Professional Documents
Culture Documents
TO
STUDENTS OF MEDICINE
HOW TO EXAMINE
A PATIENT
A POCKET GUIDE
T O STUDENTS OF MEDICINE
BY
DR. M E N I N O DE S O U Z A , M.D.
Emeritus Professor of
Grant Medical College,
and
Ex-Consulting
Physician
J.J. Hospital,
THIRD
Medicine,
Bombay,
and
Neurologist,
Bombay.
EDITION
1970
K O T H A R I
B O O K
BOMBAY
D E P O T
DR.
MENINO
First Edition
Second Edition
Third Edition
DE
SOUZA
1955
1960
1970
M . DE SOUZA
CONTENTS
CHAPTER I
CASE-TAKING
PACE
General Scheme
Case-Taking
Complaint and Duration
History of the Present Illness
Previous Diseases
Personal History . . . ."
Family History
General Examination
Consciousness and Intelligence 4; Decubitus 5; Voice
and Speech 5; General Development and Nutrition 6;
Pulse, Respiration and Temperature 11.
1
2
2
2
3
3
4
4
CHAPTER I I
RESPIRATORY
SYSTEM
General Scheme
Interrogation of Common Symptoms and Signs . . . .
Cough 16; Dyspnoea 16; Pain in the Chest 17;
Haemoptysis 17; Hoarseness of Voice 17; Hiccough 17.
Surface Markings of the Lungs
Examination of the Upper Air Passages
Nose 20; Neck 20; Larynx 20; Trachea 20.
Examination of the Chest
Inspection 21; Palpation 27; Percussion 29;
Auscultation 33.
Examination of Sputum
Examination of Pleural Fluids
Manifestations of Common Respiratory Disorders . . . .
Cough 43; Pain in the Chest 45; Epistaxis 46;
Haemoptysis 48; Hoarseness of Voice 50; Cyanosis 51;
Dyspnoea 53.
vii
15
16
18
20
21
37
41
43
viii
CONTENTS
CHAPTER I I I
CARDIO-VASCULAR
SYSTEM
PAGE
General Scheme
Interrogation of Common Symptoms and Signs . . . .
Dyspnoea 62; Praecordial Pain 62; Palpitation 63;
Syncope 63; Giddiness 63; Venous Congestion 63.
Surface Marking of the Heart
Examination of the Heart
Inspection 65; Palpation 68; Percussion 71;
Auscultation 73.
Pulse
Abnormal Pulse 82; Irregular Pulse 84.
Blood Pressure
High Blood Pressure 88; Low Blood Pressure 92.
Exercise Tolerance Test
Common Cardiovascular Disorders
Cardiac Pain 94; Palpitation 99; Syncope 100; Shock 101;
Oedema 102.
Circulatory Failure
Central (cardiac) Failure 108; Peripheral Failure 110
Enlargement of the Heart
Hypertrophy 111; Dilatation 115.
Cardiac Murmurs
Functional Murmurs 115; Mitral Murmurs 116; Aortic
Murmurs 1.19; Pulmonary Murmurs 121; Congenital
Murmurs 122; Myocardial Murmurs 123; Exocardial
Murmurs 123; Vascular and Haemic Murmurs 124.
61
62
64
65
80
86
93
94
107
110
115
CHAPTER I V
ALIMENTARY
SYSTEM
General Scheme
Interrogation of Common Symptoms and Signs . . . . .
Pain 128; Vomiting 128; Indigestion 129; Sore Tongue
129; Diarrhoea 129; Constipation 130; Haematemesis
130; Appetite 130; Thirst 130; Dysphagia 131; Jaundice
131; Blood in Faeces 131; Abdominal Swelling 132;
Flatulence 132; Eructation 132; Water-brash 132;
Heartburn 132.
127
128
CONTENTS
ix
PACF.
132
136
138
144
147
147
1 51
153
159
160
168
168
175
191
192
199
201
CHAPTER V
CENTRAL NERVOUS
SYSTEM
General Scheme
.
205
Interrogation of the Common Symptoms and Signs . . . 206
Fits 206; Fainting 207; Headache 207; Vertigo 208;
Paralysis 208; Neuralgic Pains 208; Tingling and Numbii
CONTENTS
PAGE
210
256
257
259
265
289
304
307
308
308
312
CHAPTER V I
GENITO-URINARY
SYSTEM
General Scheme
Interrogation of Common Symptoms and Signs . . . .
Haematuria 316; Polyuria 316; Oliguria 316; Dysuria
31.7; Frequency 317; Incontinence 317; Pain 317.
Examination of the Kidneys and Bladder
Examination of Urine
. . . . 3
Renal Efficiency Tests
Enlargement of the Kidneys
Abnormalities of Micturition
Common Urinary Disorders
315
316
318
1 9
329
330
332
335
CONTENTS
xi
CHAPTER V I I
HAEMOPOIETIC
SYSTEM
PAGE
General Scheme
Interrogation of Common Signs and Symptoms . . . .
Method of Blood Examination
Red Cells 360; White Cells 360; Haemoglobin 360;
Reticulocytes 361; Haematocritic determination 361; Red
Cell Indices 362; Platelet Estimation 365; Fragility Test
363; Sedimentation Rate 363; Coagulation Time 365;
Prothrombin Time 366. ,
Examination of the Bone Marrow
Blood Chemistry
Blood GroupingBlood Transfusion
Disorders of the Red Cells
Anaemias 376; Polycythaemia 380.
Disorders of the White Cells
Leucocytosis 384; Leucopenia 385; Agranulocytosis 385;
Lymphocytosis 386; Monocytosis 387; Eosinophilia 387;
Basophilia 388.
Blood Platelets and their Disorders
Lymph Glands
Generalised Enlargement 389; Localised Enlargement 390.
CHAPTER
LOCOMOTOR
357
358
358
366
368
372
375
381
388
389
VIII
SYSTEM
General Scheme
393
Interrogation
394
Muscular Disorders
394
Examination of Bones
395
Skull 395; Vertebral Column 399; Backache 400; Long
Bones 401; Small Bones 402; Nodes on the Fingers 402.
Examination of Joints
402
Arthritis
404
xii
CONTENTS
CHAPTER
SKIN A N D ITS
IX
APPENDAGES
PAGE
General Scheme
Examination of the Skin
Inspection 408; Palpation 411; Microscopic Examination
412.
Pigmentation of the Skin
Eruptions of the Skin
Haemorrhages under the Skin
Ulcers of the Skin
Examination of the Hair
Examination of the Nails
407
408
409
410
410
410
412
412
CHAPTER X
EXAMINATION
OF
CHILDREN
Family History
Present Illness
Clinical Examination
415
416
416
CHAPTER X I
EXAMINATION OF PSYCHIATRIC
PATIENTS
"Main Complaint
Family History
Personal History
General Examination
423
423
423
424
APPENDICES
428
Appendix C: Infections
Animal Reservoirs 435; Insect Vectors 435; Eruptive
Fevers 436; Infestations 437.
435
CHAPTER I
GENERAL,
SCHEME
I. NAME
Age ..
Sex
Nationality
Occupation
Marital Status
i'
Address
II. COMPLAINT AND DURATION.
III. HISTORY OF T H E PRESENT ILLNESS.
IV. PREVIOUS DISEASES.
V. PERSONAL HISTORY :
1. Marital history.
2.
Occupation.
3.
Environment.
4.
Social history.
5.
Habits.
CASE
TAKING
After entering the name, age, etc., proceed with the interrogation of the patient systematically so as to elicit the salient
features of the disease. Be accurate and comprehensive while
examining the system affected; be concise while examining the
others.
T h e mental attitude of an average patient, his ability to
answer questions and his psychological make-up is within normal
limits and hence, case-taking in most cases can be considered as
fairly reliable.
COMPLAINT
AND
DURATION
OF T H E PRESENT
ILLNESS
quality,
dissipation,
CASE
TAKING
Menstrual history.
Miscarriages and still-births.
Difficulty during delivery.
Abnormality of the child or foetus.
Financial condition.
Number
5. Habits:
(a) Foodits quality and quantity. Hours and regularity
of meals. Time taken over each meal. These details
are very necessary in Digestive Disorders.
(b) Addiction to alcohol, smoke, tea, coffee and drugs.
Their quality and intake per day.
(c) Exercise; recreation; holidays.
(d) Sexual life, if deemed relevant.
(e) Nature of sleep.
HISTORY
I.
EXAMINATION
CASE
TAKING
II.
DECUBITUS
often assume
unusual
attitude
to
any
III.
Body Configuration.
3.
4.
5.
6.
7.
8.
hands broad
with
CASE
TAKING
P L E T H O R I C T Y P E : S a m e as STHENIC
TYPE, but with florid complexion and suffused eyes. These people often suffer from heart and kidney
diseases.
P H T H I S I C A L T Y P E : S a m e as ASTHENIC
rated form with poor nutrition.
TYPE
in a highly exagge-
family history.
If rapid or gradual in onset.
The distribution of^fatif generalised or localised.
If there is any associated pain.
Habits of diet.
Exercise.
(a) CONFIGURATION
VIII.)
(b) FACIAL
OF THE
SKULL
AND
THE
FACE.
(See Chapter
EXPRESSION
T h e expression of a patient is mainly determined by the appearance of the eyes. They may be:
A N X I O U S a c u t e pain, acute illness.
APATHETICtyphoid,
psychic depression.
EXPRESSIONLESSParkinsonism,
cretinism.
BRIGHThyperthyroidism.
VACANTmeningitis, encephalitis, other conditions where consciousness
is growing dull.
WILDacute mania.
S T U P I D m e n t a l deficiency, cretinism.
SHIFTYdrug addict, masturbator, giving wrong history of the illness,
self-conscious.
RESTLESS EYESphthisis.
SELF-SATISFIED LOOKchronic
alcoholism.
FLUSHEDpneumonia.
SUNKENcholera, severe wasting, dehydration.
F I X E D SMILERisus Sardonicus
of tetanus.
OF THE
EYES
angioneurotic
cranial nerve);
oedema,
retraction
CASE
(d) COLOUR
OF THE
TAKING
FACE
(pallor).
OF THE
leucoderma.
alcoholism, cirrhosis liver.
LIPS
etc.
pneumonia,
meningitis, virus
infections.
syphilis.
OF THE
NOSE
Examine the nose especially for size and shape. Also examine
the nostrils for septal defects, polypi, ulcers and perforation.
The nose may be:
LARGEacromegaly
bulbousrhynophyma.
PINCHEDadenoids.
SADDLE-SHAPED O R W I T H
SUNKEN BRIDGEcongenital
syphilis.
10
RED-TIPPEDchronic
acne rosacea.
"BUTTERFLY"
matosus.
(g) EXAMINATION
alcoholism,
mitral
stenosis, chronic
APPEARANCE A R O U N D
OF THE
indigestion,
T H E NOSElupus
erythe
EARS
OF THE
MASTOIDmastoiditis.
MUCOUS
MEMBRANES
retraction,
pigmentation,
(See
syphilis.
blue
line
of
lead
CASE
TAKING
11
12
3.
4.
5.
The common types of fevers may be grouped under the following headings:
A.
B.
C.
FIG. I
Continuous Fever followed by Crisis. Case of Lobar Pneumonia.
CASE
TAKING
FLC. 11
Remittent Fever. Case of T y p h o i d .
FIG.
Ill
1.8
FIG. IV
Fever dropping by Lysis. Case o Broncho-Pneumonia.
CHAPTER
RESPIRATORY
II
SYSTEM
A.
INTERROGATION.
B.
C.
D.
EXAMINATION OF T H E CHEST.
I.
Inspection.
II.
Palpation.
III.
Percussion.
IV.
Auscultation.
E.
EXAMINATION OF SPUTUM.
F.
1.8
H O W TO EXAMINE A PATIENT
A.
INTERROGATION
COMMON
SYMPTOMS AND
SIGNS
Its frequency.
Duration.
When worse, when better; if seasonal.
Its characterif paroxysmal, explosive, irritating, etc.
Its toneif resonant, suppressed, husky, etc.
If with or without expectoration.
If accompanied by pain, distress, whoop, etc.
If associated with vomiting or haemoptysis.
If brought on by posture, effort, etc.
If there is any change in the voice.
Amount and character of the sputum according to the
patient.
RESPIRATORY
SYSTEM
17
5.
Colour.
5.
Duration.
2.
3.
If progressive or improving.
4.
History of tuberculosis.
5.
Habits of smoking.
6.
Occupation.
HICCOUGH
Inquire into the following:
1. History of gastric disturbanceseructation,
abdominal discomfort, etc.
2.
2
vomiting,
1.8
3.
4.
COMMON SIGNS
1. Cyanosis. Examine the lips, cheeks, ears, nose and nails
particularly (see page 51).
2.
3.
4.
5.
MARKINGS
OF T H E
LUNGS
pleura lies
but at the
cm. or so
cm. below,
T h e lobes of the lungs may be marked by drawing a line from the spine
of the 2nd dorsal vertebra to the junction of the 6th costal cartilage with
the sternum. T h i s line crosses the 5th rib in the axilla. Below it, on
each side, lie the lower lobes and above it, the upper lobes. T h e upper
margin of the right middle lobe may be defined by taking a line from the
junction of the 4th costal cartilage with the sternum to meet the previous
RESPIRATORY
SYSTEM
19
line at the mid-axillary line. It will be recognised at once that the upper
lobes and the middle right lobe are mainly accessible from the front and
the lower lobes almost entirely from the back. In the axilla, parts of all
lobes are open to examination.
FIG. V
LULLeft Upper Lobe
RULRight Upper Lobe
LLLLeft Lower Lobe
RMLRight Middle J.obe
RLLRight Lower Lobe
For the sake of convenience the surface of the chest may be divided into
the following regions:
I.
II.
2.
3.
2.
3.
4.
5.
1.8
HOW TO EXAMINE A PATIENT
III.
IV.
T w o Iaternal regions.
1.
Axillary
2.
Infra-axillary
}
)
2.
3.
4.
Important landmarks
T h e lower end of the sternum marks the 7th rib and corresponds with
the 9th dorsal vertebra behind.
T h e tip of the 9th rib is in about the mid-clavicular line.
T h e tip of the 11th rib is in mid-axillary line.
T h e most prominent spine in the back is that of the 7th cervical vertebra.
T h e lower angle of the scapula is at about the 6th or 7th interspace.
4.
5.
