Perioperative Neurosurgical Critical Care: Chris Zacko

2013 Neurocritical Care Society Practice Update
PERIOPERATIVE NEUROSURGICAL CRITICAL CARE

Chris Zacko
Penn State Hershey Medical Center
Department of Neurosurgery
Hershey, Pennsylvania
Peter LeRoux MD, FACSMain Line Healthcare
MLHS and Spine Center
Wynnewood, PA
CLINICAL CASE
A 73 year old male with poorly controlled diabetes, coronary artery disease with cardiac stents,
atrial fibrillation (non-therapeutic on Coumadin), bilateral carotid stenosis, hypertension,
hyperlipidemia, hypothyroidism and morbid obesity has just returned to your ICU after a
decompressive craniectomy for malignant MCA infarction. He is on a ventilator and muscle
relaxation was not reversed by the anesthesia team. His sodium is 132, blood pressure is
90/45, glucose is 245, and he lost 750 cc of blood during surgery. What post-operative
challenges do you face when balancing this patients medical co-morbidities, fresh surgical
wounds, and need for cerebral perfusion?
OVERVIEW
All patients who undergo neurosurgical procedures, even a well-performed operation, are in a
potentially unstable cardiopulmonary state and at risk for secondary neuronal injury.
Depending on the specific operation performed these patients can also have fresh surgical
incisions, delicate vascular anastomoses, friable resection beds, brittle patency of newly open
vessels, and/or tenuous hemostasis. All of these factors leave these patients especially
vulnerable to post-operative complications. The object of postoperative neurosurgical care is
to resuscitate, stabilize, prevent/minimize secondary neuronal damage, and to optimize
functional central CNS recovery. Therefore, the basic goals of postoperative neurosurgical care
are:
Provide smooth emergence from anesthesia
Optimize post-operative hemodynamic, volume, and electrolyte status,
Optimize airway and respiratory status,
Treat coagulopathic states and hemostatic disorders,
Optimize management of post-operative complications,
Have reliable and appropriate systemic and neuromonitoring tools
Use subtle and reproducible neurological examination methods
These goals depend on many variables and important questions to ask and answer include:
What was status (medical and neurological) of the patient before surgery?
What neurological disease is being treated?
What other neurological disorders does the patient have?
What position was the patient in during surgery?
What procedure was performed (procedure specific and expected complications)?
What happened during surgery, e.g. blood loss, vascular injury?
What anesthetic technique was used?
To manage a postoperative neurosurgical patient the neurointensivist requires knowledge of
how the CNS reacts to stress and anesthesia as well as the potential complications associated
with each specific procedure. This chapter will focus on the following topics:
1) Who goes to and who stays in the NCCU
2) The effects of anesthetic agents on the CNS and neurosurgical patients
3) Basic complications after neurosurgical procedures
4) Emergence from anesthesia in neurosurgical patients
5) Extubation in neurosurgical patients
6) Post-operative pain
7) Postoperative nausea and vomiting
8) Basic post-operative neurosurgical care
9) Postoperative monitoring
WHO GOES TO AND WHO STAYS IN THE NEUROCRITICAL CARE UNIT (NCCU)?
Postoperative neurosurgical cases account for numerous NCCU admissions. Traditionally,
patients who had craniotomies and other invasive neurosurgical procedures were nursed
postoperatively and overnight in the NCCU as a precaution. This practice is changing somewhat
as most NCCUs also have well-developed step-down or intermediate care units that can
often manage routine uncomplicated cases. Among those patients admitted to the NCCU
primarily for precautionary/observational purposes, very few patient days are created. It is
estimated that only ~15% actually require/receive active treatment. Furthermore, when a
patient stay in the NCCU is <24h, ~50% require no interventions beyond post-anesthetic care
and frequent neurologic exams. Lastly, two-thirds of these patients require no further
interventions of any kind after the first 4 hrs.
The decision to admit a given patient to the NCCU can be subjective and surgeon specific but is
often based upon: age, co-morbidities, pre-operative condition, intra-operative details (difficult
hemostasis, unexpected cerebral edema), and need for post-operative respiratory and
hemodynamic support. That said, a patient's risk for prolonged ICU stay (>1 day) can be
anticipated by: a) preoperative radiologic findings (e.g. tumor location, mass effect), b)
significant intraoperative blood loss, c) substantial intra-operative fluid requirements, and d)

the decision to keep the patient intubated at the end of surgery [1].
EFFECT OF ANESTHETIC AGENTS ON THE CNS AND NEUROSURGICAL PATIENTS
An important aspect of postoperative neurosurgical care is to distinguish residual effects of
anesthetic agents (e.g. drowsiness or confusion) from signs that indicate intracranial pathology.
While it often is believed that patients with neurological disease are prone to anesthetic
effects, this is not universally true particularly in those patients who are fully awake
preoperatively. Confusion or dementia can undoubtedly be exacerbated by anesthetic agents.
That said, some note this is a bit more unusual (but not unheard of) for focal deficits to be
aggravated by anesthesia. Excessive benzodiazepine use can be an exception and in some
situations are even felt to unmask deficits. As a general rule, however, any progressive or
fluctuating deterioration should be assumed to be a complication from the operative procedure
rather than an anesthetic effect.
The effects of anesthetic agents are complex and can depend on the agent used. For example,
increased reflexes and extensor plantar responses may be observed in 50-60% of patients who
receive enflurane or ethrane, in <30% who receive halothane, and almost never with a nitrousnarcotic mix [2]. Anesthetic associated abnormalities should return to normal when the patient
is fully awake. Non-depolarizing neuromuscular blockers may be associated with persistent
weakness or opthalmoplegia (especially in patients with underlying neuromuscular disorders)
but usually the rest of the exam is benign. However, opthalmoplegia should never be attributed
to drugs alone. Occasionally anticonvulsant toxicity, particularly Dilantin, may cloud recovery
although this is uncommon with typical therapeutic dosing. This can be considered if a patient
received excessive loading doses of certain AEDs. It is beyond the scope of this review to
address all anesthetic agents. In addition the best anesthetic regimen for neurosurgery still is
debated. Anesthetics with a short context-sensitive half-time (i.e. the time required for the
effect-site concentration of an IV drug to decrease by 50% at steady state), such as the opioids
remifentanil and sufentanil, are suitable for anesthesia when early neurologic assessment is
preferred. Several studies have compared in a randomized fashion different drug combinations,
balanced anesthesia e.g. sevoflurane-fentanyl, total intravenous anesthesia (TIVA) or
inhalational anesthesia to examine impact on recovery [3, 4]. The results are varied and
anesthetic effects may depend more on the way an agent is used rather than the specific agent
itself.
BASIC COMPLICATIONS AFTER NEUROSURGICAL PROCEDURES
Between 20-50% of neurosurgical patients may develop early postoperative complications and
about 25% will have more than one complication [5,6]. Many of these complications are
minor, the commonest being nausea/vomiting (30%), or shivering (18%). The incidence of
other complications is difficult to determine and in part depends on the procedure as well as
how the complications are classified. These include: respiratory (3%), airway trauma (4%),
cardiovascular (7%), and neurological (6%). Respiratory impairment (PaO2<90 mm Hg or
PaCO2>45 mmHg) may occur in ~25% of patients usually within the first 30 to 60 minutes. About
1% of patients require re-intubation. Overall serious complications may occur in 10% of
patients. In patients who undergo emergency surgery, or have a depressed preoperative level
of consciousness (Glasgow Coma Scale 8), this risk is greater (>40%). Being aware of some
common complications and associated management strategies is fundamental to the practice
of neurocritical care.
Craniotomies: Complications can be general or specific to the type of surgery. The most
common complications are cerebral edema, seizures, vascular injury, and post-operative
hemorrhage.
General complications after craniotomy:
a. Agitation and discomfort are common and now commonly treated quite successfully
with dexmedetomidine.
b. Cerebral Infarction: Can be due to arterial or venous injury. Venous occlusion and
infarct can occur when a bleeding vein must be coagulated or when massive cerebral
edema leads to a compressive occlusion of venous outflow. One should also be
attentive to possible venous injuries after meningioma surgery located near venous
sinuses (tentorial, parasagittal, convexity, and parafalcine). Arterial infarct can occur
with either traumatic laceration or sacrifice of an artery for hemostasis. This can
occur in TBI, glioma surgery with en passant vessels, and epilepsy surgery (i.e.
anterior choroidal artery in temporal lobectomy).
c. Seizures: particularly after penetrating TBI, epilepsy surgery, subdural empyema,
and glial resection near motor cortex, but may occur in any patient post-operatively
d. Pneumocephalus: air can be retained after craniotomy and act very much like mass
lesions. Symptoms include lethargy, confusion, nausea/vomiting, and headache.
Diagnosis is easily made with head CT. Once suspected one should actively
investigate for the presence of tension pneumocephalus and CSF fistula as this will
dictate management. Tension pneumocephalus can be urgent and is surgically
evacuated. If there is a CSF leak, the leak should be managed in typical fashion
before the pneumocephalus is addressed. Simple pneumocephalus can typically be
managed expectedly as the air normally absorbs with time. Some advocate for the
use of non-rebreathing mask with 100% oxygen for 24-48 hours. Brain sagging may
be encountered as a related phenomenon often seen after intraoperative over
drainage of CSF (e.g. during aneurysm surgery). The clinical triad consists of
pneumocephalus, midbrain crowding, and neurological symptom such as decreased
mental status improving with reverse trendelenburg
e. Postoperative hematomas: Approximately 2% of patients who undergo a cranial
procedure will develop a postoperative hematoma (PICH) with 0.8% of patients
developing a hemorrhage that requires surgical evacuation. The most common PICH
presentations include:
60% present with a decreased level of consciousness (as a result PICH should
be considered in all patients who do not recover or improve in the expected
manner after surgery).

