The effects of pethidine on the baby can be rapidly reversed immediately
after delivery by administering naloxone, an opioid antagonist, 60100 g/kg
intramuscularly. At this dose, naloxone appears to have a clinical effect for up to
48 hours and reverses the neurobehavioural effects of pethidine without any apparent
harm.
Other opioids
Morphine given via any systemic route confers no advantage and causes similar
side-effects to pethidine.
Diamorphine is used enthusiastically in a small number of units, but there is little
information comparing it with other opioids. Increased lipid solubility suggests that it
might reach the sites of action more quickly than morphine, but it is unlikely to offer
any great improvement.
Meptazinol is a mixed opioid agonist/antagonist that enjoys popularity in a small
number of units in which it is believed to be superior to pethidine. Though analgesia
may be slightly improved, side-effects are similar apart from vomiting, which is more
common.
Pentazocine is a mixed opioid agonist/antagonist that was deliberately synthesized
to minimize potential for abuse (large doses causing dysphoric side-effects). It
causes sedation and is irritant on intramuscular or subcutaneous injection. There is no
evidence that it provides superior analgesia to pethidine.
Nalbuphine is a mixed opioid agonist/antagonist similar to pentazocine. Sedation
is common and it can cause dysphoria, though less so than pentazocine. There is little
evidence that nalbuphine is more effective than pethidine.
Fentanyl is a highly lipid-soluble phenylpiperidine derivative that acts primarily on
receptors. It is approximately 80100 times more potent than morphine. Information
about systemic fentanyl in labour consists of unblinded studies and case reports. It is
unlikely that fentanyl will provide significantly better analgesia by the systemic route.
Remifentanil is an ultra short-acting opioid analgesic agent. It produces rapid
onset and offset of profound analgesia, but equally profound sedation and muscle
rigidity. It was hoped that remifentanil might be suitable for intravenous PCA in labour.
Unfortunately, although fast in onset, its peak effect does not occur until about 80
seconds after injection, when the intensity of contraction pain is declining. Reports
suggest that the dose required to provide effective analgesia during contractions
can result in a high incidence of sedation, hypoventilation and hypoxia between
contractions.
Tramadol is a weak agonist reported to have few of the detrimental side-effects
associated with other opioids. Evidence concerning maternal and fetal side-effects is
conflicting and tramadol has no clear advantages over pethidine.
Non-steroidal anti-inflammatory drugs (NSAIDs)

Compared with pethidine, ketorolac is less effective, but causes fewer maternal and
neonatal side-effects. It is unlikely that NSAIDs will gain popularity for analgesia in
labour because of the perceived risk of adverse effects on the fetal circulation, in
particular, vasoconstriction and premature closure of the ductus arteriosus.
FURTHER READING
Harrison R F, Shore M, Woods T, Mathews G, Gardiner J, Unwin A. A Comparative
Study of Transcutaneous Electrical Nerve Stimulation (TENS), Entonox, Pethidine +
Promazine and Lumbar Epidural for Pain Relief in Labor. Acta Obstet Gynecol Scand
1987; 66: 914.
Olofsson C, Ekblom A, Ekman-Ordeberg G, Hjelm A, Irestedt L. Lack of Analgesic
Effect of Systemically Administered Morphine or Pethidine on Labour Pain. Br J Obstet
Gynaecol 1996; 103: 96872.
Russell R, Scrutton M, Porter J. Pain Relief in Labour. London: BMJ Publishing, 1997.
Steer P. The methods of pain relief used. In: Chamberlain G, Wraight A, Steer P, eds.
Pain and its Relief in Childbirth: the Results of a National Survey Conducted by the
National Birthday Trust. London: Churchill Livingstone, 1993: 4967.

Pain Relief in Labour: Regional,
Epidural and Patient-Controlled
Epidural Analgesia
Robin Russell
Robin Russell is Consultant Anaesthetist at the John Radcliffe Hospital, Oxford, UK.
He qualified from Guy's Hospital, London, and trained in anaesthetics at Guy's and St
Thomas' Hospital,London, UK.
Although many methods have been used to relieve the pain of labour, regional blockade
is the most effective. In the last national UK survey of pain relief in labour conducted in
1990 by the National Birthday Trust, about 20% of women received epidural analgesia.
This figure has recently increased to 24% with a range of 540% between units.
Indications for regional analgesia
Maternal
Maternal request because labour causes many women severe pain, an
increasing number of maternity units now provide a 24-hour on-demand epidural
service.
Coexisting disease effective pain relief reduces maternal stress and the
associated neuroendocrine response which, in certain conditions such as pre-
eclampsia, may benefit both mother and baby.
Potential problems with general anaesthesia compared with regional
anaesthesia, emergency general anaesthesia carries a greater risk for both mother
and baby. Regional analgesia can be readily extended to provide anaesthesia for
operative delivery, therefore regional block is recommended for women at risk of
intervention in whom intubation is expected to be difficult or those with known
anaesthetic problems. Regional analgesia is also advisable for obese women because
they are at increased risk of requiring operative delivery. Although the procedure may
be technically challenging, the hazards of emergency general anaesthesia are avoided.
Fetal
Impaired utero-placental flow fetal well-being may be improved with epidural
analgesia because vasodilatation on both maternal and fetal sides of the placenta
improves blood flow. This is of benefit in pre-eclampsia, in the growth-restricted fetus
and in those with poor cardiotography (CTG) traces or Doppler studies.
Multiple pregnancy the risk of malpresentation, especially of a second twin, is
increased in multiple pregnancy making intervention more likely. Epidural analgesia
reduces the need for emergency general anaesthesia should operative delivery be
necessary.
Breech presentation although many breech babies are now delivered by
caesarean section, regional analgesia allows a controlled vaginal delivery with a calm
cooperative mother and, if emergency caesarean section becomes necessary, the
block may be extended.
Intrauterine death provided coagulation is normal, regional analgesia may be
suitable for pain relief.
Labour
Induction or augmentation of labour results in more severe pain. In prolonged
labour, epidural analgesia allows the mother to rest while minimizing fetal acidosis.
Operative delivery is more likely and the use of regional analgesia reduces the need
for emergency general anaesthesia.
Previous caesarean section epidural analgesia may be beneficial, although it
used to be contraindicated because of fear that the pain of scar dehiscence would be
masked. Pain is not an invariable feature of scar rupture and CTG abnormalities are
a more reliable indicator of rupture. Scar dehiscence or rupture should, however, be
considered in women with a working epidural who develop pain.
Operative or instrumental delivery any woman in whom intervention is thought
likely should be advised to have an epidural so that general anaesthesia may be
avoided.
Manual removal of the placenta in the absence of hypovolaemia, regional block
negates the need for emergency general anaesthesia.
Repair of third-degree tear effective pain relief is needed and local infiltration
may be inadequate.
Contraindications to regional anaesthesia
Maternal refusal informed consent must be obtained and, though this may be difficult
in advanced labour, every effort must be made to explain the procedure.
Lack of trained staff despite the potential benefits of regional analgesia, suitably
trained staff must be available to monitor the mother for the duration of the block.
Risk of spinal haematoma vascular trauma during needle insertion or catheter
manipulation in the presence of abnormal coagulation may lead to an expanding
haematoma, with the risk of ischaemic damage to neural tissue.
Local or systemic infection epidural abscess or meningitis may occur in the
presence of local or systemic infection. Prophylactic antibiotics may help to reduce
the risk.
Coexisting disease in certain cardiovascular conditions, such as pulmonary
hypertension, severe valvular stenosis and bi-directional shunts, regional blocks may
produce haemodynamic instability.
Uncorrected hypovolaemia sympathetic blockade in the presence of
hypovolaemia results in a dramatic reduction in cardiac output.
Allergy true allergy to local anaesthetics is rare. Alternative drugs (see below)
may be used where true allergy exists.
Pharmacology
Local anaesthetics
Local anaesthetics have a nonselective action that blocks all nerve fibres.
Bupivacaine is the most popular agent in obstetric analgesia having replaced the
shorter-acting lidocaine (lignocaine). Unlike its predecessor, it causes less motor block,
does not demonstrate tachyphylaxis and produces lower systemic levels in both mother
and baby. There have, however, been concerns regarding its safety, especially following
accidental intravenous injection when cardiac arrhythmias are more likely to occur in
doses close to those producing convulsions.
Bupivacaine is a racemic compound composed of two stereoisomers, of which the
levo form is less toxic. Although the danger of cardiotoxicity may be minimized by safe
practice (catheter aspiration and slow injection while maintaining eye and verbal contact
with the mother), a search for a safer local anaesthetic has led to the development
of new agents.
Ropivacaine is a single levo isomer which, in addition to reduced toxicity, may
produce less motor block than bupivacaine. This may be because it has only 60% of
the potency of bupivacaine. Levobupivacaine, the levo isomer of bupivacaine, unlike
ropivacaine, has a similar potency to racemic bupivacaine.
Opioids
Unlike local anaesthetics, opioids produce only selective block of nociceptive pathways.
Opioid receptors are found in the substantia gelatinosa of the spinal cord. Epidural
or intrathecal injection allows ready access to these receptors at a much higher
concentration than that which results from systemic administration. Side-effects such
as nausea, vomiting, pruritus, urinary retention and respiratory depression are dose
dependent. The lipophilic opioids are preferable because the more polar agents (e.g.
morphine) have a slow onset of action and greater potential for side-effects.
Fentanyl is the most widely used agent in the UK. On its own, it does
not produce reliable analgesia throughout labour and therefore it is usually
combined with low-dose bupivacaine. Sufentanil may be effective without additional
local anaesthetic when given intrathecally, but it is not available in the UK.
Alfentanil has been used effectively in epidural infusions, though large doses (30
g/kg/hour) have been associated with neonatal hypotonia.
Diamorphine has a much longer duration of action and, when given with a loading
dose, reduces the subsequent need for bupivacaine.
Pethidine has some local anaesthetic effect, but its duration of action is short.
Other drugs
Adrenaline (epinephrine) and clonidine both augment other analgesics through their
2-action. Adrenaline (epinephrine) also has an 1-action producing vasoconstriction,
which intensifies the action of bupivacaine, while prolonging that of lidocaine
(lignocaine). The anticholinesterase neostigmine produces analgesia, but nausea and
vomiting limit its clinical usefulness. Other agents currently under investigation include
adenosine, ketamine and midazolam.
Effects and complications of regional analgesia
Accidental dural puncture should occur in less than 1% of cases. An epidural needle
may breach both the dura and arachnoid leading to free flow of CSF or, alternatively, the
dura alone may be punctured and a catheter placed in the subdural space. A subdural
block is typically slow in onset, extends much higher than would be expected with an
epidural, but spares the sacral roots. It is often patchy with minimal motor block. Where
both dura and arachnoid are torn, epidural insertion may be attempted at another level
or alternatively the catheter passed directly into the CSF producing spinal analgesia.
With the latter, analgesia is not delayed, there is no risk of repeat dural puncture and,
provided appropriate doses are used, there is less risk of a dangerously high block.
Furthermore, the block may be safely and quickly extended for operative delivery.
As the dose for epidural analgesia is ten times greater than that for spinal use,
unrecognized spinal injection of an epidural dose of local anaesthetic results in a
rapidly ascending block with hypotension and, ultimately, apnoea and unconsciousness
total spinal anaesthesia. If this occurs, the mother must be intubated, ventilated and
circulatory support provided until the block wears off. Urgent delivery of the baby may
be required.
Local anaesthetics
Effects on the mother
Sensory block block of lower thoracic, upper lumbar and sacral nerve roots
provides pain relief in labour.
Motor block increasing motor block, which is dependent on cumulative dose,
reduces maternal satisfaction.
Autonomic block block of preganglionic autonomic B fibres produces
vasodilatation, which may lead to venous pooling with a fall in maternal cardiac output.
This is exacerbated by the supine position (supine hypotensive syndrome), which must
be avoided in women receiving regional block.
Proprioception increasing doses of local anaesthetics progressively impair dorsal
column function making ambulation unsafe.
Stress response increased cortisol and catecholamine levels resulting from
painful labour are reduced. Impaired uterine contractility from -receptor stimulation and
reduced placental blood flow from -receptor stimulation are prevented.
Temperature regulation epidural analgesia is associated with a rise in maternal
temperature. Both the mechanism and significance of this rise are uncertain, though no
adverse effect on either mother or baby has been demonstrated. Similarly, the cause of
shivering that is often observed after large epidural top-ups is not fully understood.
Bladder function difficulty passing urine is not uncommon in labour, though it is
more common in those receiving regional blocks.
Toxicity systemic toxicity (see above) may follow accidental intravenous injection
or, rarely, the administration of large epidural doses for caesarean section.
Effects on the baby

Direct effects lipophilic drugs readily cross the placenta, but adverse effects are
unlikely and observed only if the amount in the maternal systemic circulation reaches
toxic levels.
Indirect effects hypotension resulting from autonomic blockade (see above) may
reduce placental blood flow and produce fetal acidosis. Hypotension should be treated
immediately with intravenous fluids and vasoconstrictors.
Effects on the progress of labour: there remains a widespread belief that regional
analgesia has an adverse effect on the progress of labour and mode of delivery.
Retrospective analysis reveals increased duration of labour with more operative and
instrumental deliveries. However, such methodology is flawed, because women do not
choose analgesia at random, but depending on the nature of labour. Consequently,
those experiencing prolonged labour, that is more likely to end in intervention, are more
liable to request regional analgesia. Moreover, if intervention appears probable, such
as in fetal distress, women are advised to have an epidural so that emergency general
anaesthesia is avoided.
Randomized studies, in which regional analgesia is compared with systemic
analgesia, have produced conflicting results. Some studies have shown an increase in
intervention, while others have not. As these studies are not blind, observer bias cannot
be eliminated. Impact studies, in which the effects of introducing a service or increasing
the number of women receiving regional analgesia are observed, may be more helpful.
Several authors have reported little or no change in delivery outcome despite large
increases in the epidural rate. The use of historic controls may be criticized as change
in practice is not accounted for, however, it may be that this change is necessary to
prevent increased intervention.
Delay in siting an epidural before an arbitrary cervical dilatation has been reached is
not to be encouraged because no randomized data to suggest a benefit are available.
Excessive intravenous fluid loading is also unnecessary and may transiently impair
uterine contractility.
Different regional techniques (see below) appear to offer little benefit in terms
of labour outcome. However, reducing the local anaesthetic dose leads to more
spontaneous deliveries. Appropriate management of the second stage is vital and delay
in pushing, providing there is no evidence of fetal distress and analgesia is maintained,
allows descent of the presenting part. Pushing should be continued so long as there is
continued descent and intervention should occur only when definitively indicated. The
judicious use of oxytocin reduces the number of instrumental deliveries in nulliparous
women.
Opioids
Effects on the mother
Pain relief see above.
Pruritus is common, but is seldom troublesome other than with morphine.
Nausea and vomiting are common in labour. The increased incidence with opioids
is dose dependent.
Respiratory depression is unlikely if appropriate doses of lipophilic agents are
used. The potential for respiratory depression is much greater with epidural morphine.
Hypoxia minor degrees of maternal desaturation have been observed when
opioids are added to epidural solutions, though no adverse effects on mother or baby
have been demonstrated.
Bladder function urinary retention may occur as a result of blocking pelvic
parasympathetic outflow.
Gastrointestinal systemic effects, such as delayed gastric emptying are seen with
large or repeated doses.
Reactivation of herpes simplex virus has been reported following epidural
morphine.
Effects on the baby: although adverse changes in fetal heart rate have been observed
after intrathecal opioids, the significance of these findings has yet to be established.
If used appropriately, epidural opioids are unlikely to have clinically important effects
on the baby.
Other drugs
Concerns have been raised about the effects of epidural adrenaline (epinephrine)
on uteroplacental flow. Most studies have suggested that, in healthy women, its use
does not compromise intervillous blood flow, although it may be best avoided in
pre-eclampsia, when vessels are more sensitive to catecholamines. The addition of
adrenaline (epinephrine) increases motor block. Clonidine in doses much above 100 g
produces maternal sedation and hypotension, both of which are undesirable. Clonidine
does not appear to have any adverse effect on the baby.
Techniques
Before siting a regional block, informed consent must be obtained. Wide-bore

intravenous access is established, though the practice of routinely pre-loading a fixed
volume to prevent hypotension has been questioned. The procedure is performed at
the second or third lumbar interspace for epidural analgesia (the lower space is safer
for combined spinal-epidural) using a meticulous aseptic technique. Multi-hole catheters
provide more reliable analgesia and are best inserted 45 cm into the epidural space.
The advantages and disadvantages of different regional techniques are listed in
Figure 1.
Advantages and disadvantages of regional analgesic techniques
Intermittent top-up
Simple Fluctuations in analgesia
Familiar Increased risk of side-effects after bolus
Epidural infusion
Continuous ? Increased motor block
Increased safety Equipment
Decreased midwifery Decreased feedback
workload
Patient-controlled epidural analgesia

Autonomy Equipment
Satisfaction Decreased anaesthetic input
Decreased bupivacaine
dosage
Combined spinal-epidural analgesia

Rapidity Failure
Ambulation Opioid side-effects
Improved sacral block ? Increased neurological problems
Increased satisfaction
Test dose
To detect intrathecal or intravenous catheter placement, a test dose is given. No more
than 15 mg of bupivacaine is injected and the mother is observed for evidence
of hypotension, and motor and sensory block (see loading dose below). After 5
minutes, further doses may be given, though it is wise to limit each to less than
15 mg. Intravascular catheter placement is more difficult to detect as small doses of
local anaesthetic have little systemic effect. The addition of adrenaline (epinephrine)
lacks sensitivity and specificity in labouring women. For increased safety, a multi-hole
catheter should be used, and gently aspirated before each injection. Each dose should
be injected slowly while maintaining eye and verbal contact with the mother to look for
symptoms of local anaesthetic toxicity.
Loading dose
The use of low-dose bupivacaine (< 0.125%) with fentanyl, using volumes of 1520 ml
(i.e. bupivacaine, 1020 mg) in divided doses where appropriate, to ensure adequate
spread, is becoming increasingly popular. A test dose of a more concentrated solution
is unnecessary in this situation. Reducing the local anaesthetic dose minimizes motor
block thereby increasing maternal mobility. Maternal blood pressure and fetal heart rate
should be monitored closely after the loading dose.
Intermittent top-ups
Top-ups are given by either a midwife or anaesthetist as soon as painful sensations
return as each dose takes several minutes to become effective. However, levels of
analgesia invariably fluctuate and, after each top-up, hypotension is possible. Maternal
blood pressure should be checked after each top-up. Top-ups should not be withheld
early in the second stage of labour because maternal distress is increased without
improving the chance of spontaneous delivery.
Epidural infusions
Epidural infusions decrease the need for top-ups, and reduce variations in pain relief as
well as the risk of hypotension. Infusions may also be preferable to top-ups, because
intrathecal or intravenous catheter placement should produce gradually increasing
symptoms allowing more time for recognition and treatment. The workload for midwifery
staff is also reduced.
Although infusions may increase motor block and immobility compared with top-ups
of a similar concentration, infusions of more dilute local anaesthetics may be used
to maintain analgesia with ambulation still possible. This technique, however, requires
infusion pumps and delivery tubing, both of which may be expensive. Feedback on the
spread of sensory block is lost during an infusion and a careful check on block height
must be maintained.
Bupivacaine, in concentrations of 0.1% or less, is the preferred agent combined with
an opioid, usually fentanyl. An initial rate of 1012 ml/hour may be changed depending
on block height, which should be kept at T10. Block height should be checked hourly,
and maternal pulse and blood pressure noted every 30 minutes. Mothers should pass
urine every 4 hours, otherwise a catheter may be required. In the second stage, block
height and perineal sensation should be assessed. If the block is above T10 and
perineal sensation absent, the infusion rate should be decreased. If the block is at or
below T10, decreasing the rate leads to the return of abdominal pain and is of little
benefit. If the mother reports pain, it may be advisable to give a top-up and stop the
infusion.
Patient-controlled epidural analgesia (PCEA)

PCEA uses small intermittent self-administered boluses. Compared with continuous
infusions of similar concentration, bupivacaine utilization is reduced, as is the need
for supplementation. Autonomy allows women greater control and leads to high levels
of satisfaction. PCEA does, however, require sophisticated pumps and concerns have
been raised regarding the level of anaesthetic input after the initial loading dose.
Solutions containing bupivacaine 0.125% or less with fentanyl, 23 g/ml, are
preferable. The local anaesthetic dose is usually bupivacaine, 2.55 mg, with fentanyl,
1012.5 g, in a bolus of 35 ml. Lock-out time is set to 1015 minutes with an hourly
maximum dose of bupivacaine, 15 mg, and fentanyl, 30 g. Background infusion offers
little advantage and is not recommended. Mothers should be monitored as with epidural
infusions.
Combined spinal-epidural analgesia (CSEA)

A needle-through-needle technique is most commonly used for CSEA, though the use
of separate needles in either the same or different interspaces has been described.
Onset of analgesia is more rapid and the quality of sacral analgesia better than with
epidural block. Motor block is usually minimal if small intrathecal doses of bupivacaine
and fentanyl are used, and most women may ambulate safely following the first dose.
The failure rate of CSEA is up to 10% when administered by those inexperienced
in the technique. Intrathecal administration of opioids increases side-effects, especially
pruritus, nausea and vomiting. Concerns about threading the epidural catheter through
the dural hole are overstated and the incidence of dural puncture headache does not
appear to be significantly increased. The possible increase in neurological problems is
perhaps of greater concern. Although several cases of meningitis have been described
following CSEA, it is uncertain whether the technique increases this risk. The possibility
of conus damage is increased if the procedure is performed above the third lumbar
interspace.
Intrathecal loading is usually with bupivacaine, 2.5 mg, and fentanyl, up to 25 g,
although in North America sufentanil, 10 g, is often preferred. Initial analgesia usually
lasts for at least 1 hour, after which the epidural catheter must be tested and its position
confirmed.
CSEA is used routinely in some units, but many prefer to reserve its use for
advanced labour, multiparous women in whom delivery is imminent and for resiting an
unsatisfactory block in a distressed woman.
Postnatal complications
Post-dural puncture headache: see OBSTETRICS
Neurological symptoms are often attributed to the use of regional analgesia, but are
more likely to be due to labour itself. The estimated incidence of prolonged neurological
problems is 1/10,00015,000 after epidural analgesia and 1/500010,000 after spinal
block.
Chronic backache has been linked to the use of epidural analgesia in labour in
several retrospective surveys. However, no prospective study has demonstrated such
an association.
Urinary dysfunction may occur postnatally if the bladder becomes over-distended

during labour. Long-term bladder dysfunction has not been directly linked with the use
of regional analgesia in labour.
FURTHER READING
Chamberlain G, Wraight A, Steer P. Pain and its Relief in Labour. Edinburgh: Churchill
Livingstone, 1993.
Burnstein R, Buckland R, Pickett J A. A Survey of Epidural Analgesia for Labour in the

United Kingdom. Anaesthesia 1999; 54: 63440.
Paech M J. Patient Controlled Epidural Analgesia in Obstetrics. Int J Obstet Anesth

1996; 5: 11525.
Reynolds F, ed. Regional Analgesia in Obstetrics: A Millennium Update. London:

Springer, 2000.
Russell R, Scrutton M, Porter J. Pain Relief in Labour. In: Reynolds F, ed. Pain Relief in
Labour. London: BMJ Books, 1997.

Physiology of Pregnancy
Joanna C Girling
Joanna C Girling is Consultant Obstetrician and Gynaecologist with a special interest

in Obstetric Medicine at West Middlesex University Hospital, London, UK. She qualified
from Cambridge University and St Marys Hospital, London. She trained in Cambridge
and London and was taught obstetric medicine under the aegis of Professor Michael de
Swiet at Queen Charlottes Hospital, London.
Pregnancy initiates many alterations to body systems, some of them extreme. Many
of these changes are initiated within the first few weeks of pregnancy and return to
baseline values 6 weeks after pregnancy. Knowledge of these adaptations is essential
for understanding the physiology of normal pregnancy and the pathophysiology of
conditions arising in pregnant women. In addition, some pregnancy-induced changes
result in considerable adjustments to the reference ranges for many laboratory criteria;
a failure to appreciate these alterations could cause diagnostic error or therapeutic
mistakes.
The details of the physiological changes of the cardiovascular system in normal

pregnancy are debated, in part because of the difficulties of performing reliable
and safe measurements. Longitudinal studies of echocardiography with Doppler
measurement of blood flow at the pulmonary, mitral and aortic valves and in the
ascending aorta using the women as their own nonpregnant controls give the most
accurate assessment of cardiovascular changes.
The placenta creates a low resistance circulation, vasodilatation occurs peripherally
and circulating volume increases. Increased heart rate, myocardial contractility and
preload, and reduced afterload all influence cardiac performance in pregnancy, by
expanding cardiac output.
Heart rate: early in the first trimester, the heart rate increases from about 75 beats/
minute to almost 90 beats/minute. Palpitations and premature atrial and ventricular
beats are common and usually benign. Stroke volume increases significantly, from 65 to
85 ml in the first trimester, reaching a peak at 20 weeks gestation, which is maintained
until term. Cardiac output changes over a similar time from 5 to 7 litres/minute. This is
also maintained until term, and does not decrease in the third trimester; early studies
that suggested a fall at the end of pregnancy were inaccurate because they were
confounded by use of the supine position, and by changes in pulmonary vasculature
and aortic dilatation which older techniques could not account for. This increase
in cardiac output is distributed to the uterus (400 ml/minute extra), kidneys (300
ml/minute), skin (300500 ml/minute) and other sites such as breasts, gastrointestinal
tract, and cardiac and respiratory muscles.
Peripheral vascular resistance falls by almost 50% in early pregnancy even before
the low resistance placental circulation has a significant effect. The underlying
aetiology is uncertain, but oestrogen, prostaglandins, nitric oxide, relaxin and calcitonin
gene-related peptide have all been implicated. The reduced peripheral vascular
resistance, combined with the obstructive effect of the gravid uterus, contributes to the
development of varicose veins and haemorrhoids in pregnancy. It also accounts for the
susceptibility of pregnant women to supine hypotension; a left lateral tilt should always
be used when lying a pregnant woman on an operating table.
Increases in left atrial and left ventricular end diastolic volume (preload) occur in the
second and third trimesters, reflecting the increase in venous return. This combination
of increased venous return and reduced peripheral vascular resistance is achieved by a
marked increase in blood volume, which reaches a peak of 50% by the third trimester,
and a relatively smaller increase in RBC count (2040%) such that there is a reduction
in blood viscosity (this may be one mechanism offsetting the prothrombotic effects of
pregnancy; see later). The subsequent physiological dilutional anaemia of pregnancy
does not require treatment providing haemoglobin remains above 10.010.5 g/dl.
Cardiovascular examination in pregnancy

The cardiovascular changes of pregnancy that are most clinically apparent are listed
below.
Enlargement of the heart by 1015% and rotation to the left in the frontal plane.
Mild sinus tachycardia.
Apex beat displaced to the left.
Loud third heart sound caused by rapid ventricular filling.
More pronounced splitting of the second heart sound, especially towards term.
Ejection systolic murmur in more than 90% of women, caused by flow across the
pulmonary or aortic valves.
Mammary souffl (a continuous murmur in the left or right second intercostal space,
which is uncommon and can be modified by pressure with the chest piece of the
stethoscope).
ECG often reveals a Q wave and inverted T wave in lead III, which should not, for
example, be misconstrued as suggesting pulmonary embolus.
Blood pressure measurement: diastolic, and to a lesser extent, systolic blood

pressure fall during normal pregnancy. Blood pressure depends on the cardiac output
and peripheral resistance. In pregnancy, the increase in cardiac output is less than the
decrease in peripheral resistance, therefore overall blood pressure falls. The nadir is
reached at 1216 weeks gestation; systolic blood pressure falls by 09 mm Hg and
diastolic pressure by 1217 mm Hg. In the late second and third trimesters, blood
pressure increases towards levels found in the nonpregnant woman (Figure 1).
Although a blood pressure reading of 140/90 mm Hg is often considered to be
part of the diagnostic criteria for
pre-eclampsia, it is important that the measurement is interpreted in relation to
gestation. At term, 20% of women have at least one measurement of 140/90 mm Hg or
more; at 30 weeks gestation this occurs in only 1% of pregnant women, and therefore
is much more likely to reflect significant pathology.
Problems in measuring blood pressure in pregnancy include:
compression of the inferior vena cava by the gravid uterus (pregnant women should
not be supine when blood pressure is measured)
white-coat hypertension
observer error
equipment inaccuracies
uncertainty about which Korotkoff sound to use (evidence is now accumulating that
Korotkoff sound 5 (K5) is more reproducible in pregnancy than sound 4 (K4); many now
use K5 rather than K4, except in unusual cases when K5 falls to zero).
Automated devices automated blood pressure devices significantly under-read
diastolic pressure in a variable and unpredictable manner, by up to 25 mm Hg,
particularly in women with pre-eclampsia. When an automated device is used in
pregnancy, measurements should be checked against those obtained from a mercury
sphygmomanometer or an aneroid device.

Clinical Science
Obstetric haemorrhage
Obstetric haemorrhage (antenatal or postnatal) can be catastrophic and require
aggressive management from a multidisciplinary team. The increased circulating
volume of pregnancy provides some initial protection from the effects of haemorrhage.
In general, pregnant women have a healthy reactive vasculature, and are able to
compensate for blood loss by mounting a tachycardia; blood pressure falls late in the
course of obstetric haemorrhage and is an ominous sign (Figure 2).
Blood loss and shock in pregnancy

Blood loss Circulating volume Systolic blood Symptoms/signs Shock
(ml) lost (%) pressure (mm Hg)
5001000 1015 Normal Palpitations, dizziness, tachycardia Compensated
10001500 1525 Slight fall Weakness, sweating, vomiting Mild
15002000 2530 80 Restlessness, pallor, oliguria Moderate
20003000 3050 5070 Collapse, air hunger, anuria Severe
Peripheral oedema
Peripheral oedema of the legs and hands occurs in most normal pregnancies as a
result of physiological changes:
obstruction of venous return by the gravid uterus
peripheral vasodilatation
increased plasma volume
decreased colloid osmotic pressure (due to haemodilution rather than altered protein
production)
increased vascular permeability.
The presence of peripheral oedema is seldom helpful in the assessment of pre-
eclampsia, and it has been removed from most definitions of the condition.
Physiological changes in coagulation and thromboembolic risk

Physiological increases in coagulation factors I (fibrinogen), VII, VIII, IX, XII and
a decrease in some endogenous anticoagulants (antithrombin, protein S, activated
protein C resistance) occur during pregnancy, and are intended to reduce
the risk of haemorrhage, especially at delivery. However, associated with the
physiological vasodilatation of pregnancy, they contribute to a six-fold increase in
risk of thromboembolism during pregnancy. Trauma to the pelvic veins at delivery,
sometimes in association with dehydration or immobility, accounts for the additional
thromboembolic risk in the puerperium. In the UK, thromboembolic disease is the
leading cause of maternal mortality. Prevention entails assessment of thromboembolic
risk in every pregnant woman, and in particular at delivery. Caesarean section is
a major risk factor for thrombosis, and the Royal College of Obstetricians and
Gynaecologists has issued guidelines for thromboprophylaxis.
The diagnosis of acute thromboembolism should be considered in a pregnant
woman with relevant leg or chest symptoms, and care taken in the correct interpretation
of investigations. D-dimer measurement is unhelpful because it is elevated in normal
pregnancy. Duplex Doppler assessment of the femoral veins is used to diagnose deep
vein thrombosis. The amount of radiation involved in ventilation perfusion scanning is
negligible in the face of the risks to maternal and fetal well-being of an incorrectly
diagnosed pulmonary embolus.
Cardiovascular changes in labour

During labour additional physiological changes occur. Cardiac output increases by a
further 1520%, in part because of autotransfusion from the contracting uterus (Figure
3). At delivery, a further 500 ml or more of blood may be autotransfused as the placenta
is delivered; in a small group of women with volume-dependent cardiac disease (e.g.
pulmonary or mitral valve stenosis), the postnatal period may therefore be particularly
dangerous. Sympathetic nervous system stimulation through maternal pain or anxiety
results in a further increase in heart rate and possibly an increase in blood pressure.
Regional anaesthetic techniques can play an important role in assisting blood pressure
control during labour, both by providing analgesia and as a direct result of sympathetic
blockade.

BMJ

Respiratory system
In nonpregnant women, oxygen consumption is 250 ml/minute at rest. During

pregnancy, this increases by 1520% to about 300 ml/minute. The increase is mainly
to maintain the additional metabolic requirements of pregnancy; the uteroplacental
circulation and the additional work of the maternal circulation. However, ventilation
increases by 40%, such that the partial pressure of oxygen is unchanged (i.e. more
oxygen is consumed but more is acquired), remaining at about 13 kPa (100 mm Hg).
The partial pressure of carbon dioxide is considerably reduced by this increase in
ventilation, falling from 5 kPa (3540 mm Hg), to about 4 kPa (30 mm Hg); thus in, for
example, the assessment of severe asthma, an apparently normal partial pressure of
carbon dioxide may represent carbon dioxide retention. Arterial blood gas assessment
should never be performed in the supine position during pregnancy because inferior
vena caval compression by the gravid uterus and functional reduction in pulmonary
residual capacity and closing volume may give a false impression of hypoxia; the partial
pressure of oxygen falls by 2 kPa to about 11 kPa (83 mm Hg).
This increase in ventilation is achieved by increasing the tidal volume (the volume
of air moved during a normal inspiration or expiration) from 500 to 700 ml. The driving
force is progesterone, which stimulates the respiratory centre directly and increases
sensitivity to carbon dioxide. This is achieved at the expense of the inspiratory and
expiratory reserve volumes, but the vital capacity (the volume that can be inhaled from
forced expiration) is unchanged. The expanding uterus decreases the residual volume
(the volume of air remaining in the lungs at the end of forced expiration) and, therefore,
the total lung capacity, thereby reducing the dilution effect of inspired air and further
improving ventilation in the alveoli (Figure 4).
There is no change in the respiratory rate, peak expiratory flow rate or the forced
expiratory volume in 1 second. Transfer factor falls early in pregnancy, which may
account for the deterioration of some cases of severe fibrotic lung disease during
pregnancy. However, many pregnant women have a subjective sensation of shortness
of breath. It may be related to the extra work resulting from the increased ventilation
of pregnancy or to a change in the shape of the thorax as the ribs become more
horizontal and therefore at a potential mechanical disadvantage.
Clinical
Physiology in Obstetrics.
Renal tract
During pregnancy, the kidneys increase in length by 1 cm, and the renal calyces, renal
pelvis and ureter dilate. This is more marked on the right than the left side, because of
the uterine tendency to dextrorotation, but is mostly under the smooth muscle relaxing
effect of factors such as progesterone.
Renal blood flow increases in pregnancy. One consequence of this is a 50% increase
in glomerular filtration by the end of the first trimester. The filtered load therefore
increases, which is paralleled by increments in tubular reabsorption. The increase in
glomerular filtration rate (GFR) is reflected in clinical practice by a rise in creatinine
clearance; this also occurs in transplanted kidneys and often in diseased kidneys. As
a consequence, serum creatinine begins to fall early in the first trimester, reaching a
nadir in the second trimester and then increasing slightly towards term. Therefore, in
pregnancy, a serum creatinine level greater than 85 mol/litre is usually the result of
renal impairment; care must be taken to interpret renal function blood results correctly
in pregnancy.
Glycosuria is common in pregnancy and does not warrant further investigation unless
persistent and severe. It is usually a consequence of the increased GFR; the increased
amount of glucose passing into the urine may saturate the active transport system of
the proximal tubule which retrieves glucose. This is particularly likely if there has been
a significant carbohydrate load.
Uric acid is freely filtered by the glomerulus and actively reabsorbed by the
proximal tubule, the net consequence in pregnancy being a 25% fall in the
circulating levels. As pregnancy progresses, tubular function changes, net excretion
by the tubules falls, and consequently plasma levels increase towards their
nonpregnant values in the third trimester. In general, the urate concentration rises
in parallel with the number of weeks of pregnancy (< 300 mol/litre at 30 weeks,
< 350 mol/litre at 35 weeks). In pre-eclampsia, urate levels are increased compared
with normal pregnancy. This often occurs early in the course of the disease, and is the
result of impaired tubular function. Later in pre-eclampsia, glomerular function may be
altered, resulting in an increase in creatinine; interpretation of the result in relation to
normal values for pregnancy is critical.
Proteinuria: in normal circumstances, there is virtually no protein in urine. During

normal pregnancy there is an increment in proteinuria, the upper limit of normal being
300 mg/ 24 hours. This may reflect the increased GFR, changes in the glomerular
basement membrane or altered tubular function. In pre-eclampsia, proteinuria may
be marked, with values commonly reaching more than 3 g/24 hours. This is due to
(temporary) glomerular damage by pre-eclampsia and usually occurs after an increase
in uric acid.
Gastrointestinal tract
The causes of the extensive physiological changes in the gastrointestinal tract in

pregnancy are debated. Hormonal effects, including smooth muscle relaxation, and
pressure effects from the gravid uterus are likely to be important.
Changes in oestrogen and progesterone result in a fall in pressure at the lower
oesophageal sphincter. This combined with slowing of peristaltic waves in the lower
oesophagus makes it easier for stomach contents to reflux into the oesophagus.
Early in pregnancy, there is also a small increase in intragastric pressure and
80% of pregnant women experience heartburn. The pH of gastric contents and the
production of gastric acid are unchanged in pregnancy. The contractile response to
exogenous stimuli is impaired, for example protein-rich foods stimulate less production
of gastrin, resulting in decreased gastric emptying. This is marked during labour and is
exacerbated by the use of parenteral opioids. This is one of the reasons why general
anaesthesia should be avoided during labour.
Hormonal relaxation of large bowel smooth muscle contributes to the reduced
frequency of defecation in pregnancy.
Physiological effects of human chorionic gonadotrophin

Hyperemesis gravidarum is a potentially serious complication of the first half of
pregnancy. Vomiting can be of sufficient severity to cause dehydration, weight loss or
both, and the woman is likely to be dependent on anti-emetics and intravenous fluids;
thiamine supplementation is essential to prevent Wernickes encephalopathy. In at
least 25% of such pregnancies, abnormal liver or thyroid function may occur, and these
are markers of disease severity; biochemical abnormalities resolve as hyperemesis
gravidarum abates. The aetiology of the liver abnormality is likely to be a direct toxic
effect of the dehydration and starvation. The thyroid abnormality is a result of human
chorionic gonadotrophin (hCG). The subunit of hCG is identical to the subunit of
thyroid stimulating hormone (TSH), and as a consequence hCG has weak TSH-like
activity. In some women with hyperemesis gravidarum, hCG subtypes with increased
TSH-like activity are produced. This results in a biochemical picture of thyrotoxicosis,
which resolves when hCG returns to normal. It does not require treatment with
antithyroid agents.
Liver
During pregnancy, the absolute blood flow to the liver is unchanged. Oestrogen
influences the metabolism of a number of hormone-binding proteins produced by
the liver; for example, the half-life of thyroxine binding globulin (TBG) is extended
from 15 minutes to 3 days. This results in increased circulating concentrations of
TBG, and therefore of total thyroxine (T4) and tri-iodothyronine (T3). Free T4 and
T3 concentrations are essentially unchanged in iodine-replete areas, until the third
trimester when they both fall. Pregnancy-specific reference ranges must be applied,
and only free T4, free T3 and TSH should be used. Other markers of liver function
fall during pregnancy, probably because of the haemodilutional effects of pregnancy
(albumin, transaminases, -glutamyltransferase and bilirubin fall by about 20%).
However, alkaline phosphatase increases; the upper limit of normal for pregnancy is
three times greater than the nonpregnant reference range. This is because of placental
production of a heat-stable isomer. In cases of clinical uncertainty, heating the blood to
60C for 10 minutes results in destruction of the heat-labile liver isomer, and reanalysis
of the sample allows the source of the excess to be determined. Spider naevi and
palmar erythema are common physiological changes in the skin during pregnancy,
probably as a result of high oestrogen concentrations. They do not imply liver disease.
Pruritus may occur in normal pregnancy and is probably benign. It must be
distinguished from the itching of obstetric cholestasis by the finding of liver function
tests outside the normal range for pregnancy, because this condition has a 2% risk of
stillbirth.

Post-dural Puncture Headache
in Obstetrics
S M Yentis
M Rucklidge
S M Yentis is Consultant Anaesthetist at the Chelsea and Westminster Hospital

and Honorary Senior Lecturer at Imperial College School of Medicine, London, UK.
He qualified from University College Hospital, London, and trained in and around
North West London. His interests include routine and high-risk obstetric analgesia and
anaesthesia.
M Rucklidge is Specialist Registrar at the Imperial College School of Medicine,

London, UK. He qualified from St Marys Medical School, London. His interests are the
difficult airway and obstetric anaesthesia.
Post-dural puncture headache (PDPH) is a well-known complication of spinal or

epidural anaesthesia and diagnostic lumbar puncture. First described by August
Bier in 1898, it represents the most common potentially serious complication of
obstetric regional analgesia and anaesthesia. The reported incidence of accidental
dural puncture during epidural analgesia is 0.194.2% in the UK, and 46% in the
USA.
Aetiology
The precise aetiology of PDPH is unknown, though it probably involves leakage of CSF
through the dural hole. This reduces the physical buffering provided by CSF within the
skull. In the upright position, the intracranial structures settle, exerting traction on pain-
sensitive fibres attached to venous sinuses, dura and other structures. This explanation
fits with the observation that the bigger the dural hole, the greater the incidence
and severity of PDPH. There is evidence of intracranial vasodilatation associated with
PDPH, raising the possibility of similarities between PDPH and migraine, in which
cerebral vascular reactivity is also implicated.
Contributory factors
Several factors may increase the risk of PDPH following accidental dural puncture
(Figure 1). Many investigators have shown that the incidence of PDPH decreases with
increasing age. Previous studies have demonstrated increased susceptibility to PDPH
in females though recent investigations have found no relationship; the general belief
that gender affects PDPH may relate to the inclusion of young parturients in the older
studies.
Leakage of CSF through a dural tear is influenced by the size of the spinal needle
and the design of the needle tip. In obstetrics, the incidence of PDPH ranges from
under 1% with 27 G pencil-point needles to 14% with 20 G cutting needles. Sharp-point
spinal needles (e.g. Quincke) cut dural tissues and allow dural tears to persist. Non-
cutting atraumatic needles (e.g. Whitacre, Sprotte) are believed to spread dural fibres
and allow rebound closure after their withdrawal (see Anaesthesia and Intensive
Care Medicine 2:3: 106 Figure 5). The incidence of PDPH following accidental dural
puncture with a 16 G epidural needle is 7085%. Insertion of the epidural needle with
the bevel orientated parallel to the longitudinal dural fibres is associated with reduced
incidence of PDPH should accidental puncture occur, compared with insertion with
the bevel perpendicular to the dural fibres. Dural fibres are thought to close round a
longitudinal hole more efficiently than round a transverse hole.
The effect of pushing in the second stage of labour on PDPH is contentious. It was
previously common that any woman suffering accidental dural puncture was given an
instrumental delivery to avoid pushing, but this practice became unpopular in the 1990s
because any neonatal injury arising from the delivery could be traced to the accidental
dural puncture. However, a recent retrospective study found that the incidence of PDPH
and requirement for epidural blood patch were higher in women who actively pushed
in the second stage following a well-documented single accidental dural puncture,
compared with parturients who underwent caesarean section without pushing.
Predisposing factors for post-dural puncture headache
Patients characteristics
Younger age
?Female sex
Pregnancy
Characteristics of dural hole

Large size
Made with cutting, as opposed to pencil-point, needle
Bevel of needle oriented transverse to dural fibres
Subsequent management of patients

?Allowing mothers to push in second stage of labour
Presentation and diagnosis
Typically, PDPH presents 13 days after accidental dural puncture. It may be severe
and is usually occipital or frontal. Neck pain may be a primary feature or secondary to
muscle spasm. The headache may be accompanied by dizziness, vomiting and visual
or auditory symptoms. Characteristically, the headache is absent or markedly reduced
when supine and worse when upright. Following a slow CSF leak (e.g. after spinal
anaesthesia with a pencil-point 27 G needle) headache may develop 1530 minutes
after adopting the upright position.
There are many causes of headache post-partum (Figure 2), therefore it is important
to confirm the diagnosis. A history of definite accidental dural puncture and a clear
postural component to the headache make the diagnosis almost certain, with two
caveats. First, it is possible for more than one aetiology to coexist, which may confuse
the clinical picture. Second, post-partum presentation of an incidental brain tumour is
a rare but well-recognized event, so the fundi should always be examined. In difficult
cases, a useful manoeuvre, described by Gutshe in 1990, is to ask the mother to sit
up, wait until the headache returns and compress her right upper abdominal quadrant
(remembering this may be painful after caesarean section), asking her to comment on
the headaches severity. A PDPH will ease, presumably as a result of epidural venous
congestion secondary to hepatic compression.
It may be possible to diagnose a dural tear using imaging techniques (e.g. MRI)
and estimations of CSF volume, but this is not widely available. The diagnosis in most
cases remains clinical.
Causes of headache in the early post-partum period
Post-dural puncture headache

Non-specific headache
Migraine
Pre-eclampsia
Meningitis
Cerebral tumour
Subarachnoid haemorrhage
Subdural haematoma
Cerebral vein thrombosis
Management
Left untreated, most headaches resolve over 57 days, though PDPH lasting for
several months or even years has been reported. Rarely, serious neurological
sequelae may follow PDPH, including subdural haematoma and seizures. Deaths
from subdural haematoma or coning have been described following accidental dural
puncture, diagnostic lumbar puncture and spinal anaesthesia in patients without raised
intracranial pressure or other risk factors. Subdural haematoma is presumed to be
caused by shearing forces on delicate subdural vessels resulting from intracranial
hypotension in the upright position. It is thus considered important to treat PDPH in
order to prevent these serious late sequelae, though it is unknown whether symptomatic
treatment of PDPH reduces their incidence.
Few treatments of PDPH have been shown to be effective in randomized clinical
trials, though several have been described anecdotally (Figure 3).
Treatment for post-dural puncture headache1
Supportive
Avoidance of dehydration
Emotional support
Drugs
Simple analgesics
Caffeine
Sumatriptan
Adrenocorticotrophic hormone
Ergotamine
Interventional procedures
Epidural blood patch
1
Most treatments are supported only by weak, if any, evidence.
3
Supportive management
Traditional supportive management of PDPH includes bed rest and hydration. Bed
rest may temporarily alleviate symptoms but does not prevent the onset of PDPH and
there is no evidence that hydration (rather than avoidance of dehydration) helps. It is
important to offer emotional support because the headache may be incapacitating and
prevent the mother from caring for her baby.
Drug treatment
Paracetamol and non-steroidal anti-inflammatory drugs (NSAIDs) are commonly used
as first-line treatment; while paracetamol may help, NSAIDs are often ineffective
(personal observation). Paracetamolopioid combinations have not been shown to be
more effective than paracetamol alone.
Caffeine has been found to provide relief, albeit sometimes transient, in randomized
controlled trials. It may also reduce the incidence of moderate or severe headache if
given prophylactically following spinal anaesthesia. Its mechanism of action is uncertain
but may be related to its ability to increase cerebral vascular resistance and decrease
cerebral blood flow and volume. A suitable oral dose is 150300 mg every 68 hours.
Side-effects include nausea, convulsions and neonatal irritability.
5-HT, a cerebral vasoconstrictor, is important in the pathophysiology of migraine.
Sumatriptan, a 5-HT1D receptor agonist, is effective against migraine, and anecdotal
reports (but not randomized controlled trials) suggest that 6 mg subcutaneously,
repeated if necessary, may be useful in PDPH. Side-effects include pain at the injection
site and transient chest tightness; 5-HT1 agonists are contraindicated in ischaemic heart
disease.
Use of adrenocorticotrophic hormone (ACTH), 1.5 g/kg i.v., or its synthetic
analogue tetracosactide (tetracosactrin), 1 mg i.m., repeated 24 hours later if
necessary, has been described but without validated trials. A mechanism of action has
not been proposed.
Another drug that has been used is ergotamine. A combination of caffeine, 100
mg, and ergotamine tartrate, 1 mg, has been successful anecdotally but a definitive
report has not been published. In addition, ergotamine is contraindicated in pregnancy
and breast-feeding.
Epidural blood patch
Epidural blood patch is generally considered the definitive treatment for PDPH and its
effectiveness is well established. Blood is taken aseptically from the patients arm and
slowly injected into the epidural space. First reported by Gormley in 1960 using 23 ml
blood, more recent evidence suggests larger volumes are more effective; 1520 ml is
usually used as a target though injection may be limited by back pain or discomfort.
Success rates of over 90% have been quoted, with complete and instantaneous
resolution of symptoms. However, recent reports suggest success rates of 6175%
though over 90% of patients may experience initial relief. There is some evidence that
2 hours or more spent lying flat following epidural blood patch may increase the chance
of success. A second blood patch may occasionally be required.
Contraindications to an epidural blood patch are related to placement of the epidural
needle (patients refusal, coagulopathy or infection at the puncture site) or to injection
of autologous blood, primarily the potential for epidural injection of infected blood.
Pyrexia may reflect concurrent bacteraemia and, despite limited data, many authorities
advocate delaying epidural blood patch until the patient becomes afebrile.
Anecdotal evidence suggests that epidural injections of solutions other than blood
may be effective in treating established PDPH. Dextran 40, 2030 ml, has been
used with encouraging results, albeit in uncontrolled trials. Fibrin glue, a preparation
of pooled human plasma used to treat CSF leak in neurosurgery, has been injected
into the epidural space and reported to be effective. Saline has been used to provide
temporary relief and as a diagnostic measure before epidural blood patch in difficult
cases.
Prevention
Approaches to minimizing PDPH include reducing the incidence of accidental dural

puncture and reducing its severity should it occur. The first strategy involves adequate
training and supervision, because accidental dural puncture rates are higher in units
with a large number of relatively inexperienced trainees. The minimum number of
procedures required for trainees to achieve competence is unclear but attempts to
define this have been made. Other possibly preventative factors (although evidence is
weak) include the use of saline instead of air for loss of resistance and the paramedian
approach to the epidural space. There are no published prospective, randomized
controlled trials of adequate size comparing air and saline for loss of resistance. There
are, however, numerous case reports of complications associated with the use of air,
including pneumocephalus, spinal cord and nerve root compression and venous air
embolus.
Several methods for reducing the severity of PDPH after accidental dural puncture
have been proposed. Subarachnoid insertion of the epidural catheter after recognized
accidental dural puncture is an alternative to traditional management (removing the
needle and resiting the epidural at an adjacent interspace). The catheter is then used
to provide analgesia during labour. A potential benefit of this approach is suggested
largely by retrospective studies. The catheter may plug the dural tear during labour and
reduce the efflux of CSF; increased formation of fibrin around the catheter has been
described experimentally and this may also contribute if the catheter is left in situ for
24 hours. Accidental intrathecal injection of epidural doses of drugs must be avoided by
labelling the catheter and informing all relevant staff.
There is consistent evidence that prophylactic epidural saline decreases the
incidence and severity of headache after accidental dural puncture. Epidural saline
is administered either by bolus, 60 ml at 0 and 24 hours, or by continuous infusion,
5001000 ml over 24 hours. The saline is thought to tamponade the intrathecal space
and prevent efflux of CSF.
Prophylactic blood patch (i.e. via the epidural catheter before its removal) has
been used in an attempt to reduce the incidence and severity of PDPH, but this is
controversial, with poor success rates described by some authors. A possible reason
for its failure is the property of local anaesthetics to inhibit coagulation of blood.
Finally, use of neuraxial opioids has been suggested as reducing PDPH after
accidental dural puncture but the evidence is weak. A putative mechanism is unknown.
FURTHER READING
Duffy P J, Crosby E T. The Epidural Blood Patch. Resolving the Controversies. Can
J Anesth 1999; 46: 87886.
Gleeson C M, Reynolds F. Accidental Dural Puncture Rates in UK Obstetric Practice.