TRACHEA.
(a) Locate its position. Insert your forefinger in the
jugular notch between the trachea and the sternomastoid; the finger will slip to one side if the trachea
is deviated on to the other side. Displacement of the
trachea and the apex beat suggest that the position of
RESPIRATORY
SYSTEM
21
EXAMINATION OF T H E CHEST
I.
INSPECTION
1.8
R A T E OF R E S P I R A T I O N
2.
T Y P E OF
BREATHING
Normal breathing in males and in some females is abdominothoracic. It may be thoraco-abdominal in some females.
1.
2.
3.
pleurodynia
RHYTHM
RESPIRATORY
SYSTEM
PROLONGED EXPIRATIONbronchial
and renal asthma.
23
finds
disease.
chloral.
Uraemia.
4.
FORM OF C H E S T
1.8
axis vertical. The ratio between the transverse and anteroposterior diameter is 7 : 5; the subcostal angle is 70; the interspaces are broader in front than behind.
Bilateral deformities
1. Indicating proclivity to lung diseasesespecially
tuberculosis
is
in
FIG. V I
Cross Section of
Rachitic Chest
Cross Section of
Pigeon Breast
RESPIRATORY
SYSTEM 39
Unilateral deformities
(a) Bulgingfluid or air in the pleura, new growths in the lungs,
very big heart, pericardial effusion, tumours, aneurysms, empyema
necessitans, subcutaneous emphysema on one side.
(b) Unilateral depressionfibrosis, atelectasis, pleural adhesions,
emphysema.
old
M O V E M E N T S OF T H E
CHEST
ABNORMAL
MOVEMENTS
OF THE
CHEST
of
the
lungs
by
pneumonia,
tuberculosis
or
new
1.8
consolidation.
Occurs in
PRESENCE OF VEINS
RESPIRATORY
II.
SYSTEM
27
PALPATION
Apex-beat.
2.
Tenderness.
3. Fluctuation.
4. Form of the Chest.
5.
6. Vibrations.
1.
THE
APEX-BEAT
T h e apex-beat is normally felt in the 5th interspace half-aninch inside the left mid-clavicular line. Its displacement alone
without displacement of the trachea, may be due to enlargement of the heart or disorders outside the heart like scoliosis.
If both the apex as well as the trachea are shifted it- is a definite
evidence of mediastinal shift.
Z
TENDERNESS
FLUCTUATION
FORM
OF T H E
CHEST
If present, it has a
1.8
M O V E M E N T S OF CHEST
VIBRATIONS
Use the same hand on both sides because the sensitivity of the
two hands differ. Feel with the palms of the hand. Experts
may use both hands symmetrically placed on either side of the
chest and then move them to the various parts of the chest.
Feel for:
(a) Pleural frictionoccurs in early pleurisy due to rubbing
of the two pleural surfaces against each other.
(b) Rhonchal fremitusoccurs when there are catarrhal
changes in the bronchi as in bronchitis, asthma, and
pulmonary congestion. T h e "death rattle" in acute
oedema of the lungs constitutes a striking sample.
(c) Tactile vocal fremitus. Ask the patient to say some
words with a nasal sound e.g. ninety nine, and feel with
the flat of the hand for the vibrations transmitted from
the larynx through the bronchi, lungs and the chest wall.
T h e high-pitched voices of women and children do not
produce vibrations as good as the lower tones of the male
voice. In children, however, the voice, although higher
RESPIRATORY
SYSTEM
29
PERCUSSION
Percussion reveals the character of the lung tissue and the surrounding pleura.
Although percussion of the chest is one of the important parts
of the examination of the respiratory system, the limits of
percussion must clearly be borne in mind. One cannot percuss
deeper than 5 cm. It is not possible to demonstrate any pathologic lesion in the lung which is covered by a layer of air more
than 5 cm. thick or fluid 1 cm. thick. A tumour in the chest
lying deeper than 5 cm. from the surface produces hardly any
change in the percussion note. A lesion smaller than 2-3 cms.
in diameter does not cause any change in the percussion note.
Free fluid in the pleural cavity may not be detected by percussion unless it exceeds 200 c.c. in amount.
Percussion mainly determines:
1. T h e boundaries of the lungs.
2. The resonance of the lungs.
3. T h e myotatic irritability.
Percuss as follows: ,
Place the middle finger of the left hand against the surface
of the chest allowing the finger to conform to it under light
pressure. With the middle finger of the right hand flexed at a
right angle to the metacarpal bones, tap sharply against the
second or last phalanx of the left middle finger, which acts as a
pleximeter. T h e stroke should be delivered from the wrist and
not from the elbow. Over the clavicles direct percussion is to
be used.
Percuss from the resonant towards the less resonant area.
Place the longer axis of the pleximeter finger parallel to the
dull border that is being percussed. Areas to be compared
must be identical on both the sides as far as possible.
1.8
M E T H O D S OF PERCUSSION
A.
B.
C.
RESPIRATORY
SYSTEM
31
Carefully percuss the front of the chest, compare the corresponding sides, note the dullness in the cardiac and liver areas,
and the hyper-resonance over the stomach area. Next, percuss
the axillae with the patient joining his hands above his head,
and finally the back with the patient sitting up, if possible,
with arms folded and the body slightly bent forward.
Normal percussion note is resonant. This term, is however,
relative as a person with thick chest wall or much subcutaneous
fat will show less resonance than one with a thin, poorly muscled chest-wall.
1. Elicit the boundaries of the lungs.
These coincide with their surface markings. The following
points, while eliciting the borders, must be borne in mind.
(a) T h e lower border of the right lung is thin and overlaps the liver.
Hence light percussion is necessary.
(b) In older people the borders of the lungs extend beyond by one rib.
In children they are a little above.
(c) T h e liver may be enlarged upwards and give rise to dullness at the
base of the right lung.
HOW
32
T O EXAMINE A
PATIENT
(d) T h e back of the chest is less resonant due to greater musculature and
requires strong percussion.
(e) Mark the Kronig's isthmusa band of resonance connecting the
resonant areas on the back and front of the chest and which passes
over the shoulder. This area of about five cm. in width is often
reduced in early apical T.B.
3.
OF
LUNGS
RESPIRATORY
IV.
33
SYSTEM
AUSCULTATION
Vocal resonance.
points
are to be observed
while
CHARACTER OF B R E A T H
SOUNDS
34
HOW
T O EXAMINE A
PATIENT
RESPIRATORY
SYSTEM
35
FOREIGN SOUNDS
They
36
H O W TO EXAMINE A
PATIENT
VOCAL RESONANCE
RESPIRATORY
SYSTEM
37
E X A M I N A T I O N O F SPUTUM
Physical Examination
Quantity.
HOW
38
T O EXAMINE A
PATIENT
watery,
FROTHYcopious,
nary oedema.
often blood-stained.
Indicates oedema
Also indicates
of
the
pulmo-
RESPIRATORY
SYSTEM
39
(not
to be mistaken
for blood)common
in
coal-
C.
Consistency.
D.
Odour.
H O W T O EXAMINE A
40
PATIENT
Microscopic Examination.
A.
CELLULAR STRUCTURES
PUS CELLS.
ELASTIC FIBRES
ORGANISMS:
Bacteriological Examination
Perform cultures, inoculation in guinea-pigs, etc.
RESPIRATORY
41
SYSTEM
PLEURAL FLUIDS
Aspiration of fluid from the pleural cavity may be performed
as a therapeutic measure or for diagnostic purpose. Clinically
fluid can be detected if there is at least ten ounces in the
pleural space. It needs a pint of fluid to cause mediastinal
shiftan important diagnostic feature of pleural effusion.
HOW T O PERFORM PARACENTESIS
Let the patient relax on a bed-rest and ask him to raise the hand and
let it rest on the head on the side to be punctured. After aseptic precautions novocainise the tract and put in a thick-bore needle in the 5th or
6th space in the mid-axillary line or in the 8th space in the back just below
the tip of the scapula. Withdraw the fluid slowly in order to avoid respiratory embarassment. Discontinue aspiration if pain, cough or dyspnoea
develops.
HOW T O EXAMINE T H E FLUID
T h e detailed examination of the fluid is not within the purview of this
book. However, naked eye examination of the fluid invariably helps one
to gauge whether the fluid is exudate, transudate, pus containing or haemorrhagic. Blood stained fluid occurs in malignancy, pulmonary infarction
or trauma. In T . B . the fluid is straw-coloured and may 'coagulate on
standing. In empyema the fluid is opaque and is full of pus cells.
T h e common conditions that produce pleural effusion are inflammations
giving rise to transudates
or non-inflammatory conditions giving rise to
exudates.
Differentiation between exudate and transudate.
EXUDATE
TRANSUDATE
2.
Brownish-yellow.
Pale yellow.
3.
4.
5.
Clots on standing.
6.
Lymphocytes present.
1.
Malignancy
Sub-diaphragmatic
abscess. Pressure by glands
Actinomycosis
Hodgkin's malignancy
Pneumothorax
Pulmonary infarction
Pneumonia (secondary)
Malignancy
Tuberculosis
Chylous
(chyliform)
Tuberculosis
Filariasis
(chyle)
Haemothorax
(blood)
Empyema
Polyserositis
(pus)
Cardiaccongestive
Pneumonia
failure, constrictive
pericarditis Lung abscess
(transudate)
(exudate)
Tuberculosis
Non-inflammatory
Inflammatory
Etiological Classification
PLEURAL EFFUSIONS
42
H O W T O EXAMINE A PATIENT
RESPIRATORY
43
SYSTEM
Infections
COMMON COLDcough is short
paroxysmal till the mucus is cleared.
and
dry
at
first
and
later
HOW
44
T O EXAMINE A
PATIENT
B.
Mechanical Irritation
ENLARGED UVULAdry, irritating cough on lying down.
SINUSITISirritating cough with little expectoration of mucus; more
common during the first half of the day.
SMOKINGirritating cough with hardly any expectoration; there is
often associated sore throat.
PRESSURE U P O N T H E TRACHEA (aneurysm, mediastinal glands)
brassy cough.
ENLARGED HEARTmay cause cough, especially on lying down.
C.
Reflex conditions
Irritation of peripheral nervesdisordered stomach, thread worms, ear
trouble, teething, pregnancy. T h e cough is dry and irritating and
repeats at intervals.
Enlarged liver and diaphragmatic disordersthe cough is dry and
often irritating.
Nervousnesssingle, short, dry and explosive cough.
Hysteriathe cough is loud and barking, often associated with aphonia.
RESPIRATORY
SYSTEM
45
PAIN IN T H E CHEST
Lung tissue is insensitive and pain in the chest is always the
result of conditions which affect the surrounding structures. In
common respiratory diseases pain is an uncommon symptom;
when pleura is involved, however, the pain is a prominent feature, as occurs in pleurisy, lobar pneumonia, (due to associated
dry pleurisy) new growths sometimes, and pneumothorax.
The two commonest conditions that give rise to pain in the
chest are (1) lung and pleural diseases, (2) heart and pericardial
disorders. The pain in the former may be aggravated on
breathing or coughing and in the latter, on exercise.
Common varieties of pain
1. SUPERFICIALwhen cutaneous structures are involved
as by inflammation of the skin, neuralgias, herpes, adiposis
dolorosa.
2. DEEPbones, muscles, or organs involved. Myalgia,
pressure on bones by growths and aneurysms, pleurisy, pneumothorax, pulmonary embolism, coronary disease, pericarditis or
inflammation of the liverare common causes of deep pain.
3. VISCERAL. The pain is deep seated and often spasmodic in character due to involvement of hollow organs. Flatulence, stomach ulcers, gall-bladder diseases, hiatus hernia are
common examples.
4. REFERRED. This is a continuous pain, superficial in
character and localised. The pain is projected from a deep
seated point of stimulation to the sensory nerves on the surface
of the body, as occurs in cholecystitis or liver diseases at the.
right shoulder, in pneumonia in children in the abdomen, in
diseases of the spine over the chest, etc.
5. PSYCHOGENIC. Such pains occur in cardiac neurosis,
neurocirculatory asthenia or long after an industrial accident.
PAIN IN T H E CHEST MAY BE CENTRAL OR LATERAL.
The common causes of central pain are more often due to
non-respiratory than respiratory disorders. T h e common causes
are:
H O W TO EXAMINE A PATIENT
46
pain
behind
LUNG DISEASES:
PNEUMONIAthe pain is due to associated pleurisy and may be
localised or referred to the abdomen as often occurs in children.
PULMONARY EMBOLISMsudden pain with haemoptysis and collapse.
CANCER LUNGpain is not a characteristic feature unless pleura is
involved.
MASSIVE COLLAPSE OF T H E LUNGSdistress rather than pain.
2.
PLEURAL CONDITIONS:
PLEURISYpain is sharp and stabbing in character. In diaphragmatic
plcurisv it may be referred to the shoulder.
PNEUMOTHORAXsudden pain, dyspnoea and collapse.
3.
4.
5.
EPISTAXIS
Bleeding from the nose may be due to local or general causes.
It often occurs spontaneously without any obvious cause.
A.
Local causes
RESPIRATORY
SYSTEM
47
General causes
48
HOW
TO EXAMINE A
PATIENT
HAEMOPTYSIS
Haemoptysis means bleeding occuring from the lungs and not
from the mouth, nose or pharynx.
Common causes:
A.
PULMONARY DISEASES
RESPIRATORY
49
SYSTEM
Haematemesis
1.
2.
Preceded
nausea.
by
cough;
T h e blood is vomited.
no
Preceded by nausea.
3.
Usually dark.
4.
5.
Alkaline in reaction.
6.
History of
diseases.
7.
8.
lung
or
heart
HOW
50
TO EXAMINE A
PATIENT
INVESTIGATIONS
1. Exclude blood from the nose, mouth, pharynx, larynx and
stomach.
2. Suspect tuberculosis in every case of haemoptysis until the
contrary is proved.
3. Go carefully into the history of fever, cough, and loss of
weight.
4. Examine the chest for evidence of tuberculosis; heart for
mitral stenosis; and blood for dyscrasias.
5. Examine the sputum for M. Tuberculosis
times, if found negative previously.
6.
at least six
LOCAL CAUSES
Over-working of the vocal cordsshouting, singing, etc.