33% of patients develop focal neurological deficits
90% will have elevated ICP (when ICP is being monitored). By contrast in the
absence of a PICH, ICP is elevated in only 10% of post-operative patients.
In most patients (50%) clinical deterioration associated with a postoperative
hematoma occurs within 6 hours of surgery [7,8]. However, ~20% of PICH
may develop after 24 hours. Those patients at particular risk for delayed
hematomas are those who underwent posterior fossa surgery or emergency
craniotomy. Once should consider longer periods of ICU observation in such
cases. Risk factors for a PICH, particularly one that requires surgery include:
meningioma surgery; intraoperative or immediate (12 hour) postoperative
hypertension [9], intraoperative blood loss >500ml, age >70 years, hypoxia,
coughing and hiccoughs, and laboratory signs of coagulopathy (high PT, low
fibrinogen and platelet counts).
Remote hemorrhages from the surgical site can also be problematic.
Etiologies/risk factors include reperfusion hemorrhages, releasing the
tamponade effect of a contralateral hemorrhage with debulking of a mass
lesion, CSF drainage/hyperosmolar therapy causing shift of parenchyma
(especially in cerebellum), and coagulopathic states (including patients with
history of alcohol abuse).
Reoperation: Reoperation is necessary in some patients. Removal of various
types of hematomas is the most common surgical procedure at reoperation.
Outcome is favorable in about half the patients indicating the importance of
prevention. Factors associated with poor outcome include: histological type
of the tumor, clinical state at admission, GCS score before urgent
reoperation, time interval between primary surgery and urgent reoperation,
and patient age [10].
Specific complications after craniotomy:
Glioma: cerebral edema is more common after partial resection than with gross total
resection.
Epilepsy: hemiplegia can be seen if the anterior choroidal artery was injured. Word
finding difficulties can be seen with injury to the left temporal lobe. Lastly, aseptic
meningitis after depth electrode placement is a concern [11].
Pituitary and Transphenoidal Surgery: Complications to be aware of are diabetes
insipidus (DI), neuroendocrine disorders from panhypopituitarism (adrenal
insufficiency, central hypothyroid), CSF leaks, sinonasal injuries, hyponatremia, and
alterations in visual function (acuity, fields, ocular movement).
Posterior Fossa Surgery: air embolism is a classical, yet uncommon, complication of
surgery in the seated position. It is typically diagnosed and managed in the
operation room by flooding the filed with irrigation, applying bone wax to cut bone
surfaces, lowering the head of bed, placing the patient in left lateral decubitus
position (if possible), aspirating air from the left atrium via CVP catheter, and
achieving hemostasis as soon as possible. Another complication associated with
posterior fossa surgery is accelerated hypertension. Any unexpected or refractory
hypertension should warrant careful examination and a low threshold for imaging
looking for post-operative hemorrhage. Other complications include obstructive
hydrocephalus (if 4th ventricle compressed), upward herniation (via over drainage
through and EVD when the 4th ventricle is compressed), cranial nerve injuries, and
CSF leak and/or pseudomeningocele due to dependency of dural opening.
Craniotomy for securing ruptured aneurysm: this will be covered in another chapter
of this manual, but there are several strategies regarding the prevention and
treatment of vasospasm. In general terms the patient should be kept euvolemic
(please see appropriate chapter in this manual for a more complete discussion).
Arteriovenous Malformation (AVM): these cases generally have especially tenuous
and brittle hemostasis and very strict blood pressure control is crucial. In addition,
liberal use of sedation to prevent coughing and straining against the ventilator may
be critically important in the first few days after surgery. Seizures are also known to
occur after AVM surgery as these patients often have pre-operative seizure
disorders.
Transient mutism can occur with bilateral retraction of the cingulate gyrus or
division of the corpus callosum [12].
Carotid Endarterectomy (CEA)

The need for ICU management after CEA is highly variable and is dependent on surgeon
preference, anesthetic/surgical technique (local vs. general), pre-operative clinical presentation
and the patients co-morbidities. Medical complications to be mindful of are: a) cardiac
arrhythmias, b) myocardial ischemia (cardiac complications may be more common if the
procedure done under general anesthesia), c) respiratory compromise (either from soft-tissue
swelling after dissection or post-operative hematoma), d) seizures, e) hypertension (deranged
sensitivity of carotid sinus baroreceptor reflex or injury to the Hering nerve, a branch of CN IX),
and f) bradycardia (also from carotid baroreceptor injury). Surgical and neurologic
complications include:
a. Stroke: Etiologies: a) embolic from the endarterectomized surface, b) hemorrhagic
from reperfusion injury (see below), or c) occlusive from re-stenosis of the ICA (most
common cause of major stroke). If the stroke is noted directly after surgery, the
patient is typically taken immediately back to surgery for exploration without further
imaging. If the deficit is delayed, a workup is initiated and management options vary
on the findings. Options include surgery, anticoagulation, augmentation of cerebral
perfusion via blood pressure elevation, and observation with generous fluid
administration and serial examinations/imaging.
b. Post-operative hematoma: sources can be from venous bleeding in the operative
bed or from disruption of arterial suture line. The latter is an emergent situation. If
suspected, the surgeon and a dedicated team to manage the airway should
immediately be called. The patient is assessed for pulsatile swelling, tracheal