Int J Obs Anesth 1998; 7: 2426.
Lybecker H, Djernes M, Schmidt J F. Postdural Puncture Headache (PDPH): Onset,

Duration, Severity, and Associated Symptoms. Acta Anaesthesiol Scand 1995; 39:
60512.
Reynolds F. Dural Puncture and Headache. In: Reynolds F, ed. Regional Analgesia in
Obstetrics: a Millennium Update. London: Springer-Verlag, 2000; 30721.
Stride P C, Cooper G M. Dural Taps Revisited: a 20 year Survey from the Birmingham
Maternity Hospital. Anaesthesia 1993; 48: 24755.

Postoperative Pain
Management in Obstetrics
Michael Kinsella
Michael Kinsella is Consultant Obstetric Anaesthetist at St Michaels Hospital, Bristol,

UK. He trained at St Georges Hospital, London, and obtained postgraduate training
at Kingston, Queen Charlottes and Hammersmith Hospitals. His interests are the
haemodynamic effects of pregnancy, obstetric anaesthesia and analgesia.
This article concentrates on pain management after caesarean section, because this
operation makes up the bulk of obstetric anaesthetic cases. However, issues unique
to pregnancy arise in the first trimester and continue into the post-partum period. In
the UK, many drugs are not licensed for use in pregnant women. The licence for a
particular indication, or in a certain group of patients, is gained when the manufacturer
provides positive evidence of safety. Most pregnant women are healthy, therefore there
is little financial reward for pharmaceutical companies in seeking a licence for drugs
in this group of patients (with the exception of local anaesthetic drugs). Sometimes
there is no drug for a given indication that has a licence for use in pregnancy. When
presented with such a situation, it is sensible to use an old drug wherever possible
because there will be a body of evidence to support its use if problems arise.
During organogenesis, early in the first trimester of pregnancy, there is the possibility
that a drug may cause teratogenesis (the production of a structural malformation in the
fetus). No established analgesic or anti-emetic drugs that are used perioperatively are
known to have this effect. A recent paper has suggested that use of non-steroidal anti-
inflammatory drugs (NSAIDs) during early pregnancy is associated with an increased
risk of miscarriage.
Later in pregnancy, there is the possibility that analgesic drugs given to the mother
perioperatively have pharmacological effects on the fetus. There is a theoretical
possibility that long-term use of NSAIDs might cause closure of the ductus arteriosus
in utero, though this has not been found to be a problem when high-dose NSAIDs
have been used in the short term for the treatment of preterm labour. Long-term use of
NSAIDs is also associated with oligohydramnios.
It can be assumed that all drugs are transferred into breast milk, though many in
trace concentrations only. The amounts that a breast-fed neonate ingests would not
have pharmacological effects. However, many anaesthetists stopped using aspirin for
routine post-caesarean section analgesia after the Committee on Safety of Medicines
stated that it should not be used in children because of a suspected link with Reyes
syndrome.
Caesarean section
In non-obstetric practice it is common to use multimodal analgesia at the time of

operation, often given before skin incision to gain the benefit of a possible pre-emptive
effect. This is not used for caesarean section to avoid transplacental exposure of the
fetus to different drugs, especially potentially sedative analgesics.
Guidelines for the use of analgesia in patients undergoing caesarean section are
given in Figure 1.
Analgesia guidelines for caesarean section
General anaesthesia
Peroperative: morphine at least 20 mg (or morphine and other opioid)
Postoperative: morphine 1 mg (1 ml) dose given by patient-controlled
analgesia, 5 minute lockout
Spinal: elective diamorphine, 0.3 mg; very urgent case fentanyl, 25 g
Epidural top-up for caesarean during labour: fentanyl, up to 100 g
Postoperative: intramuscular morphine (up to) 1 hourly as needed first
dose not before 2 hours after spinal or epidural opioid
All cases
Diclofenac 100 mg suppository at end of operation (contraindicated in cases
of haemorrhage or pre-eclampsia)
Regular paracetamol and diclofenac for first 3 days
Source: St Michaels Hospital, Bristol, UK.
General anaesthesia
In general, strong opioid drugs are not given systemically before delivery by caesarean
section because of their depressant effect on the neonate. The use of remifentanil to
provide analgesia until delivery, with no neonatal effects, has recently been described.
This approach is potentially of major importance in a few cases in which cardiovascular
stability is crucial, but its role in routine practice remains to be defined.
Large doses of fentanyl or morphine (e.g. at least 20 mg) given after delivery are
tolerated and indeed are required. After the patient wakes, increments of morphine or
diamorphine are given intravenously until she has been made comfortable (moderate
pain or less), and then patient-controlled analgesia (PCA) is started.
Maternal deaths have occurred after general anaesthesia for caesarean section
when hypotensive or shocked patients had several doses of intramuscular or
subcutaneous morphine close together. There was a suggestion that excessive blood
levels of morphine were produced when muscle blood flow started to return to normal.
It is important to be aware of this possibility when the intramuscular route is used,
especially as recovery facilities in obstetric units may be of an inferior standard to those
in general operating theatres.
Ilio-inguinal blocks have been tried but do not confer much advantage.
When a regional anaesthetic is used for caesarean section, the analgesic options
become more flexible and more effective. The local anaesthetic block provides pre-
emptive analgesia. Opioids may be given before delivery, because the doses are lower
than those required for systemic analgesia. The ratio of the dose used neuraxially
(i.e. epidural or spinal (intrathecal)) compared with the systemic dose depends on
two factors. Spinal doses are smaller than epidural doses, and drugs that are less
lipid-soluble are used in smaller doses than those with greater solubility. The dose of
spinal morphine, which has the lowest lipid solubility of clinically used opioids, is about
one-hundredth of the systemic dose.
When there is an option of using either the spinal or epidural route, the spinal
option may be preferable because equipotent analgesia is possibly associated with
fewer minor side-effects. The serious complication of delayed respiratory depression
may also be less likely with the spinal route. The epidural space may act as a depot for
delayed absorption, whereas a lipophilic opioid placed into the CSF is rapidly cleared
into tissues. These include neural tissues, and thus lipophilic drugs given spinally also
have a rapid onset of action.
Worldwide, morphine is the most commonly used spinal opioid. Doses of 0.10.15
mg produce prolonged analgesia. It has a good safety record in obstetric practice.
However, because of slow absorption from the CSF, the drug is unlikely to have an
effect during or immediately after the operation. Thus fentanyl, 1025 g, is often
combined with morphine for its intraoperative effect.
A simpler answer is to use diamorphine. This has a rapid onset that supplements
intraoperative anaesthesia and anal-gesia. It gives postoperative analgesia of
comparable duration to morphine but with less central side-effects of itch and
drowsiness. The author currently uses diamorphine, 0.3 mg, as the best compromise
between analgesia and side-effects, but further studies may alter this. The maternal
position in which the spinal block is inserted may influence the duration of analgesia.
There is evidence that when insertion is in the sitting position, doses larger than 0.3 mg
are needed to produce a comparable effect to 0.3 mg administered while the woman
is in the lateral position.
Analgesic considerations are similar when comparing an epidural or combined
spinal-epidural, though an epidural opioid is more likely to be required before delivery
to supplement the anaesthesia produced by an epidural block on its own. When
anaesthesia is provided with local anaesthetic only in the spinal during combined
spinal-epidural anaesthesia, it is common to give a dose of opioid through the epidural
catheter after delivery of the fetus. Morphine is usually given as a single dose only,
whereas diamorphine may be repeated on several occasions.
In a small number of sick mothers, such as those with severe pre-eclampsia,
an optimum postoperative analgesic technique may promote cardiovascular stability
and therefore aid overall management. The author favours continuous infusion of a
low concentration mix of opioid and local anaesthetic, which provides analgesia and
possibly a reduction of plasma catecholamines, while avoiding the fluctuations of effect
seen with bolus doses. However, this technique is labour intensive and many units
would be unable to provide this for routine post-natal cases.
There are a number of units in which all women who have had neuraxial opioids
perioperatively are managed in a high dependency unit. Readers should check their
own local policies.
Other analgesics
The use of non-opioid analgesics is similar after general and regional anaesthesia.
NSAIDs are effective and should be used in most cases, but are contraindicated
in pre-eclampsia and if there are concerns about recent or impending haemorrhage
and hypovolaemia. It is preferable that oral analgesics (NSAIDs and paracetamol) are
prescribed on a regular basis rather than just given when requested.
Other operations
The author adapts the approach given above for other surgical procedures.
Postoperative pain may not be a feature of some procedures (retained placenta or
insertion of cervical cerclage), but can be severe after repair of episiotomies or large
perineal tears. The author uses spinal fentanyl or diamorphine in the latter cases when
spinal anaesthesia is used for surgery.
Pain management after vaginal delivery may also be greatly improved by applying a
systematic approach to analgesia similar to that used for postoperative patients.
FURTHER READING
Gould T H, Crosby D L, Harmer M, Lloyd S M, Lunn J N et al. Policy for Controlling
Pain after Surgery: Effect of Sequential Changes in Management. BMJ 1992; 305:
118793.
Howell P R, Madej T H. Administration of Drugs outside of Product License:

Awareness and Current Practice. Int J Obstet Anesth
1999; 8: 306.
Morrison J D, McGrady E M. Postoperative Pain Relief. In: Reynolds F, ed. Regional

Analgesia in Obstetrics: a Millennium Update. London: Springer-Verlag, 2000

Pre-eclampsia and the HELLP
Syndrome
Paul Howell
Paul Howell is Consultant Anaesthetist at St Bartholomews and Homerton Hospitals,

London. He specializes in obstetric anaesthesia and analgesia. He is a co-opted
committee member of the Obstetric Anaesthetists' Association and responsible for their
regular postgraduate courses.
Pre-eclampsia is a multisystem disorder of endothelial dysfunction, characterized

by widespread vasoconstriction and increased capillary permeability. About 10%
of pregnant women develop pre-eclampsia, generally leading to reduced placental
perfusion. Pre-eclampsia has a variable clinical presentation (Figure 1) and there are
no internationally agreed diagnostic criteria. It is traditionally denoted by hypertension,
proteinuria and oedema. However, many cases present with one or more of the
complications of pre-eclampsia (Figure 2) before hypertension or proteinuria are
apparent. Therefore, it is important to consider pre-eclampsia in patients with any of
these conditions even if hypertension or proteinuria has not been noted in some
patients these are late (or absent) manifestations of the pre-eclamptic syndrome. It
is important not to overlook the presence of upper abdominal pain and vomiting in
women in the third trimester, because these are symptoms of hepatic involvement and
fulminant disease, and hepatic rupture is an infrequent but dramatic cause of death in
pre-eclampsia.
Recognition of pre-eclampsia
Pregnancy-induced hypertension
Proteinuria
Generalized oedema
Excessive weight gain (> 1.0 kg/week)
Ascites
Upper abdominal pain
Vomiting
Decreased platelets
Increased packed cell volume
Increased haemoglobin
Increased plasma urate/uric acid
Increased plasma von Willebrand factor
Increased plasma cellular fibronectin
Decreased plasma antithrombin III
Fetal compromise
Intrauterine growth factor
Intrauterine hypoxaemia
Adapted from: Redman C W G, Roberts J M. Management

of Pre-eclampsia. Lancet 1993; 341: 14514.
1
Complications of pre-eclampsia
Cerebral haemorrhage
Cerebral oedema
Subcapsular hepatic haematoma/rupture
HELLP syndrome
Eclampsia
Acute renal failure (cortical or tubular necrosis)
Disseminated intravascular coagulopathy
Airway oedema
Pulmonary oedema
Retinal detachment
Placental abruption
Impaired feto-placental perfusion
Intrauterine growth factor
Fetal distress
Fetal demise
Adapted from: Redman C W G, Roberts J M. Management

of Pre-eclampsia. Lancet 1993; 341: 14514.
2
The relationship between essential (chronic) hypertension, pregnancy-induced

hypertension and the pre-eclampsiaeclampsia syndrome are unclear, and often
muddled. Oedema is usually omitted from the diagnostic criteria, because it is common
in normal pregnancy and difficult to quantify. However, clinical experience suggests
that obviously worsening oedema in a patient with pre-eclampsia is a significant clinical
marker of leaky capillaries and fulminant disease. Obstetricians often use the plasma
urate level as a marker of the progress of the condition. Rule of thumb for singleton
pregnancy: plasma urate > 0.xx mmol/litre denotes advancing pre-eclampsia (where xx
is the gestation in weeks).
Management of the woman with pre-eclampsia and associated conditions is based

on expedited delivery of the placenta (and the baby), and the provision of end-organ
protection and support for the mother. Contrary to expectation, pre-eclampsia does
not always improve after delivery of the placenta. When pre-eclampsia develops in the
preterm mother it is important to balance extra days of fetal maturity against the risks of
advancing pre-eclampsia to mother and baby. In general, the more preterm the mother
when pre-eclampsia is diagnosed, the more fulminant the condition is likely to be, and
the greater the need for expedited delivery.
Mortality
Since 1950, pre-eclampsia has been one of the two most common direct causes
of pregnancy-related death in the UK, being second to pulmonary embolism in the
19941996 data. Similar findings pertain in other parts of the developed world. For
many years most deaths from pre-eclampsia were caused by cerebral haemorrhage,
but since the mid-1980s pulmonary oedema (a poorly differentiated mix of iatrogenic
fluid overload and adult respiratory distress syndrome) has become the main cause of
death.
Pre-eclampsia protocol
To minimize mortality and morbidity a multi-disciplinary approach is essential with
open communication between obstetric, midwifery and anaesthetic teams. Establishing
a joint labour ward pre-eclampsia protocol may be useful in guiding anaesthetic and
obstetric management, particularly for staff in smaller units less experienced with pre-
eclampsia, and at points where conservative management may require more invasive
action. Suggested guidelines to be included in the pre-eclampsia protocol are shown in
Figure 3. The protocol written by Robson et al. (see Further Reading) has been used as
the basis for local guidelines in many units in the UK. Early referral of severe cases to
Regional Advisory Centres has been advocated though transfer of unstable critically ill
patients should not be undertaken lightly.
Pre-eclampsia protocol
Guidelines are required for the following
Control of blood pressure
Fluid management
Anti-convulsant prophylaxis
Acute management of eclampsia
Pain relief in labour (including management of epidural analgesia)
Anaesthesia for caesarean section
Management of oliguria
Indications for invasive monitoring

3
Haemodynamics
Women with pre-eclampsia have an elevated systemic vascular resistance and a
reduced blood volume. Most women with pre-eclampsia have a normal or high cardiac
output with a hyperdynamic left ventricle, but a few have a low cardiac output owing to
a range of causes.
Pulmonary oedema is a particular hazard owing to the combined effects of low plasma
oncotic pressure and increased permeability of pulmonary alveolar capillaries. Other
predisposing factors include impaired ventricular function, elevated pulmonary artery
occlusion pressure (PAOP) and the poor correlation between central venous pressure
(CVP) and PAOP that is seen in some patients, which may encourage iatrogenic fluid
overload.
The CVP is usually low in early pre-eclampsia. When it is low, the CVP largely
reflects left atrial filling pressures. However, when it rises (above 6 cm H2O) it often
underestimates the left atrial filling pressures, and pulmonary oedema becomes
more likely. A high-normal CVP in pre-eclampsia is a warning sign of fluid overload
or myocardial dysfunction, and provides an indication for the insertion of a pulmonary
artery catheter.
Management includes the combination of controlled vasodilatation (e.g. with

hydralazine) with limited colloid intravenous loading, a technique that improves cardiac
function and reduces vascular resistance better than using either alone.
Hypertension
In the UK, the three drugs commonly used for the acute control of hypertension in
pre-eclampsia are hydralazine, labetolol and nifedipine. Nifedipine should be used
by the oral route only, not sublingually owing to the risk of dramatic and uncontrolled
hypotension with consequent fetal and maternal compromise, particularly when used
as a second-line drug. There is little evidence that any agent or combination is to be
preferred, providing adequate reduction in blood pressure is achieved in a controlled
manner. In patients with an aggressive form of pre-eclampsia, refractory hypertension
may respond only to nitric oxide donors (i.e. nitroglycerine, nitroprusside); these
patients require invasive monitoring in an ICU.
Coagulopathy
Pregnancy and early pre-eclampsia are pro-coagulant states, but a few women
with pre-eclampsia develop coagulation disorders that put them at increased risk of
spinal haematoma formation following epidural puncture. However, the relationship
between platelet count, platelet activity and the risk of epidural haematoma following
epidural puncture is unknown. There is no evidence of increased epidural bleeding
caused by the use of low-dose aspirin in pregnancy. Thrombocytopenia is common
in pre-eclampsia, but bleeding time is probably not a useful test. Other coagulation
defects seldom occur in pre-eclampsia in the absence of thrombocytopenia, therefore
platelet count alone has been proposed as a screening test. Elevations of the partial
thromboplastin time (PTTK) in the presence of a normal platelet count are more likely to
suggest other conditions (e.g. lupus anticoagulant).
Trends may be more significant than absolute numbers. The thromboelastogram and a
new platelet function analyser (PFA 100) are being evaluated, though neither has been
validated in pre-eclampsia. The findings have been inconsistent, though data from the
thromboelastogram suggest that platelet function is largely retained with platelet counts
above 75 x 109 /litre. For many women with pre-eclampsia the benefits of epidural
analgesia outweigh the small (but potentially serious) risk of epidural haematoma
formation.
HELLP syndrome
The HELLP syndrome (Figure 4) is marked by Haemolysis (often presumed rather than
detected), Elevated Liver enzymes and Low Platelets. Subcapsular hepatic haematoma
formation may be a particular problem. As with pre-eclampsia, not all elements of
the syndrome may be apparent simultaneously, and there are no universal diagnostic
criteria. Although usually considered a complication of pre-eclampsia, it has been
questioned whether HELLP is a distinct entity. Patients with HELLP syndrome show
a marked increase in maternal morbidity (including pulmonary oedema, disseminated
intravascular coagulation, abruption and renal failure) and risk of death. There is also a
significant increase in perinatal morbidity and mortality.
Diagnostic features of HELLP syndrome
Haemolysis
Red cell fragmentation on blood film
Plasma bilirubin > 1.2 mg/dl
Elevated liver enzymes

Aspartate aminotransferase > 70 U/litre
Lactate dehydrogenase > 600 U/litre
Low platelets
Platelets < 100 x 109 /litre
Adapted from: Sibai B M. The HELLP Syndrome (Hemolysis, Elevated

Liver Enzymes, and Low Platelets): Much Ado About Nothing? Am J Obstet
Gynecol 1990; 162: 31116.
4
Management remains delivery of the placenta and aggressive supportive therapy.
Corticosteroid therapy may reduce the degree of thrombocytopenia, though expert
opinion is divided.
Labour analgesia
The benefits of well-controlled epidural analgesia in labour are well recognized,
producing excellent analgesia, a marked reduction in maternal plasma catecholamine
levels, a useful fall in blood pressure, and optimizing feto-placental perfusion. Early
studies from Finland showed that epidural anaesthesia improves the blood flow to
the fetus in pre-eclampsia, and more recent Doppler studies suggest that epidurals
produce useful vasodilatation on both the maternal and fetal side of the placenta,
optimizing feto-placental blood flow. Therefore, the early use of epidural analgesia
is recommended. Most epidural studies in pre-eclampsia have used strong epidural
solutions and studies of weak local anaesthetic and opioid mixtures are needed.
The block should be established gently to minimize hypotension (e.g. a solution of 0.1%
bupivacaine plus fentanyl, 2 g/ml) and limited colloid preloading is recommended
(though it is unclear whether preloading is desirable or necessary). The addition of
adrenaline (epinephrine) to the local anaesthetic solution remains controversial, it has
little clinical advantage, particularly when epidural opioids are used, and has several
potential disadvantages in the pre-eclamptic woman who may be exquisitely sensitive
to exogenous catecholamines. Adrenaline (epinephrine) should therefore be avoided in
epidural solutions in pre-eclampsia. Ephedrine remains the vasoconstrictor of choice.
Anaesthesia for caesarean section

Women with pre-eclampsia are at increased risk for caesarean section. Careful
assessment of the relative risks of general and regional anaesthesia must be
made. Regional anaesthesia is usually considered safer, though patients must be
assessed on an individual basis, and their coagulation status considered. Some
authors consider fulminant pre-eclampsia or eclampsia (and the risk of an eclamptic
seizure occurring during surgery) a contraindication to regional block. However, most
obstetric anaesthetists would still choose a regional technique (if there are no signs of
coagulopathy), believing that even women who have had an eclamptic convulsion may
benefit from a regional technique, provided they are alert enough to protect their own
airway, and are receiving magnesium sulphate.
Epidural anaesthesia is the preferred technique for caesarean section, and is

associated with much lower maternal plasma catecholamine and blood pressure levels
compared with general anaesthesia. If a working epidural is already present (i.e. for
labour analgesia) this should be extended for surgery.
Spinal anaesthesia is controversial; because of the potential risks of pulmonary

oedema, profound cardiovascular instability and fall in cardiac output, and the
consequent recourse to intravenous fluids and vasoconstrictors, it is not generally
recommended in pre-eclampsia. However, several recent studies suggest that
most women with pre-eclampsia who received spinal anaesthesia do not develop
catastrophic hypotension (Figure 5), and there is a growing suspicion that women
with pre-eclampsia may behave contrary to expectation following spinal anaesthesia.
There are insufficient published data to support the general use of spinal anaesthesia
in pre-eclampsia, though in individual patients with unstable or fulminant disease,
and a difficult, oedematous airway, it may be a safer technique than emergency
general anaesthesia. Scrupulous attention to detail is probably a key factor in success.
Sequential combined spinal-epidural (low-dose spinal, then epidural top-ups) may
prove useful in experienced hands.
Published studies of the use of spinal anaesthesia in pre-eclamptic women
Author Date Country Anaesthetic technique Study design Comments

Spinal Epidural General
Clark 2000 UK 20 Prospective Pre-eclampsia patients
(Abstract only) randomized required less ephedrine
than normal controls
Wood 1999 USA 103 35 Case note review ? Selection bias, unequal
group size
Sharwood-Smith 1999 UK 11 10 Prospective Study stopped

randomized prematurely owing to
poor quality epidural
Ahmed 1999 India 17 16 Case note review Some in labour
Van Bogaert 1998 S Africa 24 Case note review
Rout 1998 S Africa 49 49 Case note review Some in labour
Karinen 1996 Finland 12 Prospective Mixed severity (6/12

observational severe pre-
eclampsia) 2/12 became
hypotensive, 2/12 had
increased UA PI
Wallace 1995 USA 27 27 26 Prospective Some in labour, severity

randomized unknown.
Combined spinal-epidural
supplementation in some
Assali 1950 USA 15 Prospective Full supine position

observational procaine 0.2% or 1.0%
spinals
5
The added risks associated with general anaesthesia include airway difficulties
resulting from oedema (often aggravated by tracheal intubation), and the pressor
response to laryngoscopy and extubation. If general anaesthesia is chosen, care
should be taken to obtund the pressor response to laryngoscopy. Several techniques
have been described to abolish this, including -blockers, opioids and/or intravenous
lidocaine (lignocaine), but none is completely reliable. A bolus of magnesium sulphate
may be the most effective technique. Extubation may be hazardous because the
trauma of intubation is likely to aggravate laryngeal and airway oedema. Attention
should be paid to the degree of airway oedema at intubation, and if it is significant,
consideration should be given to the possible benefit of keeping the tracheal tube
in place postoperatively and transferring the patient, intubated and ventilated, to the
ICU for stabilization. Residual neuromuscular blockade is another problem in patients
receiving magnesium sulphate, because they are sensitive to the effects of non-
depolarizing muscle relaxants, and behave similarly to myasthenics. Very small doses
should be used with peripheral nerve stimulator monitoring.
Whatever anaesthetic technique is used for caesarean section, adequate recovery

facilities are mandatory, and these patients require high dependency nursing for at least
24 hours.
Oliguria
Most workers agree that, despite the presence of oedema, pre-eclampsia is
characterized by a vasoconstricted, hypovolaemic circulation. Moderate fluid preloading
before vasodilator therapy minimizes hypotension and improves cardiac output, and is
usual practice. Oliguria (often considered as < 0.5 ml/kg/hour) is common but generally
responds to moderate fluid load and delivery. Renal function should be checked by
regular urinary electrolyte or osmolality analysis.
Moderate oliguria in the presence of normal plasma urea and creatinine (remembering
that the values in pregnancy are usually lower than in the non-pregnant state) and
high urinary osmolality suggest appropriate renal function: conservative management
is appropriate. Other causes of oliguria include pre-renal or parenchymal renal failure
and glomerular endotheliosis. However, while renal failure in the absence of obstetric
haemorrhage is rare in pre-eclampsia, excessive fluid administration may easily
precipitate life-threatening pulmonary oedema, aggravated by the underlying pulmonary
capillary leak and low albumin levels. Oliguria generally resolves when the pre-
eclamptic process improves, therefore the author considers that these patients are best
run on the dry side and that over-aggressive fluid loading in an attempt to increase
urine output should be avoided.
Resistant oliguria occasionally requires the use of furosemide (frusemide), dopamine

and CVP or pulmonary artery catheter monitoring, but these should not be used
routinely. An agreed pre-eclampsia protocol may be useful to guide fluid administration
and the management of oliguria.
Central haemodynamic monitoring

Most patients with pre-eclampsia do not require invasive monitoring, and the indications
for CVP or pulmonary artery catheter insertion are controversial. For some years, the
use of the pulmonary artery catheter has been strongly advocated in North America
and whether the recent challenges to the use of the pulmonary artery catheter will alter
this remains to be seen.
Arterial line insertion should be associated with few complications, but the risks
of insertion of CVP and pulmonary artery catheter lines in a woman who is
probably hypovolaemic and with an actual or incipient coagulopathy should not be
underestimated. Some authors recommend avoiding the neck and using peripheral
sites for the CVP line. Other problems include the misinterpretation of data obtained
from these lines, and inappropriate management decisions based on the data
(particularly with respect to fluid management).
In pre-eclampsia, the CVP may underestimate the left atrial pressure once it has risen
to high-normal values (6 cm H2O or above), but it may be useful for dynamic fluid
challenges. In the presence of a high CVP or pulmonary oedema, a pulmonary artery
catheter is indicated.
Eclampsia
In the UK, eclampsia occurs in about 1/2000 pregnancies. The onset of eclamptic
convulsions may be unexpected, may occur before other markers of pre-eclampsia
are apparent, and, particularly in the developing world, is associated with increased
maternal and neonatal mortality. Airway reflexes may be lost, and pulmonary aspiration
and hypoxia may ensue rapidly. Intravenous diazepam may be used for terminating
seizures, but an intravenous bolus of magnesium sulphate, 4 g over 510 minutes, is
recommended.
Magnesium sulphate is the drug of choice in eclampsia, because it is more effective

than diazepam or phenytoin in preventing further fits and minimizing maternal morbidity.
All eclamptic women should receive magnesium sulphate, though the best dosing
regimen remains controversial (4 or 6 g initial bolus, followed by infusion at a rate of 12
g/hour). All labour ward staff should be trained in the basic ABC of resuscitation, and
must appreciate the importance of turning the convulsing or unconscious patient rapidly
on to her side into the recovery position.
The role of anticonvulsant prophylaxis in pre-eclampsia is controversial. For

anticonvulsant prophylaxis, phenytoin is ineffective, and older sedative treatments
with chlormethiazole and diazepam, which risk respiratory depression and pulmonary
aspiration, have largely been eradicated in the UK. Opinion on the use of magnesium
sulphate in pre-eclampsia is divided, but a rational argument suggests that if it works
in eclampsia by reversing cerebral vasospasm, a condition known to occur in pre-
eclampsia, then it seems appropriate to use it in patients with severe pre-eclampsia
before they develop eclamptic convulsions. The use of magnesium sulphate in pre-
eclampsia and eclampsia has increased markedly in the UK over the past decade.
Pre-eclamptic women are at high risk and should receive regular antacid prophylaxis
during labour or delivery (e.g. oral ranitidine, 150 mg 6 hourly) to minimize the risks of
pulmonary aspiration during an eclamptic convulsion or at general anaesthesia. u
FURTHER READING
Ahmed S M, Khan R M, Bano S, Ajmani P, Kumar A. Is Spinal Anaesthesia Safe in
Pre-eclamptic Toxaemia Patients? J Indian Med Assoc 1999; 97: 1658.
Assali N S, Prystowsky H. Studies on Autonomic Blockade. I. Comparison between

the Effects of Tetraethylammonium Chloride (TEAC) and High Selective Spinal
Anaesthesia on Blood Pressure of Normal and Toxaemic Pregnancy. J Clin Invest
1950; 29: 135466.
Clark V A, Sharwood-Smith G, Stewart A V G. Anaesthesia for Caesarean Section in

Pregnancy-induced Hypertension Haemodynamic Stability of Spinal Anaesthesia. Int J
Obstet Anesth 2000; 9: 196.
Karinen J, Rasanen J, Alahuhta S, Jouppila R, Jouppila P. Maternal and Uteroplacental

Haemodynamic State in Pre-eclamptic Patients during Spinal Anaesthesia for
Caesarean Section. Br J Anaesth 1996; 76: 61620.
Robson S C, Redfern N, Walkinshaw S A. A Protocol for the Intrapartum Management

of Severe Pre-eclampsia. Int J Obstet Anaesth 1992; 1: 2229.
Rout C C, Ward S, Rocke D A. Haemodynamic Variability at Emergent Cesarean

Section in Hypertensive Patients Spinal versus General Anesthesia. Anesthesiology
April 1998; SOAP Suppl: A50.
Sharwood-Smith G, Clark V, Watson E. Regional Anaesthesia for Caesarean Section

in Severe Pre-eclampsia: Spinal Anaesthesia is the Preferred Choice. Int J Obstet
Anesth 1999; 8: 859.
Van Bogaert L J. Spinal Block Caesarean Section in Parturients with Pregnancy

induced Hypertension. East African Med J 1998; 75: 22731.
Wallace D H, Leveno K J, Cunningham F G et al. Randomized Comparison of General

and Regional Anesthesia for Cesarean Delivery in Pregnancies complicated by Severe
Pre-eclampsia. Obstet Gynecol 1995; 86: 1939.
Wood D D, Curry R. Spinal versus Epidural Anesthesia for Cesarean Section in

Severely Pre-eclamptic Patients. A Retrospective Survey. Anesthesiology 1999; 90:
127682.

Regional Anaesthesia,
Anticoagulation and
Antithrombosis
Michael Paech
Michael Paech is Staff Specialist in Anaesthesia in a tertiary women's hospital

and a large general teaching hospital in Australia. He is an Examiner for the
Australian and New Zealand College of Anaesthetists and the Associate Editor of
the journal Anaesthesia and Intensive Care. His research interests include obstetric
anaesthesia and analgesia, regional anaesthesia, acute pain management and day
case anaesthesia.
Physiological changes during pregnancy induce a hypercoagulable state presumably

as a means of minimizing blood loss during childbirth. Venous stasis, increased
procoagulant activity (elevated levels of factors II, VII, VIII, X and XI and fibrinogen) and
reduced anticoagulant activity (increased plasminogen activator inhibitors and reduced
protein C) contribute to an approximate incidence of thromboembolism of 1/1000.
Obstetric haemorrhage causes maternal mortality in all countries, but in Australia
(19911993) and the UK (19941996), pulmonary embolism was the leading cause of
direct maternal death. In the UK, the rate of fatal pulmonary embolism (deaths/million
maternities) appears to be rising, from 14.615.1 (19851993) to 21.8 (19941996).
Anticoagulation and antithrombosis
Anticoagulation is commonly instituted during pregnancy. Awareness of

thromboembolic risk and concern were heightened by the findings and
recommendations of the recent Confidential Enquiries into Maternal Deaths in the
UK. Additionally, more patients at risk are now diagnosed and the incidence of
operative delivery (a risk factor) remains high. Some units routinely use prophylaxis
for thromboembolism following caesarean section, while others base policies on risk-
stratification (increased risk with advanced maternal age, high parity, obesity and
pre-eclampsia). Prophylaxis against thromboembolism is also initiated for many other
parturients (Figure 1). It is now appreciated that hereditary thrombophilias are not
uncommon; for example deficiencies of antithrombin, protein C or protein S; activated
protein C resistance; or the factor V Leiden mutation. The latter has a 4% prevalence
and is detected in 20% of those presenting with a thromboembolic event during
pregnancy. The antiphospholipid syndromes and systemic lupus erythematosus are
important thrombotic disorders. Many women with serious cardiac disease now achieve
reproductive status and continuous anticoagulation may be warranted (Figure 1).
Peri-partum thromboembolism and some other situations demand urgent
anticoagulation (Figure 1). This is usually initiated with intravenous unfractionated
heparin or a therapeutic dose of low molecular weight heparin (LMWH) subcutaneously
for 510 days, followed by maintenance with therapeutic LMWH for 3 months.
Thereafter, either prophylactic or therapeutic anticoagulation is continued throughout
pregnancy and 6 weeks into the puerperium. Despite a relative contraindication
because of placental abruption and post-partum haemorrhage, antifibrinolytic drugs
(e.g. streptokinase, tissue plasminogen activator) are occasionally used for massive
pulmonary embolism.
Warfarin and the vitamin K antagonists are also usually avoided during
pregnancy and reserved for anticoagulation after delivery. During organogenesis, fetal
embryopathy and cerebral haemorrhage may occur and warfarin given in the second
and third trimester may cause fetal CNS abnormalities, haemorrhage and stillbirth.
Antithrombotic and potent antiplatelet drug therapy is rare, though low-dose aspirin
therapy is used for prophylaxis against severe pre-eclampsia in certain subgroups and
for medical management after myocardial infarction and cerebrovascular disease.
Indications for anticoagulation during pregnancy
Prophylactic therapy Therapeutic therapy

Postoperative Mechanical cardiac valve
History of thromboembolism Acute thromboembolism
Low-risk thrombophilic disorder High-risk thrombophilic disorder
Antiphospholipid syndromes Arterial thrombosis
Systemic lupus erythematosus
Cyanotic heart disease, some
corrected congenital disorders,
cardiomyopathy, atrial fibrillation,
severe mitral stenosis
Critical illness
Heparin
Heparin is the anticoagulant of choice during pregnancy.
Unfractionated heparin has a long history of safe use, but evidence supporting
specific regimens in obstetric patients is lacking. Heparin does not cross the placenta,
owing to its high molecular weight (mean 1540 kDa). Maternal effects (other than
bleeding or under-coagulation) include thrombocytopenia (early, mild, transient platelet
aggregation or severe IgG antiplatelet antibody-induced). Although thrombocytopenia is
uncommon (3% after therapeutic and 0.3% after prophylactic dosing in non-pregnancy
after 14 days), the platelet count should be checked after 514 days. Following
prolonged heparinization, subclinical maternal osteopenia occurs in 20% of women,
though fractures are rare. Only the pentasaccharide fraction of unfractionated heparin
activates antithrombin III (with subsequent inactivation of factors IIa, Xa and IXa),
therefore variability in heparin effect is wide. The pharmacokinetics of unfractionated
heparin are altered in pregnancy by placental heparinase, increased plasma volume,
renal clearance and heparin-binding proteins. Consequently, requirements increase
1.52.5 times after early pregnancy, though they may fall at term with placental ageing.
Many obstetric units currently use standard (non-pregnant) prophylactic doses that are
inadequate. For example, therapeutic doses of 20,000 units t.d.s. subcutaneously or
prophylactic doses of 7,50010,000 units b.d. subcutaneously, often fail to achieve
appropriate levels.
Low molecular weight heparins (LMWH) of 45 kDa are alternatives that also do
not cross the placenta (Figure 2). In non-pregnant women, LMWH is as effective as,
or more effective than unfractionated heparin for acute thromboembolism. Therefore,
despite a lack of good evidence, LMWH is currently considered the agent of choice in
pregnant women at high risk for thromboembolism. Higher doses (e.g. enoxaparin, 40
mg rather than 20 mg daily) may be required during pregnancy and the puerperium,
probably because of increased renal clearance.
Advantages of low molecular weight heparin compared with

unfractionated heparin
Longer half-life
More predictable and non-dose-dependent bioavailability
Monitoring (anti-Xa activity) not usually required
Heparin-induced thrombocytopenia rare
Heparin-induced osteopenia less common
Regional anaesthesia and analgesia
The increasing use of regional techniques for caesarean section and labour analgesia
has meant that many obstetric patients taking anticoagulants present as candidates for
central neuraxial block. This poses a dilemma for the obstetric anaesthetist, who, in
each case, must balance the relative advantages of central neuraxial block (reduced
mortality, reduced thromboembolism or cardiac morbidity, benefits in pre-eclampsia)
against the risks (e.g. intraspinal haematoma). The use of regional techniques in
anticoagulated patients has been extensively reviewed (see Further Reading), though
points pertinent to obstetric anaesthesia were not addressed. It is essential that all
pregnant women taking anticoagulants are seen before delivery and a multidisciplinary
management plan prepared. Spinal rather than epidural techniques, and intravenous
or inhalational labour analgesia may be prudent. General anaesthesia for operative
delivery will need to be considered, despite its association with a higher risk of
postoperative thromboembolism in high-risk non-obstetric settings.
Intraspinal haematoma is rare (only seven reports in obstetric patients), suggesting

that traditional guidelines have been successful in minimizing its incidence. Both the
timing of needle insertion and catheter removal are relevant to haematoma formation.
Central neuraxial block is generally contraindicated if an antifibrinolytic has been
administered within 710 days, but is only relatively contraindicated following warfarin
which acts for 46 days until vitamin K dependent factors II and X are replenished.
Retrospective and prospective series report no haematoma formation after central
neuraxial block among hundreds of non-pregnant patients on subtherapeutic doses of
warfarin. In contrast, warfarin has been implicated in a large proportion of haematomas
after lumbar puncture and in several case reports after epidural techniques. Reversal
of warfarin using vitamin K (which takes several hours to work) or fresh frozen plasma
is seldom used except for the management of uncontrolled obstetric haemorrhage or
before urgent surgery. Ideally, aspirin should be stopped at least 3 days before a central
neuraxial block. However, in the absence of other risk factors, aspirin does not exclude
regional techniques.
The short duration of unfractionated heparin generally assists the organization
of obstetric anaesthesia when labour ensues or operative delivery is required.
Prophylactic subcutaneous unfractionated heparin peaks at 3 hours and may elevate
the APTT (therapeutic doses may do so for up to 24 hours) so testing is advisable. Two
large reviews of intraspinal haematoma (see Further Reading) suggest prophylactic
unfractionated heparin is seldom implicated and clinical experience is reassuring. A
regional technique or removal of an epidural catheter is generally considered safe
46 hours after conventional prophylactic doses (5,000 units b.d.), though even this
may be conservative practice. In contrast to experience with unfractionated heparin,
unfavourable experience with central neuraxial block in the presence of LMWH
(though not in obstetric patients) has generated concern in the USA. LMWH has weak
fibrinolytic activity and it seems appropriate to apply current general recommendations
to obstetrics (Figure 3). Local policies need to be developed, because the window of
opportunity for central neuraxial block, when anti-Xa activity is at its lowest, is brief.
Recommendations for low molecular weight heparins (LMWH) and

central neuraxial block
Avoid central neuraxial block for at least 24 hours if therapeutically

anticoagulated with LMWH
Avoid central neuraxial block for at least 12 hours after prophylactic LMWH
Discuss the timing of prophylactic LMWH preoperatively, or before induction
of labour, with the obstetrician
In patients not at high risk, or if needle insertion is traumatic, begin
prophylactic LMWH at least 12 (preferably 24) hours postoperatively
Remove the epidural catheter when activity is lowest (at least 12 hours after
the last dose)
To avoid clot disruption, do not administer LMWH until 24 hours after
central neuraxial block or catheter removal
Avoid concurrent non-steroidal anti-inflammatory drugs, antiplatelet drugs
(e.g. aspirin, dextran) and anticoagulants
FURTHER READING
Multiauthor. Reg Anesth Pain Med 1998; 23: 12993.
Paech M J et al. Anticoagulants and Regional Anaesthesia. Selected Review Course
Lectures CD IMRS 2000. 7th Congress International Anesthesia Research Society,
Cleveland, Ohio, USA, 2000.
Vandermeulen E P, Van Aken H, Vermylen J. Anticoagulants and Spinal-Epidural
Anesthesia. Anesth Analg 1994; 79: 116577.
Wulf H. Epidural Anaesthesia and Spinal Haematoma. Can J Anaesth 1996; 43: 1260
71.

Social Problems in Pregnancy
Mary Hepburn
Mary Hepburn is Senior Lecturer in Womens Reproductive Health, Glasgow

University Department of Obstetrics/Gynaecology and Social Policy/Social Work,
and Honorary Consultant Obstetrician and Gynaecologist, Princess Royal Maternity
Hospital, Glasgow. She trained as a general practitioner and then as an obstetrician/
gynaecologist. She established and is consultant in charge of the Glasgow Womens
Reproductive Health Service, a service for women with social problems. Her interests
focus on the effects of socioeconomic deprivation and associated problems on all
aspects of womens reproductive health (including pregnancy outcome) and on service
design and delivery for women with special needs.
Social factors directly and indirectly affect the health of pregnant women and their
unborn babies and should be addressed in obstetric management. Drug use is not the
foremost route of blood-borne virus infection in the UK, but because both have a social
dimension that can affect pregnancy and both illustrate management of social problems
in pregnancy they are jointly discussed here.
Problem drug use

There has been a marked increase in drug use among women of childbearing age
and consequently during pregnancy. Problem drug use with significant medical and
social consequences is closely associated with socioeconomic deprivation, which is
associated with poor health and ineffective service use and both are exacerbated by
problem drug use. Therefore, pregnant drug-using women have potentially high-risk
pregnancies but may receive less maternity care. The design, delivery and content
of obstetric care are all important in the management of drug use and associated
problems in pregnancy.
In the UK, the most commonly used drugs are opiates/opioids (including heroin,
methadone and dihydrocodeine), amphetamines and benzodiazepines. The use of
cocaine is also significant. Drugs can affect pregnancy directly and indirectly by their
effect on maternal lifestyle and general health. Injecting use carries additional risks.
Opiates/opioids: heroin is a short-acting opiate and withdrawal carries a risk of

preterm labour and reduced intrauterine growth. Therapy with longer acting methadone
reduces the risk of preterm labour. Opiate/opioid detoxification during pregnancy
is dangerous in theory, but not in practice, and can be undertaken at any stage of
pregnancy, at any speed, but only if likely to be successful. Management usually
involves a combination of detoxification/reduction and maintenance therapy with the
aim of achieving the lowest drug dose compatible with reasonable stability. Unlike
detoxification, reversal of opiate/opioid effects with naloxone can precipitate severe
fetal distress antenatally and postnatally and should be used cautiously and only if
necessary. All opiates and opioids can cause withdrawal symptoms in the neonate.
Benzodiazepines: apart from a reported association with cleft palate, benzodiazepine

use does not directly affect pregnancy. The most important consequence of
benzodiazepine use is social instability, which has implications for delivery of care and
parenting. There is no evidence of benefit from benzodiazepine sub-stitution therapy
in pregnancy but sudden withdrawal can cause maternal convulsions. Short-term
substitution (up to 7 days) to cover withdrawal is recommended. Benzodiazepine use
also causes neonatal withdrawal symptoms.
Amphetamines: chaotic injecting use carries risks for maternal health and can
be socially destabilizing. However, amphetamines per se seldom affect pregnancy
outcome, do not cause withdrawals in the neonate and there is no evidence of benefit
from substitute prescribing in pregnancy.
Cocaine use is increasing in the UK, but use of crack cocaine is less prevalent than
in the USA. In pregnancy, the vasoconstrictor action of cocaine has been reported to
cause underdevelopment of organs including limbs and gut as well as reduced brain
growth, increased rates of placental abruption, preterm rupture of membranes and fetal
death. However, there is evidence of a publication bias in favour of studies with adverse
outcomes, which seem to be largely restricted to heavy, chaotic, injecting use. Cocaine
does not cause withdrawal symptoms in the neonate and substitution is neither feasible
nor beneficial.
Neonatal withdrawal symptoms

Neonatal withdrawal symptoms (neonatal abstinence syndrome) occur with maternal
use of opiate/opioids and benzodiazepines. Their severity is largely dose related but the
many other relevant co-factors (e.g. intra-partum hypoxia, infection or other illness in
the baby) make it impossible to predict outcome for an individual baby. A combination
of opiates/opioid and benzodiazepine use is particularly problematic. Breast-feeding
reduces the severity of neonatal withdrawals and is especially beneficial in this
vulnerable group of babies. While the mothers drug use should be reasonably stable,
successful establishment of breast-feeding is in itself sufficient proof of stability. Babies
should be gradually weaned because sudden discontinuation of breast-feeding could
precipitate withdrawals in the baby.
Obstetric management
Use of opiates/opioids or benzodiazepines can reduce fetal heart rate variability and
make it difficult to interpret antenatal or intra-partum cardiotocographs. Reversal
of maternal opiate/opioid intoxication or neonatal sedation with naloxone can be
dangerous.
Methadone medication should be continued in labour if due. Opiate analgesia can also
be given and while, in theory, larger doses may be required this is often not the case
in practice. Epidural analgesia is often appropriate but venous access can be difficult,
which can also cause problems if immediate delivery by caesarean section is required.
Associated medical problems

Injecting drugs causes vascular damage and infection can lead to endocarditis and
valvular damage necessitating use of prophylactic antibiotics during labour and other
procedures likely to cause bacteraemia (Figure 1). Blood-borne virus infection is also a
risk.
1 Scarring of leg caused by injecting drug use. Mary Hepburn
Poor diet and poor oral hygiene make dental caries common. These are often
associated with bacteraemia and should be dealt with during pregnancy under antibiotic
cover.
Injecting into veins or arteries carries the risk of thrombo-embolic disease and
women with current or past episodes of thrombosis with or without embolism require
therapeutic or prophylactic anticoagulation.
Blood-borne virus infection

Women should be offered antenatal screening because they are pregnant and not
because they are perceived as likely to be infected. Testing should be offered in their
interests, not for infection control and should always be offered without pressure to
accept.
HIV infection
Known HIV-positive women should be offered interventions to reduce the risk of
vertical transmission. Antiretroviral therapy, if already started, is usually continued
throughout pregnancy but is otherwise offered during the third trimester. The aim
is to reduce maternal viral load, ideally to an undetectable level. Treatment of the
baby for the first month of life is also advocated. Elective caesarean section reduces
vertical transmission but may not carry significant additional benefit for women with
undetectable viral load. If aiming for vaginal delivery, early rupture of the membranes
and use of fetal scalp electrodes should be avoided if possible. Breast-feeding
increases the risk of vertical transmission and should be avoided.
Hepatitis B infection
Perinatal transmission of hepatitis B can be prevented by immun-ization of the baby
at birth. Babies of Ag positive mothers require active and passive immunization while
babies of Ag negative mothers require active immunization. Both groups can safely
breast-feed. Hepatitis B immunization is recommended for all injecting drug users and
for women infected with hepatitis C. A complete course can be safely administered
during pregnancy using an accelerated regimen.
Hepatitis C infection
There is no effective immunization against hepatitis C nor any intervention that
significantly reduces perinatal transmission. However, maternal screening allows
infected mothers to access specialist care and identifies babies who require follow-up.
The available evidence suggests breast-feeding does not increase the risk of vertical
transmission of hepatitis C.
Outcome of pregnancy among drug-using women

Neonatal abstinence syndrome can be a major management problem but there is
no reliable evidence to suggest that it causes permanent damage. However, low
birthweight, which may be associated with preterm delivery or fetal compromise has
long-term health implications. There is also an increased risk of sudden infant death
syndrome (SIDS). Both low birthweight and SIDS are multifactorial in origin and
socioeconomic deprivation and associated problems (including smoking) are other
aetiological factors.
Design and delivery of care

Management of maternal drug use should be provided within multidisciplinary maternity
care. Although unsuitable for midwifery-only care these women can receive much of
their care from midwives in the community. The multiple social problems associated
with drug use can tax parenting skills especially if the baby is sick. Consequently, drug-
using women often require considerable support with childcare. Careful antenatal and
post-partum assessment is essential with early introduction of support services.
Effective multidisciplinary collaboration is essential to provide integrated care that

addresses the medical and social problems. This provides the best chance of delivery
of a healthy baby that can go home with and be adequately cared for by its mother.
u
FURTHER READING
British HIV Writing Committee. BHIVA Executive Committee.
British HIV Association (BHIVA) Guidelines for the Treatment of HIV-infected Adults
with Antiretroviral Therapy. HIV Medicine October 2001; 2 (4): 276313.
British Medical Association. The Misuse of Drugs. London: British Medical Association,
1997.
Dolovich L R, Addis A, Vaillancourt J, Power J, Koren G, Einarson T. Benzodiazepine

Use in Pregnancy and Major Malformations of Oral Cleft: Meta-analysis of Cohort and
Case Control Studies. Br Med J 1998; 317: 83943.
Hepburn M. Drugs of Addiction. In: Cockburn F, ed. Advances in Perinatal Medicine.

Carnforth: Parthenon Publishing, 1997; 1204.
Koren G, Graham K, Shear H, Einarson T. Bias against the Null Hypothesis: the
Reproductive Hazards of Cocaine. Lancet 1989; 2: 14402.