ORGANIC PARALYSIS
RESPIRATORY
51
SYSTEM
and mucous
cheeks, ears,
of reduced
an excess of
HOW
52
TO EXAMINE A
PATIENT
RESPIRATORY
SYSTEM
53
54
HOW
T O EXAMINE A
PATIENT
Cardiac conditions
RESPIRATORY SYSTEM
3.
55
(a) NephritisUraemia, due to failure of the kidney to excrete non-volatile acids. The patient may even get asthmatic
attacks.
(b) Ingestion of acidifying substances such as ammonium
chloride and methyl alcohol.
(c) Diabetes mellitusdue to incomplete metabolism of fats
resulting in retention of acetone bodies in the circulation.
(d) Congestive cardiac failure and congenital heart diseases
due to excess of C 0 2 in the blood.
4.
Oxygen lack
(a) Anaemia.
(b) Co-poisoning, methaemoglobinaemia.
and
(b) Congestive cardiac failureincreased B.M.R. is one additional factor in the causation of dyspnoea in cases of congestive
heart failure.
6. Nervous hindrance to respiration
(a) Functional.
(b) Paralysis of the diaphragm.
(c) Increased intracranial pressure (Cheyne-Stoke's breathing).
PAROXYSMAL DYSPNOEA
This means that dyspnoea comes in paroxysmal attacks.
attacks are more common at nights.
The
Causes:
1. Bronchial asthma. The patient is very severely dysr
pnoeic, the breathing is laboured, the expiration is much longer
than inspiration and cooing rhonchi are heard all over the chest.
H O W T O EXAMINE A
56
2.
(a)
(b)
(c)
(d)
PATIENT
Cardio-Vascular diseases
Hypertensive heart disease.
Coronary disease.
Myocardial fibrosis.
Arteriosclerosis.
RESPIRATORY
SYSTEM
57
T h e fol-
Age
Time of onset
Mode of onset
Symptoms
Expectoration
Duration
Associated symptoms .
2.
3.
4.
5.
6.
7.
8.
Renal Asthma
Midnight.
May lastlonger.
the whole day or
immediately
fol
No sweating.
Dyspnoea only.
Nothing particular.
Sweating profuse.
lowed by cough.
Dyspnoea,
Early morning.
After forty.
History
1.
58
H O W TO EXAMINE A PATIENT
Pulse
Blood pressure
Blood
Urine
11.
12.
13.
14.
15.
in
the
Generally clear;
Eosinophilia.
there may
veins.
and
presence of casts.
No eosinophilia.
Definite albuminuria
be mild albuminuria.
No eosinophilia.
High.
Full.
Left
ventricular
enlargement; gallop rhythm.
No engorged
Engorged veins.
May be low.
Clear.
veins
Respiration
slow
and
laboured; expiration thrice
the
inspiration;
rhonchi
heard all over the chest.
engorged
neck.
10.
No
Associated signs
9.
RESPIRATORY
SYSTEM
59
CHAPTER III
CARDIO-VASCULAR SYSTEM
A.
INTERROGATION.
B.
C.
EXAMINATION OF T H E HEART.
I.
Inspection.
II.
Palpation.
III.
Percussion.
IV.
Auscultation.
D.
PULSE.
E.
BLOOD PRESSURE.
F.
HOW
62
A.
T O EXAMINE A
PATIENT
INTERROGATION
4.
If it comes in paroxysms.
5. Its duration.
6. Associated symptomscough, wheezing, oedema, giddiness,
praecordial pain, palpitation, collapse, etc.
7. Description of an attack.
PRAECORDIAL PAIN OR DISTRESS (see page 94).
Note the following:
1. Sitesubsternal, retrosternal, epigastric.
2.
3.
4.
5.
CARDIOVASCULAR
SYSTEM
63
3. If he was unconscious.
4. Associated symptomsdizziness, sweating, pallor, pain,
diarrhoea, fever, haemorrhage.
5.
6.
VENOUS CONGESTION
Look for the following:
1. Swelling. Inquire as to
(a) Where it started.
HOW
64
TO EXAMINE A
PATIENT
(b) Duration.
(c) Whether progressive or variable.
(cl) Whether weight is increasing.
Look for oedema in the legs, oxter the sacrum, genitalia and the eye-lids especially (see page 102).
2.
5.
Gastro-intestinal symptoms:
(a) State of digestionappetite, bowels.
(b) Nausea; vomiting.
(c) Distension of the abdomen or sense of fullness after
meals.
(d) Engorgement of the liver.
6.
MARKING
OF THE
HEART
CARDIO-VASCULAR
SYSTEM
65
VALVES:
1. Pulmonary valve is situated in the upper border of the 3rd left costal
cartilage.
2. Aortic valve is obliquely placed from the lower border of the 3rd left
costal cartilage to cross half the sternum.
3.
4. Tricuspid valve stretches from 4th left costal cartilage to 5th right
sterno-costal junction.
C.
EXAMINATION OF T H E H E A R T
I.
INSPECTION
heart,
(a) Apexnormally seen in the 5th space inside the left midclavicular line, limited to an area of about three-quarters
of an inch in diameter.
(b) BasePulsations in the 2nd left interspace are often seen
normally in children. Marked pulsation in the 1st and
2nd right interspace should make one suspect aneurysm
of the ascending aorta. Pulsation in the 3rd left interspace suggests diatation of the pulmonary vessels. A
marked retraction of the left lung may uncover a large
portion of the heart and produce a wide area of cardiac
pulsation.
5
66
H O W TO EXAMINE A
PATIENT
OUTSIDE T H E PRAECORDIUM:
double)
(i) Enlarged right ventricle. It is seen as a diffuse pulsation in the epigastrium and may occur in normal
persons. When the heart is hypertrophied it may be
felt as a systolic thrust on palpation.
(ii) Normal pulsation of the abdominal aorta may be felt
in nervous but otherwise normal persons, especially
when the abdominal wall is thin.
(iii) Aortic pulsation may be transmitted by a tumour
overlying the aorta such as carcinoma of the stomach.
(iv) In aneurysm of the abdominal aorta an expansile
swelling is generally felt over the pulsating area.
(v) Pulsation of the liver may occur in heart failure with
tricuspid incompetence; the pulsation is felt behind
also.
(d) Over the other bigger vesselsbrachials, femorals and
temporals. These often pulsate visibly in aortic regurgitation, anaemias, thyrotoxicosis and high blood pressure.
(e) Capillary pulsation. This is best elicited by gently compressing the lips of the patient with a slide or by pressing
CARDIOVASCULAR
SYSTEM
67
FIG. VIII
In health, vertical height of column of blood in jugular veins is
about the level with manubrium sternum (M.L.). T h e vertical
height of the column (Z.L.) is increased in congestive heart failure
to above the manubrial level (M.L.).
3. Dilated Veins
(a) In the chest. If present, suspect intrathoracic growths,
portal obstruction, right-sided failure.
(b) In the neck. If the jugular veins are prominent, measure
the column of blood filling them with the patient reclining comfortably in bed and with the head tilted forwards.
T a k e the vertical height of the venous column from the
sternal angle to the highest point of pulsation over the
jugular vein. This gives an idea of the amount of venouscongestion. Next apply light pressure over the right
hypochondrium i.e. over the engorged liver and note the
rise in the level of the venous column in the neck.
(Hepato-jugular
reflex). In normal subjects the upper
limit of the pulsation is 3 cm. above the sternal angle.
T h e venous pressure is generally elevated in congestive
heart failure, pericardial tamponade, constrictive pericarditis and mediastinal obstruction (see Fig. VIII). *
H O W T O EXAMINE A
68
II.
PATIENT
PALPATION
This confirms the position of the apex beat, gives more accurate information about the force and character of the cardiac
impulse and helps to detect the presence of thrills.
Examine the patient erect, recumbent, leaning forward and
lying on the left side, for the following:
].
FORM OF T H E PRAECORDIUM
TENDERNESS
Press gently over the cardiac area and watch the expression
of the patient; the patient winces if there is tenderness.
3.
PULSATIONS:
(a) Apex. Feel with the flat of the hand and confirm it with
the tips of the fingers.
(i) Its position. T h e apex in a normal adult is best felt in
the 5th left interspace
in. away from the midstemal line
or | in. internal to the mid-clavicular line. In children,
it is as high as the 4th space and in the aged it descends
as low as the 6th. Palpation often reveals the apex further away than by inspection. In such a case the apex
beat is taken as the lowest and outermost point at which
the finger is distinctly forced up with each beat of the
heart.
THE
APEX-BEAT
CONDITIONS:
MAY
BE
ALTERED
IN
THE
T O T H E LEFT.
(i) Hypertrophy or dilatation of the heart.
(ii) Pleural effusion or pneumothorax on the right side.
(iii) Fibrosis or collapse of the lung on the left side.
T O T H E RIGHT.
(i) Pleural effusion or pneumothorax on the left side.
(ii) Fibrosis or collapse of the lung on the right side.
FOLLOWING
CARDIOVASCULAR
69
SYSTEM
(ii) Its character. If the apex is not felt well, let the patient
sit up or even lean forward. It may be impossible to
define the character of the apex even in health in cases of
persons with thick chest wall either from muscular development or excess fat, or when it lies behind a rib. On
the other hand, the apex-beat may appear to be more
forcible than normal in people with thin chest wall and
in nervous individuals.
IX DISEASED CONDITION,
ALTERATION
IN THE
THE APEX BEAT MAY OCCUR AS
FOLLOWS-.
CHARACTER
OF
myxoedema.
heart,
right
ventricular
hypertrophy
HOW
70
TO EXAMINE A
PATIENT
THRILLS.
lesions.
It is
CARDIOVASCULAR
COMMON
CONDITIONS
HEART:
THAT
71
SYSTEM
PRODUCE
THRILLS
IN
THE
(i) A thrill at the apex is generally diastolic in time and signifies mitral
stenosis. In well-developed cases of mitral stenosis the thrill is generally presystolic i.e. felt just before the systole. Less commonly, it
may be systolic due to mitral disease.
(ii) A thrill in the aortic area is usually systolic in time signifying aortic
stenosis; less commonly it is diastolic and is due to aortic incompetence.
(iii) A thrill in the pulmonary area is invariably systolic in time and
indicates cither pulmonary stenosis or patent ductus arteriosus. In
the latter disease, it may be systolic and diastolic combined.
(iv) A thrill in the 3rd or 4th left interspace indicates inter-ventricular
septal defect and is generally systolic in time.
(v) A continuous thrill is often heard in arterio-venous communication
wherever it is situated in the body.
III.
PERCUSSION
H O W TO EXAMINE A
72
PATIENT
DULLNESS.
left.
CARDIOVASCULAR
IV.
SYSTEM
73
AUSCULTATION
CHARACTER OF T H E H E A R T SOUNDS.
H O W TO EXAMINE A
74
The character
conditions:
1. At
PATIENT
may
vary
in
several
the apex
FIG. I X
Position of the cardiac valves and auscultatory areas.
Position of the Valves: (m) mitral, (a) aortic, (p) pulmonary,
(t) tricuspid.
Position of the Auscultatory Areas:
(P) pulmonary, (T) tricuspid.
(M) mitral,
(A) aortic,
CARDIOVASCULAR
2.
SYSTEM
75
At the base
Aortic area
(a) T h e 2nd aortic sound is accentuated in conditions that
raise the systemic blood pressure, as in hypertension; so
also in aneurysm, atheroma and dilatation of the aorta.
(b) 2nd sound may be weak in the aortic area in aortic
valvular diseases, peripheral failure, weakening of the left
ventricle, anaemias and hypotension. T h e weakness in
all these conditions is due to lowering of the systemic
pressure.
Pulmonary area
(a) 2nd pulmonary sound is accentuated in conditions that
raise the pressure in pulmonary circulation, as in diseases
of the lungs, mitral disease, left ventricular failure and
some congenital heart diseases.
(b) T h e 2nd pulmonary sound is diminished in pulmonary
stenosis, right ventricular failure and massive pneumonia.
B.
R H Y T H M OF T H E H E A R T SOUNDS.
H O W TO EXAMINE A
76
PATIENT
'
Normal Sounds
GALLOP
BETWEEN GALLOP
TRIPLE
RHYTHM.
RHYTHM
Condition pathological.
Present in elderly people.
Cardiac function improper.
T h e gallop can often be felt as
well as heard.
Prognosis is serious.
RHYTHM
AND
T R I P L E RHYTHM
Condition physiological.
Present in young adults.
Cardiac function normal.
T h e rhythm can be heard, but
not felt.
Harmless condition.
CARDIOVASCULAR
SYSTEM
77
ADVENTITIOUS SOUNDS.
MURMURS
MECHANISM OF P R O D U C T I O N OF M U R M U R S
(i) Turbulence and eddy currents resulting from modification in the size
of the valve openingmore obvious when there is narrowing of the
orifice of the valve.
(ii) Increased velocity of the blood-flow as occurs in thyrotoxicosis and
anaemias.
(iii) Change of viscosity of the blood as occurs in polycythaemia
viscosity) and anaemias (low
viscosity).
(iv) Roughening of the vessel-lining as occurs in atheroma.
{high
H O W TO EXAMINE A
78
PATIENT
4.
5.
CARDIOVASCULAR
SYSTEM
Mitral Regurgitant
Murmur.
Aortic Stenotic
Murmur.
79
Mitral Stenotic
Murmur.
Aortic Regurgitant
Murmur.
FIG. X I
Conduction of Murmurs.
H O W TO EXAMINE A
80
PATIENT
PULSE
CARDIOVASCULAR
SYSTEM
81
between the beats and observe the expansion during the passage
of the pulse-wave. T h e volume depends on the cardiac output
and the calibre of the artery; hence, volume is increased in
fevers, anaemias, thyrotoxicosis and arterio-venous aneurysm.
T h e cardiac output is diminished in shock, myxoedema, mitral
and aortic stenosis, pericardial effusion, paroxysmal tachycardia
and congestive cardiac failure.
5. Tension. Estimation of "tension" of the pulse i.e. of
blood pressure within the vessel wall by palpation, is not too
reliable. However, to estimate tension press the vessel and see
how much pressure is required to flatten the vessel. T h e pulse
tension is determined by the force required to obliterate the
pulse with the fingers. When the tension is low, the artery is
easily flattened and resumes its cylindrical shape without much
resistance. When the tension is high, considerable pressure is
required to flatten the vessel. The tension of the pulse gives
an idea of the diastolic blood pressure. Hence, it is high in
hyperpiesia and low in aortic regurgitation and anaemia.