deviation and respiratory distress. If there is any hint of respiratory compromise this
is managed by OPENING THE WOUND THEN INTUBATION. If not already in the
operating room, the patient can now go to the OR and definitive repair can be
accomplished.
c. Cranial nerve injury: cited by some as the most common complication after CEA with
incidence of 8-10% [13]. Nerves at risk are the a) hypoglossal (tongue deviation,
chewing swallowing deficits); b) vagus (hoarseness, diminished cough); c)
glossopharyngeal nerve (dysphagia, nasal regurgitation, hypertension if Hering nerve
damaged); d) spinal accessory nerve (drooping shoulder), e) recurrent laryngeal
(unilateral vocal cord paralysis), great auricular nerve, and mandibular branch of the
facial nerve (asymmetry of upper lip). These injuries are generally self-limited and
recover in time.
d. Hoarseness: more likely from laryngeal edema than injury to recurrent laryngeal
nerve
e. Reperfusion Injury: a relatively rare occurrence that is possibly more prevalent after
re-opening of a high-grade stenosis in hypertensive patients especially if there is
contralateral carotid occlusion. This abrupt re-establishment of flow into an area
that is postulated to have impaired autoregulation can lead to microhemorrhages
and large ICHs. Symptoms include altered mental status, ipsilateral eye pain or
headache [14]. This has also been known to lead to seizures.
Endovascular Interventions
This is an area of tremendous advancement in recent years for the management of stroke and
vascular neurosurgery. Many of the complications to be aware of are inherent to the disorder
being treated and are discussed elsewhere. The complications specific to endovascular
procedures will be discussed below and are grouped into vascular access site and neurologic
complications.
Vascular access site complications
due to the thrombogenic effect of the catheters used in these procedures, as well as the
thromboembolic potential inherent to the conditions being treated, anti-coagulation is used
much more readily in endovascular cases vs. open procedures. This can predispose the patient
to hemorrhagic complications. Complications seen at the groin puncture site include
arteriovenous fistulas, local bleeding, pseudoaneurysm, and local nerve injury. The latter can
be emergent and require immediate attention. Any hypotension in a patient having undergone
an endovascular procedure should warrant careful inspection for signs of pseudoaneurysm.
This includes checking distal pulses, assessing for pallor in the extremity, and feeling for a
palpable pulsatile mass at the access site. Pseudoaneurysm can lead to distal ischemia in the
leg and be limb-threatening. Confirmation of a pseudoaneurysm triggers application of
prolonged pressure to the site and consultation of a vascular surgeon.
Neurologic Complications
The development of focal cerebral edema has been noted after coiling of aneurysms and
embolization of AVMs. This is typically managed with dexamethasone. Intracranial
hemorrhage can be seen after these procedures and management is discussed elsewhere.
Common sources of ICH include intra-operative rupture of an aneurysm, perforation of a vessel,
and reperfusion hemorrhage. More unique to endovascular procedures are possible
thromboembolic and thrombo-occlusive complications. The catheters used for these
procedures can physically disrupt atherosclerotic plaques causing emboli, create a dissection, or
generate thrombus due to their inherent thrombogenicity. Other sources of emboli include
microthrombotic shower after mechanical thrombectomy and glue emboli after embolization.
These emboli are often not noted until the post-operative period. Once symptoms are
suspected, urgent MRI/MRA is advised with concomitant initiation of generous fluid
administration. After diagnostic imaging is complete, treatment options include additional
endovascular therapy, anticoagulation, and/or hypertensive therapy via pressors.
Other complications of these procedures include arterial dissection, acute thrombus and
perforation. These complications are almost always noted during the procedure and
management options consist of blood pressure control, anticoagulation, and generous fluid
administration (depending on the problem encountered). For acute thrombus noted in the
procedure, treatment options include intra-arterial thrombolysis, mechanical thrombectomy,
and Reopro. Reopro is a potent glycoprotein IIb/IIIA inhibitor and has been found to be quite
effective in managing thrombo-occlusive events during endovascular procedures. The
implication to the neurointensivist is that due to Reopros effective anti-platelet activity one
need to carefully monitor for bleeding complications.
Other complications
It is important to recognize what may happen during surgery to best manage the patient after
surgery. Complications depend in part on position or the procedure. Some specific examples
include:
a. Ocular: Periorbital and/or conjunctival edema, as well as chemosis, tend to occur more
often in the prone position, during pterional approaches, or with orbitozygomatic
craniotomies. Posterior ischemic optic neuropathy or central retinal artery occlusion
also may occur (particularly with longer procedures). A third nerve palsy or blindness
may result from posterior communicating artery or carotid ophthalmic artery surgery.
b. Use of a lumbar drain may cause intracranial hypotension or remote hemorrhage
distant to the surgical site
c. Anterior cervical surgery: Soft tissue swelling can cause airway obstruction or swallowing
abnormalities
EMERGENCE FROM ANESTHESIA IN NEUROSURGICAL PATIENTS

Recovery from anesthesia and surgery is a period of intense stress for patients. The effects can
be systemic or CNS-specific.
Systemic effects
There are several physiological responses as a patient emerges from anesthesia, including: an
increase in oxygen consumption (VO2), sympathetic activation with catecholamine release,
increases in blood pressure and/or heart rate, alterations in arterial blood gases, and
hyperglycemia. Shivering, pain, and regaining awareness are additional stress factors
encountered in recovery from anesthesia.
1) Shivering occurs in approximately 40% of patients recovering from general anesthesia with a
body temperature of <36.5oC and is associated with a 200400% increase in VO2. Mild
intraoperative hypothermia can increase norepinephrine or epinephrine release, which may
extend into the early postoperative period. Forced-air skin-surface warming may reduce the
incidence and intensity of shivering. Precedex has also been used with success.
2) Pain is another stress factor and appropriate analgesic therapy may blunt the increase in
plasma catecholamines both during and after surgery. Most patients will experience moderate
or severe pain in the first two days following major intracranial surgery [15].
3) Hypertension is frequent in the early postoperative period after neurosurgery. If a >20%
blood pressure increase is considered a reasonable threshold for treatment, then 40-90% of
patients require antihypertensive therapy during emergence. Analgesics, and particularly
narcotics, reduce the sympathetic and catecholamine response to pain and extubation. Patients
with PICH are 3.6 times more likely to be hypertensive than their matched controls. In
particular there is a very strong association between intracranial hemorrhage and patients
being normotensive intra-operatively but hypertensive postoperatively [9]. Hypertension after
posterior fossa surgery should raise suspicions for possible post-operative hemorrhage.
Postoperative blood pressure generally is managed in the range of 120150 mmHg systolic.
Cerebral effects
Stressful events, including surgery and emergence from anesthesia, can alter CBF and CMRO2.
Sympathetic stimulation acting through beta-adrenoreceptors may play a role in these effects.
1) CBF: Transcranial Doppler (TCD) studies suggest that CBF velocities increase significantly
during emergence from anesthesia. The maximum increase is at extubation (as much as 60%
over preoperative value) and return to normal in about 60 minutes [16]. The CBF increase is
independent of anesthetic technique, PaCO2, or arterial pressure. This increase in CBF can
cause cerebral edema, hemorrhage, and postoperative confusion. Changes in CBF are
associated with deleterious oxygen consumption (VO2) so prevention of agitation, shivering and
coughing is important.
2) ICP: Up to 20% of patients who undergo intracranial surgery may develop increased ICP and
when it occurs half will develop clinical deterioration in large part from edema or hemorrhage
[17]. There is limited data on the specific effects of emergence and extubation on ICP.
Endotracheal suctioning has been shown to increase ICP [18]. Similarly, extubation can increase
ICP particularly when associated with coughing. The ICP increase usually lasts 2 or 3 minutes,
but is longer when intracranial compliance is reduced.
3) Hyperemia and normal perfusion pressure breakthrough (NPPB): The cerebral arteriovenous
oxygen content difference (AVDO2) often is depressed immediately after craniotomy. This is
suggestive of transient cerebral hyperemia (16). Hyperemia may result in hemorrhage or severe
edema in 312.5% of cases. An especially at-risk group is patients undergoing craniotomy for
AVM resection. Features of AVMs associated with a high-risk for postoperative hyperemic
complications, including normal perfusion pressure breakthrough, are: a) large and deep
AVMs, b) low feeding-artery pressures, c) multiple arterial inflows but only a single venous
draining vessel, and d) intense steal around the AVM nidus. Strategies used in the management
of these precarious include staged therapies (embolization and surgical), barbiturate based
anesthetic continued into the postoperative period, extremely rigorous blood pressure control
after surgery, and either invasive or non-invasive cardiovascular monitoring to optimize filling
pressure and cardiac performance
EXTUBATION IN NEUROSURGICAL PATIENTS
The goal of anesthetic emergence and subsequent extubation is to maintain stable respiratory
and cardiovascular parameters while preventing adverse CNS effects. One must be cautious as
even the physical act of extubation can cause sympathetic discharge via tracheal and laryngeal
stimulation (although it relieves the endotracheal tube stimulation itself). On one hand, a
delayed emergence with deferred extubation in the ICU may achieve better thermal and
cardiovascular stability after major neurosurgical procedures (thereby limiting secondary
insults). On the other hand, the timely diagnosis of neurosurgical complications is required to
limit CNS damage. The diagnosis of complications relies on rapid neurological examination
after early awakening and an awake patient is the best and the cheapest neuromonitoring
available. However many factors may contribute to delayed emergence including: 1)
perioperative opiate analgesia and anxiolytics, 2) metabolic disturbances (electrolyte or acidbase), 3) comorbidity, especially hepatorenal dysfunction that affect drug clearance, 4) stroke,
5) pneumocephalus or CSF hypotension and 6) seizures. Before extubation, airway and
swallowing functions should be carefully evaluated and everything should be ready for a
possible reintubation. For successful extubation, the patient should be 1) awake, 2) fully
reversed from neuromuscular relaxation and spontaneously breathing, 3) hemodynamically
stable, and 4) normothermic (Table 1 and 2).
Rapid awakening and recovery