Ophthalmology
Anaesthesia
on CD-ROM
Anaesthesia for Eye Surgery in
Paediatrics
Jonathan Lord
Jonathan Lord is Consultant Anaesthetist at Moorfields Eye Hospital, London, UK. His
specialist interest is paediatric ophthalmic anaesthesia.
Children present for ophthalmic surgery from the neonatal period onwards. Neonates
and infants generally present for cataract extraction and treatment for congenital
glaucoma whereas older children more often have strabismus, lacrimal, vitreo-retinal
or ocular plastic surgery. Many children present for repeated procedures and skilled
anaesthesia contributes to a successful result. The problems of anaesthesia are
essentially the same as those of paediatric anaesthesia in any field, however, there are
some areas that require particular attention.
General considerations
Airway: although not strictly a shared airway, most ophthalmic operations involve
draping the head and thus abolish or at least reduce access to the airway.
Intraocular pressure (IOP): normal IOP is 1022 mm Hg. The factors that affect IOP
are essentially the same as those that affect intracranial pressure. The control of IOP
is an important part of the anaesthetic management of intraocular surgery. Any sudden
increase in IOP with an open eye leads to loss of ocular contents and/or an expulsive
haemorrhage. The likely outcome of such an event is loss of vision. The main factors
involved in the regulation of IOP are the choroidal, aqueous and vitreous volumes
together with external pressure.
Choroidal volume can be affected by venous pressure, arterial pressure and
arterial partial pressure of carbon dioxide.
Venous drainage from the eye is valveless and therefore any changes in venous
pressure produce an immediate change in ocular pressure by altering the volume of
blood within the choroid. Raised venous pressure also impedes aqueous drainage via
the canal of Schlemm and causes a secondary rise in IOP. Coughing, straining and
retching all increase venous pressure. A 15 head-up tilt reduces IOP.
Mean arterial pressure has little effect on IOP but sudden increases in mean arterial
pressure produce a rapid and unpredictable rise in IOP.
Alterations in arterial partial pressure of carbon dioxide have a linear effect on IOP. A
reduction causes a fall in choroidal volume and thus in IOP and vice versa.
Aqueous volume although alteration of aqueous volume is the mainstay of
glaucoma therapy it is of limited importance during anaesthesia because without direct
drainage the volume alters slowly. Acetazolamide reduces aqueous production and
reduces IOP.
Vitreous volume is of limited importance during anaesthesia. Osmotic diuretics
(e.g. mannitol) can dehydrate the vitreous and reduce its volume.
External pressure direct pressure on the eye, for example with a mask, must be
avoided. Increase in tone of the extraocular muscles increases IOP, thus depolarizing
muscle relaxants (e.g. suxamethonium) cause an increase in IOP. The rise produced
by suxamethonium is maximal at 2 minutes and lasts for 5 minutes. Pre-treatment
with non-depolarizing muscle relaxants to prevent this has been advocated but is of
unproven value.
Oculocardiac reflex is potent in children. The afferent and efferent pathways are
shown in Figure 1. It can be triggered by increases in IOP, traction on the extraocular
muscles, trauma or pain. It usually produces a bradycardia but asystole quickly ensues
in children if left untreated. Other arrhythmias such as nodal rhythms and ventricular
fibrillation can also occur. Without any preventive treatment the reported incidence
varies from 30 to 90%. Pre-treatment with a vagolytic is protective. Oral atropine can be
given as part of the premedication, and intravenous atropine or glycopyrrolate can be
given peroperatively. Infiltration around the extraocular muscles with local anaesthesia
also reduces the reflex. It is important that a pulse monitor with an audible bleep
is used peroperatively so that both the anaesthetist and the surgeon can hear if a
bradycardia occurs.
Oculocardiac reflex pathway

Acute ocular trauma: the question of how to deal with acute ocular trauma in an
unstarved child is often discussed. Many centres avoid the problem by avoiding
emergency surgery because there is no evidence that waiting for the child to be starved
influences the outcome of surgery. However, 6 hours' starvation in a traumatized child
does not mean that the stomach will be empty and consideration must to be given to
this. Prokinetics (e.g. metoclopramide) together with H2-blockers (e.g. ranitidine) to
increase stomach pH can be given. The management of the anaesthetic is controversial
but the need to avoid suxamethonium if the eye is open is paramount because loss
of contents can occur from the rise in IOP. The authors opinion is that induction of
anaesthesia should be either intravenous with a fast-acting non-depolarizing muscle
relaxant (e.g. rocuronium) or inhalational. Intubation is preferable to
protect the airway. The child should then be extubated awake.
Postoperative nausea and vomiting (PONV): ocular procedures in general are

emetic and if consideration is not given to this a high proportion of children will have
PONV. It is produced as a result of the manipulation of the extraocular muscles, by
alterations in the IOP or by volume expansion within the orbit. Any child with persistent
vomiting following an intraocular procedure must be checked by the surgeon to exclude
raised IOP as the cause. As always, prevention is better than cure and suggested drug
treatments are shown in Figure 2.
Associated syndromes: eye abnormalities in children are often manifestations of

multisystem disorders. Many of these syndromes have anaesthetic significance and any
anaesthetist involved in paediatric ophthalmology should look out for any associated
problems. Some of the common syndromes are given in Figure 3.
Anti-emetic drugs for postoperative nausea and vomiting

Drug Dose Comments
Ondansetron 0.10.15 mg/kg (maximum 8 mg) Excellent anti-emetic; low side-effect profile
Cyclizine 1 mg/kg (maximum 50 mg) Effective but sedative
Dexamethasone 200300 g/kg (maximum 8 mg) Very effective, particularly for orbital implants
Congenital syndromes
Syndrome Ocular manifestation Anaesthetic significance
Downs Strabismus, cataract Cardiac problems, hypothyroidism, blood
dyscrasias
Goldenhars Ptosis Difficult intubation
Homocystinuria Lens dislocation Thromboembolism, hyperinsulinaemia
Marfans Lens dislocation, retinal detachment Heart valve defects, thoracic aneurysms
Sickle haemoglobinopathies Retinopathy Sickle crises
Sticklers Retinal detachment None
SturgeWeber Secondary glaucoma Epilepsy
Malignant hyperthermia is more common in ophthalmic, and in particular strabismus,

surgery. Temperature should therefore always be monitored. All anaesthetic
departments should ensure that personnel are aware of the recommendations for
treatment of malignant hyperthermia as well as the location of the necessary drugs
within the department.
Analgesia: most ophthalmic operations are not particularly painful and simple
analgesia in the form of paracetamol or other non-steroidal anti-inflammatory drugs
(NSAIDs) is all that is required. The main exceptions are strabismus surgery in which
the muscle necrosis following suturing can cause marked pain, detachment surgery
where an encircling band is used and larger procedures such as tumour resection or
eviscerations. Postoperative analgesia should be considered as part of the overall plan
of anaesthesia. A multimodal approach using local anaesthesia, paracetamol, NSAIDs
and opioids is logical. A suggested regimen is given in Figure 4. Local anaesthesia
can take the form of topical local anaesthetic drops or formal local blocks. Sub-Tenon
anaesthesia is particularly useful in strabismus and detachment surgery.
4
Specific problems
Measurement of IOP: glaucoma can be defined as a progressive optic neuropathy and
if left unchecked eventually results in blindness. The effective management of children
with glaucoma includes the accurate measurement of their IOP. In those under 5 years,
this usually requires an anaesthetic. All currently available anaesthetic agents, with the
exception of ketamine, reduce IOP. The extent of this reduction is unknown and not
repro-ducible even in the same individual. This can lead to misleading IOP readings
and have a detrimental effect on treatment.
Ketamine is the drug of choice for IOP surveillance. It is a phencyclidine derivative
that produces dissociative anaesthesia via its action at the N-methyl-D-aspartate
(NMDA) receptors. It produces either no change or a transitory rise in IOP through a
combination of its sympathomimetic effects and extraocular muscle contraction. Studies
suggest, that this rise is not seen if the child is premedicated with a benzodiazepine. A
suggested technique for ketamine anaesthesia is shown in Figure 5.
It is unnecessary to secure the airway and the child should be allowed to breathe
spontaneously in air. Supplemental oxygen is occasionally required. Premedication with
a benzodiazepine is essential because it causes amnesia (which is useful in repeated
anaesthetics in children), ketamine sparing (allowing the dose of ketamine to be
reduced) and reduces emergence phenomena. Ketamine causes excessive salivation
and should always be used in conjunction with an anticholinergic to reduce the risk
of laryngeal spasm. Ketamine is emetic and routine administration of an anti-emetic
is required. Children having multiple frequent ketamine anaesthetics can develop an
unpredictable resistance to ketamine, necessitating escalating doses. This resistance
resolves if ketamine is avoided for a few weeks.
Anaesthetic technique for measuring intraocular pressure
Premedication
Oral atropine, 30 mg/kg 1 hour preoperatively
Oral midazolam, 0.5 mg/kg 1 hour preoperatively
Ametop over convenient vein
Induction
Intravenous ketamine (50 mg/ml strength) 12 mg/kg
Onset 30 seconds
Duration 510 minutes
or
Intramuscular ketamine (100 mg/ml strength) 10 mg/kg
Onset 28 minutes
Duration 1020 minutes
Intravenous access after induction
or
Oxygen and sevoflurane up to 8%
Intravenous access
Intravenous ketamine as above
After inhalational induction it is advisable to wait 5 minutes before measuring
intraocular pressure to allow sevoflurane washout
5
Intraocular surgery: the key to successful intraocular surgery is a balanced general
anaesthetic with intermittent positive pressure ventilation. Two suitable schemes are
shown in Figure 6. The anaesthetic should be planned to try to avoid any of the factors
previously described that may increase IOP.
Extraocular surgery is mainly strabismus and lacrimal duct surgery. In general, these
are best performed with a straightforward anaesthetic allowing spontaneous breathing.
In strabismus surgery, consideration must be given to analgesia, avoidance of the
oculocardiac reflex and anti-emesis. A suggested technique is shown in Figure 7.
Anaesthesia for intraocular surgery

Premedication
Midazolam, 0.5 mg/kg orally if required
Ametop to a suitable vein
Induction
Intravenous access Inhalational oxygen + sevoflurane
Remifentanil, 1 g/kg Intravenous access
Propofol, 23 mg/kg Rocuronium 0.60.9 mg/kg
Laryngeal mask airway or tracheal tube
Maintenance
Intermittent positive-pressure ventilation with oxygen + air Intermittent positive pressure ventilation with nitrous
Remifentanil intravenous infusion 0.30.5 g/kg/minute oxide + oxygen + sevoflurane
Propofol intravenous infusion 48 mg/kg/hour
Analgesia
Diclofenac 12 mg/kg p.r.
and/or paracetamol, 2030 mg/kg p.r.
Reversal
Nil required Neostigmine, 50 g/kg + glycopyrrolate, 10 g/kg
Anaesthesia for strabismus surgery

Premedication
Midazolam, 0.5 mg/kg orally if required
Atropine, 30 g/kg orally
Ametop to a suitable vein
Induction
Inhalational or intravenous as required
Laryngeal mask airway
Maintenance
Spontaneous ventilation with nitrous oxide + oxygen + sevoflurane
Analgesia
Diclofenac, 12 mg/kg p.r.
And/or
Paracetamol 2030 mg/kg p.r.
And/or
Codeine phosphate, 1 mg/kg i.m. or p.r.
Anti-emetic
Ondansetron, 0.15 mg/kg i.v.
FURTHER READING
Mather S J. A Handbook of Paediatric Anaesthesia. Oxford: Oxford University Press,
1996.
Miller R D. Anesthesia. 5th ed. Edinburgh: Churchill Livingstone.

Care of the Eye during
Anaesthesia
Emert White
Emert White is Consultant Anaesthetist at Warwick Hospital, Warwick, UK. He

qualified from Birmingham University and trained in anaesthesia in Nottingham and
Southampton. He has a special interest in ocular physiology and anaesthesia.
Perioperative eye injuries and blindness are rare but important complications of
anaesthesia. Eye injuries account for 3% of claims against anaesthetists. A better
understanding by anaesthetists of orbital anatomy and ocular physiology and the
mechanisms of ocular injury may help to reduce injuries.
Arterial supply to the optic nerve and retina
The ophthalmic artery enters the orbit through the optic canal enclosed within the
dural sheath of the optic nerve and its first branch within the orbit, the central retinal
artery, runs along the inferior aspect of the optic nerve, exiting from the dural sheath
of the optic nerve about 10 mm behind the globe. The vascular supply to this posterior
part of the optic nerve is from pial branches of the ophthalmic artery and the central
retinal artery.
The central retinal artery divides into four major vessels at the optic disc each
supplying one quadrant of the retina. The retinal vessels are distributed within the
inner two-thirds of the retina, while the choroidal circulation supplies the outer layers
of the retina.
Two to three posterior ciliary arteries arise from the ophthalmic artery, each of which
divides into one long and 810 short posterior ciliary arteries. The short posterior ciliary
arteries pierce the sclera and form the choriocapillaris, which supplies the anterior part
of the optic nerve, the lamina cribosa and the choroid posterior to the equator.
The choriocapillaris is composed of small lobules supplied by a terminal arteriole.
Each lobule has draining venules at the periphery.
The long posterior ciliary arteries travel forward in the suprachoroidal space to the
ciliary body where they combine with the anterior ciliary arteries to form the major
arterial arcade. Recurrent branches of the long posterior ciliary arteries supply the
choroid anterior to the equator and anastomose with the short posterior ciliary arteries.
Watershed zones occur between the:
choroidal and retinal circulation
long posterior ciliary arteries
short posterior ciliary arteries
long posterior ciliary arteries and the anterior ciliary arteries
choriocapillaris lobules.
Thus, in the event of ischaemia, the pattern of visual disturbance is variable.
Ocular blood flow and perfusion
Ocular blood flow (OBF) is determined by the pressure difference between mean
arterial pressure (Pa) and mean venous pressure (Pv) and the resistance to that flow
(R).
OBF = Pa Pv
R
Retinal blood flow is about 170 ml/100 g/minute. The choroid receives 65% of the total
ocular blood flow, while the retinal circulation receives 2%.
In the upright position, the pressure within the artery entering the eye is 6070 mm
Hg, while the intraocular pressure is 1015 mm Hg, which under normal conditions
provides a perfusion pressure of about 50 mm Hg. The episcleral venous pressure is
about 37 mm Hg (78 mm Hg lower than the intraocular pressure) and increases by
34 mm Hg in the supine position. When intraocular pressure increases above 15 mm
Hg, the episcleral venous pressure rises in direct proportion to the intraocular pressure
thus reducing perfusion pressure. Retinal blood flow is maintained by autoregulation
over a wide range of perfusion pressures. Autoregulation does not occur in the
choroidal vascular system and increases in intraocular pressure reduce choroidal blood
flow.
Ischaemic optic neuropathy
When intraocular pressure increases, retinal blood flow remains constant until the
intraocular pressure reaches about 40 mm Hg. At an intraocular pressure of about 60
mm Hg, blood flow to the optic nerve at the disc ceases, but flow is maintained in the
choroidal and retinal circulation. In humans there is little correlation between occlusion
time and visual outcome, but in other primates irreversible damage occurs if ocular
ischaemia exceeds 100 minutes.
Ischaemia of the optic nerve is caused by:
arterial hypotension (hypotensive anaesthesia, haemorrhage)
elevated venous or intraocular pressure
increased resistance to flow (seen in atherosclerosis, diabetes mellitus,
hypertension, thromboembolism)
decreased oxygen delivery (anaemia).
Ischaemia of the optic nerve is classified as anterior or posterior ischaemic optic
neuropathy.
Anterior ischaemic optic neuropathy is characterized by infarction at the watershed
zones listed above, a visual field defect, a pale oedematous optic disc and oedema of
the optic nerve in the posterior scleral foramen.
Posterior ischaemic optic neuropathy occurs when the pial branches of the
ophthalmic artery become occluded. Blood flow in the posterior part of the optic nerve
is significantly less than that in the anterior part. These pial vessels are incapable of
autoregulatory control and therefore this part of the optic nerve is more vulnerable to
ischaemia in the event of a fall in perfusion pressure or anaemia. Posterior ischaemic
optic neuropathy is characterized by a slower onset of visual field defect and mild optic
disc oedema.
The incidence of ischaemic optic neuropathy varies between 1/30,000 and 1/60,000
operations. High-risk procedures are spinal surgery, cardiopulmonary bypass and
bilateral neck dissection. The primary mechanism of ocular ischaemia following bilateral
radical neck dissection is the reduction of the ocular perfusion pressure caused by the
increase in venous pressure when the normally adequate venous collateral circulation is
sacrificed to ensure adequate tumour clearance.
During spinal surgery, patients may be placed prone with the head in a dependent
position thereby elevating venous pressure and reducing perfusion pressure. In the
prone position, venous pressure may be further increased by abdominal compression
with resultant upward shift of the diaphragm. During spinal surgery, direct pressure
on the eye as a result of patient malposition has caused ischaemic optic neuropathy.
Stigmata of orbital compression are:
intraoperative bradyarrhythmias
hyperaemic conjunctiva
periorbital numbness
periorbital abrasions
periorbital oedema.
Major blood loss resulting in anaemia, intraoperative hypotension and long operative
times in combination with the above factors appears to be the cause of ischaemic
optic neuropathy following spinal surgery. It is recommended that the haemoglobin level
should be maintained above 8 g/dl and the systolic arterial blood pressure at a level
greater than 60% of its preoperative recording. Cases of ischaemic optic neuropathy
have occurred above these recommended levels.
Ischaemic optic neuropathy should be suspected when a patient complains of
painless visual loss (with macular sparing) on emergence from anaesthesia. An urgent
referral to an ophthal-mologist for advice on diagnosis and treatment should be sought.
The aims of treatment are to reduce optic nerve fibre oedema as it passes through
the posterior scleral foramen with cortico-steroids or osmotic diuretics and to optimize
oxygen delivery by maintaining normal arterial blood pressure and haemoglobin. Vision
seldom improves after ischaemic optic neuropathy.
Anaesthetists need to be aware that reductions in ocular blood flow are
multifactorial, which cumulatively can put the eye at risk. Hypotension associated
with increases in venous pressure, raised intraocular pressure and poor positioning
when prone can jeopardize the eye especially in patients at high risk (e.g. those with
hypertension, diabetes, atherosclerosis).
Central retinal artery occlusion
Central retinal artery occlusion is often caused by emboli. It may occur in conjunction
with perioperative ischaemic optic neuropathy. It presents with a painless visual
defect. Ophthalmic examination shows a pale retina with a cherry-red spot. An urgent
ophthalmic opinion is required because treatment often improves the visual defect.
Treatment options are:
vasodilator therapy; inhalation of oxygen/carbon dioxide, calcium channel blockers,
nitrates
removal of obstruction
increasing perfusion pressure; paracentesis, carbonic anhydrase inhibitor
thrombolysis
reducing blood viscosity
reducing RBC rigidity pentoxifylline (oxpentifylline)
corticosteroids.
If the cause of central retinal artery occlusion is embolic, a cardiac or carotid source
should be sought.
Aetiology of perioperative corneal abrasions
The most common complication is corneal abrasion. The incidence is 0.030.17%

depending on the method of reporting. It is most commonly caused by exposure
keratopathy, chemical injury or direct trauma.
Anaesthesia reduces the tonic contraction of the orbicularis oculi muscle, which
may cause lagophthalmus. If the anaesthetist does not ensure that the eyes are
fully closed, exposure keratopathy may occur. Anaesthesia inhibits the protective
mechanism afforded by Bells phenomena, and decreases tear production and tear film
stability, which may lead to corneal epithelial drying and lysosomal protection.
Chemical injury can result from cleaning materials on the face mask and inadvertent
spillage of antiseptic skin preparations on to the eye. The only antiseptic skin
preparation that is not toxic to the cornea is povidoneiodine 10% in aqueous
solution. It is the agent of choice when antimicrobial skin preparation of the face is
required. Antiseptic solutions with detergent readily penetrate the corneal epithelium
causing damage to the underlying iris, ciliary body, lens and blood vessels leading to
ischaemia. Chlorhexidine, cetrimide and alcoholic antiseptic solutions cause oedema
and de-epithelialization of the cornea. Trauma to the eyes can occur at any time during
the perioperative period. During induction of anaesthesia it can be caused by ill-fitting
face masks, the laryngoscope, or the anaesthetists fingers, watchstrap, identification
badge or stethoscope. After induction of anaesthesia, trauma to the eyes by surgical
drapes, surgical instruments and during patient repositioning have all been reported. In
the recovery room, the patients fingers, pulse oximeter probe, pillow or Hudson mask
may injure the eye.
Methods to prevent perioperative corneal injuries include:
manual closure of the eyelids
taping the eyelids closed
using protective goggles
suture tarsorrhaphy
bio-occlusive dressings
contact lenses
installation of ointment, methylcellulose or viscous gels.
No method is 100% effective and the various protective strategies themselves may
be associated with morbidity. Vigilance regarding the perioperative care of the eye is
required to reduce these rare but potentially devastating complications.
FURTHER READING
Hart W M. Adlers Physiology of the Eye. 9th ed. St Louis: Mosby, 1992.
Morgan J P, Haug R H, Kosman J W. Antimicrobial Skin Preparations for the
Maxillofacial Region. J Oral Maxillofacial Surg 1996; 54: 8994.
White E, Crosse M M. The Aetiology and Prevention of Peri-operative Corneal
Abrasions. Anaesthesia 1998; 53: 15761.
Williams E L, Hart W M, Templehoff R. Postoperative Ischemic Optic Neuropathy.
Anesth Analg 1995; 80: 101829.

Eye Signs in Anaesthesia and
Intensive Care
Rahul Bajekal
Rahul Bajekal is Specialist Registrar in Anaesthetics at the Hillingdon Hospital,

London, UK. He qualified from Pondicherry, India, and trained in anaesthetics in
Chandigarh, India. In the UK he trains with the North Thames (West) Deanery.
The eyes are commonly used as clinical monitors in anaesthesia because they are easy
for anaesthetists to access, and generally give well-defined responses to interventions.
Most eye signs involve motor responses or reflexes related to different parts of the
eye (Figure 1).
Eye signs in anaesthesia
Sign Implications
Local anaesthesia
Horners syndrome Cervical sympathetic block
VI nerve palsy, dilated pupils Spinal anaesthesia
Sedation
Saccades Depth of sedation
General anaesthesia
Guedels signs Ether anaesthesia
Nystagmus Ketamine
Pupillary size Opioids
Intensive care
Glasgow Coma Score Head injury
Vestibulo-ocular, oculocephalic, Brain stem death
corneal, pupillary reflexes
Sustained unreactive pupils Poor recovery following
cardiopulmonary resuscitation
Eye signs in local anaesthesia

The success of a retro- or peribulbar local anaesthetic block of the eye may be gauged
from the degree to which it achieves an anaesthetic, immobile globe.
Horner's syndrome: ocular signs as part of Horners syndrome have been used
to monitor cervical sympathetic blockade. Ptosis, miosis and enophthalmos may be
indicators of a successful stellate ganglion block. These signs may also herald possible
complications, for example if seen with brachial plexus blockade.
Spinal anaesthesia: eye signs have been reported with spinal anaesthesia though not
commonly. Abducens nerve (lateral rectus muscle of the eye) palsy has been observed
as a complication, sometimes in the absence of a typical post-spinal headache; most
cases eventually resolve without intervention. Dilated pupils seen with a high spinal
block are associated with other features including cardiovascular and respiratory effects
and loss of consciousness. The presence of non-reactive dilated pupils should not
delay or interfere with attempts at resuscitation.
Eye signs in sedation

Traditionally, simple eye signs have been used to guide the depth of sedation. Drooping
of the eyelid (Verrills sign) was used by some clinicians while administering diazepam.
Loss of eyelid and eyelash reflexes was also used to assess adequacy of sedation.
These signs are inconsistent and almost always result in unacceptably deep levels
of sedation. Verbal contact with the patient is preferred rather than relying on ocular
signs.
Saccades: a recent review has evaluated the role of saccadic eye movements as
biophysical monitors of anaesthetic sedation. Saccades have been described as rapid,
semi-voluntary, conjugate, gaze-shifting movements designed to centre a target of
interest on to the fovea. They may be monitored using electro-oculography or infrared
oculometry. Peak saccadic velocity is useful for monitoring benzodiazepine-induced
sedation but other parameters and application to other anaesthetic agents is debatable.
Eye signs in general anaesthesia
Guedel's signs: ocular signs used to be taught as part of the clinical assessment
of anaesthetic depth. What are commonly known as Guedels signs or stages of
anaesthesia were a continuum of observations extending from analgesia to overdose.
Eye signs progressed from loss of the eyelash reflex to successive abolition of the
eyelid, conjunctival and corneal reflexes. The positions of the eyeball, eye movements
and pupil size were also used to assess the depth of inhalational anaesthesia.
The advent of relaxant and intravenous techniques combined with the increasing
popularity of opioids made Guedels signs obsolete. Pupillary signs were masked by
opioids, and other signs were inconsistent with newer inhalational and intravenous
agents.
During intravenous induction, anaesthetists commonly test the eyelash reflex. This
probably indicates deep sedation though it does not predict general anaesthesia
reliably.
Nystagmus is commonly associated with ketamine anaesthesia. Some clinicians have

used this with movement and phonation to titrate intermittent boluses of intravenous
ketamine. However, isolated eye signs are not useful.
Pupillary size has been used to monitor the depth of anaesthesia and opioid
overdosage. Though various studies have used pupillometry to describe the effect of
single drugs, applicability to anaesthesia is limited. Opioids generally cause miosis and
a decrease in the velocity of the pupillary light reflex. In equianalgesic doses, there
is little difference between the various opioids. Mydriasis has been described with
pethidine intoxication.
Tears have been used as part of scoring systems for adequacy of level of anaesthesia.
Used in conjunction with other signs, they may signify light anaesthesia, but alone they
are inadequate markers.
Eye signs in intensive care
Various eye signs have been described with concurrent medical conditions. Diseases
such as myasthenia may manifest with ptosis; though pure eye signs are inadequate in
diagnosis, the constricted pupil may help differentiate a cholinergic from a myasthenic
crisis.
The effect of various drugs on the pupils may help to diagnose certain cases of
poisoning. The presence of pallor, icterus or oedema of the conjunctiva and periorbital
haematomas all aid in diagnosing underlying conditions.
The Glasgow Coma Score (GCS) uses eye signs as one of its three components.
Observations range from no eye response to spontaneous eye opening; the score for
this parameter ranges from 1 to 4. The GCS is easy to use and standardized. It does
not describe pupil size or responses.
Dilated, non-reactive pupils: the presence of a dilated pupil unreactive to light is

sometimes used as an indicator of poor prognosis after cardiopulmonary resuscitation
(CPR). During the acute phase of CPR, the administration of drugs including
anticholinergics may mask underlying pupillary responses. Complete recovery has
been seen in patients who were noted to have so-called fixed dilated pupils.
The presence of unreactive and dilated pupils in the days following resuscitation
suggests a poor prognosis. Current guidelines for CPR do not recommend cessation of
resuscitative efforts in the presence of dilated non-reactive pupils.
Brain stem death: eye signs remain a diagnostic test for brain stem death. The neural
pathways for ocular reflexes involve the brain stem and their absence, along with other
criteria, is used to confirm the absence of brain stem activity. Tests include a fixed pupil,
unreactive to light regardless of pupillary diameter along with the absence of corneal,
oculocephalic and vestibulo-ocular (to caloric testing) reflexes.
FURTHER READING
Khan O A, Taylor S R J, Jones J G. Anaesthesia and Saccadic Eye Movements.
Anaesthesia 2000; 55: 87782.

General Anaesthesia for
Ophthalmic Surgery
Nicholas C B Pritchard
Nicholas C B Pritchard is Consultant Anaesthetist at Moorfields Eye Hospital, London,

UK. He qualified from St Mary's Hospital, London, and trained in anaesthesia in
London. His special interests are oculoplastic, paediatric and intravenous anaesthesia.
The use of local anaesthesia for eye surgery is increasing but general anaesthesia will
always have a place (Figure 1). Eye conditions are seldom immediately life threatening
and it is nearly always possible to wait for the stomach to empty before giving general
anaesthesia.
Eye operations are relatively painless procedures; however, patients are often
anxious and at the extremes of age. Coexistent disease is common. Most patients
are treated on a day-care basis or require an overnight stay only. There are multiple
ophthalmic subspecialties. Good cooperation between anaesthetist and surgeon is
important and the surgeon requires a soft, motionless eye on which to operate. Clinical
strategies to ensure immobility are also vital. An analysis of closed insurance claims
by the American Society of Anesthesiologists found that 30% of claims for eye injuries
associated with anaesthesia were related to patient movement during surgery.
Patient selection for general anaesthesia
Absolute
Patient preference
Young children
Uncooperative patient (e.g. mental retardation)
Patient unable to keep still (e.g. Parkinsons disease,
dystonia, arthritis, nystagmus, tremor, cough, dyspnoea,
vertigo)
Patient unable to lie flat for duration of operation
Long procedure
Allergy to local anaesthesia
Relative
Surgery to the patient's only functioning eye
Claustrophobia
Communication problems (e.g. deaf patient, poor language
comprehension)
Bleeding disorder
1
Preparation of patients
Coexistent disease is common in ophthalmic patients and preoperative optimization of

medical conditions is required. Investigations can be arranged through the anaesthetic
clinic and liaison with appropriate specialists (e.g. cardiologists, neurologists)
organized. Eye hospitals are sometimes remote from hospital backup services such as
intensive care and CT scanners.
Blood coagulation control: the maximum acceptable inter-national normalized ratio

(INR) for a patient taking warfarin depends on the operation (e.g. cataract < 3.5, eyelid
procedures < 2). Treatment with non-steroidal anti-inflammatory drugs (NSAIDs) or
aspirin should not be stopped for cataract surgery but should be stopped at least 10
days before surgery for eyelid procedures.
Starvation: the patient should be starved of solids for 6 hours before surgery and of
clear fluids for 2 hours.
Prophylaxis for deep vein thrombosis: mechanical devices such as compression

stockings, calf compressors and ankle elevators are useful. Heparin is usually avoided
unless the patient is at high risk, especially for retinal and oculoplastic procedures.
Diabetic control: patients with diabetes should be given local anaesthesia if possible.
If they have to be given general anaesthesia, their operation should be scheduled for
early on the operating list and their morning hypoglycaemic tablet omitted. It is usually
possible for patients to eat and drink soon after surgery, therefore it may be necessary
for patients to omit only their morning insulin dose.
Drug treatment should be continued in most patients, especially cardiac drugs,

antihypertensives, bronchodilators and cortico-steroids. It should be borne in mind that
eyedrops and other ophthalmic drugs have systemic effects (Figure 2).
Systemic effects of ophthalmic drugs
Drug Effect
-blockers Hypotension, bradycardia, bronchoconstriction
Phenylephrine Hypertension
Acetazolamide Hypokalaemia
Ecothiopate Prolonged action of neuromuscular junction blockers broken
down by pseudo-cholinesterases
Premedication may be required. Give the patient anti-emetics if they have a history
of postoperative nausea or vomiting (PONV) or if they are having an emetogenic
operation. Antihistamines (H2-blockers) should be considered if gastric acidity or
oesophageal reflux are problems, particularly if a laryngeal mask airway (LMA) is to
be used. Anxiolytics may be given if needed, but should be avoided for day case
surgery. Antimuscarinics should be given to children having ketamine for glaucoma
screening. Topical anaesthetic cream should be used for children and patients with
needle phobia.
Marking the side: the surgeon must mark the correct side for surgery before the
patient leaves the ward. This is rechecked on arrival in the theatre suite and again in
the anaesthetic room before induction. The eye that does not require surgery is taped
closed after induction. The surgeon and scrub nurse should check which eye requires
surgery for a final time just before cleaning the eye in the theatre.
Induction and maintenance of anaesthesia
Airway control
A mask is required for brief procedures only and avoids airway stimulation. The LMA is
the ideal airway for most ocular procedures. Insertion and removal of a tracheal tube
causes more cardiovascular stimulation than an LMA. Breath-holding, laryngospasm,
bronchospasm and coughing are all less likely using an LMA. However, access to
the airway during surgery is not easy without serious disturbance to the surgical field,
therefore the LMA must be well positioned and stable before surgery starts. If there is
any doubt about the reliability of the LMA position, it is safest to intubate the trachea.
Tracheal intubation is required in:
the obese
long procedures
potential airway soiling nasal bleeding from lacrimal surgery and mucous
membrane graft material harvesting from inside the mouth (lower lip or palate)
LMA failure
infants having medium to long operations
low chest compliance with high airway inflation pressures.
A preformed caudally directed, or an armoured flexible, tracheal tube taped away
from the eyes, is ideal.
Intraocular surgery requires intermittent positive-pressure ventilation (IPPV). It
allows accurate control of expired carbon dioxide and therefore intraocular blood
volume and, to a lesser extent, intraocular pressure. Muscle relaxants are not usually
required with the LMA if total intravenous anaesthesia is used. Some patients
undergoing total intravenous anaesthesia do not maintain their eyes in the neutral
position, they either look up or have a divergent squint. This can happen despite
adequate depth of anaesthesia with total intravenous anaesthesia and sometimes a
small dose of non-depolarizing muscle relaxant (rocuronium, 1020 mg, in an adult)
is required to correct it and allow surgery. If muscle relaxants must be avoided the
surgeon can use a traction suture to return the eye to a neutral position.
Intravenous fluids
Provided there is little if any blood loss there is no need for intra-operative fluids other
than maintenance crystalloid solutions. A full bladder causes hypertension and elevates
intraocular pressure.
Anaesthetic maintenance drugs

Most standard methods of maintaining anaesthesia are possible. Either of the following
work well for almost any combination of ocular operation and patient:
LMA remifentanil (Figure 3) + propofol / oxygen / air
tracheal tube remifentanil + sevoflurane / oxygen / air muscle relaxant for
intubation.
The relatively unstimulating nature of most ophthalmic surgery can cause
problems during general anaesthesia. Patients often become hypotensive, and
sympathomimetics (e.g. ephedrine, methoxamine) should be used to maintain blood
pressure and heart rate. On the other hand, awareness and patient movement are
hazards if a proper level of anaesthesia is not maintained. In particular, accidental
movement of the tracheal tube by the surgeon can cause coughing. The use of a
peripheral nerve stimulator can be more of a stimulus than the operation (particularly
anterior segment procedures) and can induce movement or coughing.
The benefits of using remifentanil for ocular surgery
Produces stable, low and controllable blood pressure and heart rate and therefore
intraocular pressure
Rapidly titratable to patient needs
Avoids need for maintenance muscle relaxants
Rapid and unique recovery profile with no residual effects
Dose and duration of infusion have almost no effect on recovery ideal for long
operations
Low incidence of nausea particularly with propofol
Avoids use of nitrous oxide in vitrectomy with gas injection
Well tolerated in patients with renal and hepatic disease
Monitoring
Spirometry is useful to identify changes in the position of an LMA during surgery.
Increased peak airway pressure, decreased compliance, reduced tidal volumes and a
difference between inspired and expired tidal volume should be sought. Invasive arterial
pressure monitoring is useful if profound induced hypotension is required. Central
venous pressure monitoring is seldom required. There is an association between
malignant hyperpyrexia and oculomuscular abnormalities, however, the usual problem
is hypothermia, which may cause shivering postoperatively. Postoperative shivering
is most common after long procedures in young fit males having total intravenous
anaesthesia. Intravenous pethidine is useful to abolish shivering. It is important
to monitor the skin or nasopharyngeal temperature. Warming mattresses, warm
air blowing devices and circle breathing systems may be used to maintain body
temperature. There is seldom any need to expose the body below the neck, therefore
patients can often be kept warm with blankets.
Pain: NSAIDs and paracetamol/codeine mixtures are usually adequate to control pain.
The surgeon can perform a sub-Tenon's local anaesthetic infiltration towards the
endof surgery to provide good postoperative analgesia. Severe pain and nausea may
result from raised intraocular pressure. This may be caused by a specific surgical
complication and the patient should be examined by the operating surgeon rather than
be treated for the symptoms. Intraocular pressure can be reduced in the short term by
acetazolamide, 500 mg intravenously over 5 minutes, or mannitol, 1 g/kg intravenously
over 30 minutes.be treated for the symptoms. Intraocular pressure can be reduced in
the short term by acetazolamide, 500 mg intravenously over 5 minutes, or mannitol, 1
g/kg intravenously over 30 minutes.
Extubation is probably best performed deep with spontaneous breathing. It is

important that the patient avoids coughing and straining on the tracheal tube.
Posture: after vitrectomy with injection of intraocular gas, the patient will have to
posture as soon as they are conscious. A face-down position or with one cheek to
pillow is usual. Following oculoplastic surgery, patients are usually nursed in a sitting
position.
Specific considerations for surgical subspecialties
Vitreo-retinal
Scleral buckle with or without cryotherapy:pain, PONV, and oculocardiac reflex are
often marked, especially in young adults.
Vitrectomy: (the type of gas injected after vitrectomy, to provide retinal tamponade,
depends on the required duration of action: Figure 4.) The patient will have to posture
postoperatively so that the gas bubble lies over the appropriate area of the retina. Since
the introduction of heavy perfluorocarbon liquids in vitreo-retinal surgery, the need
for intraoperative posturing (including turning the patient prone) has been eliminated.
Patients must not travel by aeroplane nor be exposed to nitrous oxide while the gas
bubble is present. Nitrous oxide is 34 times more soluble in blood than nitrogen.
Administered nitrous oxide rapidly diffuses into the intraocular gas bubble leading to
a large increase in bubble volume and intraocular pressure, which may cause central
retinal artery occlusion and blindness. If nitrous oxide is used during the anaesthetic for
vitrectomy it must be discontinued at least 15 minutes before gas bubble injection.
Gases used for retinal tamponade
Gases used Time in eye until bubble

(all non-expansile) clears
Air 23 days
SF6 20% (with air) 23 weeks
C3F8 14% (with air) 55 days ( 15 )
Oculoplastics
Oculoplastic operations are often undergone by the elderly, or children with syndromes
such as Goldenhars. Antiplatelet drugs must be stopped for 10 days before these
procedures, particularly eyelid surgery.
Orbital
Blood loss is possible during major orbital surgery, such as three wall orbital
decompression procedures for thyrotoxic exophthalmos, and tumour resections.
Transfusion of blood is seldom required, but induced hypotension with head-up
positioning and maintenance of low to normal arterial carbon dioxide tensions all help
to improve the surgical field and reduce bleeding. Retrobulbar or sub-Tenon's local
anaesthetic infiltration is useful during enucleation surgery to reduce postoperative
pain.
Glaucoma
In patients with glaucoma, reduction of the intraocular pressure is desirable. All
anaesthetic agents except ketamine and suxamethonium reduce intraocular pressure.
Local anaesthetic injection can further compromise optic nerve function and retinal
perfusion by increasing intraocular pressure in patients with advanced glaucoma.
Intubation (and extubation) of the trachea, can cause rises in intraocular pressure of up
to 50 mm Hg. LMA insertion is much less stimulating and should be used if possible.
Cataract
Cataract operations are short and the surgical stimulus is low, therefore they are usually
carried out under local anaesthesia. The use of LMA and total intravenous anaesthesia
is good for anterior segment surgery.
Commonly mentioned topics
The oculo-cardiac reflex

Operations associated with the oculo-cardiac reflex include:
squint
scleral buckle retinal repair
orbital implant
evisceration
enucleation.
The oculo-cardiac reflex is mediated via the trigeminal afferent with vagal efferent.
It manifests as a slowing in the sinus rate, which may become irregular. Sinus arrest
with asystole can occur but recovers when the precipitating cause (usually a surgeon
pulling on the muscle) is abolished. Other arrhythmias that may be seen include
atrioventricular junctional rhythms, wandering pacemakers, extrasystole and bigeminy.
Prophylactic antimuscarinic drugs (glycopyrrolate, 35 g/kg, or atropine, 10 g/kg)
should be given after induction before the operations listed above, particularly if the
patient is having total intravenous anaesthesia or other drugs that increase vagal tone.
This pretreatment will reduce the chance of bradycardia not abolish it. Further doses
may be required.
Local anaesthetic infiltration around the muscles abolishes the afferent pathway.
Non-depolarizing muscle relaxants also reduce the incidence of the reflex by reducing
extraocular muscle tone. There is a decrease in incidence with increasing age.
The open eye

In an open eye the intraocular pressure is the same as atmospheric pressure. The
danger is of expulsion of ocular contents. It is seldom necessary to operate as an
emergency. Penetration of the eye by copper fragments may be an exception, but even
then a delay for stomach emptying is usually possible. Do not try to empty the stomach
with a nasogastric tube. An LMA can be used for open eye surgery, subject to the
restrictions mentioned above.
Avoid ketamine and suxamethonium, which increase intraocular pressure.
Aim for a smooth, rapid induction. Rocuronium, 1 mg/kg, is suitable for muscle
relaxation.
Some degree of head-up tilt may be maintained during induction.
Avoid mask pressure directly on the eye.
Do not rush intubation. Wait for the induction drugs to have full effect.
Coughing, straining or gagging during premature intubation attempts can lead to loss
of ocular contents.
FURTHER READING
British Ophthalmic Anaesthesia Society Newsletters No 2, December 1999 and No 3,
October 2000.
Greenbaum S. Ocular Anaesthesia. Philadelphia: W B Saunders, 1997.
Katz J, Stewart D. Anaesthesia and Uncommon Pediatric Diseases. Philadelphia: W B
Saunders.
Vickers M, Power I. Medicine for Anaesthetists. Oxford: Blackwell Science, 1999.

Local Anaesthesia for Ocular
Surgery
Caroline Carr
Caroline Carr is Consultant Anaesthetist at Moorfields Eye Hospital, London, UK.

She qualified from Oxford University and St Mary's Hospital, London, and trained in
anaesthesia in London. Her special interest is in teaching local anaesthetic techniques.
Most surgery of the eye and its surrounding structures can be performed under
local anaesthesia. General anaesthesia is reserved for those unable to cooperate
(e.g. children), for bilateral surgery, and for extensive or lengthy procedures. Routine
cataract surgery is usually performed under local anaesthesia and efforts have been
concentrated on finding methods that have few serious complications. Traditionally,
the surgeon administered the ocular anaesthesia as operatoranaesthetist. Recognition
of occasional serious systemic complications of ophthalmic local anaesthesia,
especially in medically compromised patients, led to involvement of the anaesthetist.
The Joint Working Party report on Anaesthesia in Ophthalmic Surgery recommended
the involvement of the anaesthetist, including performing the local anaesthetic.
Anatomy
With any local anaesthetic technique a detailed knowledge of anatomy is essential; that
is beyond the scope of this article but the relevant areas are mentioned below.
The orbit may be visualized as a quadrilateral pyramid lying on its side. The open base
forms the orbital rim at the front of the skull and the apex lies at a depth of 40 mm. The
optic canal and superior orbital fissure open into the apex and admit the nerves and
blood vessels of the orbit. The tip of the 40 mm needles used in traditional retrobulbar
blocks could reach those vital structures at the orbital apex.
The globe is roughly spherical, with an average diameter of 24 mm and is suspended

in the orbit by connective tissue. It is displaced towards the orbital roof and to the
temporal side and projects anteriorly beyond the orbital rim. Needles placed medially
and inferiorly in the orbit are less likely to penetrate the globe. The optic nerve pierces
the globe medially to the posterior pole. The equator is midway between the two poles.
The extraocular muscles: the four rectus muscles originate at the apex of the orbit
and insert into the globe behind the limbus, forming a cone within the orbit. The superior
oblique muscle originates at the orbital apex and passes through the trochlear pulley
on the medial side of the orbital roof behind the rim before passing back to insert on
the globe. Needles should be avoided in this area to prevent trochlear damage. The
inferior oblique muscle originates at the front of the orbit, on the medial side of the
floor, and passes back and up between the lateral rectus and the globe before inserting.
Inferomedial needle placement should be avoided to prevent muscle damage.
Orbital connective tissue: Tenons capsule is a thin membrane of elastic fibres

enveloping the globe from limbus to optic nerve. It adheres closely to the sclera with
fine bridging fibres. All structures that attach to or pierce the globe cross the sub-
Tenons space including the long and short ciliary nerves. Local anaesthetic placed in
this space provides globe anaesthesia. The globe is supported anteriorly by connective
tissue slings passing from Tenons capsule to the orbital wall. Posteriorly it is supported
by a diffuse matrix of connective tissue from the sheaths of the extraocular muscles.
All the connective tissue is embedded in fat. The connective tissue system allows local
anaesthetic solution placed in the orbit to diffuse throughout the contents to provide
anaesthesia of sensory and motor nerves.
The orbital blood vessels: the ophthalmic artery is a branch of the internal carotid
and supplies the globe, orbital contents and neighbouring structures of the nose and
forehead. It enters the orbit through the optic canal, crosses over the optic nerve to run
medially in the orbit as it sends out branches to the contents. Venous plexuses on the
medial wall and floor of the orbit drain via the superior and inferior ophthalmic veins
through the superior orbital fissure into the cavernous sinus. Needles must be placed
with care in the medial side of the orbit to avoid these vessels.
The nerve supply to the orbit: motor innervation is from cranial nerves III, IV, VI
and VII (Figure 1). Sensory innervation is via the ophthalmic and maxillary divisions
of cranial nerve V (Figure 2). Parasympathetic innervation is through fibres in cranial
nerves III and VII. Sympathetic innervation is from the superior cervical ganglion. The
optic nerve is cranial nerve II.
Motor innervation of the eye
Muscle Nerve supply
Inferior oblique Oculomotor (III)

Superior rectus Oculomotor (III)
Inferior rectus Oculomotor (III)
Medial rectus Oculomotor (III)
Levator palpebrae superioris Oculomotor (III)
Superior oblique Trochlear (IV)
Lateral rectus Abducens (VI)
Orbicularis oculi Facial (VII) temporal and
zygomatic branches
Sensory innervation of the eye
Structures Nerve supply
Sclera, cornea, iris and ciliary body Short ciliary nerves

Long ciliary nerves
Conjunctiva superior Supraorbital nerve

Supratrochlear nerve
Infratrochlear nerve
Conjunctiva inferior Infraorbital nerve

Conjunctiva lateral Lacrimal nerve
Conjunctiva limbal Long ciliary nerve
Periorbital skin Supraorbital nerve

Supratrochlear nerve
Infraorbital nerve
Lacrimal nerve
2
The eyelids: the orbicularis oculi muscle is a flat elliptical muscle surrounding the
orbital margin, which closes the eyelids. The levator palpebrae muscle opens the upper
eyelid. It originates at the orbital apex and passes forward between the orbital roof and
superior rectus to fan out to insert into the upper eyelid.
Methods of local anaesthesia
Topical
Topical anaesthesia provides good surface anaesthesia of the globe without the
complications of a regional block. The patient retains full eye movement. Commonly
used for superficial surgery of the conjunctiva and cornea, including removal of sutures
and small foreign bodies, topical anaesthesia alone is now often used for cataract
surgery. With the newer surgical techniques, akinesia and reduction of intraocular
pressure are not of such importance. Patients experience discomfort owing to sensation
from the iris and ciliary body but this can be abolished by intracameral preservative-free
1% lidocaine (lignocaine), up to 1 ml.
Infiltration
Local infiltration of the skin with anaesthetic is used for eyelid surgery in adults.
For anaesthesia of deeper structures, the supraorbital and infraorbital branches of
the trigeminal nerve are blocked where they emerge from the supraorbital notch
and infraorbital foramen. 0.5% bupivacaine, 12 ml, with adrenaline (epinephrine)
1:200,000 are injected subcutaneously at each site. To avoid subcutaneous
haemorrhage:
aspirin should be stopped 2 weeks preoperatively
warfarin should be stopped 3 days preoperatively
avoid injection into deeper tissues
use adrenaline (epinephrine) 1:200,000 as a vasoconstrictor in the local anaesthetic
solution.
Retrobulbar block
The classical technique of retrobulbar block provided good akinesia and anaesthesia
and was usually supplemented with a facial nerve block to paralyse orbicularis oculi.
The principle of the technique was to deposit a small volume (23 ml) of anaesthetic
solution in the muscle cone at the apex of the orbit using a 40 mm long needle.
Rare, but serious, complications occurred with these blocks, including retrobulbar
haemorrhage, globe perforation, damage to the optic nerve or ophthalmic artery and
spread of the anaesthetic to the brain stem along the optic nerve dural sheath.
Peribulbar block
Peribulbar anaesthesia was introduced in 1986 to avoid the complications of retrobulbar
block. A shorter needle is used and places larger volumes of anaesthetic solution
outside the muscle cone with the needle tip no further back than the equator. The
anaesthetic spreads throughout the orbit and provides satisfactory operating conditions.
The technique usually consists of two injections of local anaesthetic, one inferior and
one medial to the globe. These sites are selected to avoid vital structures within the
orbit. The volume used is usually enough to block the nerves to orbicularis oculi directly.
More recent adaptations of the technique have been to direct the lateral injection up into
the muscle cone just behind the globe. This produces a more rapid and reliable onset
of block with a smaller volume of anaesthetic solution, and often the medial injection
is omitted. This is the modern retrobulbar technique. However there is still a risk of
globe perforation.
Technique of peribulbar block (Figures 3 and 4)

The patient lies supine with his head on a pillow.
The eyes are in neutral gaze.
A few drops of topical anaesthetic are applied to the conjunctiva (0.4%
oxybuprocaine).
The inferotemporal injection is given first, using a 25 G
25 mm sharp needle and 5 ml of anaesthetic solution.
Insert the needle through the conjunctiva, 2 mm away from the globe, midway
between the lateral canthus and the lateral limbus.
Keep the needle tangential to the globe and advance posteriorly and medially to a
depth of 15 mm. Keep the needle tip lateral to the sagittal plane of the lateral limbus.
Following test aspiration, slowly inject 25 ml of anaesthetic. Assess orbital tension
digitally.
Withdraw the needle, close the patients eye and maintain gentle pressure for 2
minutes.
Give the medial injection using a 25 G 12 mm needle.
Insert the needle medial to the medial caruncle, with the needle bevel facing
medially.
Advance posteriorly at 90 to the face to the depth of the needle hub.
Initial resistance may be felt at the medial check ligament.
Following aspiration, slowly inject 25 ml of anaesthetic, assessing orbital tension.
Withdraw the needle, close the patients eye and maintain gentle pressure for 510
minutes.
Assess the block and for hypotony for intraocular surgery apply an oculopressor
device for 10 minutes.
Any technique using a blindly placed sharp needle may result in serious
complications threatening sight, including globe perforation. The more recently
described technique of sub-Tenons block is now commonly used for most surgery on
the globe.
3 Peribulbar block inferolateral injection.

4 Peribulbar block medial injection.
Sub-Tenons block
Local anaesthetic is introduced to the sub-Tenons space through a small incision in
the inferior nasal quadrant of the eye. Posterior diffusion of the anaesthetic blocks
sensation from the eye by direct action on the ciliary nerves as they pass through the
sub-Tenons space. If a suitable volume of anaesthetic is used, complete akinesia is
obtained as it diffuses into the muscle cone from the sub-Tenons space.
Technique of sub-Tenons block (Figure 5)

The patient lies supine with his head on a pillow.
A few drops of topical anaesthetic are placed on the conjunctiva.
A few drops of 5% aqueous iodine are placed on the conjunctiva.
A small speculum is inserted to hold the eyelids apart.
The patient looks up and laterally.
The conjunctiva and Tenons capsule are pinched firmly with non-toothed forceps
57 mm from the limbus in the inferonasal quadrant.
With round-ended spring scissors a small snip is made through both layers.
The closed scissor tips are passed through the hole and the blades opened while
gently withdrawing them to form a short tunnel.
A blunt curved 19 G 25 mm sub-Tenons cannula is passed into the sub-Tenons
space and allowed to slide round the globe, over the sclera to a depth of 1520 mm
in the inferonasal quadrant.
Up to 5 ml of local anaesthetic is injected slowly.
The cannula is withdrawn and slight pressure maintained over the closed eye for 2
minutes, when complete akinesia and anaesthesia are seen.
Sub-conjunctival haemorrhage is kept to a minimum by using topical adrenaline
(epinephrine) 1:10,000, avoiding cutting conjunctival vessels, avoiding extensive
dissection and using gentle direct pressure.
Globe perforation has not been reported with this technique and it is often used as
the technique of choice in the long myopic eye. One case of retrobulbar haemorrhage
has been reported and the anaesthetist must always be aware of this risk with any
needle or cannula technique of ocular block.
5 Sub-Tenons block.
The local anaesthetic mixture

The characteristics of a block depend on the anaesthetic solution used as well as
the technique. 2% lidocaine (lignocaine) is effective within 5 minutes and gives 3040
minutes of surgical anaesthesia. 0.5% bupivacaine has a slower onset of action but
longer duration of surgical anaesthesia (up to 4 hours). The newer local anaesthetic
ropivacaine has been used successfully in peribulbar blocks but has little advantage
over bupivacaine in the small volumes needed in eye blocks. Mixtures of lidocaine
(lignocaine) and bupivacaine are often used to provide rapid onset with delayed offset
but are of no practical advantage. Addition of 1:200,000 adrenaline (epinephrine)
reduces haemorrhage in skin infiltration techniques but is not used in orbital blocks
because the vasoconstriction may compromise retinal blood flow. The enzyme
hyaluronidase in concentrations of 530 iu/ml enhances spread of anaesthetic and
speed of onset.
Patient management
Preoperative assessment is performed as for any anaesthetic. The patients

concomitant medical conditions should be controlled before surgery. Contraindications
to ocular local anaesthesia are patient refusal, being unable to lie flat and still for the
surgery, and allergy to local anaesthetic. The technique to be used should be explained
carefully and supplemented with leaflets and other patients experiences. Preoperative
starvation is unnecessary unless the patient is at high risk. Anticoagulated patients
must maintain their international normalized ratio (INR) within therapeutic limits (23)
for ocular surgery under topical, peribulbar or sub-Tenons anaesthesia. During surgery
the patient should have intravenous access and pulse oximeter, ECG and non-invasive
blood pressure monitoring should be available if required. Trained staff should monitor
the patient and the anaesthetist should be available for resuscitation or sedation this
is a controversial point because of manpower implications.
Sedation
Most patients readily tolerate ocular surgery under local anaesthesia with careful
explanation, gentle handling and a sympathetic approach. Occasionally, an anxious
patient may require sedation. An anaesthetist provides this with the appropriate
monitoring. Various techniques may be used. A small dose of intravenous
midazolam, 0.51.5 mg, before the anaesthetic provides amnesia while allowing verbal
communication.
FURTHER READING
Barry Smith G, Hamilton R C, Carr C A. Opthalmic Anaesthesia. London: Arnold, 1996.
Hamilton R C. Techniques of Orbital Regional Anaesthesia. Br J Anaesth 1995; 75 (1):

8892.
Johnson R W. Anatomy for Ophthalmic Anaesthesia. Br J Anaesth 1995; 75 (1): 807.
Rubin A P. Complications of Local Anaesthesia for Ophthalmic Surgery. Br J Anaesth

1995; 75 (1): 936.