6. Character of the pulse wave. Note the rise and fall of
the pulse. If it rises slowly, the pulse is anacrotic in character
and suggests aortic stenosis. If it falls suddenly, it suggests
marked dicrotism (pulsus Corrigans of aortic regurgitation).
A
collapsing pulse as occurs in aortic regurgitation, anaemias,
fevers, thyrotoxicosis and arterio-venous anastomosis, is best
elicited by placing the hand around the middle of the patient's
forearm with the arm held vertically.
7. Condition of the vessel-walls. T h e condition of the
vessel-walls should be noted for evidence of arterial thickening
and undue mobility. Flatten the vessel and cause the skin of
the patient to slip up and down along the length of it. Note
if it is thickened or tortuous. Tortuosity is best noticed over
the temporal, brachial and axillary arteries. In young persons
they are more easily palpable. In arteriosclerosis they are
tortuous and like whipcord.
8. Compare the radial pulsation on both sides.
often unequal in the following conditions:
6
This is
82
H O W TO EXAMINE A
PATIENT
when
local
atheroma
complicates
the
CARDIOVASCULAR
SYSTEM
83
84
H O W TO EXAMINE A
PATIENT
and patent ductus arteriosus and which is best felt through the
musculature of the forearm raised to the level of the head. T h e
pulse is felt as a sharp impact due to rapid filling of the arteries
and rapid falling or collapse due to regurgitation of blood
through the incompetent aortic valve. Such pulse is also known
as water-hammer pulse.
4. Dicrotic pulse. In certain fevers, especially typhoid,
there is a marked relaxation of the arteries and the dicrotic
wave becomes exaggerated and can be felt as a small wave immediately following the pulse wave. It is best felt when the
diastolic pressure is low.
5. Anacrotic pulse. T h e pulse wave rises slowly, is sustained for a longer period and falls slowlypulsus tardus.
Such pulse occurs in aortic stenosis. T h e sphygmogram shows
a small wave on the ascending limb of the pulse tracing.
6. Pulsus bisferiens. This a double-crested pulse often felt
as two pulsations for each beat, usually well-sustained and of
small excursion typically seen in high-graded aortic stenosis or
in aortic stenosis and aortic regurgitation combined.
7. Pulsus alternans. T h e rhythm is normal, but a strong
beat and a weak beat occur alternately due to alternate beating
of the ventricles strongly and then weakly. Its presence indicates grave left ventricular weakness.
8. Pulsus paradoxus. T h e pulse wave is greatest at the end
of expiration and decreases or even absent during inspiration;
commonly present in pericardial effusion and in constrictive
pericarditis and is due to impediment to the normal flow of
venous return during inspiration.
9. Pulsus bigeminus. Occurs in extra-systoles. T h e waves
occur in pairs. There may also be a pulses trigeminus or
quadrigeminus,
i.e. three beats or four beats followed by a
pause.
IRREGULAR PULSE
Pulse irregularities may be caused by the following conditions:
CARDIOVASCULAR
1.
SYSTEM
85
IN
86
3.
H O W TO EXAMINE A
PATIENT
Generally
CARDIOVASCULAR
SYSTEM
87
T h e B.P. may show temporary variations with change of posture, after exertion and on excitement. In nervous patients
the second reading will represent the true pressure.
THE
FOLLOWING
ARE THE
ARTERIAL
FACTORS
THAT
PRESSURE
MAINTAIN
1.
Increased force
2.
3.
4.
5.
raises
the
blood
H O W TO EXAMINE A
88
PATIENT
HYPERTENSION).
CARDIOVASCULAR
SYSTEM
89
ARTERIAL DISEASES.
(a) Nephritis. Acute nephritis may produce high blood pressure and if neglected, may lead to chronic glomerular
nephritis resulting in persistent high blood pressure of
about 170/120. The history and presence of albumin
and casts in the urine of low sp. gr. will decide the
diagnosis. Albuminuric retinopathy is generally present.
(b) Chronic Interstitial Nephritis. This has close resemblance to benign hypertension. There is often severe
hypertension closely resembling malignant hypertension,
especially in later stages of the disease. Generally comes
on after the age of 50, but may occur at earlier age.
(c) Pyelonephritis. This leads to atrophy of one or both
kidneys resulting in hypertension which may occur even
at the age of 20. Pyelograms are distinctive. Even if
one kidney is affected the blood pressure rises.
(d) Polycystic Kidneys. This may be associated with hypertension. There may be family history and the kidneys
are easily palpable. Pyelogram is characteristic.
INTOXICATIONS.
(a) Exogenous. Alcohol, lead, arsenic, abuse of food containing excess of fat, meat and condiments.
(b) Toxaemias of pregnancy.
(c) Chronis sepsis.
90
5.
H O W TO EXAMINE A
PATIENT
H E A R T DISEASES.
the pressure
well-marked
The radial
the femoral
ENDOCRINE DISORDERS.
METABOLIC DISORDERS.
is generally
associated with
moderate
CARDIOVASCULAR
8.
SYSTEM
91
BLOOD DISEASES.
NEUROLOGICAL DISORDERS.
A.
NECESSARY
IN A CASE OF
HYPERTENSION.
History:
1. Family history of high blood pressure.
2.
5.
H O W TO EXAMINE A
92
B.
PATIENT
Physical examination:
1.
Cardio-vascular system including blood pressure, condition of the heart and arteries.
2.
C.
D.
E.C.G.
E.
F.
CARDIOVASCULAR
3.
SYSTEM
93
Endocrine disorders:
(a) Adrenals. In Addison's disease the systolic pressure
may be as low as 80.
(b) Pituitary. Simmond's disease can cause lowering of
the blood pressure.
(c) Thyroid. In myxoedema there is often lowering of
the blood pressure.
4.
Heart diseases:
(a) Severe mitral stenosis.
(b) Myocardial degeneration.
(c) Coronary infarction.
(d) Aortic regurgitationlow diastolic pressure but high
systolic.
(e) Arterio-venous aneurysmlow diastolic pressure and
generally high systolic pressure.
(f) Coarctation of the aortahigh pressure in the arms
but low in the legs.
Ask the patient to hop on one leg twenty times or ask him
to step on and off a stool eighteen inches high, twenty times in
two minutes. Take the pulse before the exercise, soon after,
94
H O W TO EXAMINE A
PATIENT
and two minutes later. If the heart is healthy, the pulse beat
should not rise by more than 10 to 20 beats per minute and
should reach normal within two minutes. This test is valueless
in patients with neuro circulatory asthenia or in other functional disorders of the heart, as they show more distress in performing this test than those with organic heart diseases.
MANIFESTATIONS OF COMMON
CARDIOVASCULAR SYMPTOMS
CARDIAC PAIN
Cardiac pain may be due to disorders of the heart or due to
extra-cardiac conditions.
1.
CARDIAC CONDITIONS.
CARDIOVASCULAR
2.
SYSTEM
95
Functional:
(a) Praecordial aching or "heartache"common in females, the pain is most marked at the centre of the
left breast, mild or severe, waxes and wanes, may
radiate over the chest or arms. The cause is sensitive
nervous system.
(b) Pseudo-anginal painsthese may occur in tobacco
excess and hyperthyroidism.
(c) Neuro-circulatory asthenia (effort syndrome)the patient complains of dull ache rather than pain. He is
anxious and neurotic. The pain has no relation to
exercise.
(d) Cardiospasmdistended stomach, especially in the
second and third decade often presses upon the heart
and causes pain in the cardiac region.
1. Aortic conditions:
(a) Aortitisthe pain is more or less continuous and has
no relation to exertion.
(b) Aortic aneurysmthe pain is boring in character and
constant in the upper thorax; it is due to pressure of
the growing sac on the bones, nerves, etc.
(c) Dissecting aneurysmthe pain is excruciating, coming on abruptly and located substernally, often
referred to the back and even legs. It is severe at the
start and may be less laterthe reverse of coronary.
T h e pulse may not be felt in the legs.
2. Pulmonary conditions:
(a) Pulmonary embolismsudden, often substernal pain,
dyspnoea and haemoptysis. T h e dyspnoea is more
severe than painthe opposite of coronary thrombosis.
(b) Pneumothoraxsudden pain, severe dyspnoea, cyanosis, and restriction of breathing.
(c) Pleurisymay give rise to stitching pain more on the
side of the chest rather than in cardiac area.
3. Mediastinal causesboring pain more or less continuous
behind the sternum.
4.
Gastro-intestinal causes.
(a) Gastric ulcerpain in relation to food, relieved when
the stomach is full and worse when empty.
(b) Acute pancreatitissevere pain with vomiting and
collapse. The pain is more central and more marked
in the upper part of the abdomen.
(c) Hiatus herniapain often shoots along the left arm;
dysphagia. The pain sometimes becomes more marked on lying down soon after food.
(d) Gall-bladder diseasestenderness is present at the tip
of the ninth right costal cartilage.
CARDIOVASCULAR
SYSTEM
97
6.
M E T H O D OF INVESTIGATION.
3.
4.
5.
Onset.
Attitude. Immobile.
Duration.
Radiation.
Shock.
Sweating.
Dyspnoea.
Vomiting.
Pulse. Unchanged.
Temperature. Normal.
B.P.
5.
li.
7.
8.
9.
10.
11.
12.
13.
14.
Leucocytosis.
E.S.R.
E.C.G.
17.
18.
Normal.
Absent.
Congestive failure.
15.
16.
Not characteristic.
Absent.
Normal or rises.
Common.
Characteristic.
Increased.
Present.
Commonly follows.
Falls.
Fever follows.
Often present.
Present.
Hours or days.
Restive.
Often at rest.
40-50 years.
Coronary Thrombosis.
Rare.
Absent.
Slight.
Absent.
Minutes.
Site of pain.
3.
4.
During exertion.
1.
2.
Angina Pectoris.
98
H O W T O EXAMINE A PATIENT
CARDIOVASCULAR
SYSTEM
99
PALPITATION
By this term is meant that the patient is conscious of his
heart-beats. Two main factors are responsible for this symptom:
1. Sensitive nervous system.
2.
Cardiac:
1. Extra systolesthe patient may be aware of the missing beat. The pause that follows the . premature
beat and the subsequent stronger beat are often perceived by the patient and are described by him as
various types of sensations. This irregularity disappears on moderate exercise.
2. Paroxysmal tachycardiasudden onset of palpitation;
rapid pulse rate of over 150; stops also abruptly
within a few hours or lasts for a day or two.
3. Auricular flutteralso appears all of a sudden but
duration is longer than in paroxysmal tachycardia.
Although the auricles beat at about 400 per minute,
the pulse is about 150. The Auricles beat innumerable number of times, but the pulse rate is about 100
to 120 per minute.
4.
Auricular fibrillationthe beats are irregularly irregular and become worse on exercise. Generally the
patient is suffering from mitral stenosis.
5. Heart blockthe pulse is slow and the increased
stroke volume causes awareness of the heart's slow
action.
6.
H O W TO EXAMINE A
100
PATIENT
II.
III.
Functional.
1. Foul ventilation, unpleasant sight or smell.
2.
5. Convalescence, starvation.
6.
CARDIOVASCULAR
SYSTEM
101
II.
III.
IV.
V.
Cardiac diseases.
In these conditions the heart fails to maintain an adequate cerebral circulation as occurs in cases of aortic
regurgitation, hypertension, coronary disease and in
conditions of the heart that produce abnormal rhythm
such as Stoke-Adam's syndrome, auricular flutter and
paroxysmal tachycardia.
Of sudden onset.
1. External injurytraumatic shock, fractures, gun-shot
wounds, severe burns, head injuries, electric shock, etc.
2.
Internal injuriessevere internal haemorrhage, perforated ulcer, ectopic gestation, rupture or torsion of an
abdominal organ, severe colic, sudden intestinal obstruction, pulmonary embolism, coronary thrombosis, big
spontaneous pneumothorax, acute pancreatitis, acute
haemorrhage in the adrenal cortex.
3.
Severe anaphylaxis.
IIOW TO EXAMINE A
102
B.
PATIENT
Of gradual onset.
].
Peritonitis.
2.
3.
4.
5.
6.
liver,
Overdose of hypnotics.
9.
CARDIOVASCULAR
SYSTEM
103
OF OEDEMA
IN
GENERAL:
CARDIAC CONDITIONS:
104
IIOW T O E X A M I N E A
PATIENT
KIDNEY DISORDERS:
1. Acute nephritis. The oedema is less influenced by gravity. The fluid accumulates in the loose subcutaneous
tissue to begin with. The eye-lids and often the face are
swollen first. It spreads rapidly causing anasarca. T h e
cause of oedema is damage to the endothelial lining of
the capillaries, retention of crystalloids and may be
water to a very limited extent. Later on there is also
fall in the plasma albumin, which further contributes to
the oedema.
2. Nephrosis. The swelling is generalised and often massive. The cause is protein depletion resulting in upsetting of the normal ratio between albumin and globulin due to excessive loss of albumin in the urine.
C.
N U T R I T I O N A L DISORDERS:
CARDIOVASCULAR
SYSTEM
105
D.
PORTAL O B S T R U C T I O N :
VITAMIN DEFICIENCY:
CIRCULATORY O B S T R U C T I O N :
EPIDEMIC DROPSY:
106
H.
HEREDITARY CONDITIONS:
LYMPHATIC OBSTRUCTION:
SCLERODERMA:
1.
OEDEMA :
Traumatic:
(a) Bruises, sprains, fractures.
(b) Frost-bite, sunburn, scalds and burns.
(c) Excessive heat or cold.
2.
Infections:
(a) Cellulitis, erysipelas, boils, carbuncles, etc.
(b) Stings and bites.
3. Metabolic:
Gout.
4. Venous obstruction:
(a) Thrombosis, varicose veins. Cardiac oedema, if confined to one leg more than on the other side, is almost
always due to venous thrombosis.
CARDIOVASCULAR
SYSTEM
107
6.
7. Lymphatic obstruction:
(a) Filariasis.
(b) Metastasis.
(c) Pressure by growths.
CIRCULATORY FAILURE
By circulatory failure is meant the condition in which the
heart muscle is unable to maintain an efficient circulation.
Circulatory failure falls into two groups.
1. Due to failure of the heart itself. (Central failure)
failure of peripheral circulation. (Peripheral failure).
or
IIOW T O E X A M I N E A
108
I.
ANGINAL
PATIENT
Anginal.
B.
Congestive.