The rationale for "rapid-awakening" after craniotomy with general anesthesia is that an early
diagnosis of postoperative neurological complications can limit potentially devastating
consequences. But extubation must be balanced by the patients perioperative neurological
status and prognosis, surgical concerns, and respiratory status. After uncomplicated surgery,
normothermic and normovolemic patients generally recover from anesthesia with minimal
metabolic and hemodynamic changes. Thus, early recovery and extubation in the operating
room is the preferred method when the preoperative state of consciousness is relatively
normal.
Delayed recovery
In the complicated or unstable patient, the risks of early extubation may outweigh the benefits.
Delayed recovery/extubation is appropriate after: long (> 6 hours) surgery, surgery for large
tumors or AVM resection, major intraoperative bleeding, preoperative altered consciousness,
severe cardiac or respiratory impairment, posterior fossa surgery where there is possible injury
to lower cranial nerves, and select cervical procedures where re-intubation may be difficult. It
is, however, often possible to perform a brief awakening of the patient without extubation to
allow early neurological evaluation, followed by delayed emergence and extubation.
Alternatively to extubation, an immediate postoperative CT may be obtained or ICP monitor
placed.
Weaning strategies and extubation failure
Standard weaning criteria includes normal mental status, and so these criteria are not always
appropriate for neurosurgery patients. To be ready for extubation, the neurosurgical patient
should successfully complete a spontaneous breathing trial. The initial trial should last at least
30 minutes and consist of either T-tube breathing or low levels of pressure support (8cmH20).
A simple leak test with cuff deflation may help to identify laryngeal edema. Further details
are provided in the recent report of the Task Force on Weaning from Mechanical Ventilation by
the 6th International Consensus Conference on Intensive Care Medicine (Table 3). The GCS and
partial pressure of arterial oxygen/fraction of inspired oxygen ratio are factors that may predict
extubation. For example the success of extubation is >75% when the GCS is 8 but ~33% when
GCS is <8 [19]. Extubation failure is diagnosed after extubation if the patient develops one or
more of the following: tachypnea (respiratory rate >25/min for 2 hours), clinical signs of muscle
fatigue or increased work of breathing, oxygen desaturation (SaO 2 < 90%, PaO2 < 80 on FIO2
>0.5), hypercapnia (PaCO2 >45 mmHg, or an increase by >20%), and acidosis (pH <7.33).
POSTOPERATIVE PAIN
Surgery and the associated tissue injury and inammation are almost always associated with
postoperative pain. Recent evidence indicates that post-craniotomy pain is reported as
moderate to severe in up to 80% of patients and may persist for several days postoperatively
[15]. Pain however often is underestimated and undertreated in neurosurgery patients. There
are several reasons for this: 1) the patient may not be able to communicate because of aphasia,
altered mental status, or cognitive impairment, 2) the side-effects of analgesic drugs are feared,
3) there is no consensus regarding the choice of the best anesthetic regimen for intracranial
surgery, 4) there is a lack of standardized, proactive protocols to assess and evaluate postcraniotomy pain and pain therapy, and 5) few studies have examined this question or validated
the benefits of post-operative pain control on outcomes and patient satisfaction.
Management of post neurosurgery pain
Analgesia needs will depend in part on the procedure. For example where there is extensive
muscle dissection (suboccipital approach, thoracolumbar spine surgery) more analgesia will be
required than procedures where there is little muscle dissection (anterior cervical discectomy
and fusion (ACDF) or frontal craniotomy). Basic postoperative analgesia consists of opiates,
non-steroidal inflammatory medicines, and acetaminophen-based preparations. Opioids are
the mainstay of analgesia. All opioids blunt the respiratory response to hypercarbia and so
there are concerns that opioid-induced carbon dioxide retention will trigger increases in
cerebral blood volume with subsequent aggravation of cerebral edema and intracranial
hypertension. In addition there are concerns that opioids may cause excessive sedation, miosis,
and/or interfere with recovery from anesthesia and postoperative neurological assessment.
For this reason codeine phosphate has traditionally been the most commonly used analgesic
post-craniotomy [20]. However, there may be better choices. When properly titrated,
morphine can be more efficacious and does not increase adverse side effects as compared with
codeine [21,22]. Furthermore, codeine is an unpredictable pro-drug and most of its analgesic
efficacy is derived from the 515% that is metabolized to morphine by hepatic CYP2D6. Interindividual and ethnic differences in CYP2D6 can influence codeines efficacy e.g., because of
genetic variation 15% of Caucasians do not experience any effect from codeine [23].
Consequently, morphine or fentanyl is recommended after surgery. With proper use, the
benefits of analgesia (e.g. blood pressure control) outweigh the risks. The non-narcotics
ketoprofen, tramadol, gabapentin, and acetaminophen-based agents (such as Fioricet) may be
useful as supplemental, opioid-sparing drugs. Pain control is reviewed by Nemergut et al [24].
POST-OPERATIVE NAUSEA AND VOMITING (PONV)
Postoperative nausea and vomiting are less common now that propofol is widely used an
induction agent. However PONV remains a common complication after neurosurgical
procedures. The incidence is uncertain since study design may influence the outcome and few
studies have looked specifically at neurosurgery PONV. Nevertheless PONV may complicate
between 30-70% of neurosurgical procedures [25]. While nausea is a source of patient
discomfort, PONV can cause major complications in post-operative patients particularly those
undergoing craniotomy. Vomiting can lead to aspiration (particularly with a compromised
swallowing reflex and impaired consciousness), electrolyte disturbances, ICP increases, and
intracranial bleeding. During the pre-ejection phase of the vomiting reflex there is sympathetic
stimulation. This can complicate control of blood pressure postoperatively. Furthermore, during
the ejection phase increased intra-abdominal (>100 mmHg) and intra-thoracic pressures
directly translates into elevated ICP [26].
General risk factors for PONV include: 1) female gender, 2) previous PONV or motion sickness,
3) non-smoker, 4) duration of surgery >60 minutes, and 5) early post-operative opioids [26].
Specific neurosurgical risk factors include: 1) surgery location (i.e., infratentorial surgery near
the area postrema at the floor of the fourth ventricle), 2) CSF cisternal space opened (chemical
meningitis), 3) awake procedure vs. general anesthesia, 4) intraoperative CSF leak and
subsequent pneumocephalus, 5) use of a fat graft for a CSF leak, and 6) a lumbar intrathecal
catheter and intracranial hypotension [27].
Management of PONV
Various pharmaceutical agents can be used to manage PONV. Serotonin (5HT 3) antagonists,
such as ondansetron, are effective but expensive. Trimethobenzamide is another popular
choice and is thought to inhibit the chemoreceptor trigger zone. Cyclizine is a cheap
antihistamine commonly prescribed whenever opiates are given. Alternatives include dopamine
antagonists, e.g. metoclopramide or droperidol. Steroids also work but there may be a ceiling
effect (5-8mg). There are synergistic effects of dexamethasone and ondansetron. Intravenous
ondansetron administration (4mg) at the time of dural closure can help reduce the incidence of
PONV and the use of rescue antiemetics. Neufeld et al [25] preformed a recent meta-analysis
of 7 prospective, randomized, placebo-controlled trials that together included 448 patients and
found that ondansetron only had a significant impact on vomiting.
BASIC POSTOPERATIVE NEUROSURGICAL CARE
Basic postoperative neurosurgical management is centered on the ABCs of care: 1) Maintain a
secure airway, 2) Adequate respiration to maintain oxygen saturation, 3) Hemodynamic
stability and fluid management. Normo-homeostasis may be regarded as neuroprotective
[28]. Other aspects of postoperative neurosurgical care (seizure control, prevention and
management of infection, venous thromboembolism, ventriculostomy care) are beyond the
scope of this review but clearly are fundamental to critical care. The typical postoperative
patient probably does not require gastrointestinal prophylaxis unless they are on steroids or
remain mechanically ventilated.
Respiratory care
Adequate oxygenation and ventilation are required to balance oxygen delivery to the brain,
cerebral blood flow, cerebral perfusion pressure, and ICP. The Brain Trauma Foundation
recommends maintaining PaO2 >60 mmHg and oxygen saturation >90% for traumatic brain
injury (TBI) patients (BTF). These are sensible goals that have carried over into postoperative
neurosurgical care of all patients. The following respiratory complications may be observed:
Airways obstruction: This may be caused by many factors e.g. laryngospasm, soft tissue swelling
around the pharynx (especially children) or laryngeal or glottic edema (anterior cervical surgery,
carotid endarterectomy), foreign bodies (loose teeth), hypotonia of pharyngeal muscles from
the remaining anesthetic, and viscous fluids (blood after transphenoidal surgery). In all patients
who develop airway obstruction, a patent airway must be achieved immediately (head tilt chin
lift, airway adjuncts, or intubation). The signs of airway obstruction include stridor, tachypnea,
tracheal tug (downward displacement of the trachea during inspiration), use of accessory
muscles, Intercostal and supraclavicular muscle recession, and reduced oxygen saturation (late
signs)
Hypoventilation
A reduced ventilatory capacity can be caused by a depressed neurogenic respiratory drive and
neuromuscular disorders. Etiologies include opioid drugs, hypothermia, metabolic alkalosis
secondary to intermittent positive pressure ventilation, or by mechanical difficulty in breathing.
Impaired chest expansion may result from parenchymal lung disease (e.g. obstructive airways
disease secondary to smoking), muscle weakness (e.g. electrolyte derangement, neuromuscular
disorders), hindered diaphragm movement (pain, obesity), and the residual effect of paralyzing
agents on the chest wall musculature.
Hypoxemia
The principal causes of hypoxemia include: 1) a reduced FiO2, 2) hypoventilation associated
with a depressed consciousness or airway obstruction and 3) ventilation/perfusion mismatch
(e.g. lung collapse, pneumonia, atelectasis, bronchospasm, pulmonary edema, pneumothorax,