Ophthalmology and
Anaesthesia
Luke Herbert
Luke Herbert is Vitreo-retinal Fellow at Moorfields Eye Hospital, London, UK
Possible eye problems in theatre
Intraocular gas
As part of the management of retinal detachment and some other retinal conditions,
long-acting gas is injected into the vitreous cavity (Figure 1). The surface tension of the
gas/fluid interface is used to close holes in the retina. However, the gas bubble has to
be positioned correctly and lying on the back is usually contraindicated.
The wrong management of patients with gas-filled eyes can cause blindness.
Several different gases can be used, the most persistent of which, C3F8, can remain in
the eye for 3 months. The gases are poorly soluble and remain in the vitreous cavity,
in equilibrium with, mainly, nitrogen. However, if a very soluble gas (e.g. nitrous oxide)
is inhaled, there is a massive influx of gas into the eye. This can cause the intraocular
pressure to rise rapidly, which can lead to blindness. Patients with gas in the eye must
never be given nitrous oxide as part of anaesthesia. A typical situation in which this
might occur is when the patient has ophthalmic surgery with long-acting gas injection
and after discharge from the eye unit, develops an acute surgical problem such as
acute retention of urine. The patient is then anaesthetized with nitrous oxide at a
different unit, and wakes up blind.
Some surgeons are also concerned about the use of nitrous oxide in the primary
surgery. If an eye is filled with gas, which the surgeon expects to be say, 16% C3F8 in
air, but the patient is anaesthetized with nitrous oxide, a large portion of the volume will
be taken up by the volume of the nitrous oxide. When the patient resumes breathing
room air the nitrous oxide rapidly leaves the eye, leaving the globe soft and vulnerable
to minor trauma, and reducing the amount of gas in the eye thus reducing the duration
of gas fill.
The total volume of gases in the eye tends to increase in the early postoperative
period as nitrogen diffuses in to the eye but C3F8 (which is poorly soluble) diffuses out
slowly. This can lead to raised intraocular pressure. It is important not to ignore pain as
a symptom of high pressure after surgery.
1 A retina: the upper half of the picture is out of

focus because there is a bubble of gas in the eye.
Silicone oil
In some patients, silicone oil is used instead of gas to plug holes in the retina. Silicone
oil floats in the eye. If the patient lies flat on their back, oil can float into the anterior
chamber of the eye (Figure 2), which can cause severe long- and short-term problems.
2 Oil has come into the anterior part of the eye and
forms a round globule in front of the iris and lens.
Odd-looking eyes
A patient waking with a fixed dilated pupil, a divergent squint and a glassy appearance
to the eye may have a prosthetic eye. Ask the patient about this before anaesthesia
it is not always easy to recognize a glass or plastic eye. Prosthetic eyes and their
sockets are unsterile, and organisms colonizing prosthetic sockets have infected remote
surgical sites.
Possible eye conditions in ICU
Mucormycosis
Mucormycosis (also known as zygomycosis) is an uncommon fungal disease. It is
often fatal and early aggressive treatment improves outcome. Orbital involvement may
need to be managed with aggressive surgical debridement including orbital exenteration
(removal of all orbital soft tissue, including the eye).
StevensJohnson syndrome
Patients with StevensJohnson syndrome have acute conjunctivitis that can lead to
acute and chronic ocular complications. Most of the acute complications are related
to exposure of the cornea and corneal drying. These can be prevented with physical
barriers such as simple eye ointment, used copiously every 34 hours, or frequent
use of lubricating drops (e.g. hypromellose 0.3% or normal saline, given every 3060
minutes). Drops given so frequently are best used unpreserved to prevent local toxicity
caused by preservatives. These drops may not be available in general hospitals in
which case normal saline for intravenous use can be used. The solution should be kept
cool, and discarded every day.
Chronic complications include scarring of the conjunctival surface. Previously,
lysis of nascent scars was encouraged in the acute phase, breaking down
conjunctival adhesions with a glass rod, but there is little evidence that this is of
benefit. Many ophthalmologists prescribe corticosteroid drops in the acute phase, but
there is little evidence of long-term benefit. Occasionally, the noninfected conjunctivitis
can become secondarily infected with a sudden increase in the purulence of the
secretions; this requires urgent ophthalmic attention.
Fungal endophthalmitis
Systemic fungal infections, typically with Candida albicans and occasionally Aspergillus
spp. can metastasize to the choroid and vitreous cavity causing a fungal
endophthalmitis (Figure 3). Patients with long-term intravenous line placement are at
particular risk of fungal endophthalmitis. They present with pain, decreased vision and
floaters. Many patients with systemic fungal infections do not develop endophthalmitis,
and many patients with endophthalmitis show no other signs of infection, especially
those who are transiently immunocompromised. Candida infections may resolve with
systemic treatment alone, usually with oral fluconazole. In patients with advanced
involvement of the vitreous, vitrectomy should be carried out to debulk the fungal
load and remove the vitreous, which acts as a substrate for further fungal growth. An
extended course of treatment is required. With appropriate management, most patients
with Candida endophthalmitis will maintain some vision. The prognosis is not as good
in Aspergillus endophthalmitis.
3 Fungal endophthalmitis; the fluffy white lesions are

balls of fungus growing within the vitreous cavity.
Ophthalmic complications related to ICU care
Conjunctival oedema (chemosis)

Patients with low plasma oncotic pressure who lie on their back tend to accumulate
fluid around the face. This can lead to profound swelling of the looser facial tissues,
particularly around the eyes. The conjunctiva is bound to the underlying sclera by a
weak meshwork of fibres. This potential space easily fills with tissue fluid causing the
conjunctiva to balloon out. This is called chemosis and can be very striking, even
preventing the eyelids from closing properly. Treatment is by raising the head of the bed.
If the eyelids cannot close, the cornea should be protected with copious amounts of
simple eye ointment to prevent drying and corneal exposure.
Corneal exposure
The cornea depends on tears, and the redistribution of tears and resurfacing of the
tear film by blinking is essential. The production of tears is reduced when the patient is
asleep or unconscious. When asleep, the eyelids can remain partly open, but in most
people the Bells phenomenon in which the eyes roll superiorly helps to protect the
cornea from drying. In the anaesthetized, paralysed patient the cornea is vulnerable
to drying, because tear production is low, the eyelids can open and the eyes remain
in the primary position.
The corneal epithelium and even the conjunctival epithelium cannot survive dry
for long. The cornea soon develops small dry spots of dead or dying epithelial cells,
known as exposure keratitis. With continued dryness or other insults, these areas
lose their epithelium to become corneal erosions, also called abrasions (Figure 4).
Once the epithelium is lost the cornea is vulnerable to infection (the conjunctival sac
is never sterile) and frank corneal ulcers can develop. This can be a problem in the
high-dependency setting where the author has seen febrile, unconscious patients with
fans thoughtfully placed to remove the last drops of moisture from the eye. The cornea
should be protected with ointment and taping.
This chronically exposed eye has developed a corneal ulcer (a). The edges of the corneal ulcer are
stained bright yellow (b) with fluorescein dye.
4
Corneal abrasion
The anaesthetist has to help protect the patients cornea from drying and trauma
otherwise a corneal abrasion may develop. Abrasions are exquisitely painful; the eye is
usually red and the vision may be slightly blurred. However, they heal rapidly, and the
pain should reduce within the first day of treatment.
Taping the eye: one way to protect the cornea is to tape the eyelid shut. Taping
vertically across the eyelid is unhelpful, because the eyelid can open under the tape
and the cornea can rub on the tape (Figure 5). The correct way to tape is from corner
to corner (Figure 6).
Venturi masks, if they are badly placed, can cause corneal abrasions and corneal
infection in debilitated patients. It is common on chronic wards to see the Venturi mask
pushed off so that an edge rubs on the eye (Figure 7).
5 The wrong way to tape an eyelid shut.
6 The right way to tape an eyelid shut.
7 Venturi mask pushed off allowing an edge to rub the

eye (this picture was posed, but this does happen).
Acute angle closure glaucoma

Anticholinergic agents allow the pupil to dilate and in susceptible patients this can lead
to acute angle closure glaucoma. This is more common in older patients who have not
had cataract surgery. The signs are of a mid-dilated pupil that does not react (direct
or consensual) to light, a slightly dull sheen to the cornea and, in conscious patients,
severe pain that can cause confusion and vomiting. Acute glaucoma is not related to
chronic glaucoma. If a patient is already receiving treatment for glaucoma it is unlikely
that they will suffer an attack because susceptible patients identified in an eye clinic
usually have immediate prophylactic laser treatment or surgery.
Systemic problems caused by ophthalmic treatment
Eye drops
Most patients do not regard eye drops as medication and it is common for patients
taking two or three eye drops to deny that they take any medication. Almost all eye
drops have some systemic side-effects, and the most important are described below.
-blockers: some topical -blockers are relatively cardio-selective. All topical -

blockers precipitate asthma attacks in susceptible patients. All -blockers reduce
exercise tolerance and can precipitate heart failure. Most -blockers are well know, the
exception is Cosopt, which contains timolol 0.5% maleate.
-agonists: adrenaline (epinephrine) used to be used as an antiglaucoma medication.

It can precipitate angina and hypertensive episodes. Adrenaline (epinephrine) and its
pro-drug, dipivefrine, are less fashionable now, but the new selective 2-adrenoceptor
agonists, brimonidine and apraclonidine, can act as systemic hypotensive agents in the
same way as clonidine.
Pilocarpine is less commonly used now, but it used to be the mainstay of glaucoma
therapy. It constricts the pupils, making assessment of pupillary function impossible.
Pilocarpine worsens asthma in some individuals and is best not used in patients with
severe reversible airway obstruction.
Latanoprost is a prostaglandin analogue used in glaucoma treatment. It can precipitate

an attack in poorly controlled or brittle asthma.
Atropine is the prototype agent for the mydriatics, including homatropine,

cyclopentolate and tropicamide. It is the agent most likely to cause problems in the
ICU because of its long duration of action in the eye. Atropine is used for painful
blind eyes, to ease ciliary spasm, to reduce pain in the postoperative period and
to facilitate examination by keeping the pupil dilated. This fixed dilated pupil can be
most disconcerting in an acute ICU setting because the dilating effects can take a week
to wear off, particularly in darker eyes.
It is possible to distinguish between atropine mydriasis and a pathologically dilated
pupil by instilling a drop of 1% pilocarpine: a pupil affected by atropine or by local
pupillary mechanical problems will not constrict, but the pupil will constrict in all
other cases. Pilocarpine wears off in about 4 hours, so it should not prevent further
examination of the pupil.
Systemic medication
Corticosteroids: ophthalmologists do not use systemic corticosteroids often, but when
they do, they tend to use high doses, particularly in temporal arteritis. Prednisolone,
80100 mg/day, is prescribed, even in elderly patients, with all the usual corticosteroid
side-effects.
Acetazolamide: some ophthalmologists routinely give the carbonic anhydrase inhibitor

acetazolamide at the end of intraocular procedures as prophylaxis against intraocular
pressure spikes. It is also used in some patients with chronic glaucoma refractory to
treatment. The use of acetazolamide, even for a few days, causes hypokalaemia and
a metabolic acidosis.
Posture
Long gone are the days when patients were immobilized for 2 weeks after cataract
surgery. However, patients who have had retinal detachment surgery with gas injection
or who have had macular hole surgery are often asked to posture for 50 minutes
every hour.
These positions are often awkward (Figure 8) and this, combined with prolonged
immobility after surgery, increases the risk of deep vein thrombosis. Ophthalmologists
are very bad at considering the systemic effects of their surgery, and a little
encouragement from anaesthetists might be useful.
8 Ophthalmologists can ask their patients to adopt

this posture for up to 2 weeks

Orthopaedics
Anaesthesia
on CD-ROM
Anaesthesia for Joint
Replacement Surgery
Rachael Craven
Robin Cooper
Rachael Craven is Specialist Registrar in Anaesthesia in Bristol. She is currently

working at the Royal Prince Alfred Hospital, Sydney, Australia.
Robin Cooper is Consultant Anaesthetist at the Gloucester Royal Hospital, UK. He

qualified from St Georges Hospital Medical School, London, and trained in the South
West Region Anaesthetic Rotation. His specialist interest is in paediatric anaesthesia.
Joint replacement surgery is a common and effective procedure for the relief of
disability due to severe joint pain and loss of function. The most common joints
replaced are the hip, knee and shoulder, but with advances in technology and surgical
techniques the range of joints that may be replaced is increasing. Most patients for joint
replacement surgery have degenerative joint disease, commonly osteoarthritis. Other
conditions necessitating joint replacement surgery include:
rheumatoid arthritis
osteoporosis and fracture
metastatic lesions and pathological fractures
avascular necrosis of the femoral head.
Most patients are elderly, and commonly have associated problems such as
hypertension, ischaemic heart disease, chronic obstructive pulmonary disease (COPD)
or renal disease. Younger people presenting for joint replacement surgery often suffer
from rheumatoid arthritis, severe osteoporosis or obesity. Presentation for revision of
previous replacement surgery is increasingly common.
Problems in multiple systems are common because most patients are elderly. The
problems of disease processes associated with orthopaedic conditions should also be
considered; the most common is rheumatoid arthritis (Figure 1).
Problems associated with rheumatoid arthritis
Skeletal
Instability of odontoid peg and atlanto-axial subluxation
Restricted mouth opening due to temporomandibular joint involvement
Respiratory
Rheumatoid lung nodules
Pleural effusions
Pulmonary fibrosis
Drugs
Corticosteroids, non-steroidal anti-inflammatory drugs, gold and methotrexate
may have significant systemic effects
Other
Anaemia of chronic disease, pericarditis and amyloid deposits causing renal
dysfunction
Assessment of co-morbidities
Cardiopulmonary reserve is most commonly estimated by assessment of exercise
tolerance. However, this may be impossible or inaccurate because joint disease may
limit exercise. In these circumstances the following may be used:
lung function tests, arterial blood gases and oxygen saturation in air
resting ECG for silent ischaemia or previous myocardial infarction
echocardiography for left ventricular function, wall movement and valvular
abnormality.
These tests are of limited relevance because they provide information only about the
function of rested, rather than stressed, cardiopulmonary systems. Dobutamine stress
tests provide information about cardiac function under stress but they are not readily
available and have associated risks.
Renal function may be impaired owing to age, hypertension or chronic use of non-
steroidal anti-inflammatory drugs (NSAIDs).
Musculoskeletal other joint involvement is common. The range of limb and neck
movements should be noted. Obesity may be a cause or consequence of degenerative
joint disease. Assessment for positioning on the table and for regional blockade should
be made. In patients with metastatic disease, the bone scan should be checked to
ensure there are no spinal deposits that may interfere with regional anaesthesia.
Hip and knee replacement
Preoperative assessment should be carried out as above.
Optimization of co-morbidities is required.
Cross-matched blood must be available.
Deep vein thrombosis (DVT) prophylaxis is required. If a regional technique is
planned, ensure appropriate timing of low-molecular-weight heparin.
Antibiotic prophylaxis (usually cephalosporin or aminoglycoside) is required.
Invasive monitoring is seldom indicated unless there is significant cardiac disease or
large blood loss is anticipated.
Large bore intravenous access is required (sited in the non-dependent arm for
laterally positioned patients).
Regional anaesthesia is probably the technique of choice because it:
reduces blood loss, leading to a decreased need for bank blood and associated
transfusion risks
decreases bleeding at the operative site, improves cement bonding and decreases
surgical time
decreases the incidence of DVT and pulmonary embolus in hip and knee
arthroplasty.
The reduction in blood loss seen with spinal anaesthesia, compared with general
anaesthesia, is thought to be due to a combination of perioperative hypotension and a
comparatively lower haematocrit level. There is a perception that regional anaesthesia
reduces the incidence of postoperative confusion and cognitive dysfunction compared
with general anaesthesia, but studies have failed to demonstrate this.
The decision to use neuraxial opiates usually depends on the presence of a

resident anaesthetist, owing to the potential risk of delayed respiratory depression
postoperatively.
Sedation is often desirable because of the duration of the operation, intraoperative

noise and patient request. Patients positioned laterally for hip replacement may become
restless and uncomfortable because of pain arising from the dependent shoulder.
Intermittent midazolam, titrated in 1 mg increments, may be used but often causes
intraoperative disorientation and confusion, resulting in patient movement. Increasingly
popular is a target-controlled infusion of propofol, 0.52 g/ml, which gives smoother,
more titratable sedation. Oxygen should be administered throughout the operative
period.
As sedation deepens, airway obstruction or snoring may occur. This is seldom a

problem in the lateral position, but some supine patients may require a nasopharyngeal
airway.
General anaesthesia: if general anaesthesia is indicated, bleeding may be reduced by

modest hypotension in carefully selected patients, using volatile agents. Unless there
is a risk of aspiration, spontaneous ventilation with a laryngeal mask airway is usually
appropriate.
For hip arthroplasty, analgesia may be supplemented by the use of a 3-in-1 (femoral/
obturator/lateral cutaneous of thigh) block. Some anaesthetists favour a lumbar plexus
block because this also blocks the sciatic nerve, which has a component supplying the
hip. For knee replacement a 3-in-1 block combined with a sciatic nerve block can be
effective.
Intraoperative problems
Patient position: in the lateral position, there is a risk of excessive lateral neck flexion
and pressure on the dependent limbs.
Hypothermia: orthopaedic theatres are often colder than other theatres, with a higher
velocity airflow leading to more rapid patient cooling. Hypothermia may cause poor
wound healing, infection, coagulopathy and cardiovascular dysfunction. Some surgeons
are opposed to hot air warming devices because of the theoretical risk of increased
wound infection, and a discussion of the balance of risks may be indicated. Fluid
warmers, blankets and patient hats should be used routinely.
Blood loss: average blood loss in total hip replacement ranges from 300 to 1500 ml
and may double in the first 24 hours post-operatively. During knee replacement surgery
with an intra-operative tourniquet, most blood loss occurs in the recovery area. Careful
fluid balance is essential because compensation for hypovolaemia is poor in the elderly.
Provided normovolaemia has been maintained a haemocue can be used to guide blood
transfusion requirements.
Cement reactions: prostheses may be cemented in place. At the time of cementing, a

drop in blood pressure and oxygen sat-uration is often seen. This was originally thought
to be caused by a directly toxic effect of the methyl methacrylate monomer component
of the cement, but it is now known to be caused by a shower of microemboli of blood,
fat or platelets forced into the circulation by high intramedullary pressure during cement
packing and prosthesis insertion. Subsequent embolization to the lungs produces a
raised pulmonary vascular resistance and reduction in left ventricular return, resulting in
hypotension. The microemboli are toxic to the lung parenchyma causing haemorrhage,
alveolar collapse and hypoxia. This may be severe enough to cause cardiovascular
collapse, cardiac arrest and death. Reactions are more common and more severe in
bilateral joint replacements and also in under-resuscitated patients; therefore it is vital
to ensure that the patient is not hypovolaemic before cementing. Fractional inspired
oxygen concentration may have to be increased. Cement reactions tend to be less
common in knee replacement.
Thromboembolism is common after joint replacement. DVTs are more common

following knee replacements than hip replacements. Following knee replacement,
most DVTs are distal calf thromboses with a low risk of pulmonary embolus. In hip
replacement surgery, extremes of movement at the hip and kinking of vessels lead to
endothelial damage and blood stagnation. These thromboses tend to be of proximal
veins with a higher risk of pulmonary embolus.
The use of a regional technique, low-molecular-weight heparin, graduated compression

stockings or pneumatic compression boots decreases the risk of DVT. Intraoperative
low-dose intravenous heparin reduces the incidence of DVT without increased bleeding
but is not commonly used. A combination of the above techniques provides the best
protection and the anaesthetist should ensure that the local thromboprophylaxis
protocol has been followed.
Tourniquet: in some patients with cardiac disease the increase in systemic vascular
resistance when the tourniquet is inflated has precipitated left ventricular failure.
However, more of a problem occurs on releasing the tourniquet, when the acidic
byproducts of metabolism are washed out of the limb causing hypotension secondary to
vasodilatation and the effects of acidosis on cardiac contractility. In knee replacement
surgery, as the duration of the operation increases, tourniquet pain can become a
problem. Additional analgesia or epidural top-up may be required.
Analgesia
Epidural analgesia is excellent, particularly in reducing quadriceps muscle spasm
following knee replacements. However, there is an increased risk of urinary retention
and the resulting catheterization may cause a bacteraemia, increasing the risk of
prosthesis infection.
Patient-controlled analgesia is the choice in many institutions. Intramuscular opiates

may also be considered.
Regular paracetamol, 1 g/6 hours, should be given orally or rectally.
NSAIDs should be used with caution especially in the elderly owing to the increased
risk of renal impairment.
Midazolam infusions or baclofen are sometimes required to ease quadriceps muscle

spasm.
Fluid balance: stringent fluid balance monitoring is mandatory because blood loss may
double in the first 24 hours. Nausea may reduce the patients oral intake.
Oxygen: perioperative ischaemia is common and generally silent. Oxygen should be

given for the first 72 hours postoperatively.
Shoulder replacement
Monitoring and intravenous access

Standard full patient monitoring is required. Large bore intravenous access is made on
the non-operative side. Non-invasive blood pressure monitoring is instituted either on
the non-operative side with a non-return valve on the intravenous line, or on the lower
leg.
The most common technique is general anaesthesia using an armoured tracheal tube
and positive-pressure ventilation. Selected patients may be managed satisfactorily
using a spontaneous ventilation technique through an armoured laryngeal mask.
Access to the patients head intra-operatively is extremely restricted. The interscalene
approach to brachial plexus blockade provides excellent intraoperative and
postoperative analgesia and improves the operative conditions with decreased blood
loss and good muscle relaxation. It commonly gives a unilateral phrenic nerve palsy, but
this seldom causes alveolar hypoventilation even in spontaneously ventilating patients.
Patient position
The patient is placed in a sitting position, with a bolster behind the shoulder blades to
improve surgical access (Figure 2). Care should be taken to ensure there is no excess
strain on the lumbar spine. The torso should be securely strapped. Many tables are
specially adapted with a built-in extension for the head ring, the height and angle of
which may be adjusted.
2 The sitting position.
The head must be securely fastened because there will be considerable pull and
movement at the shoulder. Access to the airway intra-operatively is difficult owing to the
sitting position and the presence of surgical drapes; the tracheal tube must therefore be
securely taped in place. The eyes should be taped and well padded.
Elderly patients often have poor cardiovascular compensatory mechanisms while
under general anaesthesia. At the start of the operation, while positioning the patient,
a large drop in blood pressure may accompany the change from supine to sitting and
vasopressors and a temporary return to a flatter position may be required. Patients are
at risk of air embolism from open veins at the operative site.
Shoulder replacements are extremely painful and, if possible, interscalene block should
be used, supplemented with patient-controlled opiate analgesia. Regular paracetamol
and NSAIDs (in those in whom they are not contraindicated) should also be prescribed.
Revision arthroplasty
As the number of active elderly people increases, more patients are returning for
revision of earlier replacements. As well as the problems of hip or knee replacement,
revision arthroplasties have added complications associated with prolonged surgery
and high blood loss.
Discuss the anticipated blood loss with the surgeon; this depends on the type of
previous prosthesis and the number of components being revised. Pre-donation of
autologous blood with acute normovolaemic haemodilution and the use of a cell saver
should be considered. Platelets (often not immediately available) and clotting factors
may be required.
Monitoring and intravenous access

Invasive blood pressure and central venous pressure monitoring should be considered
in view of the long duration of surgery and the likelihood of significant blood
loss. A urinary catheter should be inserted with the facility for hourly urine output
measurements.
The technique of choice is probably general anaesthesia, combined with insertion
of a lumbar epidural catheter and positive-pressure ventilation. An epidural reduces
intraoperative blood loss and improves operating conditions as well as reducing the risk
of DVT. Spinal anaesthesia is generally unsuitable because the length of the operation
outlasts its effects.
Temperature: it can be difficult to prevent perioperative hypothermia. These
operations are long and considerable volumes of intravenous fluid are transfused.
Fluid warmers, hot air blowers, humidification systems and patient hats are important
because intraoperative hypothermia can contribute significantly to coagulopathy and
perioperative blood loss.
Blood loss is often considerable. Pre-donation of 1 unit of blood in the anaesthetic

room, using acute normovolaemic haemodilution, is useful if the patient has an
adequate starting haemoglobin. Intraoperative use of a cell saver can reduce the need
for bank blood and reduce the associated transfusion risks, but once cement is in use,
cell salvage must stop. The use of a cell saver is contraindicated in patients in whom
joint replacement is for metastatic disease or infection. Platelets and fresh frozen
plasma are often required. Transfusion of pre-donated blood should wait until surgical
haemostasis is obtained. Fluid balance should be guided by surgical blood loss, central
venous pressure trends (where available), pulse, blood pressure and urine output,
with the aim of maintaining normovolaemia. The haemoglobin concentration should be
assessed often, either from blood gases or by using a haemocue device.
Should be in a high dependency unit. Oxygen should be prescribed for at least
72 hours. Analgesia should be provided by epidural infusion with regular enteral
paracetamol. Close control of fluid balance is aided by the use of central venous
pressure monitoring and hourly urine output measurement. Coagulopathies should be
treated, but the threshold to transfuse red cells depends, in part, on the presence of co-
morbid medical conditions, especially ischaemic heart disease. u
FURTHER READING
Horowitz P E. Fat Embolism. Anaesthesia 2002; 57(8): 8301.
Keith I. Anaesthesia and Blood Loss in Total Hip Replacement. Anaesthesia 1997; 32:
44450.
Kim Y H, Oh S W, Kim J S. Prevalence of Fat Embolism following Bilateral

Simultaneous and Unilateral Total Hip Arthroplasty performed with or without Cement:
A Prospective, Randomised Clinical Study. J Bone Joint Surg Am 2002; 84(8): 13729.
Shaieb M D, Watson B M, Atkinson R E. Bleeding Complications with Enoxaparin for

Deep Venous Thrombosis Prophylaxis. J Arthroplasty 1999; 14(4): 4328.

Anaesthesia for Spinal Surgery
Ian Crabb
Ian Crabb is Consultant in Anaesthesia and Intensive Care at Gloucestershire Royal

Hospital, UK. He qualified from London University and trained in anaesthesia in London
and Australia. His interests include major trauma management and cardiovascular
monitoring in intensive care.
Clinical features of spinal disorders
Intervertebral disc lesions

Prolapsed discs: lumbar backache is one of the most common causes of chronic
debility in Western society. Acute lumbar disc prolapse or chronic degeneration with
disc-space narrowing at L4/5 or L5/S1 are the most common pathologies. In acute
prolapse, the disc may bulge beneath the posterior longitudinal ligament in the mid line
(central disc) or posterolaterally with consequent distortion of the spinal canal or nerve-
root compression. Local oedema may exacerbate the problem. Symptoms result from
distortion of the posterior longitudinal ligament (chronic pain), pressure on the nerve-
root sheath (sciatica) and compression of the nerve itself (muscle weakness, numbness
and paraesthesia). Cauda equina compression may cause urinary retention, but is
relatively uncommon. Management may include rest, analgesia and physiotherapy, but
the prolapsed disc can be treated effectively only by bed rest, disc reduction (including
epidural injection or chemonucleolysis) or surgical discectomy.
Cervical disc prolapse may be precipitated by sudden unexpected flexion or rotational

movements. In most cases, there is probably a pre-existing disc abnormality. The most
common levels for prolapse are C5/6 and C6/7, and symptoms are similar to those
of lumbar disc prolapse. Treatment of the prolapse may be effected by rest, reduction
using bed rest and traction, or surgical removal, if the symptoms are severe.
Spondylosis: lumbar disc degeneration may occur following recurrent disc prolapse
or for other reasons. This results in flattening of the disc, facet-joint displacement, and
a degree of instability with limited and painful movement (spondylosis). Conservative
treatment for lumbar spondylosis is appropriate in less severe cases. However, if the
pain cannot be controlled, spinal fusion is indicated.
Spondylosis is the most common disorder of the cervical spine. In addition to disc
flattening, bony spurs may grow at the margins of the vertebral bodies, impinging on
nerve roots and producing symptoms. Physiotherapy is the mainstay of treatment, but
in severe or refractory cases anterior spinal fusion may be the definitive option.
Spondylolisthesis
If intervertebral facet joints become affected by osteoarthritic changes, dysplasia or
fractures, one vertebral body may slip forwards on the other (spondylolisthesis). The
most common levels for this to occur are L4/5 and L5/S1. Stabilization is achieved by
spinal fusion and may be necessary for symptomatic relief.
Spinal stenosis
The spinal canal may be congenitally small or narrowed by the presence of
a spondylolisthesis. Further narrowing consequent on disc degeneration and
osteoarthrosis may produce neurological symptoms, which may be unilateral (root canal
stenosis). Spinal decompression is indicated if symptoms are severe.
Rheumatoid disease
Rheumatoid arthritis affects about 1% of the worlds population. The disease causes
destruction of synovial joints, tendons and bursae, and 75% of sufferers have extra-
articular symptoms. The spine is commonly affected, most often the upper cervical
region. Erosion of the odontoid peg or cruciate ligament may result in atlanto-axial
subluxation, with the risk of cord compression. Vertical subluxation may result from
erosion of the lateral masses of the axis, causing the odontoid peg to approach or enter
the foramen magnum. Of relevance to the anaesthetist is that the disease may involve
the temporomandibular and arytenoid joints.
Assessment of atlanto-axial subluxation may be made by measuring the distance

between the anterior arch of the atlas and the odontoid peg on lateral cervical spine
radiographs. However, neither this anterior atlanto-dental interval nor the posterior
equivalent correlates well with the severity of neurological symptoms. Stabilization
procedures or surgical decompression may be undertaken to relieve neurological
symptoms, but they are hazardous, with equivocal benefit.
Spinal curvature
Scoliosis is a lateral curvature of the spine, often with a rotational element. The
deformity usually arises in late childhood and may be postural or structural. Postural
scoliosis arises as a compensatory mechanism for problems outside the spine, such
as a shortened leg or abnormal pelvic tilt. Structural scoliosis is a fixed deformity and
is always accompanied by bony abnormalities. Adolescent idiopathic scoliosis is the
most common form, presenting in the 1015 year age group. Operative treatment for
scoliosis is indicated for curvatures over 40, the surgery being potentially complex and
challenging.
Kyphosis: structural kyphosis is a fixed, excessive dorsal curvature of the thoracic

spine. It may occur in osteoporosis and ankylosing spondylitis. In Scheuermanns
disease (adolescent kyphosis), the vertebral bodies become wedge-shaped
as they grow. If the curvature exceeds 60, surgery, which carries a high risk of
neurological damage, may be indicated.
Infection
Tubercle bacilli or staphylococci may cause abscess formation within vertebral bodies.
Tubercle infection may spread to adjacent vertebrae with caseation and cold abscess
formation, resulting in vertebral collapse with a high risk of spinal cord damage.
Antibiotic therapy is the mainstay of treatment for both infections. However, abscess
drainage or spinal fusion for progressive deformity may be necessary.
Surgical procedures
Lumbar laminotomy and laminectomy: laminotomy (partial removal of vertebral
lamina) or laminectomy (complete removal) are performed to decompress the spinal
cord and/or nerve roots via a posterior approach with the patient lying prone. Should a
discectomy also be necessary, the dura is retracted to one side and the disc removed
piecemeal. During these procedures there is a risk of damage to both the dura and
retroperitoneal structures (e.g. major vessels). The extent of the procedure depends
on the underlying problem and may vary from simple laminotomy for single nerve-root
compression to decompression over several segments for spinal canal narrowing. In
such cases, a stabilization or fusion procedure (e.g. plate and screws) may also be
required.
Microdiscectomy can be performed to decompress nerve roots affected by simple

pathology; bone is not usually removed. The patient is placed prone or kneeling and the
appropriate spinal level is identified using radiographic control. A small incision is made
over the appropriate interspace and an operating microscope is used to retract the
nerve-root to allow disc material to be excised.
Thoracic laminectomy and costotransversectomy: thoracic laminectomy involves

midline removal of the vertebral lamina to decompress the thoracic spinal canal.
Costotransversectomy (removal of transverse process and rib-head) is performed for
nerve root compression. Both procedures require the patient to be prone and involve
the use of an operating microscope.
Cervical laminotomy, foramenectomy and laminectomy are used to decompress

the spinal cord or nerve roots in the cervical region. As with the lumbar and thoracic
regions, the nature and extent of the surgery depends on the underlying pathology. The
patient may be positioned prone or sitting.
Anterior cervical discectomy is a common neurosurgical procedure performed for

disc herniation or degeneration with neurological symptoms. It is often augmented by
vertebral fusion with a bone graft.
Other cervical procedures

Vertebral corpectomy is essentially an enlarged version of an anterior discectomy and
is performed as an anterior decompression procedure. If access is required above the
level of C3, a transoral approach may be used, which may involve a mandibular split
and division of the tongue.
Cervical or craniocervical fusion is indicated for spinal instability. The fusion usually
involves several adjacent vertebrae and may include fusing the occiput to the upper
cervical spine. A posterior approach is used with the patient lying prone.
Spinal reconstruction procedures: significant kyphoscoliotic deformities may benefit

from reconstructive surgery and, regardless of the underlying condition responsible for
the deformity, the surgical approach to the anterior spine is similar. Surgery to the upper
thoracic spine is achieved via a modified and extended anterior cervical exposure,
often involving resection of a clavicle, part of the manubrium and first rib. Mid-thoracic
spinal surgery is more easily performed via a thoracotomy with rib resection. One-lung
ventilation may be required. Once the vertebrae or discs are removed, the spinal cord
is at risk of damage, the degree of risk depending on the extent of the vertebral disease
and the extent of reconstruction required.
A transdiaphragmatic approach involving detachment of the diaphragm is required for

lower thoracic procedures. The lumbosacral spine is approached via a flank incision
and retroperitoneal dissection. Often the 11th or 12th ribs are resected, risking damage
to the great vessels, ureters, sympathetic chain and presacral plexus. A posterior fusion
is also often undertaken with the above procedures.
Thoracolumbar procedures (excluding corrective surgery)

Preoperative: surgical procedures on the lumbar spine for disc problems are common.
Any preoperative neurological deficit should be recorded in the patients notes,
especially if a regional technique is considered. Generally, these patients are otherwise
healthy and no special investigations are normally required.
Intraoperative: it is possible to perform simple lumbar pro-cedures under local or

regional (spinal or epidural) anaesthesia. However, this is seldom done in practice
because of medico-legal concerns that any new postoperative neurological deficit may
be blamed on the anaesthetic technique. A general anaesthetic technique involving
intubation and mechanical ventilation is more usual. For all posterior spinal procedures
the patient is placed prone or in the kneeelbow position. It is therefore advisable to
use an armoured tracheal tube to minimize the risk of kinking and to ensure that the
tube is well secured before and after turning the patient. Potential problems with the
prone position are summarized in Figure 1. Thoracoscopy is being increasingly used
for procedures on isolated regions of the thoracic spine. This requires a double-lumen
tracheal tube and for the ipsilateral lung to be deflated.
Problems with the prone position
Potential problem Comments
Eyes
Corneal abrasion Ensure eyes taped shut
Optic neuropathy Increased intraocular pressure leads to decreased perfusion
pressure
Reduce risk by avoiding compression to the eyes, hypotension, low
haematocrit
Retinal artery occlusion Avoid pressure on the eyes
Head and neck

Venous and lymphatic Careful positioning to minimize
obstruction venous obstruction
Skull fixation Insertion of pins into skull can result in a hypertensive response
that is difficult to control
Abdominal compression
Impaired ventilation Avoid abdominal compression as far as possible
Decreased cardiac output Bean-bag mattress or pillows are better than supportive frames or
kneechest position
Damage to major vessels

Aorta or inferior vena cava Accidental damage following perforation of anterior longitudinal
ligament
Produces major bleeding into wound, and presents with acute
reduction in blood pressure and electromechanical dissociation
arrest
High mortality
Iliac vessels Less acute presentation. High index of suspicion to avoid delayed
diagnosis
1
Any standard maintenance regimen is acceptable. However, blood pressure
control is important, balancing the need to ensure spinal cord perfusion with the
requirement to produce a bloodless surgical field. Sodium nitroprusside and esmolol
infusions have been widely used for this purpose, though remifentanil is becoming
popular. Blood loss is usually minimal from simple procedures, though if extensive
laminectomies and fusions are performed, cross-matched blood should be available.
Standard monitoring is appropriate for simpler procedures. However, invasive blood

pressure monitoring, a central venous pressure line and a urinary catheter should be
considered if deliberate hypotension is used or if the procedure is likely to be prolonged
and involve large fluid shifts.
Postoperative: most spinal surgery is painful and good postoperative analgesia is

important. Local anaesthetic and opioid drugs can be instilled into the epidural space
before closing. More usually, however, a regimen including patient-controlled analgesia
(PCA) combined with regular oral/rectal analgesics is successful. Postoperative
complications include persistent hypotension, haemorrhage, urinary retention, nerve
root damage and cauda equina syndrome (urinary/faecal incontinence, perineal
sensory loss and lower-limb motor weakness).
Cervical procedures
Preoperative: cervical spine fractures may cause acute spinal cord trauma and
result in acute ventilatory failure requiring emergency tracheal intubation. Cervical
spine stabilization during intubation is essential. The acute injury may additionally
produce dysfunction of the sympathetic nervous system, resulting in hypotension
and bradycardia. Simple treatment with fluids and atropine usually suffices, though
vasopressors (e.g. ephedrine) may be necessary.
Neurological signs and symptoms may be present. Nerve root compression produces
pain in the neck and arm, often associated with weakness and sensory loss. Acute cord
lesions above T1 produce paraplegia and if the lesion is above C5 the patient will be
quadriplegic.
Careful airway assessment is vital in all patients requiring cervical spine surgery.
Difficult intubation may be anticipated if there is reduced movement, swelling or
deformity. Up to 40% of patients requiring cervical spine surgery for rheumatoid
disease fall into this group. The patient may need to be prepared for an awake fibre-
optic intubation and appropriate equipment and skilled staff made available. In certain
circumstances (e.g. surgery involving maxillotomy or mandibulotomy), an elective
tracheostomy may be necessary for postoperative airway management.
Intraoperative: general anaesthesia with tracheal intubation and ventilation is required;

standard maintenance techniques are appropriate. For anterior cervical procedures,
the patient is placed supine with the neck extended and supported. For posterior
approaches, the patient is usually prone. However, the seated position is preferred
by some surgeons, because surgical access may be easier and blood loss reduced.
This position is associated with a high incidence of air embolism (2545%). If a patent
foramen ovale is present (20% of the population), paradoxical embolism may occur,
resulting in air entering the cerebral or coronary circulations. Standard monitoring may
be used for straightforward cases, but arterial and central venous pressure catheters
are useful for more prolonged procedures. Additionally, spinal cord monitoring may be
required (see below).
Extubation may be problematical and is best performed with the patient awake and able
to support their own airway. If the risk of reintubation is high, a tracheal tube exchange
catheter (e.g. Cook catheter) may be useful. The catheter can be introduced into the
tracheal tube and left in situ when the patient is extubated. Should urgent reintubation
be necessary, the new tracheal tube can be rapidly railroaded over the exchange
catheter. However, prolonged sedation and ventilation should be avoided because this
may mask postoperative neurological deterioration.
Postoperative: possible complications include airway obstruction post extubation,

which is potentially life-threatening if the patient has had a spinal fusion and is encased
in a stabilization device. Airway compromise may result from haematoma formation or
neurological deficit. Pneumothorax is an occasional cause of postoperative respiratory
distress.
Spinal reconstruction and fusion

Preoperative: spinal reconstruction is indicated for correction of kyphoscoliotic
deformities and for stabilization following trauma, infection (e.g. tuberculosis) or
metastatic carcinoma. Patients presenting for this type of major surgery require careful
preoperative assessment, because complex and chronic problems are common
(Figure 2). Preoperative management should include lung function tests (e.g. forced
vital capacity, peak expiratory flow rate), arterial blood gas analysis and review by a
cardiologist if cardiac abnormalities are suspected.
Preoperative considerations for patients undergoing major

reconstructive spinal surgery
Problem Comment
Respiratory
Reduction in total lung Reduction worse with increasing
capacity and vital capacity deformity. If vital capacity < 40%
predicted postoperative ventilation
likely. NB A further decrease in vital
capacity of up to 40% may occur
postoperatively; recovery may take up
to 2 months
Increasing V/Q mismatch Hypoxaemia more likely
Cardiovascular
Increase in pulmonary Independent of severity of scoliosis
vascular resistance
Increasing incidence of High index of suspicion
congenital heart disease
and mitral valve regurgitation
Neurological
Variable preoperative deficit Careful preoperative documentation
Musculoskeletal
Muscular dystrophy Abnormal response to muscle
relaxants
Respiratory impairment Postoperative ventilation may be
required
Nutrition
Malnourishment Likely in patients with metastatic
carcinoma
2
Intraoperative: intubation with a double-lumen tube may be necessary. Standard

maintenance techniques are applicable, although this may have to be modified (e.g.
no muscle relaxants) depending on surgical technique and spinal cord monitoring (see
below).
Major blood loss is not uncommon and suitable intravenous access should be secured.
Intraoperative blood loss may be dramatically reduced by careful patient positioning,
the use of controlled hypotension (mean arterial pressure 6070 mm Hg) and mild
haemodilution to a haematocrit of 2528%.
Intraoperative monitoring should include invasive blood pressure, central venous

pressure, and urine output measurement. Evoked potentials are used to monitor spinal
cord function (see below). If there is any indication of spinal cord ischaemia during
surgery, normal blood pressure should be restored immediately and any traction on the
cord relaxed. Strenuous efforts should be made to maintain normothermia.
Early extubation is desirable and good postoperative pain relief is essential. Epidural
analgesia is considered by many to be the gold standard. An epidural catheter can be
inserted before surgery or by the surgeon during the operation. Some patients require
planned ICU admission for elective post-operative ventilation.
Postoperative complications include the risk of respiratory failure increased by

thoracotomy, diaphragmatic injury and fat embolism. Great care should be exercised
when moving and transferring patients to prevent dislodgement of spinal fix-ation.
Careful documentation of neurological status is important because postoperative
neurological deterioration is a major concern.
Spinal cord damage

Neurological damage during surgery and anaesthesia is not limited to the site of
surgery. Paraplegia and quadriplegia have been reported as a result of poor patient
positioning. There are reports of patients with spinal disease who have suffered
neurological damage either at levels remote from the site of surgery or during surgery
unconnected with their spinal disease. However, neurological damage is more likely at
or near the site of surgery on the spine. Risk factors and methods for minimizing them
Risks of spinal cord damage
Risk related to:

length and type of surgical procedure
spinal cord perfusion pressure
underlying spinal pathology
pressure on neural tissue during surgery
Risk minimized by:

careful positioning
maintaining SCPP
SCPP = MAP CSFP
CSFP can be reduced by CSF drainage
MAP manipulated by anaesthetist
? keep systolic blood pressure > 90 mm Hg
drugs
methylprednisolone given less than 8 hours after insult
NMDA antagonists (ketamine, magnesium)
prevention of haematoma formation
careful haemostasis
stop anti-platelet medication preoperatively
withhold heparin immediately postoperatively
CSFP, cerebrospinal fluid pressure; MAP, mean arterial pressure; NMDA,

N-methyl-D-aspartate; SCPP, spinal cord perfusion pressure
3
Spinal cord monitoring

The wake-up test involves lightening anaesthesia at an appropriate point during the
procedure and observing the patients ability to move to command. The technique
requires practice and adds to the duration of surgery. In addition, it provides information
at the time of the wake-up only and misses damage occurring at other times.
Neurophysiological monitoring using somatosensory evoked potentials (SEPs) provides

a continuous picture and offers a more sophisticated approach. Electrical stimuli are
applied to the lower limbs and appropriately placed electrodes can record cortical
(SCEP) or spinal (SSEP) evoked potentials. The resulting trace can be analysed for
wave amplitude and latency with respect to a reference time zero. SCEPs are affected
by anaesthetic induction and inhalational agents, opioids and local anaesthetic drugs,
and interpretation requires care and experience. Nevertheless, a decrease in amplitude
or latency unrelated to drug administration of 3550% is thought to be significant and
indicate possible cord damage. However, even in skilled hands, interpretation can be
difficult and a wake-up test may still be required.
SSEPs can be recorded from electrodes placed into the epidural space either
percutaneously or during surgery. SSEPs are affected less by inhalational agents, but
are sensitive to temperature changes and local anaesthetic drugs. Their stability during
anaesthesia allows them to be used with more confidence during surgery than SCEPs.
Motor evoked potentials can be obtained by stimulating the motor cortex with a
transcranial electrode and eliciting a response from the distal spinal cord, peripheral
nerves or muscle. They have not been used extensively for spinal cord monitoring
because they are more difficult to achieve and are sensitive to inhalational anaesthetic
agents. u
FURTHER READING
Calder I. Anaesthesia for Spinal Surgery. Baillieres Best Practice and Res Clin
Anaesthesiol 1999; 13 (4): 62942.
Carragee E J, Samuels S I, Jaffe R A. Spine Surgery. In: Jaffe R A, Samuels S I, eds.

Anesthesiologists Manual of Surgical Procedures. 2nd ed. Philadelphia: Lippincott,
Williams and Wilkins, 1999; 791802.
Hetreed M A. Anaesthesia for Major Spinal Surgery. Curr Anaesth Crit Care 1997; 8:
2649.
Shuer L M, Larson C P. Spinal Neurosurgery. In: Jaffe R A, Samuels S I, eds.

Anesthesiologists Manual of Surgical Procedures. 2nd ed. Philadelphia: Lippincott,
Williams and Wilkins, 1999; 6177.

Preoperative Assessment in
the Elderly
Malcolm Savidge
Malcolm Savidge is Consultant Anaesthetist in the Gloucestershire Hospital Trust, UK.

He qualified from St Marys Hospital, London, and trained in anaesthesia at Northwick
Park Hospital, Harrow, Southampton and Wessex. His particular interests are medical
ethics and within anaesthesia, chronic pain, regional anaesthesia and ophthalmic
anaesthesia.
An increasing elderly population and advances in surgical technology are challenging

anaesthetists to provide safe, effective anaesthesia. The mean age of the population
continues to rise and half of all patients over 65 years will undergo surgery before
they die. Osteoarthritis is almost universal and many of these patients will require joint
replacement surgery. This article concentrates on elderly and arthritic patients and their
associated problems.
Increased age and pre-existing illness both increase the incidence of complications.
A successful outcome depends on meticulous attention to preoperative assessment
and an intelligent choice of suitable anaesthetic techniques. An understanding of the
limitations of physiological function in the elderly and rheumatic patient enables an
accurate assessment of the likely response to the stress of surgery and therefore
the final outcome to be made. The anaesthetic technique used and the choice of
perioperative monitoring often makes the difference between success and failure.
Similarly, the opportunity to improve physiological function preoperatively, where
applicable, should never be missed.
Elderly patients often present with a baffling array of pathologies. Most are chronic
effects of the ageing process and the residual effects of past illnesses. Signs and
symptoms are often masked by limitation of movement and lack of exercise because
of the pain of arthritis. This enforced immobility often leads to weight gain and obesity,
making pre-existing pathology in other systems worse and adding to the risks of
anaesthesia and surgery.
The elderly and ageing

Old age is not a disease. The elderly undergo physiological and anatomical changes
that evoke different responses to stress and anaesthesia. In 1982, the United Nations
recognized this: Support to the aged people must be provided by practitioners who
are knowledgeable in the subject of ageing, are interested in ageing people and their
families and are skilled in working with them as well as being concerned about the
quality of care given.
The process of ageing is one of continuous biological change. The number of

parenchymal cells decreases, with a concomitant increase in inactive interstitial cells,
triggering a progressive decline in physiological function. Gross morphological changes
occur with contraction of vertebral bodies and discs. Kyphosis occurs and flexion of
hips and knees. The long bones of the legs bow, but the arms remain unchanged in
length. This reverses the height:span ratio. Muscle size and bulk decrease rapidly with
advancing age, together with alterations in fat distribution. Skin becomes thinner and
more fragile.
In the heart, myofibrils enlarge but become less numerous. Collagen and fat replace
a substantial volume of the muscle mass. Deposits of amyloid and subendocardial
calcification impair conduction in the ventricle. This, combined with a reduction in
pacemaker cells, makes the elderly prone to arrhythmias.
Progressive coronary arterial sclerosis leads to a reduction in maximal coronary

artery blood flow. While the oxygen delivery is within the demand of the resting state,
relatively small increases in cardiac work index or heart rate result in ischaemia. There
is reduction in vasomotor tone; both vagal and sympathetic influences are minimized.
These changes make the heart less compliant. Stroke volume decreases; systole
time is prolonged; and with a decrease in ventricular contractility, cardiac output and
its reserve decline. Despite this, the average arterial pressure rises, with an increase
in the systolic and a slight drop in the diastolic pressures, except in obesity. The
mean arterial pressure remains unchanged. Peripheral vascular resistance increases
progressively. Vessel walls become less compliant as smooth muscle is reduced and
collagen replaces elastin. Major vessels become stretched and distended, damaging
the endothelium and baroreceptors, making blood pressures labile. Importantly, any
increase in intrathoracic pressure, passively or actively, causes greater decreases in
blood pressure with little or no rebound elevation. Degenerative vasomotor control
precipitates syncope in the presence of decreased cardiac output or peripheral
resistance. Postural hypotension can be spontaneous or an effect of drugs.
Respiratory system
Dorsal kyphosis and curvature of the thorax alter the position of the ribs, forming a
barrel chest. There is associated weakness of intercostal muscles and chest wall
rigidity. This increases the work, and reduces the efficiency, of breathing. Cellular
changes also occur in the lung parenchyma. Elastic recoil of the lungs is reduced,
increasing the lung volume at end-expiration, thus increasing the residual volume.
There is a parallel decrease in the vital capacity. Widening of the airways increases
the anatomical dead space, together with increase in the size of the alveolar ducts.
Reduction in elastic fibres in these ducts may explain why airway closure occurs at
resting functional residual capacity. This premature closure of the airways further
contributes to increases in residual volume.
Loss of recoil, increasing dependence on the diaphragm and abdominal muscles and
reduced vital capacity all produce an uneven distribution of ventilation, without change
in tidal volume at rest. The alveolararterial oxygen tension difference increases
causing a decrease in the partial pressure of oxygen in arterial blood (PaO2). The
PaCO2 remains unchanged. However, a greater contribution to progressive reduction
in arterial oxygen-ation comes from reduced perfusion. Fibrous replacement of the
muscular arterial media and reduction in the number of capillaries increases the
pulmonary vascular resistance and shunting. Maximal pulmonary blood flow, and
therefore perfusion, is lowered. The additional oxygen demand caused by increased
activity induces increased ventilation in the presence of a diminished maximum
breathing capacity. This leads to dyspnoea in the absence of underlying pulmonary
disease.
Progressive weakness of intercostal and accessory muscles reduces the ability to

cough forcibly. The bronchial mucosa degenerate because of impaired blood supply
and the cilia are not always able to keep the small airways clean. Suppressed glottic
reflexes make pulmonary infections common.
Circulation
In addition to reduced haemoglobin and haematocrit, older people have reduced
marrow iron stores and can suffer anaemia following small haemorrhages. The
temptation to transfuse red cells immediately should be resisted. One large
retrospective observational study showed no increase in mortality provided the
haemoglobin concentration was kept above 8 g/dl, even in the elderly. It recommended
that an indication for transfusion is haemoglobin below 7 g/dl. However, if elderly
patients do not respond to treatment of anaemia other causes should be sought, such
as occult malignancy, chronic infection or poor nutrition.
Other haematological changes include reduced cellular immune response because of

thymic atrophy and reduction in the number of T cells. Lymphocytosis within the marrow
results in susceptibility to proliferative disorders and infections.
Renal function
The nephron mass in the kidney can decline by 30% between 60 and 70 years of age.
This is reflected in changes in lean body mass and basal metabolic rate as a result
of loss of functioning tissue. Vascular changes may initiate this deterioration. As renal
blood flow is reduced, glomerular filtration and concentrating ability decline linearly at
1% per annum from 30 to 80 years. Large acid or alkali loads can overwhelm the ability
of the kidney to maintain acidbase homeostasis. The serum creatinine level can be
misleading because it does not necessarily increase in response to declining creatinine
clearance rates, but reflects muscle turnover when muscle mass is reduced.
Nervous system
Changes in cognitive function are multifactorial. 20% of octogen-arians have some
degree of dementia, but this diagnosis should be made only when other causes
have been excluded. Organic causes of dementia include hypoxia, infection, drugs,
hypoperfusion, hypothyroidism, constipation and impaired sight or hearing.
Temperature regulation, together with heat and cold homeo-stasis, is impaired in the
elderly; they do not often shiver. Hypothalamic hunger and thirst centres are down-
regulated and antidiuretic hormone is less effective, leaving these people vulnerable
to dehydration and malnutrition. The peripheral nervous system declines in a similar
manner. Nerve conduction velocity decreases and appreciation of pain reduces; the
elderly complain less of pain.
Care must be taken to ensure nerves are not compressed or stretched, particularly
in the neck. Many elderly patients have a reduced cerebral blood supply as a result
of atheroma or sclerosis. Vertebrobasilar insufficiency is not uncommon. Flexion or
extension of the neck can compromise cerebral oxygen delivery. Osteoporosis and
laxity of ligaments is common in old age. Care should be taken in moving the neck lest
dislocation or fracture occurs in the cervical vertebrae.
Rheumatoid arthritis
Rheumatoid arthritis is an inflammatory proliferative disease of synovium with a familial
association with the DRW 4 allogen. 70% of sufferers are female and 85% show anti
IgG or IgM antibodies. It is thought to be caused by defective cell-mediated immunity,
characterized by lymphocytic proliferation involving macrophages and complement
activation on joint surfaces giving rise to symmetrical polyarthritis with a centrifugal
distribution. Clinical features include insidious or sudden onset of pain, swelling and
stiffness in peripheral joints. Weakening of the joint capsules leads to subluxation and
permanent deformity. It is associated with tenosinovitis and muscle wasting.
Anaesthetic implications: advance of rheumatoid arthritis affects most systems. The

airway is often compromised and involvement of the temporomandibular joint restricts
mouth opening. Atlanto-occipital instability is not uncommon and 25% of patients
admitted to hospital with rheumatoid disease have subluxation of that joint.
Hyperflexion of the neck may induce vertebrobasilar insufficiency or paraesthesia.