FAILURE.
Common causes:
1. Acute coronary disease.
2. Angina of effort.
These two are the commonest conditions that give rise to
siudden failure of the myocardium associated with anginal pain.
The patient is in a collapsed state, restless or immobile, with
feeble and rapid pulse, profuse perspiration, and all other
features of peripheral circulatory failure. The less common
causes are:
3. Severe pericardial effusion causing cardiac tamponade.
4.
Severe anaemias.
5. Aortic regurgitation.
6. Stoke-Adam's syndrome.
7.
CARDIOVASCULAR
I.
SYSTEM
R I G H T VENTRICULAR
109
FAILURE.
Causes:
1. Heart diseases. Mitral stenosis, congenital heart diseases,
severe paroxysmal tachycardia, constrictive pericarditis
and other valvular diseases.
2.
Lung diseases. Chronic bronchitis, fibrosis, bronchiectasis, polycystic disease, emphysema, etc. This is the most
important group that leads to right-sided failure.
3.
4.
Primarily non-cardiac diseases. Diphtheria, toxic myocarditis, thyrotoxicosis, beri beri, severe anaemia, etc.
6.
Sub-acute form due to repeated attacks of minor pulmonary embolism by clots or malignant cells.
II.
3.
Coronary diseases.
IIOW T O E X A M I N E A
110
II.
PATIENT
In this condition there is diminution in the volume of circulating blood and the symptoms are mainly due to low cardiac
outputfeeble pulse, low blood pressure, profuse sweating,
shallow breathing, scanty urine and weak heart sounds.
Causes:
1. Neurogenicprimary
psychic stimuli, etc.
shock due
towounds,
trauma,
to
5. Cardiac conditionsacute myocarditis, Stoke-Adam's syndrome and all conditions that cause anginal failure.
6.
Pulmonary conditionsmassive
acute pneumothorax.
pneumonia,
embolism,
ENLARGEMENT OF T H E H E A R T
A heart below 200 Gm. in weight and above 375 Gm. is abnormal. The capacity of the chambers of the heart are: Left
ventricle120 cc.; right ventricle135 cc.; left auricle140 cc.;
right auricle 160 cc. The right ventricular wall is 3 mm. thick
and the left ventricular wall is 10 mm. thick.
CAUSES OF
ENLARGEMENT.
3.
Combination of both.
CARDIOVASCULAR
SYSTEM
signs of enlargement
111
enlargement
is
diagnosed,
exclude
the
E N L A R G E M E N T OF T H E L E F T V E N T R I C L E
Causes:
1.
AORTIC
DISEASES:
IIOW T O E X A M I N E A
112
PATIENT
MITRAL
REGURGITATION:
HYPERTENSIVE
HEART
DISEASE:
ENLARGEMENT OF T H E R I G H T VENTRICLE
Causes:
1.
DISEASES
(COR PULMONALE):
CARDIOVASCULAR
113
SYSTEM
HEART,
114
IIOW T O E X A M I N E A
PATIENT
ENLARGEMENT OF T H E WHOLE H E A R T
Causes:
1. Myocardial
disease.
fibrosisoften
the
outcome
of
coronary
CARDIOVASCULAR
SYSTEM
115
CARDIAC DILATATION
headingsendo-
ENDOCARDIAL MURMURS
I.
FUNCTIONAL
IIOW T O E X A M I N E A
116
PATIENT
posture and when the breath is held in inspiration. Such murmurs may be heard in fevers, anaemia, nervousness, tachycardia,
hyperthyroidism, etc.
II.
ORGANIC
congenital.
ACQUIRED
MURMURS
(c) Mitral regurgitation due to valvular disease. T h e murmur is harsh in character and conducted towards the
axilla. If it replaces the whole of systole, it is generally
known as pan-systolic tnurmur.
CARDIOVASCULAR
SYSTEM
117
Pansystolic Murmur
(Mitral Regurgitation)
Systolic Murmur
(Functional)
Fig.
XII
118
IIOW T O E X A M I N E A
PATIENT
CARDIOVASCULAR
SYSTEM
119
120
IIOW T O E X A M I N E A P A T I E N T
Systolic "diamond-shaped"
(Aortic Stenosis)
Murmur
Diastolic Murmur
(Aortic Regurgitation)
CARDIOVASCULAR
SYSTEM
121
(ii) Appears soon after the 2nd sound or replaces the 2nd
sound.
(iii) Best heard to the left of the sternum in the 3rd left
interspace.
(iv) Better heard with a flat chest-piece than with a belltype stethoscope.
(v) Better heard generally when the patient is leaning
forwards.
(vi) Conducted down to the sternum.
T H E COMMON CAUSES OF THIS M U R M U R ARE:
(i)
(ii)
(iii)
(iv)
Systolic Murmurs
122
IIOW T O E X A M I N E A
PATIENT
blood into the pulmonary arteries as in anaemia, hyperthyroidism, atrial septal defect, etc.
Common causes:
(a) Physiologicalbest heard in supine position and in full
expiration, and absent when the patient stands up; often
associated with accentuation of the 2nd pulmonary sound.
(b) Anaemiasthe murmur is soft in character and is due to
dilatation of the pulmonary arterial bed.
(c) Pulmonary hypertensioncommonly due to left ventricular failure, mitral stenosis, lung fibrosis, emphysema,
pulmonary endarteritisthe cause being dilatation of
pulmonary arteries.
(d) Thyrotoxicosisthis condition also increases pulmonary
blood-flow and hence, dilates pulmonary arteries.
(e) Congenital defects. (See pages 113 and 123.)
(f) Aneurysmsespecially of the descending aorta and of the
pulmonary artery (very rare).
(g) Transmitted aortic stenotic murmurthis murmur is
always conducted to the neck vessels, which is not the case
with pulmonary murmurs.
(h) Chest deformitiescan cause systolic murmurs in the
pulmonary area due to shifting or twisting of the heart.
2. Diastolic Murmurs
CARDIOVASCULAR
SYSTEM
123
These are generally best heard to the left of the sternum and
not exactly over the valvular areas. T h e common types of
congenital murmurs are:
1. Patent foramen ovale or atrial septal defectharsh systolic murmur heard best in the 3rd left interspace. T h e
murmur may be absent in such disorders.
2. Interventricular septal defectloud blowing systolic murmur, heard best in the 3rd and 4th interspaces just near
the left border of the sternum and often accompanied by
a systolic thrill.
3. Congenital pulmonary stenosisharsh systolic murmur
heard best in the 2nd left interspace to the left of the
sternum. Systolic thrill is also present.
4. Patent ductus arteriosuslong continuous murmur, systolic-diastolic in time (machinery murmur), best heard in
the 1st and 2nd left interspaces. There is often associated
thrill and accentuation of the 2nd pulmonary sound, with
or without cyanosis.
5. Coarctation of the Aortaa long, harsh systolic murmur
heard at the base of the heart, more towards the aortic
area, associated with large arterial pulsation in the upper
limbs, prominent intercostal arteries, weak femoral pulse
and high B.P.
6. Fallot's Tetralogya rough systolic murmur may be
heard over the pulmonary area due to associated pulmonary stenosis. (See page 113.)
7. Eisenmenger's complexthere may be a diastolic murmur
over the pulmonary area due to associated dilatation of
the pulmonary artery. (See page 113.)
124
MYOCARDIAL MURMURS
These murmurs are mainly due to temporary or permanent
damage to the myocardium.
Causes:
1. Cardiac hypertrophy with failuresystolic murmur heard
at the apex and continuous with the 1st sound.
2.
apex
3.
4.
CARDIOVASCULAR
SYSTEM
125
CHAPTER IY
ALIMENTARY SYSTEM
A.
INTERROGATION.
B.
COMMON SYMPTOMS.
C.
EXAMINATION OF T H E M O U T H AND T H R O A T .
D.
EXAMINATION OF T H E ABDOMEN.
I.
Inspection.
II.
Palpation.
III.
Percussion.
IV.
Mensuration.
V.
Auscultation.
E.
F.
RECTAL EXAMINATION.
G.
EXAMINATION OF FAECES.
H.
GASTRIC ANALYSIS.
I.
IIOW T O EXAMINE A P A T I E N T
128
INTERROGATION
T h e physical examination of the abdomen is a procedure less
exact than that of the chest. Hence, a detailed history of
symptoms is more likely to give valuable information and help
in the diagnosis of diseases of the Alimentary Tract. Carefully
inquire into full details of the symptoms, especially of those
listed below.
SYMPTOMS
PAIN (see page 168).
Note the following:
1. Its situation.
2. Mode of onsetwhether acute or gradual.
3. Duration; intervals of freedom, if any.
4. Character and
stitching, etc.
severitygriping,
gnawing,
stabbing,
5. If continuous or remittent.
6. If localised or radiatingif latter, its direction.
7. Relation to food, posture, effort; if particular type of food
worsens the pain.
8. Relieving and aggravating factorsmedicines, pressure,
vomiting, evacuation of the bladder or bowels.
9. Associated phenomenavomiting, constipation, diarrhoea,
jaundice, fever, rigors, etc.
10. Associated tenderness and rigidity.
Make sure if it is pain that the patient complains of or a sense
of fullness or discomfort.
V O M I T I N G (see page 178).
Note the following:
1. Its frequency.
2. Time of occurrence.
3. Relation to food.
ALIMENTARY SYSTEM
129
anaemia.
130
IIOW
T O EXAMINE A PATIENT
ALIMENTARY SYSTEM
131
3. If sudden or gradual.
4. Duration and progress.
5. If there is any regurgitation.
6. If there is any vomiting; i there is any blood in the
vomit.
7. If there is any loss of weight.
8. History of trauma or having taken corrosives.
JAUNDICE (see page 195).
Note the following:
1. Colour of the skin and conjunctivae.
2. If there is associated fever, pains, rigors.
3. If there are gastro-intestinal disturbances.
4. Colour of the urine and stool.
5. History of taking drugs (atebrine, atophan, arsenicals).
BLOOD IN T H E FAECES (see page 188).
Note the following:
1. Quantity.
2. Colour.
3. Frequency of stools.
4. Character of the stools.
5. If blood comes before or after evacuation or mixed with
faeces.
6. History of piles.
132
OF T H E M O U T H
AND
THROAT
MOUTH
Note the mucous membranes of the mouth, especially for
evidence of inflammation, ulcers and pigmentation.
ALIMENTARY SYSTEM
133
LIPS
Note the following:
1. Colourpale in anaemia, cyanosed in congestive heart
failure and congenital heart diseases.
2. Moisturedry in toxaemia and gastro-intestinal disorders.
3. Swellingangio-neurotic oedema, urticaria, sting-bites.
4. Fissuressyphilis, cheilosis.
5. Ulcerssyphilis, tuberculosis, malignancy.
6. Crustshealed ulcers.
7. Herpespneumonia, malaria.
TEETH
See if they are discoloured; if any are missing. Look for
evidence of pyorrhoea, caries, defective and abnormal teeth.
SOME CHARACTERISTIC
TEETH.
a.
b.
c.
d.
GUMS
Look for:
1. Colourblue line of lead sulphide, pigmentation in
Addison's disease, pallor of anaemia.
2. Consistencysponginess in scurvy.
3. Retractionevidence of pyorrhoea.
4. Bleedingpyorrhoea, gingivitis, purpura, leukaemia.
5. Hyperplasiaacute leukaemia, dilantin excess, pregnancy.
6. UlcerationVincent's angina, sarcoma.
7. Growthspolypi, epulis, papilloma, epithelioma.
134
H O W TO EXAMINE A
PATIENT
TONGUE
Ask the patient to protrude the tongue.
Note the following:
1.
COLOUR.
Paleanaemia.
Red and rawacute glossitis, pellagra, severe diabetes.
Whitishthrush, syphilis.
Blackfungus infections, intake of iron, arsenic, oral antibiotics.
Magentariboflavin deficiency.
Yellow at marginsobstructive jaundice.
Cyanosedpolycylhaemia,
disease.
heart
Strawberryscarlet fever.
PigmentedAddison's disease.
Depigmentedsyphilis,
leucoderma
sometimes.
COATING.
White with sharp red marginstyphoid.
Greyish yellowchronic gastritis.
Dry with brownish fururaemia, acute intestinal obstruction.
3.
SIZE.
Largecretinism, acromegaly, myxoedema.
Smallsprue, severe dehydration, bilateral 12th Cr. nerve paralysis.
Swollenurticaria, angio-neurotic oedema, streptococcal infection.
4.
SHAPE.
Localised swellingnew growths.
Scvthe-shapedunilateral 12th Cr. nerve paralysis.
5.
MOISTURE.
Drydiarrhoea, vomiting, fevers, belladonna poisoning.
Very moistglossitis.
6.
SURFACE.
Smoothpernicious anaemia, pellagra, sprue, iron deficiency anaemias.
Fissuredcongenital.
Glazedcongenital syphilis.
ALIMENTARY
7.
135
SYSTEM
ULCERS.
At the marginsragged tooth.
At the fraenumconstant coughing.
Ail overaphthous or follicular.
At the centresyphilis (deep 8c punched).
At the tiptubercular (not common).
At the sidemalignant (hard with everted edges).
Herpetictongue involved along with the angles of the mouth.
8.
MOVEMENTS.
Tremorschronic
alcoholism,
debilitating
diseases,
parkinsonism,
PALATE
Use a tongue depressor.
Note the following:
1. Ulcerssyphilis, malignancy.
2. Mucous patchessyphilis.
3. PigmentationAddison's disease.
4. Bleedingpurpura.
5. Perforationsyphilis.
6. Soft palate for evidence of paralysis.
SALIVARY GLANDS
Look for enlargement, tenderness and evidence of calculi.
BREATH
If smell is present it may be due to:
1. Bad teeth, stomatitis, ulcers in the gums, septic tonsils.
2. Diseases o the nose, antrum, sinuses.
3. Lung abscess, putrid bronchitis, bronchiectasis.
4. Dyspepsia, constipation, severe fermentation in the
stomach as in cancer and chronic liver diseases.
136
H O W TO EXAMINE A
PATIENT
(acetone
alcohol,
ANATOMICAL LANDMARKS OF T H E
ABDOMEN.
FIG. XIV
Division of the abdomen
into regions.
RT. HYPOCHONDRIUM.
B.
C.
LEFT HYPOCHONDRUM.
E.
UMBILICAL REGION.
F.
EPIGASTRIC REGION.