pulmonary embolism). Thoracic and abdominal surgery often may alter the chest expansibility,
and contribute to decreased oxygen saturation. This cause is less frequent after neurosurgery
(unless a thoracotomy was performed for thoracic disc or anterior decompression).
Neurogenic pulmonary edema (NPE)
NPE is a potential complication of CNS insults such as intracranial hemorrhage, SAH,
uncontrolled generalized seizures, TBI, and tumors. The postulated cause is sympathetic
discharge. The treatment is mainly supportive (mechanical ventilation possibly limiting PEEP,
alpha-adrenergic blocking agents while managing ICP).
Who should be ventilated? Intubation and mechanical ventilation is indicated in neurosurgical
patients in the following conditions: inability to protect the airway or manage secretions; need
to reduce ICP by ventilation control; PaO2 <60 mmHg despite supplemental O2; PaCO2 >50
mmHg, or pH <7.2; respiratory rate >40/minute or <10/minute; muscle fatigue; airway
compromise; and hemodynamic instability. Orotracheal intubation with rapid sequence
induction is the preferred technique. Nasotracheal intubation should be avoided particularly
when there is a basilar skull fracture or skull base surgery. Maintenance of normocapnia is the
major goal of ventilation therapy in neurosurgical patients. Whereas hypocapnia, achieved
through short periods of hyperventilation, is a potent cerebral vasoconstrictor (and can reduce
ICP) it can exacerbate brain ischemia in patients with brain injury. Hyperventilation also
decreases venous return, cardiac output, and PVO2 and may increase V/Q mismatch.
Mechanical ventilation goals have changed from achieving normal blood gases to reducing the
risks of ventilator-induced lung injury i.e. lung-protective ventilation strategy [29]. Positivepressure ventilation with a tidal volume of 6 ml/kg (or less) of an ideal body weight is used to
maintain a plateau pressure <30 cmH2O. Positive end-expiratory pressure (PEEP) is adjusted to
keep FiO2 <0.6 to prevent oxygen toxicity, with an oxygenation goal of PaO 2 >60 mmHg or SaO2
>90%. The risks and benefits of lung-protective ventilation in neurosurgical patients are unclear.
One must be aware that lung-protective ventilation may lead to permissive hypercapnia that
can be problematic in patients with elevated or borderline ICP. In addition, variable clinical
responses to PEEP may occur in neurosurgical patients secondary to PEEPs effect on
hemodynamic and respiratory variables. High levels of PEEP may decrease CPP due to
decreases in cardiac output and increases in ICP [30]. Fortunately, the influence of PEEP on ICP
is less prominent in patients with stiff lungs (e.g., acute lung injury/ARDS) as they may be the
patients who most need PEEP. PEEP should be applied carefully in patients with increased ICP,
and ICP should be monitored simultaneously.
Cardiovascular management
Cardiovascular disturbances (e.g. hypotension, hypertension, dysrhythmias and myocardial
failure) are common in patients who undergo neurosurgery. They occur as consequences of
medical or surgical therapy, central neurogenic effects on the heart and the autonomic system,
or from concurrently associated medical conditions that interact with CNS pathology. One
challenge commonly encountered in the NCCU is balancing the risks/benefits of antiplatelet/anticoagulant agents used in acute coronary syndrome against the risk of postoperative hemorrhage. Each case needs to be carefully evaluated before a treatment strategy
is initiated. Potential iatrogenic induced cardiovascular problems include: diuretic and steroidinduced hypovolemia and hypokalemia-induced ventricular irritation, bradycardia with low
cardiac output caused by surgical stimulation of the vagal nucleus in the brainstem, and a
Cushings-like response with poor venting of ventricular perfusate during endoscopic third
ventriculostomy. Prone and seated positions are associated with low cardiac output, venous
return and blood pressure.
Blood pressure control
Changes in blood pressure are common postoperative complications. Many times the surgeon
will have specific BP parameters depending on where the goal is to prevent hematomas or
preserve perfusion.
Hypotension
Fluid loss from the intravascular space (bleeding) and extravascular space (e.g. vomiting,
diarrhea, and sweating) can contribute to hypovolemia (Table 5). This may exacerbate cerebral
ischemia. Fluid therapy is discussed below. Circulation support to influence CBF is achieved best
by increasing blood pressure, as cardiac output appears not to vary with CBF. The drug of
choice to increase blood pressure is phenylephrine. With active baroreflexes, bradycardia may
occur. Careful anticholinergic administration then is necessary to augment the
sympathomimetic hypertensive action. Patients with low myocardial reserve may require an
inotrope, such as dopamine or epinephrine.
Hypertension
Increased blood pressure may be associated with pain, emergence from anesthesia, and the
underlying disease which can lead to postoperative hemorrhage and exacerbate edema. Acute
hypertension is associated with increased mortality in the NCCU (9). The precise level that
represents a risk varies and depends on patient, disease, procedure, lesion size, traumatic
disruption of vessels, and premorbid blood pressure. Strategies to limit commons irritants or
triggers of hypertension include prevention and timely treatment of bladder distention, pain
and shivering. Since sympathetic stimulation is responsible for the blood pressure increase,
beta-blocker infusions are largely used. Esmolol and labetalol are effective agents since they
have no significant effect on ICP. Cardene is a calcium-channel blocker that is used frequently
with good success. Nitroglycerin, and sodium nitroprusside are cerebral vasodilators and these
agents may increase cerebral blood volume. The specific agent used will depend on several
factors including the perceived integrity of autoregulation and management strategy being
employed for a given patient (i.e. Lund vs. Rosner theories regarding the relationship between
ICP and MAP). In patients with severe hypertension post operatively, the elevated blood
pressure also should considered to be a sign of intracranial pathology. This is particularly
important after posterior fossa surgery. Lastly, one should always carefully consider a patients
home medication regimen and be mindful of complications from that regimen being altered in
the perioperative period (such as rebound phenomena from beta blocker withdrawal).
Fluid status
Osmolality is the primary determinant of water movement across the intact bloodbrain
barrier. Reduced serum osmolality can increase cerebral edema and ICP. The goals of fluid
management after neurosurgery are: 1) maintain intravascular volume, 2) preserve CPP, and 3)
minimize cerebral edema. In neurosurgical patients, and often in the postoperative period,
intravascular volume is depleted (e.g. diuretic use, osmotherapy, or long spinal surgeries where
large volume losses may be encountered). Systemic hypotension (MAP <70 mmHg) and
negative fluid balance (<594 ml) independently aggravate outcome in TBI patients [31]. Basic
fluid and electrolyte requirements must be considered in the postoperative period. In clinical
practice, fluid management requires circulating blood volume assessment (Table 5). A patient
generally is asymptomatic until the circulating volume has decreased by at least 10%. A
persistently low urine output (<0.5 ml/kg/hour) may indicate inadequate fluid replacement and
thirst often is the first sign of reduced intravascular volume even though other vital signs are in
the normal range. However when diuretics or mannitol are given, urinary output can be
misleading. Lastly, thirst is not present if the patient is drowsy or sedated.
New technologies have also become quite helpful in hemodynamic assessment, volume
management, and the institution of more specific goal-directed therapy in ICU patients. One is
arterial pulse contour wave analyses which require invasive arterial lines to obtain data. There
are several manufacturers who make analogous equipment taking advantage of arterial pulse
pressure (PP) waveform analysis to provide continuous assessments of volume status and
cardiac hemodynamics. There is more than one methodological strategy employed to derive
such parameters including: a) calibrated PP analysis relying on thermodilution for calibration
(PiCCO) and b) statistical analysis via computer-derived algorithms (Vigileo). One of the more
common variables assessed is stroke volume variation (SVV) which is used to optimize volume
status in ICU patients such as those with subarachnoid hemorrhage. Non-invasive technologies
also exist that assist in fluid management and hemodynamic monitoring. These include
impedance cardiography (ICG) and a device that relies on bioreactivity and detecting phase
shifts that occur when an alternating current is passed through the thorax (Cheetah NICOM).
Lastly, critical care ultrasound techniques such as IVC compressibility are also used to assess
volume status. All of these technologies are crucial to the increasingly adopted goal-directed
therapy with more restrictive use of crystalloid administration (unless contraindicated) in the
perioperative period.
Fluid therapy
Complications can result from inadequate or excessive volume replacement. Inadequate
volume can cause hypotension, perfusion deficits, and acute kidney injury. Excess fluid therapy
can exacerbate heart failure, pulmonary function or cerebral edema. There are few human data
about the impact of fluids on the brain that can guide rational fluid management in
neurosurgical patients. The optimal fluid to prevent secondary brain damage after neurological
insult also is unknown. Fluid administration that reduces osmolality should be avoided. Small
volumes of lactated Ringers (13L) are unlikely to be detrimental and may be used. When
larger volumes are needed a more isotonic fluid e.g. normal saline (0.9% NS) is preferred. Rapid
NS infusion may cause a dose-dependent hyperchloremic metabolic acidosis (normal anion
gap). When large volumes are needed, a combination of isotonic crystalloids and colloids
should be considered. However Hetastarch and Dextran should be avoided since coagulation
disorders, platelet dysfunction, and kidney injury may occur. While hypertonic saline is gaining
popularity for treatment of intracranial hypertension it is not recommended for fluid
resuscitation or volume replacement. One advantage HTS seems to have over mannitol in
treating ICP is its ability to move fluid from the body's own extravascular space into the
circulation across a sodium gradient without necessarily risking hypotension from diuresis [32].
Hyperglycemia is an independent predictor of poor outcomes, and so it is reasonable to avoid
glucose-containing fluids.
Sodium balance: Sodium homeostasis is critical in neurosurgical patients. Disorders of sodium