Crico-arytenoid involvement may present with stridor. Associated lung conditions
include fibrosing alveolitis, pleural effusion and Caplans syndrome. Pericarditis can be
associated with pericardial effusions. Valvular nodules cause aortic or mitral stenosis.
These nodules are sometimes due to amyloid, which also causes nephrotic syndrome.
Renal failure can occur through vasculitis or as a result of the drugs used to treat
rheumatoid arthritis (e.g. penicillamine, non-steroidal anti-inflammatory drugs). Usually,
these patients suffer anaemia, which may be haemolytic, chronic normochromic or iron-
deficient. They may also have pancytopenia and hypersplenism (Feltys syndrome).
Fragile skin and veins are also associated with this condition together with a
predisposition to carpal tunnel syndrome, polyneuritis and neuropathy. Special care is
needed when positioning these patients for surgery.
History
Obtaining a clear history may prove difficult in elderly patients. Sensory perception
is impaired and misunderstandings occur because of failure to hear. Sight may be
compromised, distorting perception of surroundings. There may also be age-related
generalized neurological degeneration. Recall of past events is usually clear but recall
of recent episodes of illness and their significance can be hazy. Relatives often fill in
important gaps and reference to medical notes and letters is invaluable. The history
should include:
previous anaesthetics, especially any problems
previous medical history, especially heart, lungs, kidneys, blood pressure,
oesophageal reflux
allergies
current medicines
social habits (e.g. smoking, alcohol intake)
dentition.
The medical history and current medication provide important clues about the patients
underlying state of health.
Examination
The patient should be sufficiently exposed to enable accurate observation, palpation,
percussion and auscultation, while ensuring warmth, comfort and dignity. Palpation
of the pulses cannot be over-emphasized; it often reveals clear indications of severe
cardiovascular disease. Thorough examination of the cardiovascular and respiratory
systems is often rewarded by eliciting signs absent in younger patients. Cardiac
murmurs should be carefully classified according to site heard loudest, pitch,
length and timing in the cardiac cycle. Irregularities of the pulse should be noted as well
as abnormalities of the jugular venous pulsation.
Tests of respiratory function include the ability to count to 10 in one breath,

breathlessness on dressing and ability to walk up a flight of stairs. Palpation of chest
expansion, percussion and auscultation should be performed on anterior and posterior
aspects of the chest. Unexpected signs are often found, which prove important in future
management decisions. A hyper-dynamic pulse may sometimes indicate hypercarbia.
Although cognitive function is not usually directly related to anaesthetic processes,
postoperative confusion and delirium are not uncommon. A simple mental test score
such as that given in Figure 1 can be a useful marker and may highlight patients at
special risk.
Mini-Mental State Examination
Section Score Task

Orientation 5 What is the date: year, season, date, day, month
5 Where are we: country, county, town, hospital,
floor
Registration 3 Name three objects 1 second to say each, then

ask the patient to recall all three. Repeat until the
patient has learnt all three. Count and record
trials
5 Serial 7s one point for each correct. Stop after
5 correct. Alternatively spell world backwards
3 Ask for the 3 objects repeated above Give an
example of each
Language 2 Name a pencil and watch

1 Repeat the following no ifs, ands or buts
3 Follow a 3-stage command: take a piece of
paper in your right hand, fold it in half and put it
on the floor
3 Read and obey the following: close your eyes,
write a sentence, copy a design
Total score 30
Score results: 3029, normal

2826, borderline cognitive dysfunction
2518, marked cognitive dysfunction; dementia
may be diagnosed
< 17, severe dysfunction; severe dementia
From: Folstein M F, Folstein S E, McHugh P R. A Practical Method for Grading the Cognitive State
of Patients for the Clinician. J Psychiatr Res 1975; 12: 18998.
Investigations
Together with haematology and biochemistry blood assays, a recent ECG should be
available. Chest radiography may help to evaluate degrees of cardiac and respiratory
disease. Occasionally surprise findings may occur (Figure 2).
2 Chest radiograph of a
71-year-old Chinese woman
with a calcified dissected
thoracic aortic aneurysm and
aortic valve secondary to
syphilis.
The value of 2D echocardiography is limited but can be useful in valvular heart disease
in determining degrees of incompetence or stenosis. Assessment of hypokinetic
ventricular damage in ischaemic heart disease is also possible. Ejection fractions are
often not repeatable and can be misleading. If an estimation of ventricular function is
required a multigated scintigraph scan (MUGA) may give a more reliable figure. Peak
flow measurement can be easily performed. This simple test gives good quantitative
estimates of pulmonary function, and in this context, is often as valuable as formal
pulmonary function testing. u
FURTHER READING
Association of Anaesthetists of Great Britain and Ireland. Blood Transfusion and the
Anaesthetist Red Cell Transfusion. London: AAGBI, September 2001.
Davenport H T. Anaesthesia in the Elderly. London: Heinemann Medical Books,1986.

Dodds C, Murray D. Preoperative Assessment of the Elderly. Br J Anaesth CEPD Rev
2001; 1(6): 1814.

Procedures under Tourniquet
Ivan N Ramos-Galvez
Alastair McCrirrick
Alastair McCrirrick is Consultant in Anaesthesia and Intensive Care at

Gloucestershire Royal Hospital, UK. He qualified from Southampton University and
joined the Royal Air Force. He completed his anaesthetic training in Bristol and the
South West Region. He now specializes in intensive care and anaesthesia for major
bowel and vascular surgery. His particular interests include anaesthesia for carotid
endarterectomy.
Applying a pressurized pneumatic cuff to a limb can be used to prevent the central
spread of local anaesthetic during intravenous regional anaesthesia. It may also
be used to reduce bleeding and improve the surgical field when operating on an
exsanguinated limb. Using a tourniquet can induce significant physiological changes
depending on the duration of inflation and the general status of the patient.
Tourniquet application
Maintaining a bloodless field during limb surgery

The cuff should be wider than half the limb diameter and should be applied over smooth
padding. The edges of the cuff must overlap to ensure it exerts even pressure all round
the limb. Ideally, the overlap should be on the opposite side of the limb to the main
neurovascular bundle. The limb is then exsanguinated either by elevation for 1 minute
or by the application of Esmarch bandaging or a Rhys-Davies exsanguinator. (In the
presence of infection or tumour, exsanguination by methods other than elevation is
usually contraindicated.) When applied to the leg, the tourniquet is usually inflated to a
pressure 100 mm Hg above systolic arterial blood pressure; on the arm it is inflated to
50 mm Hg above systolic arterial blood pressure. The pressure required depends on
the size of the muscle mass to be compressed. During preparation of the surgical
field, skin cleaning solutions should not come into contact with the tourniquet padding.
If alcohol or iodine-based cleaning solutions soak into the padding they can cause
skin irritation. Diathermy burns have also resulted from pooling of liquid around the
tourniquet.
Intravenous regional anaesthesia

A machine equipped with two tourniquets is optimal for intravenous regional
anaesthesia. Intravenous access is obtained in the limb before application of the
tourniquet. Great care must be exercised during exsanguination to avoid dislodging
the intra-venous cannula. After exsanguination, the proximal tourniquet cuff is inflated
and local anaesthetic is introduced into the limb. (If the cuff were to fail at this stage
the local anaesthetic would spread centrally resulting in a potentially toxic plasma
concentration of local anaesthetic agent.) After a few minutes, the distal cuff is inflated
and then the proximal cuff can be let down. The result is a tourniquet compressing
a section of limb that has itself been rendered insensitive by intravenous regional
anaesthesia. This is an attempt to reduce tourniquet-related pain (see below).
The tourniquet must remain inflated for a minimum of 20 minutes to allow the local
anaesthetic time to bind to tissues. Deflation before 20 minutes may precipitate
systemic local anaesthetic toxicity.
Physiological changes
Figure 1 summarizes the physiological changes that occur during inflation and deflation
of a tourniquet.
Physiological changes
During inflation
Rising volaemia and systemic vascular resistance lead to increased
blood pressure, central venous pressure and heart rate
Temperature reduction in non-perfused limb
Anaerobic metabolites being produced
After deflation
Reperfusion of limb
Reduction in volaemia and systemic vascular resistance lead to
decreased blood pressure, central venous pressure and heart rate
Core temperature falls
Mixed acidosis, decrease in pO2 and pH while pCO2, K+ and free radicals
increase
Reactive hyper-reperfusion
1
Cardiovascular
Increases in systemic blood pressure, central venous pressure and heart rate have
been reported immediately after tourniquet inflation. These changes are related to
the sudden increase in blood volume (up to 15%) combined with a reduction in the
capacitance of the vascular bed. Reciprocal haemodynamic changes may be expected
following tourniquet deflation due to a decrease in systemic vascular resistance and
venous return while the limb is reperfusing. The magnitude of the haemo-dynamic
changes can be reduced by the use of regional anaesthesia. Preoperative ketamine,
0.25 mg/kg, moderates the rise in blood pressure after tourniquet inflation. In some
patients, who have been otherwise cardiovascularly stable, a sudden marked rise in
arterial pressure may occur about 1 hour after tourniquet inflation. In these patients, the
arterial pressure may continue to rise, despite increasing the depth of anaesthesia, and
only resolves when the tourniquet is deflated. Severe hypertension and/or concerns
about possible ischaemic limb damage are the two factors that most commonly limit the
duration of tourniquet inflation. The exact physiological mechanisms involved in this late
arterial pressure rise are unclear.
Generalized muscle perfusion remains above normal for up to 15 minutes after

tourniquet deflation. This is caused by the release of anaerobic metabolites triggering
reactive vasodilatation in capillary beds within the muscle fibres.
Temperature
While the tourniquet remains inflated, the temperature of the non-perfused limb
falls. This has some protective effect against ischaemic damage. However, during
reperfusion, blood is exposed to cold tissues and on deflation there can be a reduction
in core temperature of up to 0.6oC for each hour the tourniquet was used.
Metabolic changes
Leaving the tourniquet on for more than 30 minutes produces anaerobic metabolism,
resulting in a mixed acidosis with hypoxaemia, hypercapnia, hyperkalaemia and
formation of free radicals. These changes are normally well tolerated by healthy
individuals but may be detrimental to patients with poor cardio-pulmonary reserve.
The acidosis can be partly corrected by a short period of hyperventilation immediately
after tourniquet deflation. Maintaining anaesthesia with a propofol infusion rather than
a volatile agent may significantly reduce the formation of free radicals. Nevertheless,
caution is advised when bilateral tourniquets are required and, whenever possible,
simultaneous inflation should be avoided.
Complications
The incidence of complications is related to the inflation pressure and the duration of
inflation.
Limb ischaemia is the most serious complication. Current recommendations regarding

the upper limit for the duration of inflation vary between 30 minutes and 4 hours (30
minutes is the time taken for the onset of anaerobic metabolism). Nevertheless, after
1 hour of ischaemia, electron microscopy can detect depletion of glycogen granules in
the sarcoplasm of muscle fibres. After 2 hours, lesions associated with acidosis (e.g.
mitochondrial swelling), myelin degeneration and Z-line lysis can be identified. These
changes are reversible with reperfusion and it may be that intermittent reperfusion
exsanguination during surgery prolongs the safe limit of tourniquet application by
preventing excessive anaerobic metabolism. This may, however, be at the expense of
supplying more substrate for the production of free radicals.
Local anaesthetic toxicity: if the cuff is being used for intra-venous regional
anaesthesia it must remain inflated for at least 20 minutes after local anaesthetic has
been injected, if local anaesthetic toxicity is to be avoided. The risk of local anaesthetic
toxicity is reduced if agents with low systemic toxicity are used. For prolonged
procedures, the cuff can be deflated at intervals to prevent ischaemic damage and, if
intravenous access in the operated limb has to be retained, further, smaller doses of
local anaesthetic can be given.
Pressure-related nerve damage can be caused by a tourniquet with possible rupture

of the Schwann cell membrane. This may lead to neuralgia paraesthetica, which usually
resolves within a few weeks or months.
Excessive pressure can also damage underlying vessels, increasing the incidence of
microemboli formation in the exsanguinated limb. This increases the risk of pulmonary
microvascular injury (small pulmonary emboli). Prolonged tourniquet times have been
related to respiratory failure requiring postoperative ventilation, especially in trauma.
In a properly exsanguinated healthy limb, alterations in blood clotting physiology are
usually minimal and theoretically should have no clinical impact. The incidence of deep
vein thrombosis (DVT) may be higher when a tourniquet is used, but this has not been
substantiated in arthroscopic knee surgery. Thromboprophylaxis must be considered
in all patients aged over 40 years who have surgery performed under tourniquet
(except for arthroscopic knee surgery), especially if there are other risk factors for DVT
formation.
Tourniquet pain can occur 4560 minutes after tourniquet inflation. Patients
undergoing surgery under regional anaesthesia initially experience a dull ache in
the exsanguinated limb after about 30 minutes of tourniquet application. This may
occur even when a second cuff is inflated on an anaesthetized section of limb. As the
pain worsens, patients may become restless and eventually the pain may become
unbearable despite the presence of an otherwise satisfactory block. The pain may be
transmitted through C fibres (slow, persistent, poorly localized pain), which are more
resistant to local anaesthetic than A fibres (sharp, fast pricking pain). At the onset of
neural blockade, when the concentration of local anaesthetic is high, both are inhibited.
As the local anaesthetic is metabolized, the concentration becomes insufficient to
block C fibres despite continuing to anaesthetize A fibres. This theory is supported
by the observations that longer-acting local anaesthetic agents reduce the incidence
of tourniquet pain and that its onset is delayed if a larger dose of local anaesthetic
is used. There is also a reduction in the incidence of pain if clonidine is added to the
local anaesthetic solution. Once tourniquet pain has developed it is difficult to treat,
other than by releasing the tourniquet. General anaesthesia may need to be used if the
surgery is continuing. Opiates alone are disappointing and tend to cause side-effects
from excessive dose once the tourniquet is released and the afferent stimulus ceases.
Hypertension: patients undergoing general anaesthesia with a tourniquet in situ can

develop signs of hypertension and tachy-cardia that mimic those seen during painful
surgical stimulation. The reasons for the development of hypertension under these
circumstances are unclear and it has been traditionally ascribed to the development of
limb ischaemia, nerve compression or the development of tissue acidosis. Hypertension
developing in these circumstances is often resistant to opiates and is relieved only
when the tourniquet is deflated.
Treatment: Figure 2 lists treatments for complications. u
Treatment of complications
Easing the metabolic hurdle

Whenever possible use a regional technique, even combined with
general anaesthesia
Preoperative ketamine, 0.25 mg/kg, prevents hypertensive response to
tourniquet
Total intravenous anaesthesia with propofol helps to scavenge the free
radicals produced
Hyperventilate after tourniquet deflation to reduce acidosis
Caution with simultaneous tourniquets
Easing the tourniquet pain

Reduce tourniquet time as much as possible
Whenever possible use a regional technique, even combined with
general anaesthesia
Use longer-acting local anaesthetics to reduce incidence
Use clonidine mixed with local anaesthetic
Intrathecal opiates reduce incidence of pain
If unbearable and patient awake, convert to general anaesthesia
Caution with adjuvant systemic opiates in awake patient, they may lead
to delayed respiratory depression
2
FURTHER READING
Barash, Cullen, Stoelting. Clinical Anaesthesia. 2nd ed. Philadelphia:Lippincott, 1992.
Rogers, Tinller, Covino, Louguedler. Principles and Practice of Anaesthesiology. New
York: Mosby, 1993.

Local Anaesthetic Blocks
in Ambulatory Orthopaedic
Surgery
Patrick M Clarke
Patrick M Clarke is Consultant in Pain Management and Anaesthesia at Gloucester

Royal Hospital. He qualified at Liverpool and trained in Liverpool, Birmingham and
Bristol. He worked as Assistant Professor at Stanford University Medical Center,
California, USA. His main interests are complex pain problems and orthopaedic
anaesthesia.
More surgery is now being performed in an outpatient setting. The growing complexity
of surgical procedures challenges the anaesthetists ability to provide postoperative
analgesia. Inadequate analgesia is a cause of delayed discharge and unexpected
hospital admission. In a large prospective study, 16% of ambulatory orthopaedic
patients had severe postoperative pain. Opi-oids are associated with nausea, vomiting
and urinary retention, causing delayed discharge. Local anaesthetic techniques used
as the primary anaesthetic or as an adjuvant to general anaesthesia can provide a safe
and effective alternative to opioid analgesia.
Selection of local anaesthetic technique orthopaedic surgery lends itself to

peripheral and central neural blockade. Several questions need to be answered before
deciding on a local anaesthetic technique (Figure 1).
Can the block be used as the primary anaesthetic?
Is sedation required as well?
Can the block be used to supplement a general anaesthetic?
Is the patient happy with a local technique?
Block decision algorithm

Operation
No tourniquet Tourniquet
Will block/s1 cover Will block cover

total operative site? tourniquet?
Yes No No Yes
Operation Operation
< 10 mins > 10 mins
Patient informed and happy
Proceed with block/s sedation
Proceed to general anaesthesia

local anaesthesia adjunct
1
If bone graft is being harvested from non-blocked site general anaesthesia
is usually necessary (e.g. iliac crest graft).
If several blocks are being considered is this acceptable to the patient or is
sedation required (e.g. ankle block)?
1
Selection of a particular block depends on surgical procedure, use of a tourniquet,

patient acceptability and operator experience.
Sedation
Sedation is useful for block placement and intraoperative sedation. Some blocks
take time to site successfully and patients may become irritable and anxious
and lose confidence in the anaesthetist; sedation minimizes these problems. For
block placement the patient should be relaxed but conscious enough to report
any paraesthesia. In a paraesthesia-seeking technique less sedation should be
administered than when using a nerve stimulator to obtain motor stimulation. When a
nerve stimulator is used the patient may receive more sedation but must be conscious
enough to report major paraesthesia, which may indicate intraneural injection. Suitable
sedation for block placement may be achieved using a combination of a short-acting
benzodiazepine such as midazolam, 0.0250.05 mg/kg, and fentanyl, 0.51.0 g/kg
(i.e. midazolam, 2 mg, and fentanyl, 50 g, for a 80 kg patient).
Intraoperative sedation may be achieved with a variety of pharmacological agents

ranging from intermittent boluses of benzodiazepine/opioid combinations to an
infusional drug such as target-controlled propofol. In an ambulatory setting success is
easily achieved using bolus techniques owing to the short duration of surgery. There
is a fine balance between patient relaxation and disinhibition. It is better to have a less
sedated cooperative patient than one who is over-sedated and confused.
Patient information
Informed consent is paramount for local anaesthetic techniques used as the primary
anaesthetic or adjuvant to a general anaesthetic. To gain the patients confidence and
minimize anxiety it is important to explain the sequence of events that will take place on
arrival in the anaesthetic room or operating theatre.
Side-effects must be discussed when obtaining consent. Pain at the site of injection
occurs in about 30% of patients. 10% may experience tingling or numbness for up to
48 hours. Patients must be advised not to go near hot or cold objects and to beware of
trauma to a numb extremity for up to 48 hours. Rare complications such as infection
and bleeding should also be mentioned. Complications specific to individual blocks
should be discussed. For example, in interscalene block, hoarseness, Horners
syndrome or difficulty with coughing (secondary to phrenic nerve paralysis) should be
outlined.
Patients must be told that even with a limb blocked satisfact-orily for surgery some
sensation of movement and touch may occur otherwise they may panic when they feel
touch during surgery. The sensation can be likened to that felt following dental local
anaesthesia. Touch may be felt but pinching is not painful.
Explain to the patient that pain will occur when the block wears off and give them
advice about pre-emptive analgesia.
Choice of equipment
Needles: the popularity of needle types is often based on their likelihood of causing
trauma to nerve tissue, but the incidence of peripheral nerve injury is small. Debate
continues over the use of pencil-point needles, short bevelled needles or sharp
needles. There are no clinical outcome studies implicating bevel design as a consistent
factor in nerve injury. Evidence suggests that sharp needles cause less nerve damage,
which is more rapidly repaired. Using a short bevelled block needle gives a better feel
of deeper tissue planes. Over-zealous seeking of paraesthesia should not take place.
When used in conjunction with a nerve stimulator in a conscious, relaxed patient, a

carefully performed nerve block is unlikely to cause significant nerve injury. For single-
shot techniques with needle and nerve stimulator, the Stimuplex short bevelled needle
is excellent (Figure 2). It is available in various lengths, is well made and easy to hold.
For a continuous catheter technique the combined Braun sheathed Tuohy needle, with
side injection port and catheter is useful and well made (Figure 3). It is particularly
useful following surgery when a continuous physiotherapy machine is required (e.g.
post shoulder release).
2 The Stimuplex short bevelled

needle.
3 Braun catheter.
Nerve stimulator: there is little evidence that postoperative nerve injury is reduced
by the use of nerve stimulators. There are also few studies to verify improved success
of blocks. Ultrasound-guided block needles improve success in block placement. It is
mandatory to use a nerve stimulator in some approaches to the brachial plexus (e.g.
interscalene block because of proximity of the major blood vessels and CSF). The
negative lead of the nerve stimulator should be attached to the needle and the positive
lead attached to an ECG sticker at least 10 cm away from the limb to be anaesthetized
(Figure 4). A current of 1 mA is used initially. Once the needle tip approaches the
nerve/s to be blocked the current should be reduced to about 0.4 mA. Muscle twitching
in the appropriate muscle group at this current indicates close proximity of the needle
tip to the nerve. Muscle twitching at lower currents may indicate intraneural placement
of the needle, though the patient will usually let you know if this occurs!
4 Patient attached to nerve

stimulator.
Useful blocks in the ambulatory setting

Upper limb blocks: ambulatory orthopaedic surgery lends itself to the use of nerve
blocks as both primary anaesthetic and as an adjunct to general anaesthesia (Figure
5). The main limiting factor for use as a primary anaesthetic is the use of tourniquets.
The tourniquet must be placed on an anaesthetized part of the limb. With brachial
plexus block this is easily accomplished, but with isolated nerve blocks the use of a
tourniquet rules out blocks as the primary anaesthetic. If surgery takes less than 10
minutes a tourniquet may be tolerated, particularly with the use of sedation (e.g. carpal
tunnel decompression under local infiltration).
For proximal upper limb surgery, the block of choice is the interscalene brachial plexus
block. Shoulder arthroscopy, manipulation and arthroscopic rotator cuff repair may be
extremely painful postoperatively. Interscalene anaesthesia is ideal. It is relatively easily
performed using a nerve stimulator, the plexus usually being superficial at this level.
Most ambulatory orthopaedic surgery is performed on the distal part of the arm. In the
forearm, removal of internal fixation devices is a commonly performed procedure. For
forearm surgery the axillary approach to the brachial plexus is reliable and effective
and may be used as the primary anaesthetic. Hand surgery is easily performed under
axillary brachial plexus blockade.
The axillary approach is safe and reliable. Occasionally ab-duction at the shoulder joint
is difficult, making an axillary approach impossible. In this situation, supraclavicular,
infraclavicular or subcoracoid approaches to the brachial plexus may be used.
Both supra- and infraclavicular approaches carry the risk of pleural puncture; the
subcoracoid approach does not. In conjunction with a nerve stimulator the plexus is
easily identified and block may be successfully achieved.
Nerve blocks at the elbow may be used to supplement brachial plexus blockade.
Occasionally a nerve may be missed, requiring further block at the elbow. However,
some anaesthetists consider that the likelihood of nerve damage is increased
by attempting to block a partially anaesthetized nerve because paraesthesia is
decreased. The nerves at the elbow are superficial and paraesthesia must not be
sought over-zealously.
Upper limb block
Block Primary Adjunct Advantages Disadvantages Volume

site anaesthesia to general of local
anaesthesia anaesthetic
Plexus Interscalene Yes Yes Broad coverage Variable block 2040 ml

blocks Supraclavicular until experienced
Infraclavicular
Subcoracoid
Axillary
Block at Median Possibly Yes Add on to Does not cover 5 ml/nerve

elbow Ulnar brachial block if tourniquet
Radial patchy
Block at Median Possibly Yes Easy Does not cover 35 ml/nerve

wrist Ulnar tourniquet
Radial
Distal Ring block Yes Yes Easy None 5 ml

block
Other Biers block Yes No Easy Bloodless field 3040 ml

not obtained
Local infiltration Yes Yes
Distal nerve blockade at the wrist is usually used only as an adjunct to general
anaesthesia due to use of a tourniquet. Surgery on the finger may be performed under
ring block. A bloodless field is achievable using a finger tourniquet applied by the
surgical team following block.
Biers block is useful for simple forearm manipulations. Most surgeons do not use it for
open procedures (e.g. excision of Dupuytrens contracture) because anaesthetic may
ooze into the operative field.
Local infiltration is a useful anaesthetic tool. It may be used with a tourniquet for short
procedures. It is valuable as an adjunct to general anaesthesia and for postoperative
analgesia.
Lower limb blocks (Figure 6) are under-used. They are most appropriate when
used with a general anaesthetic. Proximal lower limb surgery is unusual other than
for removal of internal fixation devices (seldom performed in the ambulatory setting).
Removal of small screws usually benefits from simple local infiltration by the surgeon.
Most lower limb ambulatory orthopaedic surgery is distal. Commonly performed
distal lower limb orthopaedic operations include bunion and bunionette excision,
Zadeks procedure, removal of metalwork from distal tibia and fibula, excision of soft
tissue lesions (e.g. Morton neuroma). Owing to the use of proximal tourniquets local
anaesthetic techniques are not commonly used as the primary anaesthetic. However,
local blocks are an excellent adjunct to general anaesthesia. u
Lower limb blocks

Block Primary Adjunct Advantages Disadvantages Volume
site anaesthesia to general of local
anaesthesia anaesthetic
Proximal Femoral Yes Yes Useful in None 20 ml

blocks Sciatic No Yes avoiding Experience 20 ml
Lateral cutaneous central blockade required
3-in-1 block1 Yes Yes None 30 ml
At knee Sciatic No Yes Useful analgesia Sometimes patchy 15 ml

Saphenous No Yes 10 ml
C.peroneal No Yes 10 ml
At ankle 5 nerves SSSPP2 Possibly Yes In sick patients 5 injections 2030 ml
Distal Ring Yes Yes Easy None 5 ml
Other Biers block Yes No Easy No bloodless field 3040 ml

Local infiltration Yes Yes
1
Femoral, obturator, lateral cutaneous nerve of thigh; 2Saphenous, sural, superficial peroneal, deep peroneal,
posterior tibial.

Paediatrics
Anaesthesia
on CD-ROM
Acute and Chronic Airway
Obstruction
Thandla Raghavendra
Robert Walker
Thandla Raghavendra is Specialist Registrar in Anaesthesia with an interest in

paediatric anaesthesia. He has trained in anaesthesia in India and in the North West
region of the UK.
Robert Walker is Consultant Paediatric Anaesthetist at the Manchester Childrens

Hospital, UK. He qualified from Glasgow University Medical School and trained
in paediatrics and anaesthesia in Manchester. His main area of interest is the
development of fibre-optic intubation techniques in infants and children.
A baby has a large tongue in relation to the oral cavity and the larynx lies higher
than in an adult. Both features bring the tongue closer to the palate, predisposing to
obstruction. Obstruction in a baby or child due to trauma from intubation is most likely
to occur at the subglottic region because this is the narrowest part of the airway, has
a complete ring of cartilage (the cricoid) and loose mucosa (making it particularly
susceptible to oedema). Oedema can cause dramatic increases in airway resistance
and the work of breathing (for laminar flow, a 50% reduction in airway radius causes a
16-fold increase in airway resistance from Poiseuilles law). Uncuffed tracheal tubes
are less likely to cause trauma and are therefore preferred.
Physiological factors
Babies less than 5 months of age are obligate nose breathers. Obstruction of both
nasal passages (e.g. because of secretions or choanal atresia) can cause asphyxia.
Babies, especially, have a limited ability to cope with an obstructed airway because:
the chest wall, trachea and bronchi are pliable and easily deformed
the diaphragm and intercostal muscles have fewer fatigue resistant type I fibres
and tire easily
oxygen reserves are lower because of a smaller functional residual capacity (FRC)
and higher oxygen consumption (46 ml/kg/minute compared with 24 ml/kg/minute
in adults).
If the work of breathing increases, respiratory failure and hypoxaemia can develop
quickly.
Acute airway obstruction

The site of airway obstruction determines the clinical features. Agitation and crying
worsen airway obstruction by causing turbulent airflow and by worsening dynamic
compression.
Extrathoracic obstruction the calibre of the extrathoracic airways depends on the

balance between the intraluminal and atmospheric pressures. Inspiratory efforts to
overcome an extrathoracic obstruction generate large negative intrapleural pressures,
which are transmitted to the extrathoracic airway as negative intraluminal pressure.
The atmospheric pressure then exceeds the intraluminal pressure causing dynamic
compression of the airway during inspiration (Figure 1a). Extrathoracic obstructions,
therefore, cause inspiratory stridor, which may be improved by giving continuous
positive airway pressure (CPAP) to help splint the airway open.
Intrathoracic obstruction the patency of the intrathoracic airway depends on the

balance of intraluminal and intrapleural pressures. Large positive intrapleural pressures
generated during active expiration cause dynamic compression of the airways
downstream of the obstruction (Figure 1b). Intrathoracic obstructions tend to cause
expiratory stridor.
Extrathoracic
obstruction
Dynamic
compression
Intrathoracic
obstruction
Alveoli
Intrapleural space
Figures 24 list the causes, clinical features and severity of acute airway obstruction.
Causes of acute airway obstruction
Congenital Acquired
Choanal atresia (congenital Epiglottitis1
blockage of nasal passages) Laryngotracheobronchitis2
Laryngomalacia2 Bacterial tracheitis
Subglottic stenosis Subglottic stenosis
Subglottic haemangioma Burns
Webs Peritonsillar abscess
Cysts Foreign body
Tracheal stenosis Angioneurotic oedema
Vascular rings or slings Nerve palsies
Bilateral vocal cord paralysis Mediastinal masses
1
Uncommon 2
Common
2
Clinical features of acute airway obstruction
Features Implication
Stridor (noisy breathing Airway obstruction
caused by turbulent air flow)
Inspiratory stridor Supraglottic obstruction
Expiratory stridor Infraglottic obstruction

Biphasic stridor Glottic obstruction
Stridor when crying or Moderate airway obstruction
feeding
Stridor at rest Severe airway obstruction
Wheeze Small airways obstruction
Muffled cry Supraglottic obstruction
Hoarse cry Laryngeal obstruction
Unable to cry Severe obstruction
Dysphagia Supraglottic obstruction
Nasal flaring
Sternal, intercostal,
subcostal retractions Increased work of breathing
Paradoxical respiration
Head bobbing
Tachypnoea
Tachycardia Hypoxaemia
Agitation
Sitting up and unable to Severe airway obstruction

lie supine
Cyanosis Severe hypoxaemia
Sweating Hypercarbia and fatigue
Altered consciousness Severe hypoxaemia
Bradycardia or arrhythmias Collapse imminent
3
Dos and donts in stridor
Do Dont
Give oxygen Examine the pharynx
Observe closely Sedate the child
Minimize stress to the child Send for radiography
Ask for experienced help Attempt intravenous access
Maintain spontaneous respiration until help is present and
anaesthesia induced
Use muscle relaxants until
the airway is secure
4
Airway management
The primary goal of management is to secure the airway safely, which requires
general anaesthesia. The child should be kept calm, allowed to adopt a comfortable
position and given oxygen to breathe (unless this upsets them). Oxygen saturation
(SpO2) should be monitored continuously. Heliox (oxygen in helium) decreases airway
resistance during turbulent flow because of its lower density, and can be useful.
Parents should accompany the child to the induction room to avoid the distress of
separation. Appropriate equipment for emergency cricothyroidotomy or tracheostomy,
a range of tracheal tubes (including sizes smaller than that calculated) and an
experienced surgeon should be available.
An unhurried inhalational induction using either sevoflurane or halothane in oxygen is

started. Induction can be slow because of the effects of airway obstruction and VQ
mismatch caused by atelectasis. Standard monitoring is established and intra-venous
access secured once anaesthesia has been induced. Spontaneous breathing should
be preserved throughout induction (CPAP helps to keep the airway open by combating
dynamic compression and preventing atelectasis) and laryngoscopy attempted only
when the child is deeply anaesthetized. Muscle relaxants can be given safely only when
the airway is secure. The important management points are given in Figure 4.
Treating the common causes

Viral croup (viral laryngotracheobronchitis) is usually caused by either the
parainfluenza, influenza or respiratory syncitial virus. It affects children from 6 months
to 6 years of age and occurs in epidemics in late autumn and early spring. Croup is
usually preceded by several days of coryza. Respiratory obstruction develops gradually
producing stridor, which is typically worse at night (Figure 5). The child presents with
a low-grade temperature, a brassy cough and hoarse voice. About 2% of affected
children are admitted to hospital but less than 2% need tracheal intubation. Most
respond to oxygen and nebulized adrenaline (epinephrine), 5 ml of 1:1000, repeated
as required. Corticosteroids (dexamethasone or nebulized budesonide) reduce the
need for intubation. Dexamethasone, 0.6 mg/kg oral or i.v., is usually given as a single
dose but can be repeated (0.15 mg/kg). Nebulized budesonide, 2 mg, is given as a
single dose; it may be repeated but a single dose has been shown to improve outcome.
The duration of intubation varies but is on average 35 days. There is no evidence to
support the use of steam tents (which can also limit clinical observation).
Assessment of croup severity
Moderate Severe Life threatening

Alert Quiet or agitated Depressed consciousness
Stridor present Stridor present Stridor may be absent
Mild recession Severe recession Limited chest movement
No fatigue Increasing fatigue Exhaustion
Oxygen saturation Oxygen saturation Oxygen saturation

> 92% in air < 92% in air < 92% in oxygen
Steady respiratory Increasing Periods of apnoea

rate respiratory rate
Steady heart rate Increasing heart rate Bradycardia

5
Epiglottitis (supraglottitis) is a bacterial infection caused by Haemophilus influenzae
type B (HiB), which generally affects children of 26 years. The recent introduction
of universal vaccination against HiB has made this condition rare. The symptoms
progress rapidly and affected children look toxic (pale, pyrexial and shivery), have a
high temperature and inspiratory stridor. They usually sit up, leaning forward, with their
mouths open and tongue protruding, drooling saliva. They are reluctant to swallow or
speak. On laryngoscopy, the epiglottis and aryepiglottic folds appear inflamed and
swollen. Often, the only clue to the glottic opening is a small mucous bubble. After
securing the airway and obtaining blood for culture, intravenous cefotaxime, 30 mg/
kg/dose 8 hourly i.v., is given (contacts are treated with rifampicin). Airway oedema
resolves in 4872 hours. A leak around the tracheal tube (appropriate for the childs
age) is a reliable guide to timing extubation.
Bacterial tracheitis (membranous laryngotracheobronchitis) is caused by

Staphylococcus aureus. Affected children look toxic and have a brassy cough.
Respiratory obstruction can progress rapidly. On laryngoscopy, thick purulent
secretions resembling a membrane are seen covering the subglottic mucosa.
Nebulized adrenaline (epinephrine) is of little use. Anti-staphylococcal antibiotics
(e.g. flucloxacillin, 2550 mg/kg/dose 6 hourly) should be administered. Toxic shock
syndrome is a rare complication.
Inhaled foreign bodies may lodge in the larynx, trachea, main bronchi or smaller
airways. A previously well child presenting with paroxysmal cough and respiratory
distress should arouse suspicion of foreign body aspiration. Peanuts are the most
common inhaled organic objects. They absorb water, swell up, and become soft and
friable. They also cause chemical irritation of the airway and should be removed
urgently. Severe obstruction is life threatening and urgent management of the airway
a priority (Figure 6). Rigid bronchoscopy under general anaesthesia is required for
removal of a foreign body (see below). A child with a small foreign body in the larynx
may present with hoarseness or stridor. A foreign body in the lower airway may
present with persistent cough, unilateral collapse or unilateral wheeze on auscultation.
Expiratory chest radiographs are indicated in less urgent cases to locate the position
of a radio-opaque body and identify other features typical of an inhaled foreign body.
There are three characteristic patterns.
Management of choking
If a child is breathing and talking do not intervene because this could

worsen the situation
If obstruction is complete, action depends on age
< 1 year
Position child face down on rescuers lap or forearm and administer four
back blows between scapulae
If obstruction persists place supine and give 4 rapid chest thrusts
If unsuccessful attempt mouth-to-mouth resuscitation
Small child
Administer 610 abdominal thrusts with child supine and rescuer at
victims feet. Place heel of hand above umbilicus in midline and below
xiphoid process
Larger child
Treat as adult; administer Heimlich manoeuvre
If obstruction persists and medical staff are available attempt

cricothyroidotomy
6
A stop valve obstruction completely obstructs a smaller airway. A chest radiograph

shows collapse of the affected lung, mediastinal shift (towards the affected side) and
upward movement of the ipsilateral diaphragm.
A ball valve obstruction permits air entry during inspiration but stops air leaving
during expiration. This causes hyper-inflation on the affected side, pushing the
mediastinum towards the opposite side and the ipsilateral diaphragm down.
A bypass valve obstruction allows ingress and egress of air and causes no
radiological changes.
Airway burns may accompany facial burns or occur in a victim burned in a confined
space. Clinical clues include soot deposits in the mouth or nose. Other clues include
stridor, facial burns or circumferential burns of the neck and oedema of the pharynx.
When airway burns are suspected, the trachea should be intubated without delay
because facial, oral and airway oedema can occur rapidly, making intubation difficult or
impossible. It is wise to use an uncut tube to allow room for facial swelling, which may
occur later.
Laryngomalacia is a congenital laryngeal anomaly and the most common cause of

stridor in early infancy (it generally develops within a few days of birth). Obstruction is
caused by either a floppy tubular epiglottis or flabby supraglottic structures prolapsing
into the glottis, causing inspiratory stridor. Symptoms worsen during feeding, crying
or with respiratory infections, but disappear when the baby lies prone. The condition
improves with growth, usually resolving spontaneously by 1 year of age. Occasionally,
laser aryepiglottoplasty is used to treat severe obstruction but tracheostomy is rarely
indicated.
Laryngoscopy and tracheobronchoscopy

The diagnosis and evaluation of airway obstruction and removal of a foreign body
involves laryngoscopy and tracheobronch-oscopy, usually under general anaesthesia.
Preoperative imaging (CT or MR) may be required to ascertain the nature and extent of
the obstruction. Sedative premedication is avoided because of the risk of compromising
the airway further. Both laryngoscopy and tracheobronchoscopy involve sharing the
airway with the endoscopist. Spontaneous breathing is required to evaluate a dynamic
obstruction (e.g. laryngomalacia, tracheomalacia) and is safer during removal of a
foreign body.
Induction can be performed with sevoflurane or halothane (Figure 7). Sevoflurane has
a better cardiovascular profile but halothane is useful in the obstructed airway where
deepening anaesthesia is difficult. Preventing undesirable responses to instrumentation
of the airway, such as laryngospasm, breath-holding or coughing, requires a deep
plane of anaesthesia. The incidence of these problems can be reduced further by
topical anaesthesia with lidocaine (lignocaine), maximum of 3 mg/kg, to the cords (by
the anaesthetist) or carina (by the endoscopist). Anticholinergic agents (glycopyrollate,
10 g/kg, or atropine, 20 g/kg), given intravenously at induction, may reduce
secretions and prevent bradycardia (especially if using halothane).
Maintaining the airway: inserting a tube into the trachea obscures the surgeons
view and impairs the movement of laryngeal structures during breathing. There are
no specific microlaryngoscopy tubes for children, but if a tube is necessary, a size or
two smaller is selected. A common alternative is to flood the pharynx with oxygen and
a volatile agent delivered through a T-piece attached through a face mask (allowing
flexible bronchoscopy through a modified angle piece) or nasopharygeal airway
inserted into a nostril, while maintaining spontaneous breathing(Figure 7). Correct
placement of the nasopharyngeal airway (usually a softened cut-down tracheal tube)
can be verified by occluding the mouth and observing unobstructed breathing or during
bronchoscopy. Delivering anaesthesia through a nasopharyngeal airway allows easy
access by the surgeon to examine the supraglottic structures or introduce a flexible
or rigid bronchoscope through the mouth and into the trachea. Vasoconstrictor nasal
drops are useful to prevent traumatic bleeding (e.g. otrivine paediatric nasal drops or
spray which contains xylometazoline 0.05%).
7 An infant maintained on
oxygen and halothane via a
nasopharyngeal airway while
undergoing rigid bronchoscopy.
Monitoring: close observation, including movement of the chest and reservoir bag
(once the breathing system is attached to the rigid bronchoscope) and SpO2 monitoring
are essential during the procedure to ensure adequate ventilation and oxygenation. The
patency of the airway and movement of the cords can also be assessed by watching
the endoscopic image on the screen. Leak of gases from the mouth makes end-tidal
CO2 monitoring less reliable.
The bronchoscope: the T-piece can be directly connected to the side arm of the
Storz bronchoscope (Figure 8), allowing the bronchoscope to function effectively
as a tracheal tube once passed through the cords. Positive-pressure ventilation or
assisted breathing can also be delivered if the lesion is fixed. However, other rigid
bronchoscopes do not permit ventilation (e.g. the Hopkins rod). Anaesthesia is
maintained with a nasopharyngeal airway delivering oxygen and a volatile gas.
b b
8 Rigid bronchoscope showing: a

the Storz ventilating bronchoscope;
b the Hopkins rod; and c the Storz
laryngoscope.
During removal of foreign bodies from smaller airways, inadequate ventilation and
hypoxia can occur. The surgeon should withdraw the bronchoscope to the trachea to
improve ventilation.
Chronic airway obstruction

Causes of chronic airway obstruction are given in Figure 9. Obstructive sleep apnoea
syndrome may complicate chronic airway obstruction. The features include:
snoring
apnoea
fragmented sleep
daytime somnolence
failure to thrive
recurrent respiratory infections.
Causes of chronic airway obstruction
Adenotonsillar hypertrophy Micrognathia/retrognathia

Macroglossia Pierre Robin syndrome
Downs syndrome Treacher-Collins syndrome
Beckwith-Wiedemann syndrome Goldenhars syndrome
Hypothyroidism Moebius syndrome
Glycogen storage disorders Hallermann-Streiff syndrome
Mucopolysaccharidoses
Neuromuscular disorders Obesity

Duchenne muscular dystrophy Praeder-Willi syndrome
Cerebral palsy
Syringobulbia Maxillary hypoplasia
Arnold-Chiari malformation Aperts syndrome
Crouzons disease
Laryngomalacia
Laryngeal papillomatosis
(Figure 10)
9
Right heart failure may occur in severe obstructive apnoea, the pathophysiology of
which is given in Figure 11.
If obstructive sleep apnoea is suspected, the ECG should be examined for signs of right
ventricular hypertrophy. Echocardiography helps to assess right ventricular hypertrophy
and pulmonary pressures and detect tricuspid regurgitation. If heart failure is present,
preoperative nasal CPAP and diuretics may optimize the childs condition.
Surgery should be deferred, if possible, in the presence of respiratory infections.

Sedative premedication should be avoided because of the risks of oversedation and
airway obstruction.
a The normal infant larynx. b Laryngeal papillomatosis.
10
Airway laser surgery

Laser beams are used to vaporize papillomata (see Figure 10b), and occasionally other
pathology, but is associated with scarring. To enable the surgeon to aim the laser with
precision, the target area should be still. Although neuromuscular blockade and tracheal
intubation can ensure this, a laser beam can set fire to a normal polyvinyl chloride tube.
Special metal-coated, laser-resistant tubes are expensive and their external diameter
(ED) exceeds that of ordinary tracheal tubes of the same internal diameter (ID). The
smallest laser tube has an ID of 3.0 mm and an ED of 5.2 mm (compared with 3.0 mm
and 4.2 mm for a standard tube) and is suitable only for children over 1 year of age.
Narrowing of the airways further limits their use. The dangers of airway laser surgery
are discussed elsewhere.
Pathophysiology of right heart failure in obstructive

sleep apnoea
11
Alternative anaesthetic techniques

Jet ventilation down the bronchoscope or operating laryngoscope, combined with
total intravenous anaesthesia and muscle relaxants. The flow generated decreases
with smaller injector needles. A 16G needle is commonly used in children, but great
care must be taken to avoid barotrauma. A pressure-regulating device is now available
which should be used to decrease the pipeline pressure (4 bar) to a lesser amount and
thereafter deliver a more suitable volume to a small child. Pneumothorax, though rare,
is a complication. Dissemination of the papilloma virus is a theoretical consideration but
as yet is not described.
Apnoeic techniques: the surgeon uses the laser intermittently and the anaesthetist
intubates and ventilates the patient for short durations between successive applications
of laser.
Deep volatile anaesthesia delivered through a nasopharyngeal airway:

for supraglottic and subglottic laryngeal lesions the combination of deep volatile
anaesthesia with topical local anaesthetic (as described for laryngoscopy above) allows
spontaneous respiration and can provide excellent conditions. u
FURTHER READING
Mather S J, Hughes D G. A Handbook of Paediatric Anaesthesia. Oxford: Oxford
Mayer C M, Cotton R T, Shott S R. The Pediatric Airway. An Interdisciplinary Approach.

Philadelphia: J B Lippincott, 1995.

Anaesthesia for ENT Surgery
Charles Stack
Charles Stack is Consultant in Paediatric Anaesthesia and Intensive Care at Sheffield

Childrens Hospital, Sheffield, UK. He qualified from the Middlesex Hospital, London,
and trained in anaesthesia in Southampton, Nottingham and Great Ormond Street.
In the UK, routine ENT surgery accounts for a high proportion of children requiring
anaesthesia. Tonsillectomy is undertaken in 2.3/1000 children under 12 years of age.
Postoperative haemorrhage occurs in up to 4% and carries a risk of death.
Adenotonsillectomy
Indications for adenotonsillectomy include:
recurrent tonsillitis
recurrent otitis media
obstructive sleep apnoea
upper airway obstruction leading to pulmonary hypertension, right ventricular
hypertrophy and right heart failure
quinsy
tuberculous cervical adenitis
The two main surgical techniques are guillotine tonsillectomy (which involves snaring
the tonsil and excising it rapidly), and dissection tonsillectomy (which involves dissection
and uses diathermy or surgical ties to control bleeding points). For either technique, the
airway has to be secured, with a tracheal tube or a laryngeal mask airway (LMA). The
surgeon inserts a BoyleDavis mouth gag to keep the mouth open, the tongue blade of
which (the Doughty tongue blade) has a groove to keep the tracheal tube or LMA out
of the surgical field. It is important to ensure that the airway remains patent when the
gag is opened because kinking of the tracheal tube or LMA can easily occur.
Preoperative assessment and premedication it is important for the anaesthetist to

ask specifically about:
upper respiratory tract infections (adenotonsillectomy should be avoided during
active infections because the risk of bleeding increases with adenoidal or tonsillar
inflammation)
features suggesting a bleeding diathesis
obstructive sleep apnoea.
Children with obstructive sleep apnoea are particularly liable to respiratory depression
after sedatives (therefore avoid sedative premedication) and general anaesthesia.
Improvement after surgery is not immediate and takes several weeks. Postoperative
care on a high dependency unit or ICU is usually required.
Airway protection the standard method for maintaining the airway during
tonsillectomy has been intubation with a south-facing, preformed, disposable tracheal
tube followed by a spontaneously breathing anaesthetic technique. However, the results
of a study using airway endoscopy showed no soiling of the trachea with blood when
using an LMA compared with soiling in over 50% when using a tracheal tube. The LMA
and tracheal tube for tonsillectomy are compared in Figure 1. The LMA is preferable
because it affords better airway protection from blood until the patient is awake, but the
choice depends on the anaesthetist and surgeon.
Use of tracheal tube or laryngeal mask airway (LMA) for tonsillectomy in

children
Tracheal tube LMA

Definite placement in trachea Better airway protection
Smaller size No muscle relaxants required
Not in surgical field Protection of the lower airway until awake
Easier to take over respiration Reduced incidence of postoperative
vomiting
Blood in trachea in > 50% of Large size may impair surgical access
children Placement may encroach on surgical field
Greater stimulation on insertion Can be difficult to position correctly
May need muscle relaxation for
intubation
Removal of airway protection
when deeply anaesthetized if
extubated deep
1
Postoperative bleeding the main complication of tonsil-lectomy is blood loss in the

airway. If an anaesthetic technique that involves extubation under deep inhalational
anaesthesia is used, it is important to suction the pharynx fully under direct vision (this
also allows assessment of whether the surgeon needs to consider further attempts to
control bleeding). The patient should be extubated head down on their left side (the
tonsillar position) and should remain in this position to allow blood to trickle away from
the larynx. Mean blood loss is about 4 ml/kg, but it is usually underestimated because
most is swallowed.
Primary postoperative haemorrhage usually occurs within 8 hours of surgery. Children

should be observed closely post-operatively to detect signs suggesting haemorrhage,
such as:
increased swallowing
pallor or prolonged capillary refill time
unexplained tachycardia
restlessness
sweating
signs of airway obstruction
hypotension (occurs late).
Bleeding tonsil
Death can occur from a bleeding tonsil (usually due to hypotension) following induction
of anaesthesia after inadequate resuscitation. Mortality from tonsillectomy is about
1/10,000. The patient loses blood steadily, often quietly swallowing the blood before
vomiting. Blood loss is always considerably more than that measured in the vomit;
careful preoperative assessment is essential.
Before surgery the child should be given oxygen and resus-citated with intravenous
fluids and blood (when available). A full blood count, clotting screen and cross match
are required.
Adequate fluid resuscitation with colloid and blood products is essential before
inducing anaesthesia.
Restlessness is often due to hypovolaemia, therefore sedation preoperatively should
be avoided.
Abnormal clotting may occur, therefore non-steroidal anti-inflammatory drugs
(NSAIDs) should be avoided and replacing clotting factors considered.
Blood in the airway may cause obstruction or hinder the view at laryngoscopy.
Blood in the stomach increases the risk of gastric aspiration at induction.
The airway may be narrower due to tracheal edema, if so a tracheal tube half a size
smaller should be considered.
Care should be exercised when using anaesthetic agents that may cause
vasodilatation and hypotension.
The effects of the previous general anaesthetic and peri-operative opiates should be
considered.
The recommended anaesthetic techniques are compared in Figure 2. Two suckers

should be available at induction because haemorrhage can be brisk. Attempts should
be made to empty the stomach before cessation of anaesthesia to reduce the risk of
postoperative aspiration.
Uses of rapid sequence induction (RSI) or gaseous induction in the left

lateral, head-down position for the child with a bleeding tonsil
RSI Gaseous induction

Rapid induction Maintenance of spontaneous
Rapid control of the airway respiration
Less likelihood of regurgitation during Inhalation of blood less likely
induction
Blood in airway Blood in airway may precipitate
Patient may inhale blood laryngospasm
May not visualize cords after paralysis Slow
Cardiovascular depression from Less experience with this
induction position therefore intubation
difficult
Restlessness during induction
Respiratory depression from
previous anaesthetic
Cardiovascular depression from
gaseous induction
2
Analgesia
Adenotonsillectomy is painful. Traditionally, opiates have been avoided because of
their respiratory depressant and sedative effects (particularly in those with obstructive
sleep apnoea) though codeine phosphate, 1 mg/kg i.m., has been used. NSAIDs are
as effective as opiates but may increase the risk of primary postoperative haemorrhage
(particularly ketorolac). Paracetamol alone is often insufficient.
In one study, the combination of paracetamol and ibuprofen as premedication reduced

early requirements for supplementary analgesia compared with paracetamol alone
(though pain scores were similar by 4 hours). Primary postoperative haemorrhage
occurred but the numbers were too small to be significant. Median blood loss increased
during adenotonsillectomy but was not statistically significant in the group receiving
ibuprofen.
Most anaesthetists use perioperative opiates with a combination of NSAIDs and

paracetamol at operation and then regularly postoperatively. A comparison of fentanyl
(intravenous) and morphine (intramuscular) showed reduced frequency of vomiting in
the fentanyl group (median: 1 episode versus 2 episodes) but not a reduced incidence
(70 versus 78%). 52% of the fentanyl group and 41% of the morphine group required
rescue opiate.
Postoperative nausea and vomiting occurs in 578% of patients. Vomiting causes

distress, delayed discharge, dehydration and possibly bleeding from the tonsillar bed.
Swallowed blood is emetogenic. Factors that reduce vomiting following surgery in
children are:
propofol induction and maintenance
use of LMA
routine use of anti-emetics
midazolam, dexamethasone
adequate analgesia
avoidance of opioids
intravenous fluids.
Day case tonsillectomy

The advantages of day case tonsillectomy are mainly socioeconomic; it involves
less family disruption and reduces cost. The operation must be in the morning and a
significant overnight admission rate may be expected. The disadvantages are the risk
of primary postoperative haemorrhage (14%), the need for adequate analgesia (over
40% require postoperative opioids) and a significant rate of postoperative nausea and
vomiting (578%). Distance from hospital, availability of transport and appropriate
family circumstances also have to be taken into account. Children with a history of
obstructive sleep apnoea should not be admitted as day case patients. Overall, it is
probably safer for patients to remain in hospital overnight after tonsillectomy.
Myringotomy
Myringotomy with insertion of grommets is a common day case operation. An
anaesthetic technique with spontaneous respiration (usually via a face mask) is used
and the head held to the side during examination. Theoretically, nitrous oxide increases
the pressure in the middle ear by diffusion of the gas into the air-filled cavity. Mild-to-
moderate pain occurs afterwards for which perioperative paracetamol is useful. u
FURTHER READING
Pickering A E, Bridge H S, Nolan J, Stoddart P A. Double-blind, Placebo-controlled
Analgesic Study of Ibuprofen or Rofecoxib in Combination with Paracetamol for
Tonsillectomy in Children. Br J Anaesth 2002; 88: 727.
Williams P J, Bailey P M. Comparison of the Reinforced Laryngeal Mask Airway and

Tracheal Intubation for Adenotonsillectomy. Br J Anaesth 1993; 79: 47881.