End of ileum.
Caecum.
Vermiform appendix.
G.
HYPOGASTRIUM.
I.
Coils of ileum.
Coils of jejunum and ileum.
Upper part of rectum.
Sigmoid flexure.
Sigmoid loop.
Urinary bladder.
Gravid uterus.
H.
D.
A.
ALIMENTARY SYSTEM
137
138
H O W TO EXAMINE A
PATIENT
EXAMINATION OF T H E ABDOMEN
1.
INSPECTION
ALIMENTARY
SYSTEM
139
(a) Skin. Smooth and glossy skin indicates great distension; wrinkled skin suggests old distension, now
relieved.
(b) Striae. Indicates old
repeated pregnancies.
distension,
especially
after
PALPATION
140
H O W TO EXAMINE A
PATIENT
pating hand should first feel the abdomen in some part away
from the suspected area.
Look for:
1. Tenderness and test for hyperesthesia. Gently press
over the suspected area and note the expression of the
patient. T h e patient winces if he feels the pain; note
the degree and extent of tenderness. Tenderness is
usually found over the region where the inflamed viscus
is situated. Cutaneous hyperaesthesia is often associated
with deep tenderness. Use the point of a pin to elicit
hyperaesthesia.
2. Rigidity. Feel gently for the muscle guard, after gaining confidence of the patient. Ask the patient to open
the mouth and breathe quietly. Abdominal rigidity is
due to muscular contraction which often occurs reflexly
as a part of defence mechanism over an inflamed organ.
Localised rigidity is common in appendicitis, cholecystitis, etc., and generalised rigidity is found in peritonitis
as after typhoid perforation, etc.
3. Splashing and gurgling sounds. Place one hand on each
side of the stomach and suddenly press inwards the
finger-tips of each hand alternately. Splashing felt three
hours after meals suggests dilatation of the stomach. It
forms an oval swelling in the epigastrium and left
hypochondrium.
4. Evidence of tumour. If a lump is felt, try to move the
abdominal wall over it in order to exclude lumps
attached to the wall which move freely along with it.
See if the lump is tender and note its relation to respiratory movements. Note its position, size, shape, surface
and consistency (see page 166).
5. Evidence of fluid. Dip the fingers into the abdomen
sharply; fluid is momentarily displaced and the solid
tissue is felt easily. In the presence of ascites, a tumour
underneath may be difficult to palpate, but by this method
the dipped fingers often locate the growth.
ALIMENTARY
141
SYSTEM
6. Prominence of veins. Note the direction of the bloodflow by emptying "milking" a section of the vein and
pressing each end of the emptied part with a finger.
Next release one finger and note if the vein is filled.
Repeat the performance by removing the finger at the
other end. Blood enters more rapidly from the direction
of the blood-flow.
7. Hernial rings. Ask the patient to cough, preferably
standing, and feel if there is any prominence in the
inguinal areas.
8. Viscera. Examine especially
spleen and kidneys.
the
liver,
gall-bladder,
III.
PERCUSSION
l 4 2
HOW TO EXAMINE A
PATIENT
FIG. XV
Demonstration of shifting dullness in ascites.
FIG. XVI
Demonstration o a fluid thrill in ascites.
ALIMENTARY
SYSTEM
143
Test for thrill after asking the patient to place the edge of
his hand firmly in the middle of the abdomen while percussing,
in order to damp down vibrations transmitted by the abdominal
fat which is fluid at body temperature, and, hence, capable of
transmitting thrill especially in fat individuals. Place the hand
on one side of the abdomen and tap with the fingers of the
other hand on the opposite side. A distinct impact will be
felt to pass from one hand to the other when there is fluid in
the peritoneum.
IV.
MENSURATION
AUSCULTATION
144
H O W TO EXAMINE A
PATIENT
the fluid enters from the pharynx into the oesophagus; the
second as it passes from the oesophagus to the cardiac sphincter.
Between these two sounds there is usually an interval of 5 to
10 seconds; in oesophageal obstruction, considerable delay may
occur or the second sound may be absent.
EXAMINATION OF T H E VISCERA
1.
STOMACH
2.
Feel for the lower border first by placing the hand flat over
the abdomen and feeling at different levels, preferably from
below upwards with the tips of fingers gently inserted beneath
the costal margin. Ask the patient to take a deep breath while
palpating. If the edge is felt, note if it is smooth, irregular or
sharp. Normally the edge is not palpable, but may become
so from slight displacement of the viscus without any important disease; deformities of the chest as a result of rickets or
kyphosis and also tight-lacing often displace the liver downwards. In infants too, the liver may be palpable normally. In
all such cases the border is sharp, firm and regular. When
the liver is enlarged due to fatty changes, its edge is soft and
difficult to feel. In passive congestion of the liver the edge is
firmer than normal, while in malignant disease and syphilis it
ALIMENTARY
SYSTEM
145
146
H O W T O EXAMINE A
PATIENT
ALIMENTARY
SYSTEM
147
PHYSICAL APPEARANCE
A. Quantity:Average is about 100 Gms. per day. In vegetarians it is more. In starvation it may be reduced to even 10
Gms. per day. Only 25% of the faecal matter is solid constituents and consists mainly of food residue and bacteriathe
latter constituting l/3rd of the weight of dried faeces. The
quantity of faeces may be considerably increased by intake of
indigestible food, in pancreatic diseases, obstructive jaundice
and steatorrhoeas.
B. Colour:It is due to stercobilin derived from bilirubin
and varies from light-yellow to dark-brown normally.
HOW
148
TO EXAMINE A
PATIENT
Bilirubin
It requires at
least 100 c.c. of blood from the upper intestinal tract to produce tarry
stool.
Black stool may also result after ingestion of iron and bismuth.
in
colon
or rectum
(piles,
cancer,
polypi,
JELLYintussusception.
STREAKS OF BLOOD
ulcerative colitis.
WITH
PLENTY
OF
MUCUS
AND
PUS
ALIMENTARY
SYSTEM
149
Abnormal substances:
Vegetable fibresoften present normally.
Animal mattermuscle fibres and connective tissue. If muscle fibres
are found in large numbers it suggests some defcct in protein digestion.
Connective tissue fibres being not easily digested are often found in
the stool in fairly large quantity.
Starchexcess suggests error in carbohydrate metabolism.
becomes blue on adding iodine.
T h e stool
Fatneutral fat is not found normally in the stool; fatty acids arc
found in small amountabout 20% of dried faeces, ! Its presence in
excess is suggestive of obstructive jaundice, pancreatic disorders and
steatorrhoeas.
Foreign constituentsgall stones, fruit, stones, etc. may be present
in the stool.
H O W T O EXAMINE A PATIENT
150
MICROSCOPIC EXAMINATION
A.
IS.
CELLS.
1.
2.
irritation.
3.
CRYSTALS.
1.
Calcium oxalate,
normally present.
fatty
acid
crystals
and
triple
phosphates
2.
3.
in
groups
are
are
U N D I G E S T E D FOOD.
1.
2.
3.
4.
normally.
CULTURE EXAMINATION
This is very necessary in enteric fevers, cholera and bacilla-ry
dysentery.
ALIMENTARY SYSTEM
151
GASTRIC ANALYSIS
Chief indications:
1. Addison's anaemia.
2. Peptic ulcer.
3. Gastric cancer.
4.
Unexplained diarrhoea.
PHYSICAL
EXAMINATION.
H O W TO EXAMINE A PATIENT
152(j
intimately mixed with the gastric contents may be due to haemorrhage from
an ulcer, cancer or oesophageal-varix. Blood present in the stomach generally becomes darkish brown (coffee ground) due to conversion of haemoglobin into acid haematin. Such changes in the blood are strongly suggestive
of cancer stomach.
Bile colours the gastric juice yellow or dark green; the latter may simulate
altered blood. Addition of water makes the green colour of bile more
apparent whereas altered blood remains dark. Bile is often present in the
gastric juice and may be found in the last few specimens when the stomach
is nearly empty. Its presence in earlier samples suggests premature relaxation of the pylorus and also occurs after gastroenterostomy and partial
gastrectomy.
3. ODOUR:Normal gastric juice has a characteristic penetrating
smell, which is often absent in achlorhydria. In pyloric stenosis the gastric
contents has a sour, smell and in intestinal obstruction, faecal smell.
B.
CHEMICAL EXAMINATION
MICROSCOPIC EXAMINATION
contents.
Look
4.
16 7
ALIMENTARY
SYSTEM
GASTRIC ACIDITY
1.
HYPERCHLORHYDRIA
CAUSES:
HYPOCHLORHYDRIA
CAUSES:
HYPOCHLORHYDRIA
154
ACHLORHYDRIA
1. Gastriccancer, chronic
syphilis of the stomach.
gastritis,
atonic
dyspepsia,
secondary
4. Deficiency diseasespellagra.
5. Endocrine disordersAddison's
myxoedema, diabetes mellitus.
disease,
thyrotoxicosis,
BILL
MUCUS
&LOOD
trtrace.
STARCH
HOURS
Fractional test meal of a normal subject. The stippled area represents the
limits of free HC1 in 807o of healthy people.
FIG. XVII
GASTRIC JUICt
ALIMENTARY SYSTEM
155
GASTRIC ANALYSIS
Present.
Present.
Nil.
Lactic acid.
Nil.
Present.
Boas-Oppler bacilli
Present.
Excess.
Present.
Excess.
Nil.
Traces.
Nil.
Bile.
Blood.
Pus.
Traces.
Mucus.
5 to 30 c.c.
Significance.
anaemia.
Peptic ulcer.
Chronic gastritis, cancer, pernicious
Cancer stomach.
Cancer stomach.
Pyloric obstiuction.
Cancer, gastritis.
Duodenal ulcer.
Peptic ulcer, cancer, acute gastritis,
oesophageal varix, trauma by the
stomach lube.
Increased.
Decreased.
Achlorhydria.
Offensive.
Cancer.
Faecal.
Intestinal obstruction.
Ammoniacal.
Uraemia.
Pyloric obstruction.
Abnormal.
Above 50 c.c.
Present.
No smell.
unpleasant.
Below 50 c.c.
Pungent and
Free. HC1
Odour.
Volume.
Normal.
GASTRIC CONTENTS
156
H O W T O EXAMINE A PATIENT
Common.
Mid-epigastric.
Variable.
X-rays.
Gastric analysis.
Mclacna.
Haematemcsis.
obsessional.
"Crater" seen.
Rare.
Always hyperchlorhydria.
May occur.
Generally hyperchlorhydria.
'
By food, alkalis.
comfort.
Rare.
line.
Rare.
Common.
Relief of pain.
Anxious,
Robust.
After 40 years.
30-40 years.
Radiation.
Site.
Onset of pain.
Temperament.
General development.
Social condition.
Age.
Sex.
Duodenal Ulcer.
Gastric Ulcer.
Features.
ALIMENTARY SYSTEM
157
30-45 years.
X-rays.
Gastric analysis.
Tumour.
Common.
Lost.
Not so.
Hyperchlorhydria.
Not felt.
STOMACH.
Achlorhydria.
May be palpable.
May be present.
Vomiting.
CANCER
Cancer Stomach.
AND
After 45 years.
ULCER
Males.
Not s0-
Not lost.
Characteristic.
Predominantly males.
PEPTIC
Peptic Ulcer.
BETWEEN
Appetite.
Relief.
Periodicity.
Sex
Age_
DIFFERENTIATION
158
H O W T O EXAMINE A PATIENT
16 7
ALIMENTARY
SYSTEM
OF OBTAINING
ABDOMINAL
SPECIMEN.
PARACENTESIS.
Let the patient empty the bladder; catheterize, if necessary. Let the
patient sit upright on the bed or on a high-back chair. Apply abdominal
bandage if all the fluid is to be removed. Insert a trochar and cannula
midway between the umbilicus and symphysis pubis in the middle line
after aseptic precautions. Keep on tightening the bandage as fluid comes
out through the cannula in order to maintain the intra-abdominal pressure
and thereby the flow of the fluid. When the fluid stops draining the
cannula is removed and a sterile dressing and adhesive tape are placed
over the puncture as the latter shows tendency to drain.
EXAMINE
A.
THE FLUID
AS FOLLOWS:
PHYSICAL EXAMINATION.
1.
2.
3.
The
a.
b.
c.
d.
e.
f.
upon
b.
c.
d.
e.
4.
5.
160(j
B.
HOW
TO
EXAMINE
PATIENT
CHEMICAL E X A M I N A T I O N .
This may be necessary in certain cases, especially for proteins. Transudates have under 2.5 Gms. of proteins per 100 mi. of fluid and exudates
over 2.5.
C.
CYTOLOGICAL EXAMINATION.
Transudates have less than 5000 cells per cm. and exudates over 5000.
A large number of red cellsover 50,000 per cm. is suggestive of metastasis.
A few red cells may be found in tuberculosis.
P E R I T O N E A L FLUID
DIFFERENTIATION
BETWEEN
TRANSUDATE.
EXUDATE AND
TRANSUDATE.
EXUDATE.
1.
Non-inflammatory.
Inflammatory.
2.
3.
4.
5.
Odournil.
6.
7.
May coagulate.
8.
Sero-mucin absent.
Sero-mucin present.
9.
Result of inflammation or
malignancy.
MAINLY LIQUIDS.
1. Ascites.
2. Distended bladder.
3. Cystichydatid, pancreatic, ovarian.
4. Hydronephrosis.
three
ALIMENTARY SYSTEM
B.
16
MAINLY SOLIDS.
1. Obesity.
2. Accumulated faeces.
3. Gravid uterus.
4. Fibroids.
C.
MAINLY GASES.
1. Tympanitis.
2. Phantom tumour.
ASCITES
Ascites means accumulation of fluid in the peritoneal cavity.
M E T H O D OF INVESTIGATION:
A.
A.
B.
C.
PHYSICAL EXAMINATION.
162(j
H O W T O EXAMINE A PATIENT
EXCLUDE SIMULATING
CONDITIONS.
FIG. XVIII
Distinction between an ovarian cyst (left) and ascites (right)
by percussion of the abdomen.
16 7
ALIMENTARY
SYSTEM
There
ETIOLOGY OF ASCITES:
1. Diseases of Peritoneum.
(a) Tuberculosis. This is the commonest cause of ascites
in children. T h e abdomen contains fluid which may be
free or loculated. T h e omentum may be thickened and
felt iike a sausage-shaped mass. Mesenteric glands may
be palpable. A doughy feel may be elicited over the
lower abdomen where the skin is wasted and shiny.