metabolism including diabetes insipidus, syndrome of inappropriate ADH secretion (SIADH) and
cerebral salt wasting syndrome need to be diagnosed and treated. This important topic is
discussed in a separate chapter of this manuscript.
POSTOPERATIVE MONITORING
Systemic and neuromonitoring are essential after neurosurgery to help identify patients who
may deteriorate. However relatively few studies describe how postoperative monitoring
influences outcome. Therefore, in most patients decisions about monitoring should be based
on the patients presentation, the surgical procedure, and clinical judgment. The most
important monitor after elective neurosurgical procedures is the repeated clinical examination.
Neurological evaluation
Postoperative neurological evaluation is focused on two characteristics - consciousness and
focal neurologic findings. The procedure may determine the specific focal finding to
concentrate upon. For example, assess for foot drop after an L4/5 discectomy. Objective
scoring instruments are useful since they can limit inter - and intra-observer variability and
objectify some examination findings making communication among practitioners easier. That
said nothing replaces a detailed neurologic examination for detecting subtle changes in
neurologic function. Common instruments include: the Glasgow Coma Score, Full Outline of
UnResponsiveness (FOUR score), Reaction Level Score, and NIH Stroke Scale.
Systemic
Hypoxia and hypotension are the two most important systemic secondary insults in TBI
patients, and it is reasonable to presume this also is true for postoperative neurosurgical
patients. Therefore, oxygen saturation by pulse oximetry and blood pressure should be
continuously monitored. Continuous EKG also should be considered (e.g. severe arrhythmias
may occur after SAH). Other cardiovascular monitors (e.g. pulmonary artery catheters, invasive
pulse pressure contour monitors, non-invasive impedance cardiography ) may be necessary for
patients with pre-existing cardiac disease, neurogenic pulmonary edema, SAH with stunned
pericardium, or Takatsubos cardiomyopathy. The arterial partial pressure of CO2 (PaCO2) is an
important determinant of CBF. A PaCO2 change can be determined by blood gas analysis or
estimated from end-tidal CO2 (ETCO2). There, however, is debate about ETCO2 reliability in
neurosurgical patients.
Intracranial Pressure
The incidence of elevated ICP after neurosurgical procedures has had little study and most likely
is underestimated. In addition, the impact of elevated ICP on outcome after neurosurgery has
not been examined despite management of cerebral edema and elevated ICP being critical
components of perioperative craniotomy care. Postoperatively elevated ICP can be expected in
about 15% of patients. An ICP monitor should be considered in the following circumstances:
large vascular tumors, severe edema, trauma surgery, deeply sedated patients where an exam
cannot be obtained (or a patient fails to wake up), known operative complications (e.g.
aneurysm rupture, known vessel occlusion), and large fluid shifts are expected.
Other monitors
For most patients the extent of specialized neuromonitoring should be based on the clinical
presentation and the experience of the responsible physician. This includes 1) bedside CBF
assessment (e.g. jugular bulb oximetry, Transcranial Doppler sonography [TCD] Thermal
diffusion flowmetry, Near infrared spectroscopy [NIRS]), 2) Microdialysis and brain tissue
oxygen tension (PbtO2) and 3) Electroencephalography (cEEG).
Imaging
Imaging is a snap-shot in time. CT investigations in critically ill neurosurgical patients are useful
to monitor the course of the illness and for the early detection of complications and should be
considered when neurological deterioration occurs or the expected postoperative
improvement does not occur. When early detection of ischemia is necessary MRI is superior to
CT since diffusion weighted imaging (DWI) can recognize ischemic injury within 30-60 minutes
of onset. In addition, CT-angiograms and CT-perfusion scans are rapidly improving technologies
that are broadening diagnostic imaging options for practitioners. There is a well-documented
risk of transporting patients to scanners and portable CT scanners are becoming increasingly
adopted in NCCUs.
Surgical drains
Many procedures require use of post-operative drains. This can entail hemovacs or JP drains
left after craniotomy or lumbar drains left after spinal surgeries where there is a concern for
CSF fistula formation. The neurointensivist should always communicate clearly with the
surgical team to fully understand what compartment the drain was left in (subgaleal, epidural,
subdural). This is crucial to evaluating both the quality (blood, CSF) and quantity of drain
output. It is advisable to never remove a post-operative drain until you have specifically
discussed its purpose with the surgeon.
CONCLUSION
Following a neurosurgical procedure, the patient remains vulnerable to secondary CNS injury
because of the pathological changes associated with the disease, the nuances of the procedure
itself, and the physiological changes associated with management. The level of care after
surgery should be no less than that given during the procedure. Whereas the surgeon may
influence patient's anatomy, it is the neurointensivist role in collaboration with the
neurosurgeon to ensure the patient's physiological stability and to navigate the transition from
pre- and intra-operative care through recovery and return to the ward.
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Table 1. Systemic and brain conditions necessary for rapid postoperative awakening and
extubation after a neurosurgical procedure
Brain Conditions
Normal pre-operative level of consciousness
Surgery < 6 hours
Systemic Conditions
Normothermia (~36oC)
Normovolemia, normotension
(70 mmHg < MAP< 120 mmHg)
No major CNS or vascular injury
Spontaneous ventilation and PaCO2 <50
mmHg
No brain swelling
Normoglycemia (glucose 4-8 mmolL)
Antiepileptic prophylaxis when indicated
Normosmolality (>280 mOsm/kg)
Intact lower cranial nerves (IX,X,XII) - airway Hemoglobin ~9g/dl
protection
Normal coagulation status
No major swelling of face and tongue
Table 2. Checklist before extubation of a neurosurgical patient.