Assessment of Pain in
Children
Neil S Morton
Neil S Morton is Consultant in Paediatric Anaesthesia, Intensive Care and Pain

Management at the Royal Hospital for Sick Children, Glasgow, UK. He qualified from
Aberdeen University and trained in Glasgow, Dundee and Montreal, Canada. His
interests are in developing pain management services for children and improvements in
the management of children undergoing diagnostic and therapeutic procedures.
Pain is difficult to measure precisely and reliably in children and many pain
measurement tools and scores have been developed (Figure 1). The clinician needs a
pragmatic system that reliably tracks both the childs pain experience and the efficacy
of pain control over time.
Pain assessment is a broader concept than pain measurement and takes into
account cognitive, physiological, sensory, behavioural, affective, sociocultural and
environmental factors. The assessment must be appropriate for the childs stage of
development, the severity and chronicity of the childs illness, the surgical or medical
procedure and the medical environment.
Self-reported assessment pain assessment is most accurate when children can
tell staff about their pain. It is possible for children from age 3 years to self-report
the location, severity and nature of pain using words appropriate to their stage of
development.
Observed assessment to detect the symptoms and signs of pain in the younger
child (or in the older child with mental or physical disabilities), behavioural cues and
physiological values are used. These are open to misinterpretation; for example the
same changes may be caused by things other than pain (e.g. hunger). Experienced
paediatric staff are better at interpreting these cues than novices, and parents are often
better than nurses.
Pain assessment must be linked to appropriate interventions based on the
assessment with the aim of ensuring that the child experiences no pain or only mild
pain. Measurement with pain tools or scores should be regarded as an aid to this more
complex holistic assessment process. For severe or acute pain that is likely to persist
over a number of days it is important to assess anxiety and depression.
Whichever scoring system is used, pain assessments should be repeated regularly,
appropriate interventions should be prescribed and their effectiveness should be
documented.
Pain scoring
Pain measurement Appropriate Clinical utility Indicators included Advantages Disadvantages
tool age range
Behavioural and physiological signs of distress

Objective Pain < 3 years Acute postoperative Blood pressure Easy to use
Scale (OPS) pain Crying Validated
Movement Reliable
Agitation Tracks pain over time
Verbal expression Scores decrease with
Body language analgesia
CRIES Score 3260 weeks' Neonates and infants Cry Easy to remember Uses oxygenation as
(Cry, Requires gestational age For acute procedural Oxygen saturation and use measure which can be
oxygen, Increased and postoperative and requirements Validated affected by many other factors
heart rate and pain Heart rate and blood Reliable Blood pressure
blood pressure, pressure Tracks pain over time measurement may upset
Expression, Expression Scores decrease with the baby and falsely
Sleeplessness) Sleeplessness analgesia increase the score
COMFORT 017 years Distress in paediatric Alertness Validated Complicated

Score intensive care Agitation Reliable Unsuitable for intubated
Calmness Tracks pain over time or paralysed patients
Respiratory response Scores decrease
Physical movement with analgesia
Blood pressure and/or sedation
Heart rate
Muscle tone
Facial tension
CHEOPS 17 years Acute postoperative Cry Validated Complicated

(Childrens Hospital pain Facial expression Scores decrease May not track
of Eastern Ontario Venepuncture pain Verbal expression with analgesia postoperative pain
Pain Scale) Torso position or over time in 37
movement year age group
Touching wound because pain behaviours
Leg position and become inhibited
movement or habituated
TPPPS 15 years Acute postoperative Verbal expression Tracks pain relief Seven categories to
(Toddler-Preschool pain Facial expression score
Paediatric Pain Scale) Body language
Self reporting tools

Poker chip tool > 4 years Procedural pain Four tokens to Validated Unsuitable for the
(Figure 2) Acute postoperative indicate pieces of Easy to use critically ill or sedated
pain hurt corresponding child
to nil, mild, moderate
and severe pain
Four faces scale > 4 years Procedural pain Four faces from Validated Unsuitable for the
(Figure 3) Acute postoperative neutral to sad Easy to use critically ill or sedated child
pain corresponding to nil,
mild, moderate and
severe pain
Vertical colour > 4 years Procedural pain Vertically oriented Validated Unsuitable for the
analogue slide-rule Acute postoperative coloured wedge Easy to use critically ill or sedated child
(Figure 4) pain Calibrated 0100
Horizontal linear > 7 years Procedural pain Horizontal 100 mm line Validated Unsuitable for the
analogue Acute postoperative No markings as anchor Easy to use critically ill or sedated child
pain
Adjectival self-report > 4 years Procedural pain Key words with Validated Unsuitable for the
Acute postoperative four choices Easy to use critically ill or sedated child
pain
Source: Finley G A, McGrath P J, eds. Measurement of Pain in Infants and Children. Progress in Pain Research and Management. Vol. 10. Seattle: IASP, 1998.
Children younger than 3 years
In the assessment tools used for children younger than 3 years, observations of
behaviour (e.g. facial expression, body position, mobility, crying, sleep pattern),
skin colour and vital sign measurements (e.g. arterial pressure, heart rate, arterial
haemoglobin saturation) are given numerical scores that are added to give a total.
This static assessment is much less useful than a dynamic one, in which the nurse
is looking for the total score to improve in response to comforting, analgesia or
sedation. This responsive (or interactive) scoring can be used to guide, for example,
the titration of analgesic drugs. Good documentation of the score, the intervention used
and its effect is important.
Many scores of this type are confounded in the less mature, sick or sedated,
paralysed, intubated or ventilated child, so it is reasonable to assume that such children
who have had surgery may be in pain and ensure that adequate analgesia is given.
Pain-related behaviour in toddlers may be all-or-nothing in nature. They can often
locate pain precisely (e.g. by grabbing at the site of operation). This suggests that a
simple scoring system (e.g. pain present/absent) may be enough to guide analgesic
therapy in this age group.
Children older than 3 years
Many children over 3 years can differentiate between the presence or absence of
pain, and indicate its nature, intensity and site. They can categorize pain reasonably
accurately into one of four choices corresponding to nil, mild, moderate or severe.
Many children can explain whether they are feeling pain and indicate how bad it
is providing they understand the language and phrases used. They can comprehend
the concept of pieces of hurt as used, for example, with the poker-chip tool
(Figure 2).
Indicating severity using a faces scale can work well, but the choice of faces is best
limited to four, with the first face appearing neutral rather than happy (Figure 3). Some
children are unable to relate the faces to their own pain experiences, while others tend
to choose those at the extremes of the scales.
Many children relate to previous pain experiences to indicate whether their current
experience is worse or better, for example by comparing it with a previous injury.
These earlier experiences may influence their assessments (e.g. the same injury may
be scored as severe by a young child with no previous pain experiences, while an
older child, who has had a worse pain before, may score the pain as mild). Some
children who have undergone repeated, painful procedures may be sensitized and have
a lowered pain threshold.
Poker chip tool The four faces scale
Nil Mild Moderate Severe Very severe Nil Mild Moderate Severe
Tokens acting as pieces of pain are stacked by the child to

indicate how much pain they are experiencing Note: the first face should be neutral, not happy
2 3
Children older than 5 years
Visual analogue tools and scales can be operated successfully by children from the
age of 5 years, however, the classical 100 mm horizontal line is not well understood
by younger children.
Adding colour gradations is helpful and making the scale into a vertical colour wedge
is best (Figure 4).
Vertical colour analogue slide-rule tool
FURTHER READING
Ambuel B, Hamlett K W, Marx C M, Plummer J L. Assessing Distress in Pediatric
Intensive Care Environments. The COMFORT Scale. Pediatr Psychol 1992; 17:
95109.
Beyer J E, Wells N. The Assessment of Pain in Children. Pediatric Clinics of North
America 1989; 36: 83753.
Finley G A, McGrath P J, eds. Measurement of Pain in Infants and Children. Progress in
Pain Research and Management. Vol. 10. Seattle: IASP, 1998.
McGrath P J, Unruh A M, Finley G A. Pain Measurement in Children. IASP Pain Clinical
Updates 1995: 3: 14.

Central Blocks in Children
Edward Doyle
Edward Doyle is Consultant Paediatric Anaesthetist at the Royal Hospital for Sick
Children, Edinburgh, UK. He qualified from Oxford University and trained in paediatric
anaesthesia in Glasgow and Edinburgh. His research interests include postoperative
analgesia and regional anaesthetic techniques in children.
The use of central neural blocks in children is now a routine part of paediatric
anaesthesia. In selected children they reduce the morbidity associated with surgery
and anaesthesia and can favourably influence the postoperative course. These
techniques often result in dense intraoperative and postoperative analgesia, reduced
requirements for volatile agents, minimal postoperative vomiting and a reduction in
opioid use. The same standards of preoperative assessment used in adults, regarding
contraindications, technical competence, sterility and postoperative monitoring are
required in children. In most patients, a central block is combined with general
anaesthesia. There is an incidence of predictable side-effects and a low incidence
of potentially serious complications. Most of these are easily managed if competent
personnel and appropriate facilities are available.
Subarachnoid and epidural blocks in young children seldom result in hypotension
unless there is significant hypovolaemia or a high thoracic block. This is probably
because children under 8 years of age have a reduced sympathetic tone and reduced
blood volume in the splanchnic circulation and lower limbs, compared with older
children and adults. Consequently, fluid loading or the administration of vasopressors
are seldom necessary and this can make the practical conduct of central blocks easier
than in adults. In older children, who have a more adult physiology, there is occasionally
a variable decrease in both heart rate and blood pressure.
Subarachnoid (spinal) anaesthesia
Subarachnoid anaesthesia has a rapid onset, produces profound sensory and motor
block without systemic effects, and when used alone avoids volatile anaesthetic agents
or tracheal intubation. It provides definite benefits compared with general anaesthesia
in certain children at high risk (e.g. infants born prematurely) but requires experience
and the ability to manage any complications that may occur.
The most common indication is probably inguinal hernia repair in infants who were
premature. 30% of premature infants with a birth weight less than 1000 g develop
an inguinal hernia. Postoperative apnoea occurs in 3040% of these babies if they
undergo general anaesthesia for repair and is particularly common in those less than
44 weeks postconceptional age.
Three prospective, randomized, controlled studies have demonstrated a significant
reduction in the incidence of postoperative apnoea, episodes of bradycardia and
hypoxia, or requirement for postoperative ventilation, when subarachnoid anaesthesia
rather than general anaesthesia is used in infants who were premature. In one study,
in which a subgroup received sedation as well as subarachnoid anaesthesia, over
80% developed prolonged postoperative apnoeas with bradycardia and this technique
probably offers no advantages over general anaesthesia in reducing the incidence of
respiratory complications.
Other indications for subarachnoid blockade include most operations below the
umbilicus (though it has also been used for upper abdominal or thoracic surgery). In
combination with general anaesthesia, the technique has been used for spinal and
cardiac surgery to reduce the requirements for opioids or postoperative ventilation in
high-risk children, and to minimize the perioperative stress response to surgery. In
many centres outside the UK, the technique is not restricted to high-risk patients but is
also used in ASA I and II patients having lower- body surgery, simply because of the
good anaesthetic and surgical conditions it provides.
Short narrow-gauge spinal needles ranging from 22 G to 24 G are available for
use in children. Narrower-gauge adult needles may also be used in older children
particularly if post-dural puncture headache is a concern. Hollow hypodermic needles
or intravenous cannulae should not be used because they may introduce a core of
epithelial tissue into the subarachnoid space. Injection should be performed at a low
lumbar interspace because the neonatal spinal cord usually reaches the L3 vertebral
level. Injection is often performed with the baby in the sitting position restrained by an
assistant who also ensures that episodes of airway obstruction do not occur during
the procedure.
Drugs
Bupivacaine is the local anaesthetic used most commonly in Europe whereas tetracaine
(amethocaine) tends to be used in North America (Figure 1). Larger doses of local
anaesthetic on a mg/kg basis are required than in adults. Children, and especially
neonates, have a larger volume per kg of CSF than adults, with a higher proportion
contained in the lumbar region, resulting in more dilution of the local anaesthetic. The
greater cardiac output relative to body weight in infants and neonates results in more
rapid systemic uptake of local anaesthetic contributing to a relatively short duration
of subarachnoid anaesthesia compared with adults (usually about 50120 minutes).
The addition of adrenaline prolongs the duration of effective subarachnoid blockade
by 2040%.
There is limited pharmacokinetic data concerning subarachnoid bupivacaine in
children. The mean plasma bupivacaine concentration in neonates 10 minutes after
intrathecal administration of isobaric bupivacaine, 1 mg/kg, was 0.31 g/ml (range
0.130.79 g/ml) and 0.25 g/ml (range 0.10.38 g/ml) after intrathecal administration
of isobaric bupivacaine, 1 mg/kg, with 1/200,000 adrenaline (epinephrine). Bupivacaine
is extensively bound to plasma proteins, mainly albumin and 1 acid glycoprotein.
Neonates have lower levels of these proteins than adults, resulting in a decreased
binding capacity for bupivacaine and an increased risk of toxicity from free bupivacaine.
The mean free bupivacaine levels in this study were 0.047 g/ml (range 0.010.11 g/
ml) in the group receiving bupivacaine alone and 0.062 g/ml (range 0.030.1 g/ml)
in the group receiving bupivacaine and adrenaline (epinephrine). These values are
reassuringly low.
Local anaesthetics and doses for subarachnoid anaesthesia in infants
Drug Dose range1 (mg/kg)

0.5% tetracaine hyperbaric plain 0.32
0.5% tetracaine hyperbaric plus adrenaline (epinephrine) 0.50.6
0.5% bupivacaine isobaric plain 0.751.0
0.5% bupivacaine plain with or without adrenaline (epinephrine) 0.61.0
1
Recommendations from different authors
1
Problems
The technique of subarachnoid blockade in neonates and infants has a significant
incidence of problems. The duration of the block is short and is reliable only for
procedures lasting less than 1 hour. There is no significant postoperative analgesia
and alternative analgesia must be provided. There is a failure rate of about 10%
and an incidence of high blockade, which can cause respiratory compromise. These
problems are well demonstrated in a series of 164 infants, who were premature,
undergoing subarachnoid anaesthesia. In 137 patients (83.5%) there was a block
that was adequate for surgery. Successful lumbar puncture could not be performed
in 12 patients (7.3%). A further 15 (9.1%) required supplementation with infiltration
anaesthesia, systemic analgesia or anaesthesia. Two patients became apnoeic during
the lumbar puncture and five developed a high block producing respiratory weakness.
Postdural puncture headache is seldom a clinical problem in children aged less than
10 years, but does occur in older children. Efforts to prevent this include the use of a
pencil-type or a fine cutting needle. Hypotension during a subarachnoid block is also
unusual in babies or children and if it occurs may indicate unanticipated hypovolaemia
or a high block.
Epidural analgesia
The introduction of paediatric epidural needles (5 cm long, either 19 G or 20 G)

and fine epidural catheters has made epidural analgesia feasible in the smallest
of children. Single injection or infusion epidural analgesia at the thoracic or lumbar
levels has become popular and often allows the use of light anaesthesia and
minimal opioid administration, and may help avoid postoperative ventilation in some
high-risk patients. Children in whom these techniques are particularly important
include those with gastro-oesophageal reflux undergoing fundoplication, children with
respiratory disabilities undergoing abdominal surgery or neonates undergoing repair of
oesophageal atresia. In neonates and infants it is possible to thread a catheter from
the sacral hiatus to the thoracic region and to provide analgesia for abdominal or
thoracic surgery. This technique is popular because it allows the epidural space to be
cannulated below the spinal cord. However, attempts to thread catheters to the thoracic
region from the caudal hiatus or a low lumbar approach are generally ineffective in
children aged over 2 years.
Conservative doses for epidural infusion in children after a loading dose of
bupivacaine, 22.5 mg/kg, are a maximum of 0.20.25 mg/kg/hour in neonates or
0.30.4 mg/kg/hour in older children. Data from various sampling studies during
continuous infusion of extradural bupivacaine of less than 0.5 mg/kg/hour are generally
reassuring. Mean plasma concentrations are usually low and less than 24 g/ml, a
level often associated with the risk of toxicity. However, concentrations in individual
patients may sometimes be high. There is particular concern about toxicity in children
aged less than 6 months in whom drug elimination is variable as a result of diminished
clearance and prolonged half-lives and prolonged infusions are associated with rising
plasma levels of bupivacaine.
The simultaneous use of other analgesics such as opioids or non-steroidal analgesic
drugs, increases the efficacy of epidural analgesia and reduces the dose of local
anaesthetic required. After major surgery, an opioid (commonly fentanyl, morphine or
diamorphine) is usually required in addition to local anaesthetic. This acts synergistically
with the local anaesthetic to improve analgesia and to reduce the requirement for local
anaesthetics. It will also treat discomfort from areas of the body that are not covered by
the epidermal block and provide a mild degree of sedation. Opioids are conventionally
given mixed with the local anaesthetic solution but may also be given systemically.
Opioids have also been used alone by intermittent injection or continuous infusion to
provide epidural analgesia.
Problems
Common problems associated with epidural anaesthesia in children are listed in Figure
2. The incidence of dural tap is variable and is influenced by various factors including
the experience of the anaesthetist, the technique used, the age of the patient and
the type of epidural needle used. More dural punctures occur if inappropriately large
epidural needles are used or if air, rather than saline, is used to detect loss of
resistance. The incidence of dural tap is usually quoted at less than 10%.
Technical problems with epidural catheters may occur and cause premature
discontinuation of epidural analgesia. The incidence of problems is considerably higher
with the fine catheters (e.g. 23 G) designed for babies or small children, than with the
larger catheters (e.g. 21 G). Potential problems include leakage at the site of entry
of the catheter through the skin, misplaced or occluded catheter and disconnection
between the epidural catheter and the bacterial filter.
Common potential side-effects include urinary retention, leg weakness, nausea and
vomiting. Intravenous or subarachnoid injection, epidural haematoma or infection are
uncommon, but possible. Lack of sensation may cause problems if not anticipated
and heel blisters or pressure sores may occur in analgesic skin unless patients are
repositioned regularly.
When epidural opioids are used there is a possibility of respiratory depression. This
is a particular risk if the child is aged under 1 year, is given concurrent parenteral
opioids or large doses are used. Appropriate doses associated with a low incidence
of respiratory depression are fentanyl, 0.10.5 g/kg/hour, or morphine, 5 g/kg/hour.
The best method of detecting respiratory depression at an early stage is the use of
continuous pulse oximetry while the patient is breathing air.
Postoperative nausea and vomiting in infants and young children tends to be less
common and severe than in adults, though older children behave more like adults.
The use of epidural opioids probably makes this problem worse, but it is impossible
to quantify this effect in children. The incidence of postoperative nausea and vomiting
during epidural infusions containing fentanyl has been reported as 080%. This should
be compared with the significant incidence when systemic opioids are used to provide
analgesia after major surgery.
The incidence of urinary retention is unknown because many patients are
catheterized perioperatively. The reported incidence varies with age, opioid use and the
criteria used to define urinary retention. The reported incidence is zero in neonates,
18% in infants and 62% in those aged 1017 years. The relative contributions of opioid
and local anaesthetic are difficult to determine because it occurs when both types of
analgesic are used alone.
Epidural abscess or haematoma associated with the use of epidural analgesia for
acute pain have not been reported in children. Other serious complications that result
in permanent neurological deficit or death have a low incidence (5 of 7200 epidurals in
a retrospective survey of practice between 1982 and 1991 of members of the Society
of French Speaking Paediatric Anaesthetists). Risk factors for serious complications in
this study included multiple traumatic attempts at epidural cannulation, age less than 3
months, or the use of the loss of resistance to air technique for identifying the epidural
space.
Common problems of epidural analgesia in children
Problem Incidence1 (%)

Dural puncture < 10
Catheter disconnection or obstruction 017
Respiratory depression <1
Hypotension < 10
Urinary retention 060
Nausea and vomiting 080
1
Composite figures from a number of series
2
Caudal epidural blockade
Single-injection caudal epidural blockade is a simple technique with a high success rate
and a low incidence of serious complications. It can be used to provide intraoperative
anaesthesia and postoperative analgesia for many operations below the umbilicus. It
reduces the requirement for volatile anaesthetic agents and opioids, which reduces
the incidence of postoperative nausea and vomiting. Children may then resume oral
intake and take oral analgesics after quite major surgery without the need for parenteral
analgesic drugs. In most patients, the caudal block is combined with light general
anaesthesia, though it has been used as the sole technique for inguinal hernia
repair in infants who were premature. It has also been combined with simultaneous
subarachnoid block to provide prolonged anaesthesia after a subarachnoid block has
worn off.
Injection is performed through the sacral hiatus, well below the termination of
the spinal cord, therefore there is little risk of serious neurological damage during
caudal epidural blockade. The main potential for serious complications comes from
the possibility of intravenous injection or dural puncture followed by a subarachnoid
injection. This is especially the case in small children in whom the termination of the
dural sac may lie as low as the second sacral vertebra. Both of these problems can be
almost eliminated if the initial puncture of the sacral hiatus is performed with a needle
without the syringe of local anaesthetic attached (Figures 3 and 4). If this needle is
left open to the atmosphere for a few seconds, blood or CSF will appear if there has
been a puncture. This will prevent the injection of local anaesthetic into the CSF or a
vein. If the needle is not left open to the atmosphere for a few seconds then it may
be impossible to aspirate blood or CSF and an injection of local anaesthetic into the
wrong compartment may be given.
3 Initial puncture of sacral hiatus performed with a needle without the

syringe attached.
4 Slow injection of local anaesthetic without moving the needle.
Drugs
Local anaesthetics: bupivacaine is the local anaesthetic agent used most
commonly for caudal epidural blockade. Pharmacokinetic data show that single
epidural doses of bupivacaine, 22.5 mg/kg, are associated with low plasma
levels of the drug (Figure 5).
Plasma levels of bupivacaine after caudal epidural injection
Drug Dose Number C max mean (range) Tmax mean (range)

(mg/kg) of children (g/ml) (minutes)
Bupivacaine 2.5 6 1.25 (0.961.64) 29 (1938)
Bupivacaine 2.5 13 0.97 (0.551.93) 28 (1060)
Bupivacaine 3.0 45 1.4 (maximum 2)
Bupivacaine 2.0 14 0.9 16
Bupivacaine plus adrenaline 3.7 10 0.67 45
(epinephrine)
Reprinted from Anaesthesia 1998; 53: 9801002 with permission from Blackwell Science Ltd, Oxford, UK.
Additives to local anaesthetic solutions have been used in an attempt to prolong the
duration of caudal analgesia provided by a single injection of local anaesthetic.
Adrenaline (epinephrine) vasoconstrictors decrease the rate of vascular
absorption of local anaesthetic and increase the density and duration of the block. The
most common is adrenaline (epinephrine) in a concentration of 5 g/ml (1/200,000).
When used for caudal epidural injection the effects of adrenaline (epinephrine) tend
to be less pronounced with longer-acting local anaesthetics (e.g. bupivacaine) than
with more hydrophilic drugs (e.g. lidocaine (lignocaine)). The high lipid solubility of
bupivacaine causes it to be deposited in epidural fat and released slowly and adrenaline
(epinephrine) tends to have little effect in prolonging its duration of action.
Opioids the administration of caudal epidural opioids usually produces profound
long-lasting analgesia. The median duration of analgesia after caudal morphine, 0.1
mg/kg, for lower-body surgery is 12 hours (range 424 hours) compared with 5
hours (range 3.524 hours) for 0.25% bupivacaine, 1 ml/kg, plus 1/200,000 adrenaline
(epinephrine) and 45 minutes (range 0.324 hours) for intravenous morphine, 0.1
mg/kg. Side-effects of caudal epidural opioids include nausea, urinary retention,
pruritus and respiratory depression. The latter is particularly worrying because its onset
may be delayed for several hours after opioid administration, particularly if morphine is
used. The largest reported series of children given caudal epidural morphine reported
11 cases of clinically important hypoventilation in 138 cases (8%). Of these, eight
patients were younger than 3 months of age and seven received parenteral opioids
in addition to caudal morphine. Assays of blood for plasma morphine levels after the
administration of caudal epidural morphine show levels much less than those required
for analgesia after systemic administration and strongly suggest that the synergistic
effect of epidural opioids on analgesia results from a local action at spinal cord level as
opposed to an effect after systemic absorption.
Clonidine also prolongs the duration of caudal epidural blockade produced with
a local anaesthetic solution. Three groups of 15 patients undergoing lower-body
general or urological surgery under combined general anaesthesia and caudal epidural
blockade were given caudal injections of 0.25% bupivacaine. Two groups had added to
this clonidine, 1 g/kg, or adrenaline (epinephrine), 5 g/ml. The quality and duration
of postoperative analgesia assessed as the time to first analgesic requirement using
an objective pain score was significantly longer with clonidine (mean 16.5 hours) than
with bupivacaine (mean 7.6 hours) or bupivacaine plus adrenaline (epinephrine), (mean
6.3 hour). In a comparison of 0.25% bupivacaine, 1 ml/kg, with or without clonidine, 2
g/kg, for lower-limb orthopaedic surgery, there was a significantly increased duration
of postoperative analgesia in the group given clonidine (mean 9.8 hours) compared with
the group receiving bupivacaine (mean 5.2 hours).
Ketamine a comparison of ketamine, clonidine or adrenaline (epinephrine) added
to 0.25% bupivacaine showed that ketamine, 0.5 mg/kg, provided a longer duration of
postoperative analgesia after orchidopexy (median duration 12.5 hours) than clonidine,
2 g/kg (5.8 hours) or adrenaline (epinephrine) 5 g/ml (3.2 hours). There were
no differences between groups in the incidence of urinary retention, motor block or
postoperative sedation.
Problems
The incidence of failed caudal block has been reported to be as high as 11%. Failure
appears to be more common in children weighing less than 10 kg in whom there may be
difficulty identifying the sacral hiatus and in children aged over 7 years. Failure may also
result from using an inadequate volume to block the required nerve roots.
The incidence of motor block as shown by leg weakness is variable after caudal
blockade. Moderate weakness of the legs is common and occurs in about 30% of
patients given 0.5% bupivacaine to block lumbar dermatomes. The incidence is less
than 10% if more dilute solutions of bupivacaine are used. The optimal concentration
of bupivacaine for caudal epidural blockade in children may be 0.125%. This has been
shown to produce a block with an equal duration of analgesic effect and the same
requirements for supplementary analgesia as 0.25%, but with a much lower incidence
of leg weakness.
Venous puncture has an incidence of 1.610.6%. This is reduced when experienced
anaesthetists, rather than trainees, perform the procedure and if short bevelled, rather
than hypodermic, needles are used. There are no reports of extradural haematoma
after caudal epidural blockade in children. The incidence of dural tap has been
described as 1/500 and 1/1100 in various series. Negative aspiration for CSF is
possible despite a dural puncture. A total spinal block is uncommon but has been
reported.
FURTHER READING
Cook B, Doyle E. The Role of Additives to Local Anaesthetics for Caudal Epidural
Analgesia in Children. Paed Anaesthesia 1996; 6: 3539.
Flandin-Blety C, Barrier G. Accidents following Extradural Analgesia in Children. The
Results of a Retrospective Study. Paed Anaesthesia 1995; 5: 416.
Peutrell J M, Mather S J. Regional Anaesthesia for Babies and Children. Oxford: Oxford
Rowney D, Doyle E. Epidural and Subarachnoid Block in Children. Anaesthesia 1998;
53: 9801002.
Tobias J D. Spinal Anaesthesia in Infants and Children. Paed Anaesthesia 2000; 10:
516.

The Child with Associated
Medical Disease
Ann E Black
Ann E Black is Consultant Paediatric Anaesthetist at Great Ormond Street Hospital,

London. She trained in anaesthesia in London and Philadelphia. Her interests include
preoperative preparation, day care, audit and the strategies for management of the
difficult paediatric airway.
Anaesthetists often have to deal with a child suffering from a common medical
condition such as upper respiratory tract infection or asthma. Less commonly, a
child may have a medical condition presenting early in life that may have important
anaesthetic implications. This article addresses some common medical conditions; a
textbook should be consulted for unusual or rare conditions.
Respiratory disease
Wheezing in children may be caused by:

asthma
infection (especially respiratory syncytial virus bronchiolitis in those less than 2 years
of age)
foreign body aspiration
cystic fibrosis
laryngotracheomalacia
chronic lung disease (e.g. bronchopulmonary dysplasia, bronchiectasis, recurrent
gastro-oesophageal reflux).
Asthma
Asthma affects about 10% of children, leading to reversible obstructive airways disease.
Symptoms include wheezing, intermittent cough or dyspnoea. The incidence of asthma
may be increasing owing to environmental changes and pollution. Most children with
mild asthma become asymptomatic as they grow older. A smaller number continue to
require long-term medication, including corticosteroids, and have severe exacerbations
of the disease requiring repeated hospital admissions. Asthma attacks may be
precipitated by respiratory infections, environmental factors, anxiety or stress.
Management: preoperative management of children with asthma includes optimizing

lung function with bronchodilators, disodium cromoglycate and corticosteroids. Regular
peak flow charts may be useful to assess the severity of the disease. An anaesthetic is
planned to avoid histamine-releasing drugs. The use of diclofenac in asthmatic children
has not been shown to be associated with drug-induced asthma or change in measured
respiratory function therefore non-steroid anti-inflammatory drugs (NSAIDs) are not
contraindicated for short-term use in children with mild asthma.
Upper respiratory tract infection (URTI)

On average, children have two to nine episodes of URTI per year. It may be difficult to
decide whether to proceed with anaesthesia for elective surgery if a child has had a
recent URTI. The evidence of additional morbidity associated with general anaesthesia
is conflicting. Although severe morbidity, and even mortality, have been reported in
children with URTI caused by severe lung infection, pulmonary collapse or myocarditis,
this is rare. Most large studies have dealt with children undergoing day-case surgery,
who are healthy or have mild systemic disease (ASA groups I and II), with minor
symptoms of URTI. The adverse outcomes noted during anaesthesia in children with
URTI include laryngospasm, apnoea, bronchospasm, cough, arterial desaturation, and
postoperative stridor. Some studies suggest that complications with anaesthesia are 11
times more common if a child has an URTI or recent symptoms of URTI. The reasons
include an increase in bronchial sensitivity, increased airway secretions and a tendency
for closure of the small airways. Infants under 1 year of age are at increased risk of
complications, particularly croup, and some studies have shown that children who are
intubated may also be at additional risk.
Management: a child who is obviously systemically unwell with a high fever, chest
signs or malaise, should have his surgery postponed. However, there is a large group
of children in whom the benefit of cancellation is unclear. In general, the decision to
postpone elective surgery can be made on history and examination (including WBC
count and radiography), particularly taking into account the view of the parent. The
length of postponement is also debated. It has been recommended that elective
surgery is postponed for 36 weeks after an URTI. However, if this were implemented
in some children with frequent mild URTI symptoms it would be difficult to find any
period in the year when the child is considered free of the potential risk of complications
associated with an URTI.
Cystic fibrosis
Cystic fibrosis is an autosomal recessive condition that affects 1/2000 live births.
It is a progressive, multisystem disease affecting mainly the lungs and pancreatic
exocrine function. Babies may present with meconium ileus, but infants tend to
present with recurrent respiratory symptoms or failure to thrive. A diagnostic sweat test
reveals a high sodium content of the sweat. The respiratory effects of cystic fibrosis
include respiratory failure as a result of increasing ventilationperfusion mismatch,
bronchiectasis and pulmonary haemorrhage. Other sequelae include cor pulmonale,
clubbing, cirrhosis, portal hypertension, malabsorption or failure to thrive. Diabetes
occurs in about 10% of children with cystic fibrosis.
Management includes physiotherapy, bronchodilator therapy and systemic and inhaled

antibiotics. Preoperative preparation involves maximizing these therapies. Pulmonary
function tests show a mixed obstructive and restrictive pattern and quantify the degree
of impairment. A chest radiograph reveals the extent of chronic lung damage (Figure 1).
The ECG may indicate right heart hypertrophy. If liver function is affected, clotting may
be abnormal and require preoperative correction.
Premedication is not contraindicated, but some of these children will not tolerate
sedation and anticholinergics are often avoided because they make secretions more
difficult to clear. Pancreatic supplements, salt supplements and vitamins are continued.
Following intubation, physiotherapy and suctioning of the bronchial secretions in the
anaesthetic room is useful, particularly if surgery is likely to take a long time. Tracheal
tubes and suction catheters must be used with a careful aseptic technique. Intravenous
fluids are given routinely and prolonged periods of fasting avoided.
Postoperatively, frequent chest physiotherapy and effective pain management are
essential. Supplementary regional analgesia is useful if coagulation is normal.
1 Chronic changes of cystic fibrosis seen on a chest radiograph include

hyperinflation of the lung fields, bronchiectasis and peribronchial thickening.
Neurological and muscular disease
Developmental delay and autism

Many conditions result in a child who has difficulties with understanding or behaviour,
and the effects vary. Causes of developmental delay include genetic abnormalities,
severe cerebral palsy, complicated epilepsy or following head injuries or trauma. Autism
is a disease of unknown cause that has a distinctive pattern of behaviour, starting
in early childhood, which results in the child being unable to relate to other people.
Children with autism tend to be quiet, have a short attention span, be withdrawn and
solitary and appear unconnected to their environment. These children may find the
process of admission to hospital very stressful.
Management: regardless of their disability, children must be treated sympathetically.

The family will be able to indicate the best way to help the child feel comfortable and
prepare for anaesthesia. It is important to involve the child whenever possible and a
play specialist can be helpful. Assessment of the cause of any apparent distress can
be difficult and many systems in routine use (e.g. pain scores) are of little use in these
children. Some children benefit from premedication, but in others behavioural difficulties
may increase following sedation. Fasting policies may be difficult to implement and
these children are often best treated early on a theatre list and allowed home as soon
as their family feel ready to continue their care.
Cerebral palsy
Cerebral palsy is a non-progressive neurological disorder that results in abnormalities
of motor function. Learning difficulties occur in over 50% of these children. The disorder
can be associated with birth asphyxia, preterm delivery and cerebrovascular insults
(including intraventricular haemorrhage, congenital infection or metabolic disorders);
however, in many cases the cause is unknown. The resultant physical and neurological
effect in the child is variable. Limb spasticity is common, as is scoliosis, poor mobility,
restrictive lung disease secondary to chest abnormalities, seizure disorder, gastro-
oesophageal reflux, feeding problems and failure to thrive. Intelligence may be normal,
but speech may be seriously affected and there is often developmental delay. Particular
issues to consider include respiratory compromise, restricted lung function, associated
infection, frequency of fits, developmental delay, sensory compromise and nutritional
status.
Management: preoperative respiratory care with physiotherapy and bronchodilators,

if used, is beneficial. There may be an increased risk of respiratory depression and
aspiration (owing to oesophageal incoordination), therefore sedative premedication
should be used cautiously. Some children are sensitive to the respiratory and sedative
effects of opiates. Anti-epileptic medication is continued. Positioning for surgery can be
difficult. Postoperative apnoea can occur and oxygen saturation monitoring is useful.
Analgesics, such as paracetamol, diclofenac and codeine, are advised. Assessment
of postoperative pain can be difficult because routine pain assessment tools are often
unusable. An epidural is often successful as an adjunct to general anaesthesia during
major abdominal or hip surgery. Painful muscular spasms are common, particularly
after orthopaedic surgery, and are best treated with benzodiazapines. Intensive care
may be needed postoperatively and weaning from the ventilator following major surgery
can be difficult if restrictive lung disease is significant.
Hydrocephalus
Hydrocephalus can be congenital (associated with meningomyelocele as in the Arnold
Chiari malformation), acquired (as in post-haemorrhagic ventricular dilatation) or less
commonly the result of tumours, cysts or meningitis. In the neonate and young infant,
the skull can increase in size to accommodate additional fluid, but in the child with
fused cranial sutures, signs of raised intracranial pressure, such as vomiting, headache
or decreased level of consciousness, occur earlier. Treatment requires insertion of a
ventriculoperitoneal shunt if the cause cannot be cured.
Management: preoperative assessment of the childs level of consciousness is

important. Excessive vomiting may result in electrolyte disturbance. A blood cross-
match is usually required. Tapping the CSF in the neonate provides temporary relief
and a ventriculoperitoneal shunt is usually inserted later when the neonates naturally
high CSF protein levels have decreased and the risk of obstruction of the shunt is
reduced, though there is no consensus in management. If a temporary external
ventricular drain is used, the resultant loss of CSF volume must be replaced with
intravenous saline.
Neuromuscular disease includes muscular dystrophies, myotonias, myopathies and
myasthenia. In many children the cause of the myopathic disease is unknown. Common
operations in this group of children include muscle biopsy, surgery for scoliosis, squint
or talipes repair.
General considerations include the presence of associated conditions, particularly
respiratory, cardiac or airway abnormalities. Abnormal responses to anaesthetic drugs
can occur, including the potential for severe reactions to suxamethonium or other
relaxants, sensitivity to sedatives or the risk of precipitating malignant hyperthermia.
Duchenne muscular dystrophy

Duchenne muscular dystrophy is a dominantly inherited, sex-linked disorder. It produces
progressive muscle weakness resulting in death in late adolescence, usually as a result
of respiratory failure or cardiac disease. It is the most common muscular dystrophy and
occurs in about 1/3300 live male births. Presentation is with weakness, slow walking,
clumsiness and classically pseudohypertrophy of the calf muscles.The associated
features significant to anaesthesia are summarized in Figure 2. It is not associated
with malignant hyperpyrexia though there have been some reports of a malignant
hyperpyrexia-like syndrome occurring in children with Duchenne muscular dystrophy.
Suxamethonium is contraindicated because it can cause acute hyperkalaemia, resulting
in cardiac arrest, and is also associated with rhabdomyolysis. Preoperative assessment
includes ECG, echocardiography, pulmonary function test, physiotherapy review, full
blood count and urea and electrolytes.
Myopathies
Myopathies are a mixed group of conditions and present a wide spectrum of disease,
which can be difficult to diagnose. The potential for metabolic instability, drug sensitivity
to opiates, sedatives or muscle relaxants, and the associated risk of malignant
hyperthermia, must be considered. Specific types should be reviewed in specialist
textbooks. Of the congenital myopathies, central core disease is of most relevance to
the anaesthetist because it is associated with malignant hyperthermia.
Associated features in Duchenne muscular dystrophy
Features Effect
Respiratory muscle weakness Recurrent chest infection, sputum
retention, long-term ventilation
Scoliosis
Cardiac Arrhythmias, mitral valve prolapse,
ventricular dysfunction, sudden death
Gastric distension Risk of aspiration
Sensitivity to sedation
Suxamethonium Produces hyperkalaemia, cardiac
contraindicated arrest, muscle
rigidity, rhabdomyolysis
Myopathies
Myopathies are a mixed group of conditions and present a wide spectrum of disease,
which can be difficult to diagnose. The potential for metabolic instability, drug sensitivity
to opiates, sedatives or muscle relaxants, and the associated risk of malignant
hyperthermia, must be considered. Specific types should be reviewed in specialist
textbooks. Of the congenital myopathies, central core disease is of most relevance to
the anaesthetist because it is associated with malignant hyperthermia.
Other conditions
Downs syndrome
Downs syndrome is one of the most common chromosomal disorders. It results in
characteristic facial features, developmental delay, and problems with the airway, heart
and joints. Specific anaesthetic issues include behavioural problems and difficulty with
vascular access.
Snoring or sleep apnoea may be present and preoperative sedation is sometimes
contraindicated because of the risk of obstruction. Both post-intubation stridor and
subglottic stenosis are more common in children with Downs syndrome. Congenital
heart disease (e.g. atrioventricular septal defects, Fallots tetralogy) is present in 40%
of children with Downs syndrome. Assessment by a paediatrician or cardiologist
and echocardiography or ECG are useful. Antibiotic prophylaxis for the prevention of
bacterial endocarditis is essential for most cardiac lesions.
Laxity of the ligaments of the neck at the atlanto-axial joint occurs in 1518% of
patients with Downs syndrome and the risk increases with age. C1C2 dislocation and
spinal cord damage can occur (Figure 3). Some centres routinely screen the cervical
spine at regular intervals, but this practice is not widespread. Any child with Downs
syndrome who has neurological symptoms, such as paraesthesia of the hands or motor
instability, must be screened with flexion and extension views of the neck. Additional
care must be taken with positioning these children during anaesthesia.
3 MRI of a child with Downs syndrome showing

C1C2 instability with spinal canal narrowing
(arrow).
Renal disease
The most common cause of renal impairment in infants is pelvic renal dilatation from
either posterior urethral valves or pelviureteric obstruction. In children, the causes
include congenital abnormalities, glomerulonephritis or nephrotic syndrome. In the
child with established renal disease and a degree of chronic renal failure, symptoms
are unusual until the glomerular filtration rate is less than 25% of normal. Then chronic
anaemia, failure to thrive, renal osteodystrophy, hypertension, metabolic effects of
uraemia, acidosis, salt loss or hyperkalaemia become more common.
Management: Preoperative assessment includes haemoglobin level, urea and

electrolytes and creatinine. Fluid and electrolyte requirements are variable and should
be assessed and discussed with the renal team before surgery. A child on dialysis
will require post-dialysis bloods, including clotting studies (if heparin is used as in
haemodialysis). Surgery should be avoided soon after dialysis so that time is given for
fluid shifts to occur. Arm vessels are preserved because they may be required later for
vascular shunts.
Drugs best avoided in children with significant renal impairment include known
nephrotoxic drugs (e.g. aminoglycosides, diclofenac) and drugs dependent on renal
excretion. Suxamethonium is contraindicated in the presence of hyperkalaemia
because of the potential of producing severe hyperkalaemia. Renal patients should
not be fasted excessively and fluid replacement should be maintained carefully.
Perioperative hypotension should be avoided. Regular antihypertensive medication
should be continued. If hypertension is poorly controlled a review of medical
management before planned surgery is wise.
Diabetes
Type 1 diabetes occurs in about 1/500 children and most commonly presents at
67 years or at puberty. Control of blood sugar levels can be difficult because of the
changing nutritional and insulin needs of the growing child and because older children
may be non-compliant with their therapy. The long-term complications of diabetes
(retinopathy, autonomic neuropathy or nephropathy) do not occur in children before
puberty and good metabolic control minimizes their development in adulthood.
Management: routine surgery in diabetic children usually requires that they be

admitted the day before surgery. Their diabetes should be under good control and
ideally they should be scheduled first on the theatre list. Preoperative measurements
of urea and electrolytes and blood sugar are taken. Preoperatively, bedside blood
sugar estimates are checked regularly and the urine screened for sugar and ketones.
The morning dose of insulin is omitted and an infusion of 10% dextrose with added
potassium is started with an infusion of soluble insulin (e.g. 50 ml syringe with 1 unit
of insulin per ml), with the rate adjusted according to hourly sugar results. This is
continued until the child returns to a normal diet and his insulin regimen is restarted.
If diabetic control is poor, or emergency surgery is required and the child is
systemically unwell and has a high blood sugar (with or without ketoacidosis) it is
best to treat the metabolic condition first because surgery in the ketoacidotic child is
associated with a high morbidity.
Sickle cell disease

All children from ethnic groups with a high incidence of sickle cell disease should be
screened preoperatively, unless their sickle cell status is known. Routine screening
is with a Sickledex test, which, if positive, must be followed by haemoglobin
electrophoresis to identify the relevant haemoglobin types present. Sickledex tests are
unreliable in babies less than 3 months of age because they have a high percentage
of fetal haemoglobin, therefore electrophoresis should be carried out instead. Sickle
haemoglobin may occur in association with other haemoglobinopathies, such as
thalassaemia. Sickle cell trait is associated with a normal haemoglobin level and HbS
and HbA on electrophoresis. These children are managed routinely and do not have
additional risks during carefully conducted general anaesthesia.
Management: the preoperative management of children with sickle cell disease is

under review. All cases should be discussed with the haematologist so that the risks
and benefits of blood transfusion before surgery are considered. Blood transfusions
are avoided if possible, so that the development of antibodies and other complications
related to blood transfusion do not occur. These would make later management of the
disease more difficult, particularly if a bone marrow transplant were required. Many
children with sickle cell disease have a mild course and few symptoms.
For minor surgery, exchange or top-up transfusion is not routine, though some
centres will give blood to increase the haemoglobin levels to 10 g/dl.
For more extensive surgery, or in children with a history of severe disease (e.g.
painful crises of the bones, joints, spleen, lung or brain) a regimen of exchange
transfusion is undertaken in the weeks before surgery to raise the haemoglobin level
above 10 g/dl and the percentage of HbS to less than 30%. In all these patients,
careful anaesthesia is essential, ensuring that the child is kept warm, well hydrated and
that additional oxygen is administered perioperatively and even transient episodes of
hypoxia avoided. Use of tourniquets is contraindicated owing to the risks of acidosis
and tissue hypoxia in the exsanguinated limb. In these children, most surgery requires
antibiotic cover. Effective pain management is important so that mobility is encouraged
and early chest physiotherapy can be used to minimize the likelihood of a sickle crisis
occurring.
Mucopolysaccharidosis
There are many different forms of mucopolysaccharidosis, which are genetic
abnormalities resulting from an inborn error of metabolism. The most common are
Hurlers syndrome and Hunters disease. Children with Hurlers syndrome have
characteristic facies and often have obstructive airway symptoms. Depending on the
abnormality present they develop learning difficulties, cardiac disease, kyphoscoliosis,
respiratory failure and neck instability. The airway can be difficult to manage during
anaesthesia (Figure 4).
4 Child with Hurlers syndrome illustrating the

typical coarsened facial features that are associated
with difficulties in managing the airway.
Oncological disease and chemotherapy

Many childrens cancers are now treated successfully. Common childhood oncological
diseases include leukaemia (most commonly acute lymphocytic leukaemia), cerebral
tumours, neuroblastoma and Wilms tumour. In most patients, care is shared between
the tertiary referral centre and the local hospital. Anaesthetic implications are related
to the disease or to the effect of treatment such as corticosteroids or cytotoxic drugs,
some of which have specific renal, haemopoietic or cardiac toxic side-effects.
Management: most children require chemotherapy, multiple blood tests, blood

component therapy and repeat anaesthesia. To assist this management, indwelling
catheters (e.g. Hickman catheters, Portacath) are placed early after diagnosis. Children
can become quite fond of their catheters. An aseptic technique is essential when
accessing these catheters and if carefully looked after they may be kept for many
months. These children are frequent attenders at hospital and they often have particular
requests about the conduct of their anaesthesia and need sensitive management.
A full blood count should be available preoperatively. Additional investigations may
include urea and electrolytes and clotting studies. Blood component therapy is often
required before or during surgery. Blood products may need to be leucodepleted and
irradiated in these children, and this should always be discussed with the oncology
team. The requirements depend partly on the intended surgery and on local clinical
guidelines. A platelet count of at least 100,000 is required for the insertion of indwelling
intravascular catheters or general surgery. For a lumbar puncture, a platelet count
above 50,000 is acceptable, providing the clotting results are normal. Epidural and
caudal anaesthesia are often contraindicated because of coagulation abnormalities.
These children are often immunocompromised and great care is needed to avoid
potential infection. Suppositories are contraindicated if the child is neutropenic owing to
the risk of infection.
Latex allergy
Sensitivity to latex products is the most common cause of anaphylaxis during
anaesthesia. It is a type 1, IgE-mediated hypersensitivity reaction and can be severe.
Children most at risk include those with:
a history of sensitivity to latex (e.g. balloons, toys)
atopy
specific food allergies (e.g. kiwi fruit, chestnuts, avocado, banana) owing to cross-
sensitivity to specific food proteins
a history of repeated surgery (particularly urological surgery)
spina bifida.
Children at risk should be screened with a radioallergosorbent test (RAST) and enzyme
linked immunosorbent assay (ELISA). These tests are non-specific and up to 45%
of patients with negative RAST tests have a positive skin test to latex, so this should
be considered if the history is strong. The management of children at risk from latex
allergy is debated. In many centres, children at risk from latex allergy are admitted
for preoperative treatment with methylprednisolone, ranitidine and chlorpheniramine,
each given 6-hourly intravenously, started 12 hours preoperatively and continued for
24 hours postoperatively. This management precludes the use of day-care surgery
and therefore the use of such regimens has been questioned and in some centres
abandoned in favour of providing a latex-free environment for all children in the group
at risk. It would seem wise to try to prevent sensitization of any patients by avoiding
exposure of a child in an at-risk group to latex.
Long-term corticosteroid use