(b) Simple Chronic Peritonitis. This is generally a sequel
to repeated paracentesis abdominis.
It is generally
associated with peri-hepatitis and thickening of the peritoneum over the diaphragm, liver and spleen which
block u p the pores through which the peritoneal fluid
normally drains away.
(c) Polyserositis. This is an inflammatory condition of the
peritonium, pleura and pericardium often associated
with fluid in all the sacs.
164(j
H O W T O EXAMINE A
PATIENT
16 7
ALIMENTARY
SYSTEM
5. Cardiac diseases
(a) In congestive heart diseases the dependent parts are
swollen first. There will be signs of failure in the heart,
congestion in the lungs and distension of the neck veins.
The liver may pulsate synchronously with the heart.
(b) Adherent pericardiumthere may be history of former
pericarditis. The heart is very large. There is often
retraction of the left lower ribs synchronous with the
heart beat.
(c) Pick's disease. Constriction of the superior and inferior
vena cavae along with ascites and engorged liver in a
young subject with oedema of the legs, distended jugular
veins, but no cardiac lesionsuspect Pick's disease. Calcification often occurs in the pericardium and is often
noticed early by X-rays.
6. Renal diseases
(a) Nephritisthe swelling appears on the face first followed
by general anasarca. Urine examination will reveal
albuminuria and casts.
(b) Nephrosisthe swelling is extensive and there is massive
albuminuria.
7. Severe anaemia. The swelling in the abdomen generally
appears after the diagnosis has been made on the grounds of
pallor, glossitis and changes in the blood. There is generally
a haemic murmur in the heart.
8. Severe malnutritionthe ascites in such cases is part of
the general oedema. There is often associated anaemia, well
marked wasting, dermatosis, glossitis, etc.
9. Lymphatic obstruction. Milky white fluid is found in
the peritoneal cavity and is due to obstruction to the main
-abdominal lymphatics and is common in filariasis. In rare
16(j
HOW
TO EXAMINE A PATIENT
2.
S.
of
tuberculosis,
4.
5.
heart
disease,
anaemia,
mal-
ABDOMINAL TUMOURS
For detection of a tumour in the abdomen the following
points should be observed.
1. Position. Describe their situation with reference to the
anatomical areasepigastric, umbilical, hypogastric, hypochonclrial, lumbar and iliac. Ascertain with which organ the tumour
is connected.
A swelling in the epigastric region is commonly due to a dilated stomach.
Less frequently it is due to cancer stomach, liver abscess, pancreatic cyst,
tumour of the transverse colon, T . B . omentum or an aneurysm.
A prominence in the umbilical region is often caused by T . B . omentum,
gastroptosis, enlarged mesenteric glands, retro-peritoneal tumour or an
aneurysm. A swelling in the hypogastric region is generally due to a dis-
ALIMENTARY
SYSTEM
16 7
fibroids,
ovarian cysts
168(j
H O W T O EXAMINE A PATIENT
Cancer of the head of the pancreas can cause tenderness in the epigastric
region in later stages.
Salpingitis, pelvic and psoas abscess produce painful lumps in the iliac
regions.
Tubercular caecum, appendicular abscess and cancer of the colon in late
stages produce pain in the right iliac fossa; and cancer of the sigmoid colon
may cause pain in the left iliac fossa.
ABDOMINAL RIGIDITY
Rigidity suggests that the patient has severe pain in the
abdomen, generally due to irritation of the peritoneum or
rupture of an organ.
The extent of rigidity depends upon the number of nerves
involved and the nature, duration and degree of the stimulus.
T h e stimulus may arise from the brain, but more commonly it
comes from the peripheral nerves.
COMMON CAUSES OF RIGIDITY:
3. Pancreasacute pancreatitis.
4. Intestinestrangulation, perforation of an ulcer, appendicitis, volvulus, diverticulitis.
5. Peritoneumacute peritonitis.
6. Female Genital Organstwisted ovarian cyst, ruptured
ectopic gestation, acute salpingitis, torsion of a fibroid.
7. Referred painpneumonia, pleurisy, Pott's disease, etc.
ABDOMINAL PAIN
An adequate stimulus is necessary to give rise to pain in the
abdomen and it may be:
(a) Strong contraction of the smooth muscles as in intestinal,
biliary, ureteric or uterine colicall these give rise to
intermittent pain.
(b) Irritation or inflammation of the peritoneum as occurs
in perforation of a peptic ulcer or appendicitisthe pain
is continuous in character.
16 7
ALIMENTARY
SYSTEM
1. Visceral
(a) Due to distension of a hollow viscus. Abdominal viscera
are so poorly supplied by sensory fibres, that stimuli, like
pinching, cutting, stitching, etc., are not adequate to
produce pain. T h e pain to be effective, the stimulus
must be a sustained one and applied to a wider area.
(b) Due to stretching of the capsule of a solid viscus, e.g.
liver and spleen, which cause localised tenderness rather
than pain which is often referred to some other part of
the body.
2. Peritonealdue to irritation of the peritoneum.
DIFFERENTIATING FEATURES BETWEEN VISCERAL AND
PERITONEAL PAINS
VISCERAL PAIN
PERITONEAL PAIN
1.
2.
N o tenderness.
No rigidity.
3.
4.
5.
6.
7.
Not localised.
No hyperesthesia.
Pain waxes and wanes.
Temperature generally normal.
Restlessness.
Tenderness.
Rigidity.
Generally localised.
Hyperaesthesia.
Pain constant.
Fever.
Patient is quiet.
170(j
H O W T O EXAMINE A PATIENT
A.
splenic
coronary
16 7
ALIMENTARY
SYSTEM
172
4. Mucous colitisthe patient who is generally ne urotic, passes flakes of mucus now and then.
III. Peritoneal conditions
Chronic peritonitisvague pain in the abdomen,
tenderness, doughy feel, localised masses may be felt
due to rolling up of the omentum. There may be
ascites, emaciation and fever. The cause is tuberculosis.
IV. Involvement of the abdominal organs
1. Livercongestion, hepatitis, liver abscess.
2. Gall-bladderchronic cholecystitis.
3. Pancreaschronic pancreatitis.
V. Referred pain
1. Spinal cariesespecially in children.
2. Pleurisy.
COLICKY PAIN
Typically this is a pain which makes the patient want to roll
about to procure ease. The pain comes on in spasms, passes off
after some time, only to come: back again. It is believed that
colicky pain is caused by the excessive and spasmodic contraction of plain muscle, as happens, for example in the segment
of the bowel just above an obstruction.
CHIEF VARIETIES OF COLICS:
Al I M E N T A R Y
SYSTEM
173
4. Large-intestine colica dragging pain, with slow fluctuations in intensity. The lower the site of origin of the colic the
more easily can the patient localise the pain, especially in the
transverse colon, the sigmoid or the rectum. The cause of pain
in these areas is generally growths which may be clearly felt;
there may also be signs of intestinal obstruction like vomiting
of faecal matter.
5. Appendicular colicthe pain is localised in the right
iliac fossa often associated with vomiting. There is local
tenderness and rigidity. The patient is generally constipated.
6. Biliary colicpain is very severe, "like a red-hot poker"
maximal in the right hypochondrium but spreads all over the
right side of the abdomen and chest and radiates through to the
back and between the shoulder-blades. The pain usually remains
constant for several hours and then passes off fairly suddenly.
7. Renal colicvery severe, knife-like pain, maximal in the
loin; radiates down the course of the ureter towards the genitalia or the inner side of the thigh.
8. Uterine colicsevere or moderate pain, aching in character, increasing up to a maximum and then dying away, maximal
being low down in the pedvis or in the sacrum.
ABDOMINAL PAIN IN CHILDREN
Causes:
A.
Abdominal diseases:
1. Indigestionthere may be vomiting and diarrhoea.
2. Gastro-enteritissevere
tion.
vomiting,
3. Intussusceptionsevere
stool.
pain,
diarrhoea,
dehydra-
collapse, blood in
the
IIOW T O E X A M I N E A
174
FATIENT
Specific fevers:
1. Enterictenderness in the right iliac fossa may
Slow pulse, leucopenia, mental torpor, positive
test are characteristic features. Perforation is
borne in mind when there is severe pain, fall of
rature, fast pulse and rigidity of the abdomen.
occur.
Widal
to be
tempe-
Blood diseases:
1. Henoch's purpuramay affect the intestine and cause
pain, vomiting, blood in the stools resembling intussusception. In the latter, pain comes first and then
Al I M E N T A R Y
175
SYSTEM
2.
Age.
(a) In children suspect intestinal intussusception.
(b) In adolescentssuspect
appendicitis.
(c) In adultshernia.
(d) Middle agepeptic ulcer.
(e) Old agecancer, diverticulosis, volvulus.
3.
4.
5.
6.
Site of stimulus.
Causative agent.
Location of pain.
1.
Cerebral cortex or
basal ganglia.
Affects
the
whole
abdominal wall; varies
in intensity; abolished
easily.
2.
Lower 6 dorsal
nerves.
Pleurisy, pneumonia,
infection of the chest
wall.
3.
Nerve-endings in
the abdominal
wall.
Injury or infection of
the muscles.
Limited to the
affected part.
4.
Nerve-endings in
the peritoneum.
Inflammatory exudate,
blood or contents of a
hollow viscus.
176
IIOW
TO EXAMINE A
FATIENT
ETIOLOGY:
A.
MECHANICAL
OBSTRUCTION
IN THE
OESOPHAGUS.
MECHANICAL
PALATE
DEFECTS
OP THE
MOUTH,
TONGUE
AND
PAINFUL
SWELLING.
NERVE
DYSFUNCTIONS.
Al I M E N T A R Y
SYSTEM
177
CAUSES:
1. Functionalcardiospasm.
2- Post-diphtheritic neuritis.
3. Bulbar paralysispoliomyelitis, progressive bulbar paralysis, syringobulbia, post-encephalitis.
4. Pseudo-bulbar paralysisprogressive muscular atrophy,
motor neurone diseases.
5. Hydrophobia.
6. Botulism.
7. Myasthenia gravis.
8. Thrombosis of posterior inferior cerebellar artery.
9. Tetanus.
INVESTIGATIONS
1.
HISTORY IN G E N E R A L :
(a) Age and sex.
In children exclude cleft palate, foreign bodies and diphtheria.
young females suspect hysteria and Plummer-Vinson syndrome.
old people suspect cancer of the oesophagus.
In
In
mechanical
obstruction;
and
for
PHYSICAL EXAMINATION:
(a) Mouth and throatfor stomatitis, mechanical defects, malignancy of
tongue.
(b) Neck for thyroid gland.
(c) Chest for evidence of aneurysm, enlarged heart, mediastinal growths.
(d) Central Nervous System for bulbar lesions, laryngeal paralysis.
(e) Blood for anaemia.
3.
SPECIAL INVESTIGATIONS:
(a) Laryngoscopy.
(b) Barium swallow.
12
I I O W T O EXAMINE
178
A FATIENT
(c) Oesophagoscopy.
(d) X-rays of the cliesf.
VOMITING
Mechanism of vomiting, depends upon the following:
1.
2.
4.
the spinal
VOMITING.
ALIMENTARY T R A C T :
obstruction,
gall-
NERVOUS CONDITIONS:
Al I M E N T A R Y S Y S T E M
179
REFLEX:
]. All colics.
2. Stimulation of pharynx.
3. Shock.
4. Severe pain.
D.
TOXAEMIA:
Uraemia, alkalosis, ketosis, hypoglycaemia, toxaemia of pregnancy, specific fevers, Addison's disease, hyperthyroidism, acute
yellow atrophy.
E.
MECHANICAL:
Severe cough.
FEATURES
OF SOME TYPES OF
VOMITING.
1. Sudden onset:
(a) With nauseaacute abdominal diseases, acute specific
fevers, toxic poisons.
(b) Without
nauseaincreased
intracranial
tension
(especially tumours), gastric crisis, neurosis.
1. Faecal vomitingintestinal
peritonitis.
obstruction: sometimes
in
3. Time of vomiting:
(a) Early morningpregnancy in early stages, chronic
alcoholism, chronic gastritis, uraemia sometimes.
IIOW T O E X A M I N E A
180
FATIENT
COLOUR:
(a) Bright redliaematemesis commonly due to peptic ulcer, splenic
anaemia, cirrhosis liver.
(b) "Coffee-ground"cancer of the stomach.
(c) Yellowish greenexcess of bile. T h e addition of water makes
the green colour of bile more apparent.
(d) Jelly likeexcess of mucus.
4. REACTIONgenerally
and in pernicious anaemia.
acid.
Chronic gastritis.
HAEMATEMESIS
Haematemesis or vomiting of blood has to be differentiated
from haemoptysis. (See page 49 for distinguishing features.)
Before arriving at a conclusion that blood comes from the
stomach, always make sure that it is not swallowed by the
patient as often occurs in epistaxis, haemoptysis and bleeding
from the mouth.
ALIMENTARY SYSTEM
ETIOLOGICAL
A.
181
CLASSIFICA TION:
FROM T H E OESOPHAGUS:
There will
FROM T H E STOMACH:
is generally
epistaxis
82
C.
DUODENUM :
1. Ulcersduodenal
liaematemesis.
ulcer
causes
melaena
rather
than
LIVER DISORDERS ( P O R T A L O B S T R U C T I O N ) :
ACUTE INFECTIONS :
BLOOI) DISORDERS:
A.
ALIMENTARY SYSTEM
I.
183
II.
diseases,
Weakness of the intestinal musculature or more probably inhibition of the muscular activity:
1. Congenital.
2- Senile.
3. Fat or flabby abdomen.
III.
B. Dyscheziapassage through the colon is normal but evacuation from the pelvic colon and rectum is inadequately performed.
1. Obstruction by the faeceshard and dry faecal matter;
less consumption of water.
2. Neglect to respond to call of nature due to faulty habits,
unclean closets, false modesty.
3. Weakness of muscles of defaecation or obstruction lower
down in the intestinestrictures, diverticulosis.
C.