Discuss expected postoperative course and potential complications and agree with the
neurosurgeon about postoperative management
Check antiepileptic prophylaxis
Infuse analgesics before the end of anesthesia
Check respiratory and cardiovascular parameters
Check adequate recovery of muscle strength if muscle relaxants were used
Check pupil size and awareness
Prepare IV antihypertensive agents for blood pressure control
Check adequate spontaneous ventilation with end-tidal CO2 < 50 mmHg
Check the vacuum system
Be prepared to give supplemental oxygen after extubation
Assess adequate recovery of neurologic function
Table 3. Factors associated with readiness to wean ventilator support in neurosurgical patients.
Clinical assessment
Adequate cough
Absence of excessive tracheobronchial secretions
Resolution of disease acute phase for which the patient was intubated;
Normal intracranial pressure (ICP)
Objective measurements
Clinical stability
o Stable cardiovascular status (i.e. heart rate 140beats/min; systolic BP 90-160
mmHg, no or minimal vasopressors)
o Stable metabolic status
Adequate oxygenation
o SaO2 > 90% on FIO2 0.4 (or PaO2/FIO2 150 mmHg)
o PEEP 8mmHg
Adequate pulmonary function
o Respiratory rate 35 breathes/minute
o Maximal inspiratory pressure -20 to -25 cm H2O
o VT >5 mL/kg
o VC >10 mL/kg
o Rapid shallow breathing index <105 breaths/min/L
o No significant respiratory acidosis
Abbreviations: BP = blood pressure; FIO2 = inspiratory oxygen fraction; PaO2 = arterial oxygen
tension; PEEP = positive end-expiratory pressure; SaO2 = arterial oxygen saturation; Rapid
shallow breathing index = respiratory rate/VT; VT = tidal volume; VC = vital capacity.
Adapted with permission from Boles J, Bion J, Connors A, et al. Weaning from mechanical
ventilation. Eur Respir J 2007; 29:103356.29
Table 4. Spontaneous breathing trials in neurosurgical patients: failure criteria