The long-term use of corticosteroids may occur in severe asthma, juvenile arthritis,
nephrotic syndrome, in many chemotheraputic regimens and in replacement therapy for
adrenal or pituitary failure or congenital adrenal hyperplasia. Long-term corticosteroid
therapy can result in steroid facies, hypertension and diabetes. Children at risk of
having inadequate endogenous corticosteroid production require additional cover
during surgery. The dose of replacement corticosteroids is debated and more is
probably given than is required.
Give children taking regular corticosteroid therapy, hydrocortisone, 1 mg/kg i.v. on
induction and 6-hourly until their routine corticosteroid treatment restarts.
In children who have used corticosteroids in the last 2 months give hydrocortisone, 1
mg/kg i.v. until 2448 hours postoperatively.
Children who have had inhaled corticosteroids, for example in asthma medication,
do not require additional corticosteroid perioperatively.
FURTHER READING
Gregory G A. Pediatric Anesthesia. 3rd ed, New York: Churchill Livingstone, 1994.
Jones K L. Smiths Recognisable Patterns of Human Malformation.5th ed. Philadelphia:
Saunders, 1997.
Katz J, Steward D J. Anesthesia and Uncommon Pediatric Diseases. 2nd ed.
Philadelphia: Saunders, 1993.
Steward D J. Manual of Pediatric Anesthesia. 4th ed. New York: Churchill Livingstone,
1995.
ACKNOWLEDGEMENTS
Thanks to Dr K McHugh for the radiograph of cystic fibrosis,Dr A Mackersie for the MRI
scan of Downs syndrome and Dr A Velodi for the picture of Hurlers syndrome

Cleft Lip and Palate
John Currie
John Currie is Consultant Anaesthetist at the Royal Hospital for Sick Children,
Glasgow. He qualified from Liverpool University and trained in Paediatrics in Edinburgh,
and then in anaesthesia in Liverpool; Great Ormond Street, London; and the Childrens
Medical Centre, Dallas, Texas. His interests include paediatric plastic surgery, spinal
surgery and chronic pain in children.
Cleft lip and palate occur in 1.5/1000 live births. Cleft palate alone has an incidence
of 0.5/1000 live births. Accompanying congenital abnormalities may be present (e.g.
Pierre Robin syndrome). Often there are supernumerary teeth or absence of the incisor
in line with the cleft. There may also be widening of the middle portion of the face
(telecanthus) or even true hypertelorism. Several operations may be required to correct
these abnormalities.
Cleft lip
Cleft lip is best repaired in the neonatal period. This produces a better scar and
reduces the mothers emotional stress. Babies with congenital abnormalities are often
premature and surgery should be delayed until feeding is well established and any
other congenital abnormalities, respiratory problems or jaundice have been identified
and treated. A detailed history of the babys post-natal progress is essential.
Anaesthesia babies with cleft palate tend to have enlarged tongues and
micrognathia. Therefore, an inhalation induction may be preferred. Once the
anaesthetist has confirmed that he can ventilate the lungs, a muscle relaxant may be
given to facilitate intubation (a south-facing RAE tube is preferred to give good surgical
access). A mouth pack is then inserted in case of intraoperative bleeding. Perioperative
analgesia can be provided with an infra-orbital block, though the surgeon may prefer to
inject local anaesthetic and adrenaline (epinephrine) to optimize the field. At the end of
surgery, it is essential to remove the tracheal tube when the baby is awake to prevent
laryngeal spasm.
Surgery also involves improving the appearance of the ipsilateral nostril (which is
always flattened) by moving tissue medially from the lateral side of the cleft and
repositioning the displaced cartilage. To maintain this position, the surgeon often sews
a piece of sponge into the nostril. This may impair breathing postoperatively, so a small
length of feeding tube should be included in the sponge, to provide an airway.
Postoperative care babies may have difficulty feeding postoperatively and be

unsettled (perhaps due to numbness of the lip from local anaesthetic). This can be
helped by giving codeine phosphate, 1 mg/kg i.m., before extubation. Once feeding is
re-established, paracetamol (regularly for 24 hours) maintains analgesia.
Cleft palate
Cleft palate should be repaired ideally at about 6 months of age. This is when the baby
is learning to imitate speech, and is using the levator palatini and the aponeurotic tensor
palatini muscles to close the velo-pharangeal aperture to make oral (as distinct from
nasal) sounds. Modern techniques involve repositioning these muscles to obtain normal
palatal function.
Anaesthesia no premedication is required and (in the absence of other serious

airway anomalies) intubation seldom presents a problem. A south-facing RAE tube
is preferred. Before repair, the surgeon inserts a BoyleDavies gag to open the
mouth and provide access. It is essential to check the tracheal tube position carefully
because it is often kinked or pushed into a main stem bronchus by the gag. Bilateral
air entry should be checked by listening with a stethoscope after the gag has been
positioned. Local anaesthetic and adrenaline (epinephrine) help to produce a dry field
and analgesia. However, it is also wise to give an opiate (e.g. fentanyl, 1 g/kg) to
avoid tachycardia if the surgeon strays beyond the blocked area (particularly likely
when making lateral relieving incisions to facilitate a difficult repair). Codeine, 1 mg/
kg i.m., before extubation is useful, especially if combined with rectal diclofenac at
induction. Diclofenac and paracetamol should then be given regularly for 24 hours, with
paracetamol as required thereafter.
Postoperative care the repair tends to lift the palate towards the roof of the
nasopharynx, narrowing the airway (which may be worsened by spasm of the levator
palatini) and causing upper airway obstruction after extubation. The obstruction may
be overcome by inserting a nasopharyngeal airway (usually a tracheal tube one
size less than that used for intubation). Ideally the surgeon should insert this before
removing the gag if the repair is tight. The nasopharyngeal airway must be kept patent
postoperatively (e.g. by suction). These babies should be nursed on a high dependency
unit.
Fistula repair
The child may require further operations if it is impossible to close the cleft completely
or the repair breaks down. Occasionally, a tongue flap is needed to provide enough
tissue to close an anterior fistula. Initially, the surgeon fashions the flap and attaches
it to the defect in the roof of the mouth. These children should be nursed on a high
dependency unit for 24 hours. The child returns 2 weeks later for division of the flap.
Intubating a child with its tongue attached to the roof of the mouth is challenging
and best achieved fibre-optically by the nasal route. This can be practised during
anaesthesia for the first stage to determine the most suitable nostril and the optimum
position for the best view.
Alveolar bone graft

The final stage of repair is to close the defect in the alveolar arch (usually at about
89 years of age) using bone from the iliac crest. Postoperatively, infusion of local
anaesthetic subcutaneously at the donor site provides excellent analgesia. u

Common Local Anaesthetic
Techniques in Children
Pam Cupples
Roddie McNicol
Pam Cupples is Fellow in Paediatric Anaesthesia at the Royal Hospital for Sick
Children, Glasgow, UK.
Roddie McNicol is Consultant in Paediatric Anaesthesia at the Royal Hospital for Sick
Children, Glasgow, UK.
Paediatric regional anaesthesia is not a scaled-down version of adult practice. It is

important to be aware of the anatomical and pharmacological differences between
children and adults and to apply that knowledge appropriately so that regional
anaesthesia becomes an integral part of day-to-day practice.
In children, regional analgesia is usually combined with a general anaesthetic to
provide balanced anaesthesia. The depth of anaesthesia can be reduced because
regional blocks provide excellent intraoperative analgesia and a predictable period
of postoperative pain relief. Local anaesthetic techniques combined with mild-to-
moderate oral analgesics, such as paracetamol or non-steroidal anti-inflammatory
drugs (NSAIDs), decrease the requirements for opioids and reduce the incidence
of unwanted side-effects (e.g. nausea and vomiting, respiratory depression, excess
sedation).
The advantages of regional anaesthesia in the postoperative period are shown in
Figure 1. Both children received similar anaesthetics, but different analgesics. The boy
given the penile block had excellent pain relief for almost 8 hours before he became
uncomfortable and required simple analgesics. The girl given papaveretum had poorer
pain control complicated by side-effects (e.g. vomiting).
Contribution of regional anaesthesia during and

after surgery
12-year-old girl given papaveretum during and after surgery
As bad as
can be 10
Sleepy Awake
9
8
7
Drink Papaveretum
Pain score
6
5
4
3
2
1
No pain 0
0 1 2 3 4 5 6 7 8 9 10
Postoperative period (hours)
5-year-old boy given a penile block
As bad as
can be 10
9
Sleepy Awake
8
1
1
7
Pain score
6
5
4 Drink Drink Paracetamol
3
1
2 Lunch Up to play
1
No pain 0
0 1 2 3 4 5 6 7 8 9 10
Postoperative period (hours)
Applying local anaesthesia
Topical anaesthesia
The ability of local anaesthetics to penetrate intact skin and produce anaesthesia and
analgesia proved to be a difficult pharmacological challenge until the development
of a eutectic mixture of local anaesthetic (Emla cream) in the 1980s. Emla is an
oily emulsion containing 25 mg/ml each of lidocaine (lignocaine) and prilocaine.
Eutectic refers to the lowering of the melting points, the physical transformation that
occurs when lidocaine (lignocaine) and prilocaine crystals are mixed together in equal
quantities. When applied to the skin under an occlusive dressing for 6090 minutes, the
emulsion produces analgesia of the skin which is useful for:
venepuncture
division of prepucial adhesions
myringotomy and ventilation tube insertion when applied to the tympanic membrane
minor surgical procedures when given before superficial infiltration of local
anaesthetic.
Emla occasionally causes transient blanching of the skin owing to vasoconstriction
of blood vessels, and erythema and oedema, which can make cannulation difficult.
Ingestion of the occlusive dressing and Emla cream have both been described, and
methaemoglobinaemia has occurred in a child following application of Emla cream over
a large area, leading to systemic absorption and toxicity.
A new alternative to Emla is tetracaine (amethocaine) 4% gel (Ametop), which
provides more rapid and longer-lasting analgesia before venous cannulation.
Mucosal analgesia
Topical analgesia of mucosal surfaces is simple and effective, and can be used for
the following indications:
strabismus surgery, using 0.4% oxybuprocaine hydrochloride eye drops into the
conjunctival sac before the conclusion of surgery
circumcision, using 2% lidocaine (lignocaine) gel applied at the end of surgery or
during the postoperative period
anal stretch for the treatment of anal fissures, using lidocaine (lignocaine) gel.
Instillation of local anaesthetics

Local anaesthetics can be instilled directly into wounds (e.g. inguinal hernia). The
analgesia is of shorter duration, but can equal that produced by an iliohypogastric/
ilioinguinal nerve block.
Local anaesthetic can also be instilled before cleaning or suturing small superficial
wounds in the Accident and Emergency Department. The local anaesthetic can be
applied either by dropping it on to the wound or applying a swab soaked in the local
anaesthetic. Solutions of either lidocaine (lignocaine) or bupivacaine combined with a
vasoconstrictor, such as adrenaline (epinephrine), are most commonly used.
The technique of instillation can be useful in children requiring regular dressing
changes (e.g. split skin graft donor sites); the wound dressing can be soaked with
a combination of local anaesthetic and adrenaline (epinephrine). Alternatively, an
epidural catheter can be incorporated into the wound dressing and local anaesthetic
(e.g. 0.125% or 0.25% bupivacaine with 1:400,000 adrenaline (epinephrine)) can be
continuously infused on to the wound at a rate of 13 ml/hour. Care must be taken not
to exceed the maximum recommended dose of 0.5 mg/kg/hour or 2 mg/kg/4 hours.
Infiltration
The infiltration of local anaesthetics, alone or combined with vasoconstrictors, is used
regularly to provide anaesthesia and analgesia for many operations (e.g. suturing
superficial wounds, or excision of cysts, accessory auricles, naevi). It is particularly
useful in the neonate undergoing pyloromyotomy; infiltrating the wound edge before
completion of surgery can produce excellent postoperative analgesia. Combined with
paracetamol, this avoids the use of opioids and reduces the incidence of side-effects,
particularly respiratory depression or apnoea.
Peripheral nerve blocks

A variety of needles is available for regional block or subcutaneous infiltration of
nerves. The ideal needle should give good perception of the different fascial planes,
but have a low incidence of nerve damage. Short bevelled needles allow the user to
appreciate these changes in resistance and are less likely to impale a nerve than a
long bevelled needle. Nerve stimulators are useful in children because their anatomy is
variable and most children are anaesthetized before the block therefore the technique
of paraesthesia cannot be used.
Great auricular nerve block is used for pinnaplasty; a common operation in children.
The sensory supply of the ear is largely from the great auricular nerve derived from the
superficial cervical plexus (Figure 2).
The great auricular nerve divides into pre- and post-auricular branches, which can
be blocked by infiltrating the tip of the mastoid process anteriorly and posteriorly with
23 ml of local anaesthetic (Figure 3). A branch of the mandibular division of the
trigeminal nerve, the auriculotemporal nerve, supplies the external auditory meatus
and the temple region. This can be blocked by infiltrating a further 23 ml of local
anaesthetic anterior to the external auditory meatus.
Great auricular
nerve block
Auriculotemporal
nerve
Lesser occipital
nerve
Great auricular
nerve
Infraorbital nerve block is excellent for providing analgesia for neonates undergoing
cleft lip repair. It removes the need for opioids and reduces the risk of respiratory
depression or apnoea. This is particularly important because these neonates are often
either preterm or have associated congenital anomalies.
The infraorbital nerve is a branch of the maxillary division of the trigeminal nerve
and provides the sensory innervation to the skin and mucus membranes from upper
lip to the lower eyelid and medially to the side of the nose. The landmark for locating
the infraorbital nerve is found by drawing a line from the angle of the mouth to the
midpoint of the palpebral fissure; the nerve is situated about halfway along this line and
can be approached either percutaneously or buccally (Figure 4). For the percutaneous
technique a 25 G needle is used and is introduced perpendicular to the skin and
advanced until bony resistance is felt. The needle is then withdrawn slightly and,
following a negative aspiration test, the local anaesthetic (usually 0.5% bupivacaine,
0.50.75 ml with 1:200,000 adrenaline (epinephrine)) is injected.
3 Site of great auricular nerve block.
4 Landmarks for infraorbital nerve block. A line is

drawn from the angle of the mouth to th emidpoint
of the palpebral fissure. The nerve is situated
about half way along this line.
5 Ilioinguinal and iliohypogastric

nerve block. X marks the position of
the anterior superior iliac spine.
Combined ilioinguinal and iliohypogastric nerve block provides anaesthesia

and postoperative analgesia for operations in the groin. These nerves are derived
from T12, L1 and L2. A 22 G short bevelled needle is inserted at a point one patients
fingerbreadth medial to the anterior superior iliac spin (Figure 5). The needle is inserted
perpendicular to the skin. A pop is felt as the needle passes through the aponeurosis
of the external oblique. After a negative aspiration test, about one-third of the local
anaesthetic is injected at this point. The needle is then withdrawn and redirected
caudally and laterally until it strikes the ilium, and a further third of the solution is
injected. The remaining local anaesthetic is injected as the needle is withdrawn.
Genitofemoral nerve block: if the child is undergoing an orchidopexy, the genital

branch of the genitofemoral nerve has to be blocked. Depositing one-third of the
solution adjacent to the pubic tubercle and infiltrating subcutaneously across the
midline blocks the genital branch and any innervation from the contralateral nerve.
0.25% bupivacaine, 2 mg/kg, is the recommended safe dose. In the older child, 0.5%
bupivacaine may be used.
6 Penile block.
Penile block: the dorsal nerve of the penis is the terminal branch of the pudendal
nerve (S2, 3 and 4) and is commonly blocked to provide postoperative analgesia
following circumcision. The patient lies supine and a short bevelled needle is inserted
0.51.0 cm lateral to the pubic symphysis (Figure 6), depending on the age of the child.
The needle is advanced posteriorly, caudally and medially; a pop is felt twice as the
needle penetrates the superficial fascia then Scarpas fascia. Plain 0.5% bupivacaine,
0.1 ml/kg, is then injected. Vasoconstrictors should never be added to the local
anaesthetic solution because of the risk of ischaemia.
Fascia iliaca block: the femoral, lateral cutaneous and obturator nerves can be
blocked with a single injection using the fascia iliaca compartment block devised by
Dalens. It has superseded the femoral 3 in 1 block because it is a simple technique
with a high success rate (particularly in children) and lower complication rate. The
fascia iliaca block can be used for a number of operations on the hip and thigh, for
example femoral osteotomy, reduction of femoral fracture, surface operations on the
thigh, femoral biopsies and the removal of metal screws and plates from the femur. The
child lies supine and an imaginary line is drawn between the anterior superior iliac spine
and the pubic tubercle (Figure 7).
C B
This line is divided into thirds and the junction of the lateral with the medial two-thirds
is located. A short bevelled needle is inserted at an angle of 60 about 0.5 cm below
this point. As the needle is advanced, two pops are felt as the needle penetrates the
fascia lata then the fascia iliaca. The needle is aspirated to ensure that it is not lying
intravascularly and the local anaesthetic is then injected. 0.25% bupivacaine can
be used alone or in combination with 1:200,000 adrenaline (epinephrine) and the
recommended doses are given in Figure 8.
Dosing guidelines for fascia iliaca nerve block
Weight of child Total volume of local

(kg) anaesthetic (0.25%
bupivacaine ml/kg)
< 20 0.7
2030 15
3040 20
4050 25
> 50 27.5
Metacarpal and metatarsal blocks are used for operations on the fingers and
toes, respectively. These techniques are simple and provide good intraoperative and
postoperative analgesia. They are preferred to blocks within the digits because the
digits are small and injecting large volumes into a confined space can damage the
end artery, producing ischaemia or distorting anatomy and impairing surgical access.
The common digital nerves are derived from the ulnar and median nerves, and divide
into dorsal and ventral branches in the distal palm. They run on the dorsolateral and
ventrolateral aspects of the digit, respectively, and are accompanied by the digital
vessels.
To perform a metacarpal block, a short bevelled needle is inserted through the skin
on the dorsal aspect of the hand adjacent to the proximal end of the metacarpal bone
and advanced until it can be felt by the operators hand on the palmar surface (Figure
9). Following a negative aspiration test, 0.25% bupivacaine , 0.51.0 ml, is injected
until a small swelling is felt. The technique can be repeated at several interspaces,
depending on the number of digits involved.
Analgesia of the toes can be obtained similarly with a metatarsal block. A needle
is inserted through the skin on the dorsum of the foot at the proximal end of the
metatarsal bone. 0.25% or 0.5% bupivacaine, 0.51.0 ml, is injected. Vasoconstrictors
should not be added because of the risk of ischaemia.
9 Metacarpal block.
Central neuroaxial blocks
There are important anatomical differences between babies, children and adults (Figure
10). Following neuroaxial blockade in children, there is less haemodynamic instability
because of the immaturity of the sympathetic nervous system and less pooling of blood
in the legs.
Differences between newborn and adult spines
L1 L1
Spinal
cord
Newborn L2 L2 Adult
L3
Dural
L3
sac
L4 L4
L5
Epidural
L5
space
S1
S2
S3
The tip of the spinal cord lies at L3 at birth and the dura extends to S23.
Only at the age of 1 year does the cord assume the adult position of the
L12 interspace and the dural level of S2. The intercristal line in the
neonate lies at the level of L5S1 and in the slightly older child at L5
10
Spinal anaesthesia
Spinal anaesthesia is most commonly used in neonates or ex-premature babies for
operations of short duration on the lower abdomen (e.g. hernia repair, orchidopexy).
There is a 10% absolute failure rate for this technique as well as a 10% rate of
inadequate blockade.
In the neonate, the CSF pressure is low and many therefore recommend the use of
a 22 G Quincke point needle, which allows better flow of CSF once in the spinal canal.
A short bevelled needle allows better perception of the pops as the needle traverses
the posterior spinal ligaments and dura. Atraumatic tipped spinal needles (Whitacre
needles) are not recommended for neonates because of the tendency of the orifice of
the needle to straddle the dura. The incidence of post-dural puncture headaches is low
in neonates, but increases as the child ages. It is therefore prudent to use a smaller-
gauge needle (e.g. 26 G) in older children and adolescents.
Either hyperbaric or isobaric 0.5% bupivacaine can be used. If hyperbaric
bupivacaine is used, the appropriate dose can be calculated using the formula: 0.06
ml/kg + 0.1 ml. If isobaric bupivacaine is used, the dose is 1 mg/kg. As a guide, the
distance from the skin to the subarachnoid space is 10 mm in a full-term baby and 7
mm in a premature baby. Spinal anaesthesia lasts for 20110 minutes, but the block is
unreliable for operations longer than 40 minutes.
One of the main indications for performing spinal anaesthesia is to reduce the
incidence of postoperative apnoea, which can be a problem following general
anaesthesia. If spinal anaesthesia is used, it is of paramount importance to monitor the
baby postoperatively for oxygen saturation and apnoea.
Epidural anaesthesia
Epidural analgesia (usually combined with general anaesthesia) is useful for
orthopaedic surgery on the legs, orchidopexy and operations involving the perineum.
Commercially available paediatric epidural kits are available (i.e. 18, 19, 20 G Tuohy
needles with 21 G, 23 G and 24 G catheters, respectively; Figure 11). The 18 G Tuohy
needle with its 21 G catheter can be used in babies weighing more than 3 kg; the larger
gauge of catheter allows better flow of blood, if the catheter has breached an epidural
vessel, or CSF, if the catheter has traversed the dura inadvertently. There are fewer
technical problems, such as kinking and blocking, with the larger gauge of catheter.
A guide to the depth of the lumbar epidural space in children can be calculated
according to either their age or weight (e.g. (body weight in kg + 10 ) x 0.8 mm).
Alternatively, for children 6 months to 10 years of age, the distance to the epidural
space is about 1 mm/kg body weight.
In children, the epidural space can also be accessed through the sacral
intervertebral spaces, because the sacrum does not ossify until the age of 2530
years.
The complications following epidurals in children are similar to those seen in adults
and include:
dural puncture with total spinal block
post-dural puncture headache age increases incidence
hypotension uncommon in children less than 6 years old
nerve damage occasionally the catheter may press against nerve roots
infection
urinary retention
unilateral or patchy blocks.
11 Paediatric epidural kit containing

19 G, 5 cm Tuohy needle with 23 G
catheter.
Epidurals are most commonly inserted in the lumbar region and then threaded to the
appropriate dermatomal level. The epidural space in children contains gelatinous fat
globules instead of the densely packed fat divided by fibrous bands found in adults.
This allows more longitudinal spread of local anaesthetic within the space and makes
it possible to thread a catheter the entire length of the vertebral column. The volume
of local anaesthetic required can be calculated using the formula devised by Takasaki
for caudal anaesthesia (Figure 12), which may also be applied to lumbar epidural
anaesthesia. Alternatively, 0.25% bupivacaine, 0.51 ml/kg can be used for lumbar
epidurals and half this dose for a thoracic block.
Formulae for calculating the volume of local anaesthetic for caudal block
Armitage
Lumbosacral blocks = 0.5 ml/kg of 0.25% bupivacaine
Thoracolumbar = 1 ml/kg of 0.25% bupivacaine
Mid-thoracic = 1.25 ml/kg of 0.25% bupivacaine
Takasaki
Volume = 0.05 ml x body weight x no. of spinal segments to be blocked
12
Caudal anaesthesia
Caudal anaesthesia is a simple and safe technique. It is performed by injecting local
anaesthetic through the sacral hiatus, which is easily palpated as a dimple flanked by
the sacral cornua (Figure 13).
Single-shot caudal blocks can be performed using either a short (2.5 cm) 23 G
intramuscular needle, a short bevelled needle with a solid obturator, or a 22 G cannula.
However, the risks of vascular penetration or the production of a dermoid cyst due
to implantation of skin are recognized problems that favour the use of the cannula
technique. The technique of insertion is different depending on the age of the child. In
babies, the needle should be inserted in the centre of the hiatus at an angle of 15 to
the skin because of the flatness of the sacrum. In older children, the needle is placed at
the apex of the hiatus at an angle of 45 to the skin. For continuous caudal anaesthesia,
a 20 G intravenous cannula can be used ensuring the cannula is not advanced too
far up the caudal space for fear of damaging the dura. A catheter (23 G) from a 19 G
epidural set can then be passed easily through the cannula to the desired dermatomal
level.
Caudal block
Landmarks for caudal block in babies
Posterior superior iliac spines
Intercristal line Sacral
Dura hiatus
L5/S1
S2S3
Site of caudal block
13
ACKNOWLEDGEMENTS
Figures 3, 5, 6, 9 and 13 are reproduced from Morton N S, Raine P A M, eds.
Paediatric Day Case Surgery. Oxford: Oxford Medical Publications, 1994, by kind
permission of the publisher.
FURTHER READING
Arthur D S, McNicol L R. Local Anaesthetic Techniques in Paediatric Surgery. Br J
Anaesth 1986; 58: 76078.
Cousins M J, Bridenbaugh P O, eds. Neural Blockade in Clinical Anaesthesia and
Management of Pain. 3rd ed. Philadelphia: LippincottRaven,1998.
Dalens B. Regional Anaesthesia in Children. Anaesth Analg 1989; 68: 65472.
Dalens B J. Paediatric Regional Anaesthesia. Florida: CRC Press, 1990.
Finucane B T. Regional Anaesthesia: Complications and Techniques. Can J Anaesth
1991; 38: R316.
Morton N S, ed. Acute Paediatric Pain Management: A Practical Guide. London: W B
Saunders, 1998.
Morton N S, Raine P A M, eds. Paediatric Day Case Surgery. Oxford: Oxford Medical
Publications, 1994.
Peutrell J M, Mathers J. Regional Anaesthesia for Babies and Children. Oxford: Oxford
University Press, 1997
. 2002 The Medicine Publishing Company Ltd

Congenital Heart Disease
Monica Stokes
Monica Stokes is Senoir Lecturer in Paediatric Anaesthesia and Honorary Consultant

at University Hospital, Birmingham, UK, and Birmingham Childrens Hospital. She
qualified from the University of Nottingham and trained in anaesthesia in Cambridge,
Bristol and Birmingham. She has held Fellowships in Australia and the USA. Her
clinical interests include anaesthesia for paediatric cardiac surgery, neonatal surgery
and ethical issues in contemporary anaesthesia practice.
The incidence of congenital heart disease (CHD) is about 68/1000 births, and is
more common in premature infants. There is a broad range of lesions and severity,
with differing implications for morbidity and life expectancy. The multifact-orial causes
include known teratogens such as maternal alcohol, rubella, and diabetes. In some
instances there is an association with a chromosomal abnormality (e.g. trisomy
21, Downs syndrome), or other recognized pattern of malformation or syndrome.
Significant musculoskeletal defects such as diaphragmatic hernia, exomphalos,
tracheo-oesophageal fistula, and imperforate anus may co-exist.
The pathophysiological effects of CHD vary with the nature of the lesion and change
as time passes. Some septal defects, for instance, close spontaneously without medical
intervention. Other lesions tend to worsen as the child grows, and some are lethal
without intervention. Therefore, regular evaluation of anatomical and functional status
is essential. There is often an optimal time for surgical intervention to achieve the best
outcome, and many defects are palliated or treated at an early age.
Pathophysiology
Classifications of CHD based on detailed anatomical descriptions are unhelpful for

practical purposes because it is the pathophysiology that determines the presentation,
natural history and management of a particular condition. A simple distinction between
cyanotic and acyanotic is too broad, however, because it gives no sense of the potential
for systemic and pulmonary circulatory patterns to change. It is more useful to consider
whether the dominant lesion is a shunt between systemic and pulmonary circulations,
with increased or decreased pulmonary blood flow, or obstruction to systemic or
pulmonary blood flow (Figure 1).
Simple classification of congenital heart disease
Lesions causing primary left-to right shunts

Patent ductus arteriosus
Atrial septal defect
Lesions causing primary right-to-left shunts

Transposition of the great vessels
Tetralogy of Fallot
Tricuspid atresia
Lesions obstructing ventricular function

Left heart
Coarctation of the aorta
Aortic stenosis
Mitral stenosis
Right heart
Pulmonary stenosis
1
Shunts
A shunt is a communication between systemic and pulmonary circulations. It may occur

outside the heart (e.g. collateral vessels, patent ductus arteriosus) or within it (at atrial,
ventricular, or great artery level). It may be a component of the congenital heart lesion
or be created to palliate it. (A conduit, by contrast, is a channel fashioned between
vessels or chambers normally in continuity.)
The magnitude and direction of blood flow across a shunt are determined primarily
by the size of the communication and by the relative resistances of the pulmonary and
systemic circulations.
A dependent shunt is one where the flow varies according to the relative resistances
of the vascular beds. It may be left-to right or right-to-left.
A small communication may be restrictive in that systemic and pulmonary vascular
resistances are less important in determining the amount of shunting. This is usually the
case in children with mild heart disease that is asymptomatic or minimally symptomatic
(e.g. small artial septal defect, ventricular septal defect, patent ductus arteriosus).
A non-restrictive defect is defined as one across which no pressure gradient exists,
the direction and degree of shunting being determined by the relative compliances of
the two atria and ventricles.
An obligatory shunt occurs when resistances are fixed and flow occurs because of
pressure differences of an order of magnitude.
Shunting may be essential for survival: a patent ductus arteriosus for instance, may
supply the pulmonary blood in pulmonary atresia or the systemic flow in aortic atresia.
In other words, where there is partial or complete obstruction to a circulatory path, a
communication at another level is necessary.
Left-to-right shunts
Children with left-to-right shunts are typically pink with pulmonary plethora on chest
radiography. The physical signs reflect the shunt volume. The cardiac chambers
enlarge and hypertrophy to cope with the excessive volume and increased flow across
a valve causes a murmur.
Unchecked, volume overload can lead to ventricular failure, and sustained high
pulmonary blood flow damages small peripheral pulmonary arteries. This damage
consists of medial hypertrophy of the arterial wall, followed by intimal damage and
ultimately elevated pulmonary vascular resistance, which may be irreversible. At this
point, flow through the shunt diminishes and eventually reverses, the patient becoming
cyanosed (Eisenmenger reaction).
Atrial septal defect

The secundum atrial septal defect is the most common type of interatrial
communication. It is a true defect of the atrial septum, unlike the more complex
ostium primum septal defect. The direction of blood flow is determined by the relative
compliances of the two atria and ventricles, which in the newborn are equally thick
walled. Shunting between the atria does not occur until the pulmonary vascular
resistance has fallen after birth, and the right ventricle has become more compliant.
Of the excessive blood returning to the left atrium, enough enters the left ventricle
to sustain a normal systemic output
but a greater volume is recirculated through the atrial defect, right heart and lungs.
Flow through the pulmonary circulation can be three times that through the systemic
circulation, producing the characteristic mid-diastolic tricuspid flow murmur, pulmonary
ejection murmur, and prolonged right ventricular ejection.
Some infants with isolated interatrial communications develop symptoms of
intractable congestive heart failure and failure to thrive. Many children are initially
asymptomatic but with time, particularly if a large shunt (2:1 or greater) persists through
childhood, pulmonary vascular disease and arrhythmias can develop.
Large defects may be closed surgically but it is possible to occlude smaller defects
with devices placed percutaneously under radiological imaging, avoiding the need for
cardiopulmonary bypass.

In ventricular septal defect, blood flows from the left to the right ventricle in systole and
recirculates through the lungs. Both ventricles and the left atrium dilate and the liver
enlarges secondary to right ventricular volume overload.
A large defect may present in early infancy with tachypnoea and failure to thrive,
because the lungs are stiff and non-compliant. The high left ventricular pressure is
transmitted to the pulmonary circulation and the hypertensive pulmonary arteries may
compress small airways. Therefore, respiratory tract infections are common. Both
ventricles enlarge making the chest wall bulge and the apical beat is typically forceful.
The characteristic murmur is pansystolic, and when the pulmonary flow is more
than about twice systemic, a mitral diastolic murmur appears. As pulmonary vascular
resistance increases, the pulmonary artery diastolic pressure rises; pulmonary flow
decreases, and the mitral diastolic murmur disappears. Eventually, when the pulmonary
vascular resistance approaches systemic levels, the pansystolic murmur shortens and
disappears. On chest radiography the enlarged heart becomes small and the plethoric
lung field become oligaemic with pruning of the peripheral vessels.
Medical management depends on the size of the defect. Most defects are small and
close spontaneously. About 10% of the larger defects will also close. In some patients,
obstruction to the right ventricular outflow tract develops. These patients become
cyanosed, the physiology coming to resemble that of tetralogy of Fallot. Pulmonary
vascular disease develops if the defect remains large so surgery is often performed
in infancy.
Patent ductus arteriosus

Patent ductus arteriosus is a shunt at arterial level and flow occurs during both systole
and diastole. The magnitude of shunting is dependent on the size of the duct and the
relative resistance of the pulmonary and systemic vascular beds. There is a continuous
flow of blood from the aorta to the pulmonary artery, producing a continuous murmur.
If the ductus is large, pulmonary venous return is high, the left heart is overloaded and
so the apical impulse is prominent and a mitral mid-diastolic flow murmur is heard.
During diastole the blood steals from the aorta to the pulmonary artery, and therefore
the aortic diastolic pressure is low and the upstroke of the pulse is abrupt as blood is
ejected into an empty aorta. This produces the characteristic bounding pulse.
Most children with patent ductus arteriosus are asymptomatic. Premature babies,
however, are often symptomatic. The work of breathing is increased and attempts to
wean from mechanical respiratory support are unsuccessful.
Treatment with indomethacin is often successful in promoting closure of the
ductus but when it fails, surgical ligation is indicated via a left thoracotomy. It is
extremely unlikely that a patent ductus arteriosus will close spontaneously after 1 year.
A large duct can lead to progressive pulmonary vascular disease, while those with
smaller shunts are at risk for endocarditis, aneurysm, calcification and paradoxical
emboli. Nowadays, it is common for ducts in older children to be occluded by devices
placed percutaneously at cardiac catheterization.
Pulmonary venous obstruction

Patients with pulmonary venous obstruction may be cyanosed or acyanotic but have
signs of pulmonary oedema clinically and on chest radiography.
Obstruction to pulmonary venous return can occur at several places; in the
pulmonary venous pathway (obstructed total anomalous pulmonary venous drainage),
within the atrium (cor triatriatum) or by obstruction to left ventricular inflow at
supravalvar, valvar, or submitral level. Children with pulmonary venous obstruction
usually present in early infancy with cyanosis and dyspnoea caused by pulmonary
oedema. In less severe cases, presentation is with failure to thrive and respiratory
symptoms.
The major effect of total anomalous pulmonary venous drainage is that all systemic
and pulmonary venous return is to the right atrium. The pulmonary veins drain into a
confluence behind the heart and from there to the right atrium, usually indirectly via
the innominate vein, coronary sinus or portal system. Saturated and desaturated blood
mixes in the right atrium; sufficient oxygenated blood crosses an atrial sepal defect
to support the systemic circulation while the remainder re-enters the right ventricle.
The long pulmonary venous pathway is usually obstructive, causing pulmonary venous
hypertension and pulmonary oedema and contributing to a high pulmonary vascular
resistance. This is a life-threatening situation requiring emergency corrective surgery.
Obstruction to systemic perfusion
The dominant features of an obstruction to systemic perfusion are poor peripheral

pulses and metabolic acidosis. This can be a result of aortic obstruction (interrupted
aortic arch and coarctation) left ventricular outflow tract obstruction (aortic valve
stenosis) or low left ventricular stroke volume (hypoplastic left heart syndrome). Even
when the anatomical obstruction is severe, the fetus survives because the right
ventricle can provide systemic perfusion through the ductus arteriosus. Once the
duct starts to close in early neonatal life, systemic hypoperfusion, or lower body
hypoperfusion in coarctation, develops. The pulses become impalpable, urine output
diminishes, metabolic acidosis develops and a vicious cycle of generalized organ
dysfunction develops.
Resuscitation includes maintaining the patency of the ductus with prostaglandin
infusion. Mechanical ventilation and inotropic support of the failing left ventricle is often
required.
Coarctation of the aorta

Narrowing of the aortic lumen usually occurs at the level of the insertion of the ductus
arteriosus. In neonates, the pressure load on the left ventricle may produce congestive
failure, metabolic acidosis and respiratory insufficiency.
Older children are usually asymptomatic but have diminished femoral pulses and
upper limb hypertension. Collateral vessels tend to be well developed: enlarged
intercostal arteries produce the characteristic rib notching seen on chest radiography in
older children and adults with coarctation.
Tetralogy of Fallot
The tetralogy of Fallot is the combination of a ventricular septal defect and obstruction
to pulmonary blood flow (usually at the outlet of the right ventricle, the infundibulum).
There is secondary right ventricular hypertrophy and an abnormally positioned aortic
outflow, which overrides the ventricular septal defect.
Blood flow to the lungs is reduced but by variable amounts some children have
very few symptoms unless stressed, whereas others present early in infancy with
cyanosis, particularly if the pulmonary arteries are also small. Cyanotic spells are a
result of spasm of the infundibular muscle and cause an increased shunt across the
ventricular septal defect to the systemic circulation (right to left). It is this dynamic
aspect of the obstruction to pulmonary blood flow that accounts for both the intermittent
nature of spells, and therapeutic interventions that may curtail them. Intraoperative
spells are detected by desaturation, a reduction in end-tidal carbon dioxide and
systemic hypotension.
Management is directed towards improving forward pulmonary blood flow including:
hyperventilating with 100% oxygen to reduce pulmonary vascular resistance
optimizing intravascular volume with a bolus of colloid
increasing venous return by elevation of the legs
increasing systemic vascular resistance by administering phenylephrine or
noradrenaline (norepinephrine).
Analgesia and -blockade are also helpful (Figure 2).
Transposition of the great arteries

In transposition of the great arteries, the aorta arises from the right ventricle and the
pulmonary artery comes off the left ventricle. To be compatible with life, mixing must
occur through a septal defect or patent ductus. If the neonate has an intact septum, an
atrial communication is made by percutaneous balloon septostomy.
Transposition of the great arteries is usually lethal without cardiac surgery. There
are two surgical approaches.
Anaesthetic considerations in tetralogy of Fallot
Give preoperative hydration (see right-to-left shunts)

Prescribe sedative premedication (helps reduce spells)
Hypoxia and hypotension on induction should be avoided because they tend
to increase shunting
Intraoperative desaturation and reduced end tidal carbon dioxide tension
values occur in other acute situations such as hypovolaemia and air embolus
Treatment of infundibular spasm
Oxygen
Pain relief
blockade (propranolol, 0.1 mg/kg i.v.)
Intravascular volume replacement
agonist (e.g. phenylephrine, noradrenaline
(norepinephrine)) to increase systemic vascular resistance
Risk of embolization
Physiological correction: a physiological correction involves making channels in the

atria such that venous blood returning from the body is diverted into the left ventricle,
and then into the pulmonary artery (the Mustard or Senning procedures). Longer term,
the right ventricle is unable to power the systemic circulation indefinitely and right
ventricular failure eventually occurs.
Anatomical correction: an anatomical correction can be made, in which the aorta and
pulmonary arteries are switched and the coronary arteries are reimplanted. Although
technically complicated, cardiovascular function is usually good afterwards.
Anatomy and function of the heart are variable, therefore each patient must be
assessed individually (Figure 3). A thoughtful approach to anaesthetic management will
avoid unnecessary upset of the childs cardiorespiratory balance. Sedative, anxiolytic
premedication is very useful, for instance, but large doses of opioid premedication
should be avoided because of the potential for respiratory depression. The aim is
for a smooth induction of anaesthesia, with impeccable airway control and balanced
pulmonary and systemic vascular resistances.
Children with mild-to-moderate functional impairment tolerate inhalation induction
and intravenous induction well. Intravenous ketamine is a useful alternative for more
severely impaired patients because it has little effect on either systemic or pulmonary
vascular resistance.

Level of activity (cardiac reserve) and symptoms
Murmurs, peripheral pulses and skin temperature
Investigations
Chest radiography (heart position, size and shape; increased or decreased
pulmonary vascular markings)
ECG (R axis deviation is normal in infancy; evidence of ventricular
hypertrophy)
Echocardiography (anatomy, function, cardiac output)
Cardiac catheterization (site and size of shunts, pressures, saturations)
Haematocrit (increased in cyanotic lesions; significant risk of thrombosis
if > 60%).
Medications
Diuretics, digoxin, captopril
Warfarin, aspirin
Antibiotics (endocarditis prophylaxis)
Previous surgery
Review records
Note airway problems
Review dental hygiene
Left-to-right shunts
An increase in systemic vascular resistance increases left-to-right shunting. An
increase in pulmonary vascular resistance reduces left-to-right shunting.
Intravenous induction may be prolonged because of recirculation in the lung.
Uptake of inhalational agents is not really influenced by left-to-right shunt unless
there is poor cardiac output. An agent with low blood gas solubility coefficient will
then show increased speed of uptake. Pulmonary congestion increases the risk of
atelectasis.
Right-to-left shunts:
Prolonged starvation times should be avoided. Dehydration produces
haemoconcentration, worsening the effects of the high haematocrit associated with
cyanotic heart disease (e.g. increased risk of thrombosis and stroke). Consider starting
intravenous fluids if the time of surgery is uncertain.
Accidental air embolization should be avoided.
The aim is not to make the shunt any worse (e.g. by hypoxia or hypotension).
Raised intrathoracic pressure decreases pulmonary blood flow.
Cyanotic patients have an abnormal response to hypoxia because they do not
increase breathing rate in the same way as healthy individuals.
Intravenous induction is rapid, however, the dose should
be reduced to avoid a large drop in systemic vascular resistance.
Uptake of volatile anaesthetic gases is slow
FURTHER READING
Burrows F A. Anaesthetic Management of the Child with Congenital Heart Disease for
Non-cardiac Surgery. Can J Anaesth 1992; 39(5): R605
Cote, Ryan, Todres, Goudsouzian eds. A Practice of Anesthesia for Infants and
Children. 2nd ed. Philadelphia: W B Saunders, 1993.
Lake C ed. Pediatric Cardiac Anesthesia. 2nd ed. Stamford, CT: Appleton and Lange,
1993 .

Equipment for Paediatric
Anaesthesia
Christopher J Vallis
Christopher J Vallis is Consultant Anaesthetist at the Royal Victoria Infirmary,

Newcastle upon Tyne, UK. He works full time in paediatric anaesthesia and intensive
care, and is also involved in medical education.
There are physiological and anatomical differences between babies, children and
adults, therefore the anaesthetic equipment required for each needs to be different.
Differences are greatest for neonates (under 4 weeks old) and infants (under a year).
The laws of physics also determine that the behaviour of some equipment depends on
size. However, cultural differences between centres, which sometimes seem to have
little scientific basis, may dictate which anaesthetic equipment is used.
Environment
A child-friendly environment is important. However, when designing paediatric

anaesthetic or recovery areas, it should be remembered that 13-year-olds may be
insulted if they are put in an area better suited to 3-year-olds. Fashions change and
durable cartoon characters are more suitable than current fads that may soon be
outdated.
Temperature maintenance
Infants have a high surface area/body mass ratio and therefore lose heat rapidly,
mainly by radiation, though convection, conduction and evaporation also have a role.
Strategies to maintain temperature should take account of all these. In general, the
following factors should be considered:
warming the patients environment
warming and humidifying inhaled gases
limiting evaporative heat loss
warming topical and intravenous fluids.
Even within the hospital, neonates should travel in a heated incubator. Paediatric
theatres should be warm, but temperatures above 25C are uncomfortable for staff;
therefore, the microenvironment of the patient needs attention. For infants, a radiant
overhead heater should be used during induction and reversal of anaesthesia and
during application of skin preparation, when heat loss (through the latent heat of
vaporization) is high. Manufacturer's guidelines concerning patients' proximity to the
heater should be followed to avoid overheating or burns. Forced-air warming systems
blow filtered, warm air from a cover or mattress and can be used throughout the
operation. When draped, the patient lies in a microenvironment of warm air. Simple
techniques are also available; for example, partial wrapping in aluminium foil reduces
radiant heat loss, and wrapping in cotton wool padding reduces conductive and
convective losses.
Humidification of gases
Some active water-bath humidifiers incorporate a heating wire in the patient tubing.
This reduces rain-out condensation that occurs when gases cool below the dew
point. A temperature sensor at the patient end of the tubing prevents the gases
overheating beyond 35C. Use of sterile water and disposable components reduces
bacterial colonization.
The heat and moisture exchanger (HME), or condenser humidifier, is a passive
humidifier using a membrane that is hygroscopic (water absorbing) or hydrophobic
(water collects as surface droplets). The membrane warms during expiration, both from
the expired gases and the release of latent heat of evaporation. HMEs are efficient with
small tidal flows (with larger tidal volumes the membrane may saturate before expiration
ends). Efficiency over short periods is limited but improves with time after 1 hour the
humidity of the inspired gases may be 30 g/m3 (equivalent to 95% relative humidity in
the trachea at 32C). Modern HMEs are small, adding less dead space and less flow
resistance (even when saturated), and are suitable for paediatric use.
Viruses can be transmitted via the breathing system, mainly in liquid secretions.
Heat and moisture-exchanging filters act as barriers to all microorganisms and may
allow single-use systems to be re-used. However, their volume adds dead space and
they are not suitable for neonates.
Intravenous infusions
Cannulae
Cannulae are available in sizes as small as 26 G. Nicking the skin before insertion
reduces the chance of a fine cannula buckling. An extension set can be attached via
a three-way tap to facilitate drug administration. Using a narrow-bore extension (100
cm long, 0.8 ml volume) avoids having to give large volumes of flush each time a drug
is given. Giving fluids to babies by syringe (either manually or using a syringe driver)
allows small volumes to be given accurately and reduces the possible danger of the
fluid from a full burette inadvertently running into the patient.
Intravenous filters
Care should be taken to exclude bubbles from the system. In the case of a patient
with a known atrioventricular malformation or atrial septal defect, an air filter is
recommended because there is a risk of air emboli entering the left side of the
circulation. However, blood cannot be given through air filters.
Fluid warmers
Various types are available. Some use a special concentric double-tubing system. The
infusion in the central tube is kept warm by heated water circulating in the outer tube,
which also prevents gases coming out of solution and forming bubbles. However, the
tubing sets are expensive.
Guedel airway
a b c
A Guedel airway is unnecessary if the airway can be managed without it. Sizing guide: with the flange at the centre of the lips, the end should
be nearly at the angle of the jaw (c). An incorrectly sized airway will make matters worse (a and b). Sizing and colour-coding is not consistent
between manufacturers.
Adapted from: Advanced Life Support Group. Advanced Paediatric Life Support. 2nd ed. London: BMJ Publishing Group, 1997. BMJ Publishing Group, 1997.
Anaesthetic machines
An air flowmeter allows mixtures containing less than 100% oxygen to be given when
nitrous oxide is contraindicated. Availability of carbon dioxide is controversial, but
is some-times useful in preventing hypocarbia. Some flowmeters are limited to 0.5
litre/minute to prevent excessive carbon dioxide administration.
It is a good idea to have a pressure blow-off valve at the fresh gas port of the
anaesthetic machine, functioning at 56 kPa, to avoid inadvertently exposing the patient
to high pressures.
Equipment for managing the airway
Face masks
The Rendell-BakerSoucek mask, designed specifically for babies, is shaped to give
a low dead space, but can be difficult to use. Because most anaesthetists intubate
babies, a face mask is used principally during ventilation before intubation, so a good
seal is more important than low dead space. Round masks with moulded face seals,
often made of clear silicone rubber, are increasingly popular for this reason.
Laryngeal mask airways (LMAs)

The wide LMA tube has a low resistance to gas flow during spontaneous breathing
compared with a small tracheal tube, thus reducing the work of breathing. This is
indicated by a lower incidence of paradoxical respiratory movements. (The Hagen
Poiseuille equation states that the laminar flow is proportional to the fourth power of
the radius.)
A range of sizes is available, down to size 1, recommended by the manufacturers
for babies less than 6.5 kg (see Figure 1, Anaesthesia and Intensive Care Medicine
1:1: 33). However, LMAs are not used routinely in neonates because dead space is
excessive, obtaining a laryngeal seal is difficult, and most anaesthetists use intermittent
positive-pressure ventilation (IPPV) delivered through a tracheal tube. However, LMAs
have been used for neonatal emergencies and difficult airways such as the Pierre
Robin syndrome.
In small children, it has been suggested that the LMA is easier to insert with the
cuff partially inflated, or inserted sideways and then rotated 90. Positioning is not
always satisfactory, and gas leaks are common. Reinforced LMAs have made their use
practicable for adenotonsillectomy.
In view of the potential for distending the stomach with gas, LMAs are not
recommended for IPPV in small children.
Laryngoscope blades
Seward
Robertshaw
Magill
Intubation equipment
Straight-bladed laryngoscopes are usually preferred in younger patients. There are
several designs (Figure 1), which may be broadly divided into open designs (e.g.
the Robertshaw and Seward), and those with a semi-circular blade (e.g. the Magill).
Open blades are often easier to use, especially when using forceps to place nasal
tubes. Laryngoscopes are better balanced if a lightweight paediatric handle is used.
Fibre-optics give superior illumination. Green bands indicate International Standards
Organization compatibility with interchangeable blades and handles from different
manufacturers. The age of the child at which the straight blade is replaced with a
curved adult blade is a matter of personal preference, but is often around 5 years.
Infants have relatively large heads, therefore the traditional adult sniffing the
morning air position with the head on a pillow is inappropriate. An infants head should
be flat on the trolley or table. A rolled-up pillowcase under the nape of the neck helps
stabilize the head.
With straight open blades, intubation technique is a matter of choice. There are three
possible techniques:
the tip of the blade placed in the vallecula
the epiglottis lifted with the blade
the tip of the blade initially placed in the oesophagus, then withdrawn until the cords
appear.
Tracheal tubes
In infants and children the airway narrows beyond the cords, at the cricoid ring (Figure
2), and the tracheal mucosa may be damaged by excessive tube or cuff pressure,
resulting in temporary swelling or even permanent subglottic stenosis. With modern
materials and soft cuffs it is debatable whether cuffed tubes do much harm for short-
term use. However, absence of a cuff may allow a slightly larger tube size, improving
gas flow. It is still normal practice to use uncuffed tubes and there are no rigid rules
about the age at which to switch to cuffed tubes, though 810 years is reasonable.
Disposable tubes are often made of polyvinyl chloride (PVC), which is implantation
tested in rabbit paravertebral muscle or tested in cell culture. Tubes are marked IT
or Z-79 to indicate this. PVC softens at body temperature, conforming to the patients
airway. (Tubes soften when repeatedly handled. If practising intubations on manikin
heads, they are best kept in iced water). Thin-walled paediatric tubes kink easily.
Tube sizing: a correctly sized tube passes easily through the cords, giving a slight leak
at maximum, or just over maximum, inflationary pressure. The necessity for significant
leaks at normal ventilator pressures is less emphasized than previously. Suggested
tube sizes for infants are shown in Figure 3.
Infant airway anatomy showing narrowing at cricoid
Cricoid
Adult Infant
Tube sizes for infants
Age Weight (kg) Tube size (internal diameter, mm)

Small premature < 0.7 2.0
Premature 0.71.5 2.5
Small term 1.53.0 3.0
Term 3.04.0 3.5
6 months 7 4.0
1 year 10 4.5
For older children: tube size (mm) = age (years)/4 + 4.5. For emergencies, a tube
size of age/4 + 4 should be used (a small tube is usable, whereas one that is too big
is useless). It is also sensible to have ready a smaller and a larger tube than the one
planned.
A formula for the length of an oral tube in a child older than 12 months is: [12 (age
in years) + 12] cm. In some countries it is usual to leave a length protruding from the
mouth and different formulas are used. In emergencies it may better to leave a tube
uncut, because one cut too short is useless.
The ideal position for the tip of the tube is the mid-trachea. This can be obtained by
passing a 3.0 or 3.5 mm tracheal tube 3 cm, a 4.0 or 4.5 mm tube 4 cm, or a 5.0 or 5.5
mm tube 5 cm through the cords. However, the tube position should always be checked
by auscultation (and radiography for long-term ventilation).
Reinforced tubes can simply be folded over the lip and stuck down, making
adjustment of the intratracheal length simple (Figure 4). Some anaesthetists use them
routinely. An intubation stylet is needed for insertion. Overall tube diameter depends on
wall thickness, therefore reinforced tubes (with thick walls) may need to be half a size
smaller than predicted.
Reinforced tracheal tube
The use of a reinforced tube allows easy adjustment of length,

and the tube can be securely stuck down to the upper lip
Other tubes: double-lumen tubes do not exist in infant sizes and single lung
anaesthesia is achieved by endobronchial intubation. Cole pattern tubes have wider
bores, narrowing at a shoulder to a section that passes the cords. They may be easier
to use for neonatal emergency intubation but have associated problems. Airflow is
turbulent at the shoulder, increasing flow resistance. If the tube slips and the shoulder
presses on the glottis, there is a risk of damage.
Connectors: standard 15 mm connectors are bulky when used with small tracheal
tubes. For this reason, neater 8.5 mm systems were developed. However, the
small demand has led to limited commercial success and their future is uncertain.
Nevertheless, awareness of different connectors is important, particularly for
transportation between centres.
Breathing systems
Paediatric breathing systems should be lightweight with low dead space. For
spontaneously breathing patients, resistance to flow should be low (though the greatest
resistance will be at the narrow endotracheal tube). It is desirable to have a low
compressible volume of gas, particularly for ventilation at small tidal volumes, and stiff,
non-compliant tubing.
Breathing systems may be divided into absorber and non-absorber systems. Non-
absorbing systems have had greater use in paediatrics.
Mapleson classification: this is the usual classification of semi-closed systems .

There are no unidirectional valves to direct gas flow, and no absorbant, so the fresh gas
flow (FGF) must wash away the carbon dioxide.
The Mapleson A system is efficient for spontaneously breathing patients, and low
gas flows, equivalent to the alveolar ventilation, may be used (alveolar ventilation in
litre/minute 0.6 bodyweight in kg). However, the system is inefficient for ventilated
patients.
The Mapleson D and F systems are the most efficient for use with IPPV. The
Humphrey ADE system is a combination of three systems Lack (Mapleson
A), Mapleson D and Mapleson E, and has been used successfully in paediatric
anaesthesia.
The T-piece
Ayres original form was a Mapleson E system. It was later modified by Jackson Rees,
by including an open-ended reservoir bag and using a longer reservoir tube. In this form
it is a Mapleson F. The Jackson Rees modification is commonly used for patients under
about 20 kg, though with a high enough FGF and an expiratory limb greater than tidal
volume there is no upper weight limit. It has several advantages:
lightweight
low flow resistance
suitable for spontaneous or controlled ventilation
simple design with no valves.
It also has some disadvantages:
exhaust gases difficult to scavenge
obstruction of expiratory limb exposes patients to high pressures
high FGF required in larger patients.
Carbon dioxide elimination is affected by several factors:
FGF
tidal volume
rate of ventilation.
Classically it was taught that an FGF of two-and-a-half to three times the patients
minute ventilation should be used. The patients minute ventilation is not known, thus
the FGF is estimated from bodyweight (BW); for example: FGF = 3 x (1000 + 100
ml/kg) for an intubated patient who is breathing spontaneously. Alternative formulas are:
FGF = 2BW for spontaneous respiration; FGF = BW for controlled ventilation. It is
now usual to monitor end-tidal carbon dioxide and make adjustments accordingly.
Increasing FGF pushes expired alveolar gas further down the reservoir tube,
reducing rebreathing of exhaled gases during inspiration. Above a certain FGF there is
no rebreathing of alveolar gas. Increasing FGF beyond this point is wasteful. The use of
high gas flows in a T-piece results in a degree of positive end-expiratory pressure, as a
result of the pressure needed to expel gas through the expiratory limb.
At low FGFs it is largely the FGF that determines the degree of rebreathing and
hence the elimination of the patients carbon dioxide. If the patient is ventilated,
increasing the tidal volume may have little effect on carbon dioxide. This characteristic
allows generous tidal volumes to be given to the patient, reducing basal atelectasis,
without blowing off excessive carbon dioxide.
Increasing the rate of ventilation may not increase carbon dioxide exhaled gases to
be driven out of the reservoir tube.
A simple increase in rate may even lead to paradoxical carbon dioxide retention unless
the FGF is also increased.
Circle systems
Paediatric circle systems are not widely used in the UK because of concerns about flow
resistance, dead space and leaks around the uncuffed endotracheal tube. Disposable
circle systems are also expensive. However, many of these concerns are spurious.
Recognition of physiological differences has led most anaesthetists to use controlled
ventilation during anaesthetia in infants. The use of filters reduces infection risk and
small paediatric soda lime canisters and narrow-bore tubing reduce compressible
volume.
It is important to monitor gases within the circle, because there may be significant
differences between the composition of fresh gas compared with gas in the circle.
Ventilators
Paediatric ventilators can be classified under familiar headings (e.g. power source,
cycling mechanism, pressure or flow generator). Most mechanical ventilation in
small children is defined by the fraction of oxygen in inspired air (Fi O2), inspiratory
and expiratory times (or inspiratory/expiratory ratio and rate), and the pressures
(maximum, mean and end-expiratory). Ventilation is not usually defined by setting
tidal volume. Tidal volume is unknown with pressure-controlled ventilation, but will
be reasonably constant with unchanging compliance. In practice, ventilation is set up
according to sensible predicted values and then modified according to the monitoring
figures.
T-piece occluding ventilators

Ventilation requirements in the operating theatre are different from those in the ICU. In
the ICU, compliance changes are usually gradual, and the chest wall can be observed.
The lowest acceptable mean airway pressure is used to prevent barotrauma. ICU
ventilators are often time cycled, pressure limited, pressure pre-set and of the T-piece
occluder type (e.g. Sechrist). There is no separate driving gas. Gas flows continually
in the T-piece and the ventilators function by occluding the T-piece outflow, when
gas flows into the patient. The patient can always make spontaneous breaths, with
low resistance to flow. In effect, the patient is always given intermittent mandatory
ventilation. High fresh gas flows are often used in the ICU to maintain a rapid upsweep
in inspiratory pressure, allowing optimal recruitment of alveoli.
In the operating theatre, ventilators with a separate driving gas are favoured,
because simple T-piece occluders are not ideal. Compliance and tidal volume can fall if
one of the surgical team leans on the chest or splints the diaphragm. The endotracheal
tube may block or kink and this may cause tidal volume to fall without much change
in the ventilator pressure display.
Bag squeezer
Gas-driven, bag-squeezing, ventilators are easily connected to a T-piece or Bain
system, replacing the anaesthetists hand squeezing the bag. Some are pure flow
generators and produce a constant tidal volume (provided the safety blow-off pressure
is not exceeded).
The PenlonNuffield anaesthesia ventilator is used in many centres in the UK and
Australasia, and in some centres in the USA. It is a gas-driven flow generator. It is fitted
with a Newton valve for use in infants, which introduces a fixed leak and has a pressure
relief valve set at 40 cm H2O. With the Newton valve the Nuffield ventilator works
predominantly as a flow generator at low pressures and as a pressure generator at
higher pressures. A drawback is the slow inspiratory pressure rise, because with short
inspiratory times this gives sub-optimal alveolar recruitment.
A bag squeezer can provide stable ventilation that is unaffected by small changes
in compliance. As discussed earlier (see page 58), at low fresh gas flows it is the FGF
that governs the elimination of carbon dioxide in the T-piece or Bain system, not small
changes in patient tidal volume. In contrast, using high gas flows with no rebreathing,
where carbon dioxide elimination is determined by adjusting minute ventilation, may
produce unstable ventilation that needs frequent fine-tuning in theatre.
Other ventilators
Complex intensive care ventilators with a variety of volume or pressure modes may be
used for theatre ventilation. However, these ventilators, though flexible, are not always
ideal because the alarms are easily triggered.
Adult circles, with bag-in-bottle ventilators using volume control, are not
recommended for infants because accurate control of tidal volume is impossible as
a result of the large compressible volume of gas in the system. Smaller bellows and
tubing are used to reduce compressible volume in paediatric circles.
Disconnection alarms
Some T-piece occluders require a separate alarm that detects pressure cycling. The
alarm limits are adjusted by the user; if set incorrectly, system leaks may not be sensed.
It is also possible that a high flow rate through a small tracheal tube will generate
sufficient pressure for an accidental extubation to go undetected.
Hand ventilation
Once practised, hand ventilation is easy and reliable with the T-piece.
Advantages
Pressure on the chest or diaphragm is felt immediately.
The educated thumb can detect disconnection, or occlusion of the tube (assuming
the system is non-compliant).
The anaesthetist stays near the patient.
There is useful back-up in case of ventilator problems.
Disadvantages
The anaesthetist will need assistance for some manoeuvres (e.g. giving drugs or
changing fluid bags).
The technique is suitable for the T-piece only. Hand ventilation is possible with other
circuits, but the higher compressible volumes mean that problems are detected less
reliably.
Resuscitation equipment
Pocket resuscitation masks

Pocket resuscitation masks are of one adult size only, but may be used upside down in
infants by forcibly folding the nose end over the chin.
Self-inflating bags
Three sizes are available: neonatal (240 ml), child (500 ml) and adult (1600 ml). With
care, the child size may be used on neonates. It is essential to have one available
during transportation, when exhaustion of the oxygen cylinder would render a T-piece
unusable. A reservoir limb or bag should be attached to deliver a high inspired oxygen
concentration.
Defibrillators
Defibrillators are seldom needed in paediatrics. If the patient is less than 10 kg,
paediatric (4.5 cm) paddles are used, often revealed by sliding off the adult paddles.
Separate paediatric paddles clipped over adult ones are easily lost.
FURTHER READING
Booker P D. Equipment and Monitoring in Paediatric Anaesthesia. Br J Anaesth 1999;
83: 7890.
Dorsch J E, Dorsch S E. Understanding Anaesthesia Equipment. Baltimore: Williams
& Wilkins, 1994.
Hatch D J, Hunter J M. Editorial. The Paediatric Patient. Br J Anaesth 1999; 83: 12.
Hughes D G, Mather S J, Wolf A R. Handbook of Neonatal Anaesthesia. Philadelphia:
Saunders, 1996.

Fluid and Electrolyte Balance
for Children
Grant Rodney
Grant Rodney is Consultant Anaesthetist and Honorary Senior Lecturer at Ninewells

Hospital, Dundee, UK. He qualified from the University of Cape Town, South Africa, and
trained in anaesthesia in Cardiff, with a year of paediatric anaesthesia in Vancouver.
His interests are in paediatric anaesthesia and resuscitation.
Applied physiology
Renal function matures rapidly from 34 weeks gestation. At birth, term babies have
a glomerular filtration rate one-third that of the adult, rising to mature values by 1218
months of age. Infant tubular function is poorly developed at birth and matures over
the first months of life. Function can be regulated only under physiological conditions.
Neonates in the first week of life are unable to tolerate large acute water or salt loads.
Equally, faced with fluid restriction, neonates are able to concentrate to only half of the
adult capacity. Preterm neonates have a much slower increase in glomerular and tubular
function after birth. Greatly reduced renal function persists until at least 18 months
postconceptional age, reaching mature values only by 8 years of age.
Glucose homeostasis: neonates have reduced hepatic glycogen stores and are at
risk of developing hypoglycaemia. They usually require fluids containing 10% glucose.
Critically ill neonates may require greater concentrations of glucose. However, the
stress response to surgery or illness may cause hyperglycaemia. With reduced
glomerular filtration, the ensuing glycosuria may cause an osmotic diuresis. Neonates
should be closely monitored for both hypo- and hyperglycaemia.
Body water: total body water of a term neonate is 80% of body weight or 800 ml/kg.
This value falls to 60% (600 ml/kg) by 1 year of age. The intracellular fluid (ICF) volume
is constant, at about 40% of body weight. The extracellular fluid (ECF) comprises the
plasma volume within the circulation and the interstitial fluid volume. In relative terms,
the ECF volume falls to 20% by 1 or 2 years of age (Figure 1). Most of the decrease
in ECF results from a decrease in interstitial fluid. Plasma volume within the circulation
is one-third to one-quarter of the total ECF volume, the remainder consisting of the
interstitial fluid volume. Blood volume is 90100 ml/kg at birth, falling to 80 ml/kg at
1 year of age and to 70 ml/kg by adulthood.
Fluid compartments as percentage of body weight
Total body Extracellular Intracellular

water (%) fluid (%) fluid (%)
Neonate 80 40 40
Child (2 years) 60 20 40
1
Acute loss of circulating fluid as in blood loss (trauma, surgery) or plasma loss
(burns) can be replaced with rapid infusion of relatively small volumes of fluid (i.e.
20 ml/kg boluses). Dehydration is usually of slower onset with loss of fluid from all
fluid compartments. The vascular compartment is maintained unless fluid loss is
rapid (overwhelming diarrhoea in small children) or has exceeded compensatory
mechanisms. Evidence of dehydration is not clinically apparent until the overall loss is
greater than 5% of body weight (50 ml/kg).
Normal fluid and electrolyte requirements

Normal daily fluid intake is variable. Urine output is adjusted to account for diminished
or excessive fluid intake. Maintenance fluids are required to compensate for water
losses from skin, respiratory tract and stools, water for essential urine output and
growth, and to maintain a reasonable diuresis. Water requirements can be calculated
by one of three methods.
Body surface area (BSA) this requires measurement of weight and height and the
use of nomograms. Measuring height in neonates and infants is difficult and in children
under 3 kg BSA errors of 20% occur.
Calorie requirements metabolism of 1 calorie requires 1 ml of water, therefore

knowledge of a childs calorie requirement can be used to determine fluid requirement.
Body weight is the simplest method of calculating fluid and electrolyte requirements
(Figure 2). Continuing measurement of body weight also gives a reliable indication of
changing volume status.
The examples in Figure 3 show that maintenance fluid volumes are easily calculated.
However, calculated requirements are an initial estimate and, when based on body
weight, do not take account of variations in lean body mass, metabolic rate and variable
growth rates.
Normal fluid and electrolyte requirements
Body weight Daily requirement Hourly requirement Sodium1 Potassium1

(ml/kg) (ml/kg) (mmol/kg/day) (mmol/kg/day)
First 10 kg 100 4 24 1.52.5
Second 10 kg 50 2 12 0.51.5
Subsequent 10 kg 25 1 0.51 0.20.7
1
Printed with permission of Advanced Life Support Group.
Calculating daily maintenance fluid and electrolyte requirements
5 kg infant
Water100 ml/kg for the first 10 kg of body weight = 500 ml
Sodium 24 mmol/kg for the first 10 kg of body weight = 1020 mmol
Potassium1.52.5 mmol/kg for the first 10 kg of body weight = 7.512.5 mmol
The fluid that best meets this requirement is 500 ml of 0.18% saline in glucose,
which would supply 15 mmol sodium (0.18% saline contains 30 mmol/litre of
sodium). Potassium requirement could be met by addition of 10 mmol KCl to each
500 ml bag of fluid, assuming adequate urine output and need for continuing
parenteral fluid
16 kg child
Water100 ml/kg for the first 10 kg of body weight
+ 50 ml/kg for the second 10 kg of body weight
= 1000 ml + 300 ml = 1300 ml
Sodium24 mmol/kg for the first 10 kg body weight

+ 12 mmol/kg for the second 10 kg body weight
= (2040) + (612) mmol = 2652 mmol
Potassium1.52.5 mmol/kg for the first 10 kg of body weight

+ 0.51.5 mmol/kg for the second 10 kg body weight
= (1525) + (39) = 1834 mmol
1300 ml of 0.18% saline would supply 39 mmol of sodium/day

Adding 20 mmol/litre of KCl would supply 26 mmol of potassium
Dehydration
Dehydration reflects whole body fluid loss in excess of fluid intake and compensatory
mechanisms. Severity of dehydration is classified as mild (5% of body weight or less),
moderate (510%), or severe (10% or greater) (Figure 4).
Clinical signs of dehydration
Signs/symptoms Mild Moderate Severe

< 5% 510% > 10%
Decreased urine output + + +
(beware watery diarrhoea)
Dry mouth +/ + +
(mouth breathers are dry)
Decreased skin turgor +/ +

(use several sites)
Sunken anterior fontanelle + +

(crying increases pressure)
Sunken eyes + +
Decreased eyeball turgor +/ +

(difficult in young)
Tachypnoea +/ +
(acidosis and pyrexia
worsen this)
Tachycardia +/ +
(hypovolaemia plus pyrexia
and irritability cause this)
Drowsiness, irritability +/ +
Printed with permission of Advanced Life Support Group.
Mild dehydration is associated with up to 50 ml/kg fluid deficit and can usually be
managed with oral rehydration.
Moderate to severe dehydration always requires intravenous fluid replacement. It

is important that an initial assessment of circulatory status is performed. Most of the
childs body weight consists of water, therefore 10% dehydration equates to a 10%
reduction in body weight caused by fluid loss. This value in grams is equivalent to
millilitres of fluid deficit (Figure 5). Large volume and/or particularly rapid fluid loss
may precipitate shock. When dehydration exceeds 10%, shock is invariably present.
The child with sunken eyes, dry mouth, tachypnoea, tachycardia, cool peripheries,
prolonged capillary refill and drowsiness or irritability requires rapid intravascular
volume replacement. Treatment of shock involves administration of high flow oxygen,
attention to airway and breathing, and administ-ration of a fluid bolus (20 ml/kg).
Crystalloids, either 0.9% saline or Ringers lactate are given initially. These fluids are
isotonic and restore the ECF volume. Once the circulatory status has improved (based
on continuing assessment and repeat fluid bolus if necessary) further fluid therapy is
initiated to correct the associated dehydration. This requires calculation of fluid deficit
and maintenance fluid requirements (Figure 6). Blood samples are taken to calculate
electrolyte values to guide fluid therapy, particularly speed of rehydration.
Estimating fluid deficit in a dehydrated child
A 10 kg child with diarrhoea is estimated from clinical assessment

to have 10% dehydration
The fluid deficit is therefore 10% of 10 kg = 1 kg = 1000 g

1000 g = 1000 ml of fluid deficit (100 ml/kg)
This can be more easily calculated as % dehydration body

weight (kg) 10 ml
Types of dehydration
The three types of dehydration are isotonic, hyponatraemic and hypernatraemic. All
are associated with water and sodium loss but the speed of replacement depends on
serum sodium values.
Calculating fluid requirements in dehydration
Fluid requirements for a 4 kg baby with pyloric stenosis and an estimated

10% dehydration
Maintenance fluid requirement (see Figures 2 and 3)

100 ml/kg/day = 400 ml/day
Ideally given as 0.18% saline in glucose
Deficit fluid requirement (see Figure 5)

4 (wt in kg) 10 (% dehydration) 10 = 400 ml/day
This should be given as 0.9% saline, reflecting the predominant loss of

extracellular fluid volume in dehydration (gastric fluid is isotonic and has
large quantities of sodium, chloride and hydrogen ions)
Combined fluid requirement = 800 ml
The deficit can be replaced over 24 hours, assuming the child is not
hypernatraemic. Continuing fluid type and volume needs adjustment based
on clinical assessment of hydration status and electrolyte values
6
Isotonic or hyponatraemic dehydration: the baby with pyloric stenosis (Figure 6)

could be given maintenance fluid using 400 ml of 0.18% saline (which gives 12 mmol
sodium ions/30 mmol/litre) while replacing the fluid deficit caused by de-hydration with
400 ml 0.9% saline (150 mmol/litre), to give an additional 60 mmol of sodium ions. A
total of 72 mmol sodium ions would then be infused over 24 hours. However, it is more
practical to infuse a single type of fluid to provide both maintenance and deficit volumes
and sodium requirements. By calculating the sodium ion concentrations, it can be
seen that a solution of 0.45% saline (75 mmol/litre) matches best. For example, giving
800 ml of 0.45% saline in 5% glucose would deliver 60 mmol sodium ions and provide
adequate sodium requirement for fluid maintenance and deficit requirements. This
solution is isotonic and prevents hypoglycaemia.
For more complex situations (e.g. children with severe cardiac or renal dysfunction,
particularly the critically ill) it may be appropriate to provide separate infusions for
maintenance requirement, fluid deficit and continuing losses. In these situations,
frequent measurements of serum and urinary electrolytes and clinical assessments of
hydration are required.
Hypernatraemic dehydration: if the serum sodium concentration is above 145 mmol/

litre, rapid infusion of fluid causes the serum sodium concentration to fall. Water then
moves into cells to maintain osmotic equilibrium and there is a risk of cerebral oedema
and death. The serum sodium concentration should be lowered by no more that 5
mmol/day to avoid this and the values measured every 4 hours. The aim is to correct
dehydration over 48 hours.
Colloids or crystalloids?
The relative merits of colloids and crystalloids for volume replacement during surgery
and intensive care are still debated.
Isotonic crystalloids (e.g. normal saline, Ringers lactate) are used to restore the
intravascular volume but are distributed evenly within the ECF volume. As plasma makes
up only one-third to one-quarter of the ECF volume, only one-third of the infused fluid
remains in the intravascular space, the remainder lying in the interstitial fluid space.
Therefore, if crystalloid is used to replace blood loss, then three times the volume of
blood lost is required as crystalloid therapy. There is concern that excessive crystalloid
fluid administration may result in overhydration of the interstitial space with resultant
oedema formation. On the other hand, faced with plasma volume depletion, fluid shifts
from the interstitial space into the circulating volume so that in hypovolaemic states
there is generalized depletion of ECF volume. The whole of the ECF volume requires
resuscitation and therefore crystalloids are most appropriate.
Crystalloids are readily available, cheap and generally free of adverse reactions. They
are widely used as first choice therapy in the USA. In other countries, colloids are
preferred to treat hypovolaemia, particularly in neonates who have large body water
volumes, susceptibility to oedema and inability to deal with water and solute loads.
Human albumin solution is most widely used because there is concern about the
effects of synthetic colloids such as gelatin and hydroxyethyl starch (accumulation in the
reticuloendothelial system) on the newborn and young children. A recent review of 30
published studies suggested a higher mortality in patients receiving albumin. However,
there is criticism of some of the studies included and no published comparisons of
crystalloids with colloids in children. Albumin is still preferred for intravascular volume
replacement in critically ill children, especially neonates. For older children, the choice
of initial fluid is less important than recognizing circulatory compromise and treating it
promptly.
Perioperative fluid requirements

The volume and type of fluid required perioperatively depends on:
the duration of preoperative fasting
additional preoperative deficits from abnormal loss of fluid and electrolytes (e.g.
diarrhoea, vomiting, ileus, burns, blood loss)
intraoperative losses include evaporation from the wound (e.g. during laparotomy)
or airway (if anaesthetic gases are not humidified), blood loss, and third-space loss
associated with surgical manipulation and tissue trauma
retention of water and sodium postoperatively, due to the stress response to surgery.
The stress response to major surgery includes release of aldosterone and antidiuretic
hormone with retention of salt and water. It is important to limit the use of non-
crystalloid solutions (e.g. 5% glucose) because of a tendency to cause haemodilution
and hyponatraemia. This is particularly relevant because third-space fluid losses, blood
loss and the circulatory effects of anaesthesia (including reduced cardiac output and
vasodilatation) mandate crystalloid fluid therapy.
Intraoperative fluids are given based on maintenance fluid requirements and

replacement of pre-existing deficits (e.g. because of fasting) and additional losses
during surgery (e.g. bleeding or extravasation of fluids in major surgery). For simple
surgical procedures, the fluid deficit can be replaced by resuming oral fluid intake
postoperatively. For more major surgery, starvation fluid deficit can be calculated by
multiplying hourly maintenance fluid requirement by the duration of fast in hours. Half
the deficit is replaced in the first hour and a further quarter in the subsequent 2 hours
given in addition to the hourly maintenance fluid.
Perioperative administration of glucose: neonates have inadequate glycogen

stores and a tendency to hypoglycaemia. They require infusion of 10% glucose at
maintenance rates. Additional crystalloid and colloid may be needed depending on
the type of surgery. Sick neonates may require higher concentrations of glucose. If
fluid restriction is required, glucose may have to be given centrally in 20% or 50%
concentrations. Sometimes, the stress response causes hyperglycaemia. It is important
to monitor blood sugar concentrations closely to avoid hypo- or hyperglycaemia.
Older children, unless fasted for prolonged periods, or critically ill, are able to maintain
adequate blood sugar levels by metabolism of glycogen stores. Crystalloids are
indicated for perioperative fluid infusion. Infusion of crystalloid with low concentrations
of glucose (2%) avoids hypo- and hyperglycaemia in children receiving variable fluid
infusion rates. Such fluids are not available commercially and must be prepared, as
required, by adding 20 ml of 50% glucose to 500 ml of 0.9% saline.
Practical fluid administration in the operating room

Neonates should receive 10% glucose at maintenance rates and additional crystalloid,
colloid or blood, as necessary. The blood glucose should be monitored carefully.
Children having day case or body surface surgery do not require intravenous fluids
because of liberal fluid fasting policies (2 hours preoperatively for clear fluids), minimal
fluid loss and the ability to take oral fluids rapidly after surgery.
Children having prolonged surgery (over 1 hour duration) or those having major
surgery (especially within a body cavity or associated with blood loss exceeding 10%
of the circulating volume) require intravenous fluids perioperatively. Other factors to
consider include the age of the child and the likelihood of rapid return to oral intake. If
large intraoperative fluid losses are not anticipated, then 0.18%/0.45% saline in glucose
can be infused at maintenance rates. If larger losses or fluid shifts are predicted,
Ringers lactate (with or without additional glucose) may be administered. Hourly fluids
infused at up to 23 times maintenance rates may be required. It is important that the
cardiovascular variables (e.g. peripheral perfusion and capillary refill time, heart rate
and blood pressure) are continually reviewed in the light of fluid administration. Invasive
monitoring of arterial and central venous pressures may be indicated if large fluid shifts
are predicted.
Hypervolaemia
Hypervolaemia is usually secondary to cardiac or renal failure. Occasionally, it results
from deliberate excessive ingestion of water. The signs of hypervolaemia are those
of heart failure, which is treated by fluid restriction and diuretics. Patients with water
intoxication present with confusion, convulsions and coma from cerebral oedema and
hyponatraemia. The treatment is to restrict fluids and manage the symptoms.
Specific electrolyte abnormalities
Sodium abnormalities are linked with dehydration or over-hydration, and are

considered above.
Potassium the usual daily requirements are listed in Figure 2. The upper limit of
normal is 5.8 mmol/litre for neonates and 5.0 mmol/litre for infants and children. High
values are found at birth and are tolerated without ECG changes. The clinical features
(especially the ECG abnormalities) and causes of hypo- and hyperkalaemia are given
in Figure 7. Treatment for hyperkalaemia is described in Figure 8.
Features and management of hypo- and hyperkalaemia in children
Hypokalaemia Hyperkalaemia
Clinical features
Muscle weakness Tingling
Hypotonicity Paraesthesia
Ileus Muscle weakness
Ventricular and atrial Flaccid paralysis
tachycardias
ECG changes
Prolonged PR interval Peaked T waves
T wave inversion Prolonged PR interval
Prominent U waves Widened QRS complex
Deep S wave and eventually asystole
(arrhythmias rare < 7.5 mmol/litre)
Causes
Inadequate intake Excessive intake
Abnormal losses Endogenous release
Gastrointestinal (e.g. diarrhoea) Burns
Renal (e.g. hyperaldosteronism, Rhabdomyolysis
diuretic therapy, volume Haemolysis
depletion) Decreased renal excretion
Compartmental shift Renal failure
Alkalosis Drugs (e.g. potassium-sparing
Insulin therapy diuretics, ACE inhibitors)
2-agonists Compartmental shift
Acidosis
Insulin deficiency
Succinylcholine administration
Treatment
KCl, oral or i.v. slowly (centrally See Figure 8
if concentration > 40 mmol/litre)
Guidelines for potassium administration

Total daily maintenance dose = 2 mmol/kg (0.08 mmol/kg/hour)
K to be replaced = weight x (CD CM) x 0.3 = mmol required

where CD = serum concentration desired; CM = serum concentration measured
Max concentration for i.v. administration = 20 mmol/500 ml fluid
KCl, 2 mmol/ml, is diluted in 5% dextrose or 0.9% saline
Maximum infusion rate = 0.5 mmol/kg/hour
Higher infusion rates (up to 2 mmol/kg/hour) used in cardiac ICU
Electrolyte status and ECG should be monitored
Oral K supplements can be given as effervescent or slow release tablets 12 mmol/

kg/day in up to 3 divided doses given with or after food
7

Yes
Arrhythmia Calcium, 0.1 mmol/kg i.v.
No
Consider specific
arrythmia protocol
Nebulised salbutamol,
2.510 mg
Falling
Calcium
Repeat serum resonium, Plan dialysis
potassium 1 g/kg p.o. if necessary
or p.r.
After Remains
bicarbonate high
Assess pH
pH < 7.34 pH > 7.35
Sodium bicarbonate Dextrose 0.5 g/kg/hour

2.5 mmol/kg i.v. Insulin 0.05 units/kg/hour
< 2.5 years 2.5 mg

2.57.5 years 5 mg
> 7.5 years 10 mg
Printed with permission of the Advanced Life Support Group

8
Calcium abnormalities, particularly hypocalcaemia, are associated with acute

illness including septicaemia or renal failure. Hypocalcaemia can produce muscle
weakness, tetany, hypotension and arrhythmias, or convulsions. Treatment is of the
underlying condition but intravenous calcium may be required. It is best administered
as a continuous infusion via a central line using calcium gluconate 10% (0.225 mmol
calcium/litre). The total daily dose is 1 mmol/kg given as 0.2 ml/kg/hour of 10%
solution. However, calcium gluconate should be diluted in 5% dextrose or 0.9% saline
to at least a 2% (20 mg/ml) solution. Doses for neonates are halved. Hazards include
precipitation, if given with sodium bicarbonate, tissue necrosis, if the drug extravasates,
and the possibility of cardiac arrhythmias, if given with cardiac glycoside drugs.
Hypercalcaemia is treated with volume expansion using 0.9% saline. u
FURTHER READING
Advanced Life Support Group. Advanced Paediatric Life Support, The Practical
Approach. 3rd ed. London: BMJ Books, 2001.
Hatch D J, Sumner E. Paediatric Anaesthesia. London: Arnold, 1999.
Gregory G. Paediatric Anaesthesia. London: Churchill Livingstone,1989.

Cardiorespiratory Arrest
Pauline M Cullen
Pauline M Cullen is Consultant in Paediatric Anaesthesia and Intensive Care at the

Royal Hospital for Sick Children, Glasgow, UK. She qualified from National University
of Ireland, Dublin, and trained in anaesthesia in Glasgow, Bristol and Melbourne,
Australia. Her special interests include paediatric intensive care and paediatric
resuscitation.
Cardiorespiratory arrests in children are uncommon and their aetiology differs from
those in adults. Progressive respiratory insufficiency accounts for 60% of all paediatric
arrests. This may result from upper or lower airway disease (e.g. croup, bronchiolitis,
pneumonia, asthma, foreign body aspiration) or respiratory depression caused, for
example, by prolonged convulsions, raised intracranial pressure, neuromuscular
disease or drug overdose. Other important causes include sepsis, dehydration and
hypovolaemia.
Primary cardiac arrest in children is rare and ventricular fibrillation has been reported
in less than 10% of cases. Many children have a relatively long pre-arrest phase
(i.e. cardiac arrest following prolonged physiological deterioration). Impending
cardiopulmonary arrest may be averted by early recognition of the childs distress and
prompt intervention. Once cardiac arrest occurs, the outcome is dismal with survival
rates of 317%. Often the child is resuscitated only to die of multi-organ failure in the
ICU or to survive with significant neurological impairment.
Guidelines for paediatric life support are published by several national organizations.
The most recent recommendations are those of the International Liaison Committee on
Resuscitation (ILCOR) in 1997 and the European Resuscitation Council in 1998. The
cardiopulmonary resuscitation (CPR) algorithms described in this article are based on
these guidelines. The CPR sequence and general resuscitative principles are similar for
infants and children. An artificial line is generally drawn between infants (< 1 year) and
children (18 years). Older children and teenagers should be resuscitated using adult
algorithms and techniques.
Basic life support

Basic life support (Figure 1) refers to maintenance of the airway and support of
respiration and circulation without the use of equipment.

Head tilt, chin lift
or jaw thrust

OK

Look, listen, feel
None

2 effective breaths reposition airway
reattempt
up to 5 times

treat as for
airway obstruction

OK
10 seconds maximum
None

5 compressions:
1 ventilation
100 compressions/minute
Initial approach and assessment of responsiveness

Before starting resuscitation it is important to evaluate the site for any danger or
physical hazards. Only in extreme situations should the child be moved. The first step in
any resuscitation is to assess the level of responsiveness. If the child does not respond
to voice or gentle shaking, a rapid cardiopulmonary assessment should be performed
(Figure 2). Assessment should take no longer than 10 seconds. Infants should not be
shaken vigorously. If trauma is suspected, the cervical spine should be immobilized.
Resuscitation should start immediately and help should be summoned.
Rapid cardiopulmonary assessment
A Airway
Patency
B Breathing
Respiratory rate
Work of breathing
Stridor
Wheeze
Air entry
Skin colour
C Circulation
Heart rate
Pulse volume
Capillary refill
Skin temperature
Mental status
D Disability
Conscious level
Posture
Pupils
2
Airway
The tongue is the most common cause of airway obstruction in children. Simple
head tilt, chin lift or jaw thrust manoeuvres may relieve the obstruction. Infants are
primarily nose breathers; this is an inbuilt mechanism to overcome obstruction
caused by a relatively large tongue. Only the jaw thrust procedure is recommended in
suspected spinal injury. If a foreign body is obstructing the airway it should be removed
carefully under direct vision. The blind finger sweep technique used in adults is not
recommended because it may cause trauma and bleeding or displace the foreign body
further into the trachea.
Breathing
The adequacy of breathing should be assessed by looking for chest movement,
listening over the airway for breath sounds and feeling for exhaled air over the mouth
and nose. If the child is not breathing despite an adequate airway, expired air ventilation
should be started. The mouth of the rescuer should cover the nose and mouth of
the infant. In the child, mouth-to-mouth expired air ventilation is recommended. A
minimum of two, but up to five breaths, may be required for effective ventilation in
the hypoxic child. The breaths should be delivered slowly, over 11.5 seconds, with
a force sufficient to make the chest rise. By giving the breaths slowly, an adequate
volume is delivered at the lowest possible pressure thereby avoiding gastric distension
and possible regurgitation of gastric contents. If chest movement does not occur or is
inadequate, the airway position should be readjusted and the possibility of a foreign
body considered.
Circulation
Check the presence, rate and volume of the pulse. In infants, the brachial or femoral
pulse is easiest to feel. In older children, the carotid should be palpated. It may be
difficult to locate a pulse in a collapsed child owing to the intense vasoconstriction. If no
detectable pulse is felt within 10 seconds or the rate is less than 60 beats/minute in an
infant, chest compressions should be started.
The chest is compressed over the lower half of the sternum and the technique differs
slightly between age groups.
In infants, the chest is compressed using two fingers placed one fingers breath
below an imaginary line joining the nipples.
In the child, the heel of the hand is used and positioned one fingers breath up from
the xiphisternum.
In the child over 8 years, the two-handed compression technique is recommended.
The chest should be compressed to one-third its resting diameter at a rate of 100/
minute. One breath should be given after each five compressions.
Airway obstruction from a foreign body

If upper airway obstruction due to foreign body aspiration is witnessed or strongly
suspected, special measures to clear the airway must be undertaken (Figure 3). If
the child is breathing spontaneously, their own efforts to clear the obstruction should
be encouraged. Intervention is necessary only if these attempts are ineffective and
respiration is inadequate. The manoeuvres suggested for removing impacted foreign
bodies are:
back blows
chest thrusts
abdominal thrusts.
The choking infant or child
Infant Child
Blind finger sweep is contraindicated 5 back blows
5 back blows 5 chest thrusts
5 chest thrusts Check airway
Check airway 5 back blows
Repeat if 5 abdominal thrusts

necessary
Check airway
Repeat if
necessary
3
A combination of back blows and chest thrusts are recommended for infants.
Abdominal thrusts are not recommended because damage to the abdominal contents
may occur. In children, back blows with alternate cycles of chest thrusts and abdominal
thrusts are preferred. After each cycle, the mouth should be checked for the presence
of a foreign body and ventilation attempted.

As soon as skilled help and equipment arrive, advanced life support should be started
(Figures 4 and 5). The aim of advanced life support is to restore spontaneous cardiac
activity. Asystole is presumed to be the primary arrhythmia because ventricular
fibrillation has been documented in less than 10% of paediatric cardiac arrests.
Monitoring equipment (including a pulse oximeter, ECG and end-tidal carbon dioxide
analyser) should be attached as soon as possible. The priorities are to secure the
airway and provide adequate oxygenation and ventilation followed by vascular access
and drug administration.

Ventilate/oxygenate
Attach defibrillator/monitor
Assess rhythm
check pulse
Ventricular fibrillation/ Non ventricular

ventricular tachycardia fibrillation/non ventricular
tachycardia
Asystole; pulseless
electrical activity
Defibrillate Adrenaline (epinephrine)

as necessary
CPR 1 minute CPR 3 minutes

Tracheal intubation Hypoxia
Intraosseous/vascular access Hypovolaemia
Hyper/hypokalaemia
Electrode/paddle positions Hypothermia
and contact Tension pneumothorax
Tamponade
Adrenaline (epinephrine) every Toxic/therapeutic
3 minutes disturbances
Thromboemboli

Consider giving bicarbonate
4
Perform basic life support algorithm

Ventilate the lungs with 100% oxygen
Establish a secure airway by intubating the trachea
Establish reliable vascular access
Administer adrenaline (epinephrine) every 35 minutes
If resuscitation attempts exceed 15 minutes, consider giving sodium
bicarbonate
Correct reversible causes
5
Airway and ventilation

A secure airway and effective ventilation are vital in advanced life support. Respiratory
failure is the primary cause of paediatric cardiac arrest, therefore the highest available
oxygen concentration should be given immediately by bag, valve mask ventilation. An
oropharyngeal airway may be used to aid airway management in the short term.
Tracheal intubation is the most effective method of securing the paediatric airway
during CPR. It allows optimum ventilation, protects the airways from aspiration of
gastric contents, and provides a route for drug administration. Intubation should be
achieved rapidly. Any attempt lasting longer than 30 seconds should be abandoned
and the childs lungs reoxygenated before further attempts are made. The position of
the tracheal tube should be checked and the tube secured to prevent dislodgement or
displacement. The place of the laryngeal mask airway in paediatric resuscitation has
yet to be established.
Circulation
Rapid vascular access is critical in paediatric resuscitation for drug and fluid
administration. In small children this may be difficult owing to the extreme
vasoconstriction. The intravenous or intraosseous routes are preferred for drug delivery.
Intravenous access: the choice of venous access is determined by the skill of the
resuscitator and the relative risks of the procedure. In practice, the largest, most
accessible vein that does not require the interruption of CPR is used. Attempts at
peripheral venous cannulation should be limited to 90 seconds. Useful central venous
routes during resuscitation include the femoral and external jugular veins. The internal
jugular and subclavian routes require interruption of external cardiac compressions and
are prone to serious complications in young children. Drugs administered centrally act
more rapidly than those administered peripherally.
Alternative routes of drug and fluid administration: when rapid venous access
is impossible an intraosseous cannula should be inserted. This is relatively easy to
perform, safe and usually rapidly achieved. Drugs and fluids can be administered by
this route and gain rapid access to the central circulation.
The trachea is often intubated early in the resuscitation and is a useful alternative
route for drug administration. It is best used when there has been, or is likely to be,
a significant delay in establishing venous access. Lipid-soluble drugs, adrenaline
(epinephrine), atropine, lidocaine (lignocaine), naloxone and diazepam are suitable
for this route. Animal studies suggest that peak plasma concentrations of drugs are
significantly lower than those achieved by intravenous administration, hence a tenfold
increase in the adrenaline (epinephrine) dose is recommended for the tracheal route.
Depot storage of adrenaline (epinephrine) in the lungs may cause prolonged post-arrest
hypertension.
Drug and fluid therapy

Adrenaline (epinephrine) is the most useful drug during paediatric CPR. The -
adrenergic action increases systemic vascular resistance, elevates aortic diastolic
pressure and thereby improves coronary perfusion. The recommended initial dose
is 0.01 mg/kg, intravenously or intraosseously, or 0.1 mg/kg by the tracheal route.
Because the outcome of asystolic arrest in children is poor and a beneficial effect of
higher dose adrenaline (epinephrine) has been demonstrated in some studies, second
and all subsequent doses should be 0.1 mg/kg regardless of route of administration. As
the action of adrenaline (epinephrine) is short lived, it should be repeated every 35
minutes during resuscitation. If there is no return of spontaneous cardiac activity after
two doses, despite adequate CPR, the outlook is likely to be dismal.
Sodium bicarbonate: after the initial treatment of cardiac arrest (ventilation, chest
compression, adrenaline (epinephrine)), severe acidosis is treated with sodium
bicarbonate. Its use remains controversial because it has not been shown to improve
survival. Nevertheless, during prolonged resuscitation (i.e. over 15 minutes), sodium
bicarbonate, 1 meq/kg, may be administered intravenously or intraosseously.
Other drugs: neither calcium chloride nor atropine is recommended in the treatment of
asystole or pulseless electrical activity.
Fluids: expansion of the circulating blood volume is vital in children who are
hypovolaemic secondary to fluid loss or fluid maldistribution. The intravascular fluid
of choice is isotonic crystalloid. An initial bolus of 20 ml/kg is given and repeated until
there is an improvement in circulatory status.
Treatment algorithms
Non-ventricular fibrillation/non-ventricular tachycardia: asystole and pulseless
electrical activity are the most common rhythms in childhood cardiac arrest. Profound
bradycardia should be treated in the same way as asystole. The drug of choice is
adrenaline (epinephrine), 0.01 mg/kg, intravenous or intraosseous or 0.1 mg/kg via
the tracheal route. This should be followed by 3 minutes of CPR. If the child does
not respond to the initial dose of adrenaline (epinephrine), another dose of 0.1 mg/
kg should be given. All subsequent doses should be the higher dose of 0.1 mg/kg
intravenous or intraosseous.
Any underlying reversible cause of the arrest should be treated and resuscitation should
not be abandoned until reasonable attempts have been made to do so. Reversible
causes of pulseless electrical activity include:
hypovolaemia
tension pneumothorax
cardiac tamponade
drug overdose
electrolyte imbalance.
Ventricular fibrillation and ventricular tachycardia are relatively uncommon in

infants and children; they are treated by defibrillation. The recommended sequence is
to give two rapid defibrillatory shocks of 2 joules/kg, followed by a single shock of
4 joules/kg. If the initial third shock fails, CPR should be continued for 1 minute and
adrenaline (epinephrine), 0.01 mg/kg, given. The heart is then defibrillated with
three further shocks at 4 joules/kg. The cycle of defibrillation and 1 minute of CPR is
repeated until defibrillation is achieved. In children there is often an underlying cause
and correction of hypothermia, drug overdose and electrolyte imbalance should be
considered.
Post-arrest stabilization
Following a cardiac arrest, children are often poorly perfused, hypotensive and very
acidotic. Most require continuing pharmacological support to maintain blood pressure
and improve tissue perfusion. Management is similar to the general management of
critically ill infants and children in cardiogenic shock. The goals are rapid restoration
of blood pressure, effective organ perfusion, and correction of hypoxia and acidosis.
Normocapnic ventilation should be continued until cardiorespiratory stability is
achieved.
Cerebral resuscitation aims to provide a sufficient supply of oxygenated blood to the

brain to meet its demands. Hypo-glycaemia and hyperglycaemia should be avoided,
and factors that increase cerebral oxygen requirements (e.g. hyperthermia, inadequate
analgesia, seizures) should be treated. Mild hypothermia (34oC) is beneficial after
global brain ischaemia. In animal studies, lowering brain temperature from 36 to 33C
with local cranial cooling during the first hour of post-ischaemic recirculation improves
neuronal survival. The protective effect of mild hypothermia is presumably multifactorial
as it cannot be explained by the modest reduction in oxygen consumption. The clinical
impact of mild hypothermia on long-term outcome remains to be tested. It is probably
wise to avoid aggressive rewarming of patients in the early post-arrest period. Cerebral
resuscitative strategies such as thiopental (thiopentone), calcium channel blockers and
steroids do not improve outcome.
Outcome
The combined mortality and morbidity rate of children who are pulseless on arrival
in the accident and emergency department approaches 100%. Children who have a
delayed response to resuscitation have little chance of surviving without neurological
damage. The length of resuscitation is another predictor of outcome. Prolonged
resuscitation requiring more than two doses of adrenaline (epinephrine) leads to
a dismal outcome and attempts beyond 25 minutes are unsuccessful. Respiratory
arrest alone is associated with a better outcome. The most effective treatment of
cardiorespiratory arrest is prevention. The early recognition and aggressive treatment of
impending cardiac or respiratory failure in children is essential. u
FURTHER READING
Advanced Life Support Group. Advanced Paediatric Life Support Manual. 3rd ed.
London: BMJ Books, 2001.
Paediatric Advanced Life Support: An Advisory Statement by the Paediatric Life

Support Working Group of the International Liaison Committee on Resuscitation.
Resuscitation 1997; 34: 11527.
Ushay M H. Pharmacology of Pediatric Resuscitation. Ped Clin N Am 1997; 44: 207

29.
Zaritsky A L. Recent Advances in Pediatric Cardiopulmonary Resuscitation and

Advanced Life Support. New Horizons 1998; 6: 20111.
Ziderman D A. Paediatric and Neonatal Life Support. Br J Anaesth 1997; 79: 18897.

Intraosseous Cannulation
Jane M Peutrell
Jane M Peutrell is Consultant Paediatric Anaesthetist at the Royal Hospital for Sick
Children, Glasgow, UK. She qualified from the University of Newcastle upon Tyne in
1982 and after a medical SHO post in Durham, trained in anaesthesia in Leeds, the
South West of England, and the Netherlands. Her main interest is regional anaesthesia
in babies and children. She also instructs regularly on APLS courses.
The technique of obtaining vascular access through intraosseous cannulae became

popular during the 1940s but was forgotten as equipment and methods for venous
cannulation improved. The technique was rediscovered in the 1980s for use during
paediatric resuscitation and quickly became accepted practice because:
access is rapid
landmarks are easily identified
success rates are high (85% of babies, 50% of adults) and complications infrequent
a variety of drugs and fluids (including all those given during resuscitation) can be
injected.
Intraosseous cannulation is now indicated in babies or children during resuscitation

or in an emergency when intravenous access cannot be obtained quickly or after two
failed attempts. However, it is essentially a resuscitation technique and conventional
intravenous access should be obtained as soon as possible (certainly within 24 hours)
to reduce the risk of complications, particularly osteomyelitis.
Applied anatomy
The marrow cavity in long bones contains a spongy mesh of non-collapsible venous
sinusoids, which drain into a wide central venous canal. The central canal leaves
the bone through nutrient veins (running with the arteries) or sometimes through
independent emissary veins that pierce the shaft elsewhere.
The skeleton of a baby contains very vascular red marrow, which is gradually replaced
by less vascular yellow marrow from about 5 years of age. Although intraosseous
cannulation is recommended for children less than 6 years of age, it is useful
throughout childhood. Even adults have numerous venous sinusoids, allowing infusion
rates of 2025 ml/minute (sufficient for drug administration).
Technique
Equipment: intraosseous cannulation using hypodermic, spinal, or standard bone
marrow needles has been described, though specifically designed equipment is also
available. Cook have developed two types (Figure 1).
Intraosseous needles developed by Cook a T45 (45 trochar) Two laterally

a A smooth external, non-threaded needle with inner opposed
stylet showing the standard tip (left) and one with two side ports
lateral side ports (right). This needle is available in
different gauges (18/16/14), lengths (2.5/3/4 cm) and
tips (35 lancet/pencil-point/45 trochar). Having two
Positioning
laterally opposed side ports allows flow if the end-
mark
hole obstructs. b Threaded, self-tapping needles with
Tri-faceted tip
large or small handles are available in either 15G, b
1.8 cm (for babies < 9 months) or 12G, 2.3 cm (for
children > 9 months). They have trifaceted cutting
tips, relatively short lengths (therefore low centre of
gravity making them easier to handle) and two lateral
side ports. The screw thread allows controlled and
atraumatic access to the marrow and better
Side ports
stabilization (reducing the risks of dislodgement,
leakage, or penetration of both cortices) Needle with small needle handle Needle with large needle handle
Site: the proximal tibia is the most common site for insertion (Figure 2). The sternum is
no longer used because of the risk of mediastinal damage.
Cannulation: as far as practicable, use an aseptic technique. The landmarks and

technique of insertion in the proximal tibia are shown in Figure 3.
Recommended sites for intraosseous cannulation
Common
Proximal tibia most common site in children, but difficult to access
in adults
Distal tibia just above the centre of the medial malleolus, better
access to red marrow in adults
Distal femur approached from the anterior aspect
Others
Clavicle
Humerus
Ilium
2
Intraosseous cannulation at the proximal tibia
Tibial tuberosity
Anterior
border
Needle inserted
at 90 to medial
surface
The site of needle insertion is 13 cm (children) or 0.51 cm

(babies) below and just medial to the tibial tuberosity on the
flat, medial aspect of the tibia where the bone lies
subcutaneously. Support the leg on a firm surface, grasping
the thigh and knee above and lateral to the site of insertion.
Insert the needle at right angles to the coronal plane, directing
the needle tip slightly caudally and away from the tibial growth
plate. To prevent dislodgement, carefully immobilize the
cannula and splint the limb
3
To insert the needle, use a boring, twisting, or screwing action (depending on design),
applying axial pressure through the needle shaft. Avoid rocking movements (which
produce a larger diameter hole than the needle) or repeated attempts, which can cause
leakage of drugs or fluid during infusion. Stop once there is a loss of resistance and
then unscrew the cap or handle. Try aspirating to confirm correct placement and to
obtain marrow for laboratory investigations. Test the position by injecting 10 ml of 0.9%
saline. Signs suggesting correct placement include:
a sudden loss of resistance as the needle tip passes through the cortex into the
marrow (does not occur with screw-threaded needles)
aspiration of marrow (reassuring, but not always possible despite correct placement)
the needle remains upright without support
fluid can be injected easily, without evidence of extravasation (e.g. increased limb
circumference or tissue firmness).
Intraosseous cannulation should take about 2 minutes. If unsuccessful on one side,

make the second attempt on another limb or bone to prevent leakage through the
original hole.
Contraindications include fracture of the ipsilateral, proximal limb; repeated attempts

in the same bone; local infection; osteogenesis imperfecta; osteoporosis; osteopetrosis
and osteomyelitis.
Complications are uncommon, but include:

dislodgement of the cannula (10%)
extravasation around the needle or through a secondary site (e.g. previous attempts
in the same bone, penetration through the posterior cortex) or failure to penetrate
the cortex, producing:
- haematoma
- severe tissue necrosis, particularly with hypertonic solutions (e.g. bicarbonate,

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Topics covered in each 3-year series include:

Alcohol Anxiety Child psychiatry

The inguinal region

Horizontal section through the inguinal canal

Inferior epigastric vessels Deep inguinal ring

Inguinal canal showing anterior wall

External oblique aponeurosis

It is covered anteriorly by the external oblique aponeurosis which is reinforced laterally

Inguinal canal with external oblique removed

Structures lying deep to the inguinal ligament

Femoral nerve Anterior

The larynx consists of articulating cartilages linked together by ligaments. It lies

Anatomy of the trachea

Features of the throat

Laryngotomy or cricothyroidotomy (Figure 3) an incision is made through the

Position for cricothyroidotomy and tracheostomy

First tracheal ring

Tracheostomy (Figure 3) an incision is made midway between the cricoid ring

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Sympathetic reflex arc

The autonomic nervous system

Somatic fibres are distributed as grey, non-myelinated, postganglionic rami

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Lymph nodes of the axilla

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Coronal section through the brain showing relations

Left hemisphere functional localization

Pre central motor

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There are two plexuses of nerves in the neck:

The cervical plexus

The brachial plexus

Surface anatomy of the brachial plexus emphasizing

Neck First rib

Relationship of the brachial plexus to the axillary

Ventral rami (roots) C5

Branches of the brachial plexus C5

Brachial plexus block

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A typical cervical vertebra: superior aspect

Atlas: superior aspect

Axis: superior aspect

A typical thoracic vertebra (Figure 4) has a wedge-shaped body that is shallower

A typical thoracic vertebra: lateral and

A typical lumbar vertebra: superior aspect

Joints and ligaments

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John S P Lumley is Professor of Surgery and Honorary Consultant at St

Olfactory nerve (I)

Optic nerve (II)

Oculomotor (III), trochlear (IV) and abducent (VI) nerves

With abnormalities of the IIIrd nerve, there is:

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Facial nerve (VII)

The greater petrosal branch

The chorda tympani branch