Clinical assessment and subjective indices
Agitation and anxiety
Deterioration in mental status
Diaphoresis
Cyanosis
Evidence of increasing effort
o Increased accessory muscle activity
o Dyspnea
Objective measurements
Agitation and anxiety
PaO2 50-60 mm Hg on FIO2 0.5 or SaO2 < 90%
PaCO2 > 50 mmHg or an increase in PaCO2 by >8 mmHg
pH < 7.32 or a decrease in pH 0.07 pH units
Respiratory frequency >35 breath/min1 or increased by >50%
Rapid shallow breathing index >105 breath/min/L
HR >140 breath/min1 or increased by >20%
Systolic BP >180 mmHg or increased by >20%
Systolic BP <90 mmHg
Cardiac arrhythmias
Abbreviations: BP = blood pressure; FIO2 = inspiratory oxygen fraction; HR= heart rate; PaCO2 =
arterial carbon dioxide tension; PaO2 = arterial oxygen tension; SaO2 = arterial oxygen
saturation..
Adapted with permission from Boles J, Bion J, Connors A, et al. Weaning from mechanical
ventilation. Eur Respir J 2007; 29:103356.29
Table 5: Clinical assessment of volume status in a 70 kg patient

Blood loss (ml)
Blood loss (% of blood volume)
Heart rate (beats/min)
Blood pressure
Pulse pressure
Capillary return
Respiratory rate (breaths/min)
Urine output (ml/hour)
Mental status
750
15
<100
Normal
Normal
Normal (<2 s)
14-20
>30
Normal
750-1500
15-30
>100
Normal
Reduced
Prolonged
20-30
20-30
Anxious
1500-2000
30-40
>120
Reduced
Reduced
Prolonged
30-40
5-15
Confused
2000
40
140
Reduced
Reduced
Prolonged
35
Negligible
Drowsy
PERIOPERATIVE NEUROSURGICAL CRITICAL CARE QUESTIONS

1. A patient with a lumbar drain who was awake and doing well after an endoscopic skull base
procedure to remove an olfactory groove and parasellar meningioma suddenly deteriorates.
Immediate management may include:
a) Give antibiotics
b) Administer mannitol
c) Clamp the lumbar drain
d) Give ativan
e) Restrict sodium intact
2. A 73 year old man with COPD, asthma, and obstructive sleep apnea is admitted to the NCCU
after CEA under general anesthesia. Within 3 hours of arrival the nurse calls you and
informs you the patient is complaining of breathing difficulty. When you arrive at the
bedside, the patients neck is swollen and he is stridorous. The most appropriate next step
to take is:
a) Give him supplemental oxygen and racemic epinephrine nebulizer
b) Immediately order a carotid duplex
c) Immediately call the surgeon and anesthesia so that they can open the wound
and then intubate the patient
d) Immediately call the surgeon and anesthesia so that he can be intubated and
then taken to the operating room
e) Immediately order a neck CT and CT-angiogram
3. Adequacy of pulmonary ventilation is assessed by
a) FiO2
b) Oxygen saturation
c) PaCO2
d) Partial pressure of O2 in the blood
e) Tidal volume
4. All but the following are associated with successful extubation
a) RR <35 breaths/minute
b) Negative Inspiratory Pressure of at least -20 to -25 cm H2O
c) Rapid Shallow Breathing Index (RSBI) of >105
d) VC >10-15 mL/kg
e) PF Ratio >200
5. Match the anesthetic agent with the description. Each response may be used once, more
than once or not at all
a) Enflurane
b) Etomidate
c) Halothane
d) Isoflurane
e) Ketamine
f) Thiopental
1.
2.
3.
4.
5.
6.
Increases CBF and CMRO2

Of the volatile anesthetic agents increases CBF the least
Induces seizure discharges
Dissociative anesthetic
Decreases CBF and CMRO2 and produces cardiovascular depression
Decreases CBF and CMRO2 and suppresses adrenocortical response to stress
6. Risk factors for postoperative intracranial hematomas include the following except
a) Blood loss >500mls
b) Young age
c) Postoperative hypoxia
d) Meningioma surgery
e) Seizure
7. A 63 year old woman is now 32 hours s/p subocciptial craniectomy for resection of a
cerebellar metastasis (primary being melanoma). She continues to be awake and alert but
the nurse notes she has been struggling to control her blood pressure. She has given
labetolol twice and now has started a Cardene infusion to control the blood pressure. You
were called as the Cardene drip was started because her blood pressure remains 192/100
and she is beginning to look uncomfortable. The next step in the management should be:
a) Give her another prn dose of labetolol
b) Increase the Cardene until you control the blood pressure
c) Place an EVD
d) Carefully examine the patient and order a head CT
e) Give 4mg intravenous morphine
8. True or false: Postoperative nausea and vomiting is more common in:
a) Males
b) Non-smokers
c) Surgery <60 minutes
d) Posterior fossa surgery
e) CSF leak
9. All the following statements are true about lung-protective ventilation strategy except:
a) Tidal volumes of 5-7cc/kg of ideal body weight are recommended
b) Permissive hypercapnia should be avoided as it may exacerbate intracranial
hypertension
c) Elevated PEEP may help reduce FiO2 to <0.6 and improve gas exchange
d) Plateau pressures should be kept <30cm H2O
e) The use of pressure control ventilation may prevent barotrauma but at the
expense of variability in tidal volume
10. A patient has recently returned from the angio suite to your ICU after elective coiling of a
complicated bi-lobed anterior communicating artery aneurysm. There was some concern of
a prolapsed coil, although complete obliteration of the aneurysm, so the patient was
started on Reopro overnight. A few hours after arrival you are notified the patient is
hypotensive and diaphoretic. The next most appropriate step in the management of this
case would be:
a) Order and EKG and cardiac biomarkers
b) Order a fluid bolus
c) Obtain a stat head CT
d) Order neosynephrine to raise SBP to 140
e) Inspect the groin-site and distal pulses
PERIOPERATIVE NEUROSURGICAL CRITICAL CARE ANSWERS

1. The correct answer is C. Sudden deterioration should trigger the thought of over drainage
with parenchymal shift due to the lumbar drain. Infection is not likely to cause sudden
deterioration without systemic red flags preceding the event. Seizure is possible but not as
likely as meningiomas are extra-axial tumors and there was not physical signs of seizure
activity. Mannitol may worsen the condition. Hypernatremia is unlikely to cause an abrupt
decline and sodium restriction will not quickly reverse the issue even if related.
2. The correct answer is C. This is an emergent situation. Ideally the patient could be taken to
the operating room before opening the wound, but in this case bedside hematoma
evacuation seems prudent. Intubation will likely be extremely difficult until the pressure
from the hematoma is relieved. The clinical scenario described clearly rules out time for
diagnostic studies. Epinephrine and oxygen are inappropriate and do not reflect a
treatment for the problem at hand.
3. The correct answer is C. Choices a, b, and d relate to oxygenation. Tidal volume affects
ventilation but it cannot be used to assess ventilation.
4. The correct answer is C. An RSBI < 105 is predictive of successful extubation.
5. The correct answers are 1-a, 2-d, 3-a, 4-e, 5-f, 6-b.
6. The correct answer is B.
7. The correct answer is D. Refractory hypertension after posterior fossa surgery should
always raise suspicions about a post-operative hematoma. Further attempts to control BP
may cause one to lose valuable time to intervene while the hemorrhage is expanding.
Hydrocephalus is a possible complication and will be seen on head CT, but placing an EVD
without radiographic evidence is not recommended. Sedation may decrease BP in some
patients who are in pain, but one must rule out more serious pathology first.
8. The correct answers are a-False, b-true, c-false, d-true, e-true.
9. The correct answer is B. Permissive hypercapnia is a known effect of lung-protective
ventilation strategy. This should be carefully considered and the risk accepted when this
ventilation strategy is initiated. One can try to limit the increase in PaCO2 but it should not
be avoided all together in serious cases such as ARDS where this ventilation strategy is
crucial. All the other choices are accurate features of lung-protective ventilation strategy.
10. The correct answer is E. This has all the features and red flags of a pseudoaneurysm. The
groin should be inspected and pressure held on the site. Vascular surgery is often involved
early. The other options may be appropriate once pseudoaneurysm has been ruled out.

Perioperative Neurosurgical Critical Care: Chris Zacko

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2013 Neurocritical Care Society Practice Update