IlOW T O E X A M I N E A
184
PATIENT
DIARRHOEA
Too frequent evacuation of liquid faeces is a symptom and
not a disease per se. Hence, in every case an attempt must be
made to discover the underlying cause. T o attain this, it may
be necessary, in addition to routine physical examination, to
employ one or all of the following special methods:
1. Digital examination of rectum.
2. Sigmoidoscopic examination.
3. Gastric analysis.
4. Detailed examination of faeces.
5. X-ray of the alimentary tract.
Before considering a case of genuine diarrhoea it is desirable
to exclude faecal impaction in the colon which may give rise to
"spurious diarrhoea" due to secondary putrefaction of the
impacted faecal matter.
ETIOLOGICAL CLASSIFICATION:
A. Gastrogenous: T h e origin is in the stomach and diarrhoea occurs due to deficiency of hydrochloric acid in the
gastric juice. In all these conditions the diarrhoea tends to
occur in bouts chiefly in the mornings. The stools are loose,
alkaline and contain undigested matter.
CAUSES:
1. Addison's anaemia.
2. Gastric cancer.
3. Simple achlorhydric anaemia.
4.
5. Nutritional anaemia.
6.
Pellagra.
Al I M E N T A R Y
COMMON
SYSTEM
185
CAUSES:
1. Dieteticunbalanced diet,
tion in diet, idiosyncrasy.
indigestible
food,
indiscre-
Colonic diarrhoeas.
COMMON CAUSES:
200
IlOW
TO
EXAMINE A
PATIENT
DIARRHOEA IN INl-ANTS
Acute diarrhoeas in infants is either dyspeptic, infective or
reflex in origin. In infectious types the patient generally shows
signs of toxaemiacollapse, pinched skin, sinking of the fontanelles and fever. If the stool contains blood one should also
suspect acute intussusception.
I.
DIETETIC ERRORS:
1. Over feeding.
2. Excess of fatsthe stool becomes loose, curdled, sour
smelling.
3. Excess of carbohydratesstool is loose, green, frothy and
acid in reaction.
4. Allergy to certain foods.
II.
INFECTIONS:
1. Bacterialstool is loose, 5-10 per day, greenish and offensive; there may be fever.
2, BacilVavystools watery, 10 or more per day, and odourless. There is generally fever and vomiting. In later
stages there may be dehydration.
III.
REFLEX:
STEATORRHOEAS:
Al I M E N T A R Y
AETIOLOGY
I.
SYSTEM
187
Causes:
1. Jaundice of obstructive or infective typein both, the
skin and conjunctivae are yellow and bile is found in
the urine.
2. Gall-stonesthere is generally bilary colic. There is
more often constipation than diarrhoea.
Hence,
steatorrhoea is not common.
III.
Split
similar
INTESTINAL DISORDERS
1. Sprueassociated with frothy stools, wasting of the
tissues, shrinking of the liver and macrocytic anaemia.
Common at the age of about 30-40 in tropics.
188
IlOW T O
EXAMINE
PATIENT
D I F F E R E N T I A T I O N BETWEEN I D I O P A T H I C S T E A T O R R H O E A
SPRUE.
Idiopathic
Steatorrhoea.
Tropical
AND
Sprue.
Age.
Adults.
Middle age.
Climate.
Temperate.
Present.
Tropics.
Bone deformities.
Clubbing.
Present.
Not present.
Megacolon.
Present.
Absent.
Morning diarrhoea.
Absent.
Diarrhoea.
General features.
Wasting common.
Prognosis.
Not good.
Fairly good.
BLOOD IN T H E STOOL
The appearance of blood in a stool may be bright red or
tarry.
CAUSES OF BRIGHT
A.
RED BLOOD
IN A
STOOL-.
RECTAL CONDITIONS :
Al I M E N T A R Y
SYSTEM
189
2. Prolapse of the rectumblood also appears after evacuation; there is associated tenesmus.
3. Anal fissurequantity of blood passed is small; there is
excruciating pain while passing stool.
4. Proctitissevere tenderness while passing stool, which is
blood tinged. Proctoscopic examination is indicated in
most cases.
5. Rectal polypicommon in children. Rectal examination and sigmoidoscopy reveal the true nature of the
disease.
6. Cancer rectumpresence of blood in an old man may be
the first evidence. Rectal examination and sigmoidoscopy is essential.
B.
1.ESIONS OF T H E LARGE I N T E S T I N E :
LESIONS OF T H E SMALL I N T E S T I N E :
BLOOD DYSCRASIAS:
Shallow.
Sharp.
Serpiginous.
Inflamed.
Sigmoidoscopic Examination:
Depth of ulcers.
Deep.
Edge.
Undermined.
Appearance. Flask-shaped.
Imcnening mucosa.
Normal.
Microscopic examination:
Ai>e.
Not common in children.
Common in children.
Onset.
Insidious.
Sudden.
frequency.
5 to 10 stools per day.
Several.
lever.
Rare.
Present.
Toxaemia.
Slight or none.
Present.
Abdominal pain.
Right side.
Left side.
Tenesmus.
Absent.
Present.
Complications.
Perforation; liver abscess.
Toxaemia; dehydration.
Appearance of the Stool
Reaction.
Acid.
Alkaline.
Odour.
Offensive.
Not so.
Faecal matter.
Present.
Hardly any.
Blood & mucus.
Present; more mucus.
Blood and mucus intimately mixed.
more blood.
190
IlOW TO EXAMINE A PATIENT
SYSTEM
19!
MELAENA
This is a term applied to black or tarry stools resulting from
haemorrhage higher up in the intestine. When the stool is
dark in appearance exclude intake of iron, charcoal, bismuth,
black-berries and excess of bile.
COMMON
A.
STOMACH CONDITIONS:
C.
D.
INTESTINAL CONDITIONS:
BLOOD DISORDERS:
IN T H E LL.M1.N OI T H E INTESTINE.
1. Impacted faeces.
2. Gall-stones.
192
IlOW
TO EXAMINE A
PATIENT
3. Round worms.
4. Foreign bodies.
B.
IN T H E WALL.
1. Intussusception.
2. Tumours.
3. Strictures.
4. Diverticulosis.
C.
OUTSIDE T H E WALL.
are
ALIMENTARY
193
SYSTEM
abdominal muscles, the lower edge may be felt on deep inspiration, more
so in the upright position.
Many conditions quite unconnected with the liver cause an apparent
alteration in its size and, hence, the organ may be palpable below the
costal arch as in the following conditions:
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
All these
size of the
conditions
liver.
of an increase
in
the
ENLARGEMENT OF T H E LIVER
CLA SSIFICA TION:
A.
GENERALISED
I.
ENLARGEMENT.
With jaundice.
1. Regular enlargement.
(a) Stone in the common bile duct.
(b) Cancer of the head of the pancreas.
(c) Arsenical poisoning.
(d) Catarrhal jaundice.
(e) Acholuric jaundice.
2. Irregular enlargement.
(a) Late secondaries.
(b) Syphilis (jaundice not common).
alcoholic,
Banti's,
bronzed
IlOW T O E X A M I N E A
194
PATIENT
Hodgkin's
disease,
LOCALISED ENLARGEMENTS.
1. Hydatid cyst.
2. Amoebic abscess.
3. Riedel's lobe.
4. Actinomycosis.
TENDERNESS OVER T H E LIVER MAY BE MET W I T H I N :
1.
2.
3.
Early cirrhosis.
4.
Actinomycosis.
5.
Visceroptosis.
6.
7.
3.
Sprue.
In emphysema
and right-sided pneumothorax
the
upper border of the liver cannot be percussed and in
perforative peritonitis and in excessive gaseous disten-
Al I M E N T A R Y
SYSTEM
dullness
195
is
apparently
2.
3.
4.
5.
congestive
heart
JAUNDICE
Jaundice is a term used to indicate yellow colouration of the
skin, conjunctivae, mucous membranes, most of the tissues and
fluids of the body due to increased concentration of bile pigments in the blood. Normally the ratio in the circulation of
bile to blood is 1:100,000. As soon as it rises to above 1:50,000
the urine reveals bile pigments.
Bile pigments are primarily formed by the breakdown of the
red cells in the R-E system of the liver, spleen, bone-marrow,
etc. T h e immature bilirubinic acid thus produced, if present
in excess, causes mild jaundicehaemolytic jaundice.
Such
jaundice occurs in blood diseases like acholuric jaundice, pernicious anaemia, etc., where excessive amount of haemoglobin is
set free in the circulation and the liver cells cannot convert the
whole amount into bilirubin as the amount is too far in excess.
Van den Berg's reaction in such cases is indirectly positive.
Ordinarily the immature bile passes through the liver cells
where the acid radicle is held back and pure bilirubin is
formed, which is excreted from the biliary passages along with,
bile salts. If obstruction occurs in any part of the biliary system,
the bile instead of flowing into the duodenum is dammed back
into the liver and absorbed in the bloocl stream giving rise to
obstructive jaundice.
The Van den Berg's reaction in such
cases gives an immediate direct reaction (a quickly producing
violet colouration).
196
IlOW T O E X A M I N E A
PATIENT
In some conditionshepatogenous jaundicethe liver parenchyma is damaged by toxic agents. T h e damaged liver cells
are incapable of dealing adequately with the bilirubinic acid
presented to them for conversion into bilirubin and exit of any
formed bile is impeded by the inflamed and swollen liver cells.
The Van den Berg's reaction in such cases is biphasic.
RED CORPUSCLES
RET1CUL0-ENDOTHEUAL
SYSTEM-
KBEKO-fclURUMN
IN 6LOOO
FIG. X I X
OBSTRUCTIVE JAUNDICE:
Causes:
1. In the lumen of the bile ductsgall-stones, worms.
2. In the wall of the ductsstrictures, neoplasms.
Al I M E N T A R Y
SYSTEM
197
HEPATOGENOUS JAUNDICE:
Causes:
1. Infectionshepatitis, yellow fever, Weil's disease, acute
yellow atrophy, malaria, catarrhal jaundice.
2. Chemical poisonsarsenic, sulpha, atophan, chloroform,
carbon tetrachloride, gold, etc.
3. After blood transfusion (virus infection).
4. Deficiency of specific food factorsmethionine, choline
and cystine. These deficiencies probably play a part in
the production of necrosis of hepatic cells.
5. Icterus gravis in infants.
C.
HAEMOLYTIC JAUNDICE:
Causes:
1. Anaemias, especially where there is excessive destruction
of red cellshaemolytic. anaemias, pernicious anaemia,
etc.
2. Familial acholuric jaundice.
3. Icterus neonatorum.
4. Snake venom.
5. Incompatible blood transfusion.
6. Chemicalssulpha.
The commonest cause of jaundice is infection, next being
gall-stones and cancer of the head of the pancreas.
INVESTIGATIONS:
1.
AGE.
(a) In new-bornsuspect icterus neonatorum or gravis.
(b) In infantsinfective jaundice, congenital syphilis.
(c) In children and in adultsinfective hepatitis (catarrhal jaundice).
(d) In middle agegall-stones.
(e) In old agecancer.
2.
SEX.
198
IlOW T O E X A M I N E A
PATIENT
3.
4.
5.
6.
7.
LABORATORY INVESTIGATIONS:
(a) Examine the urine for bile salts and pigments.
(b) Stool for neutral fats, fatty acids and occult blood.
(c) Blood plasma for the following tests:
]. VAN DEN BERG'S TEST is not so reliable to distinguish the three
types of jaundice as was once believed. T h e agents used for the test are:
Reagent "A" containing hydrochloric acid and sulplianilic acid, and reagent
"B" containing sodium nitrite.
METHOD-.
Draw 5 c.c. of blood and immediately centrifugalize it so as to get
plasma of the patient for the necessary test. Divide it into two parts.
In the first half, add 2 c.c. of diazo solution (in the proportion:25 c.c.
of "A" and 0.75 c.c. of "B") and note the colour:
Immediate blue colourationobstructive
jaundice.
Al I M E N T A R Y
SYSTEM
199
GALL-BLADDER
Palpation is the best method of examination in detecting an
enlarged gall-bladder. One may feel an oval, smooth swelling
moving downwards when the patient breathes just near the tip
of the 9th costal cartilage.
An enlarged gall-bladder may be mistaken for the following
other swellings:
1.
LIVER:
RENAL T U M O U R S :
IlOW T O E X A M I N E A
200
PATIENT
more freely movable of the two; the upper pole of the kidney
may be palpable which is not the case with the gall-bladder.
There may be jaundice in gall-bladder diseases and urine may
be abnormal in kidney disorders.
3.
T U M O U R S OF T H E NEIGHBOURING ORGANS:
1. Infections:
(a) Typhoid may cause empyema. History of remittent
fever and positive Widal test will reveal the true
diagnosis.
(b) Catarrh of the cystic duct may lead to a mucocele.
2. Gall-stones may cause impaction of the cystic duct leading
to mucocele.
3. Cancer of the head of pancreasgenerally causes enlargement of the gall-bladder associated with persistent and progressive jaundice, sometimes pains resembling gall-stone
colics. T h e commonest cause of enlargement of the gallbladder after middle life is cancer of the head of the
pancreas.
4. Cancer of the gall-bladdergenerally there is no ascites
unless the liver is involved secondarily. This disease is
extremely difficult to diagnose. The rapidity of the enlargement of the gall-bladder in absence of any definite cause
will suggest growth particularly in a person of cancer age;
the gall-bladder may also not be very smooth to the feel.
Al I M E N T A R Y
SYSTEM
201
SPLEEN
An enlarged spleen is likely to be mistaken for other structures round about the organ. Hence, the following points must
be borne in mind while examining the spleen:
1. Spleen moves with respiration.
2. T h e organ is situated very superficially.
3. T h e sharp edge and the splenic notch can be easily felt
when the gland is enlarged.
4. Fingers cannot be passed between the organ and the left
costal arch.
5. There is dullness on percussion over the gland.
6. T h e dullness posteriorly does not extend as far as the
middle line.
COMMON CAUSES OF E N L A R G E M E N T :
I. Infections.
1. Acuteenteric fever, typhus, most of the specific
infections.
2. Protozoalmalaria, kala-azar.
3. Sepsis.
4. Infectious mononucleosis.
5. Granulomatoussyphilis.
II. Blood diseasespernicious anaemia, leukaemia, polycythaemia, acholuric jaundice, Hodgkin's disease, purpura, splenic anaemia, Von-Jackson's anaemia, haemolytic
anaemia.
III. Diseases of the liverportal cirrhosis, haemochromatosis,
biliary cirrhosis.
IV. Diseases of the vascular system.
1. Congestive heart failure.
2. Infarctionsubacute bacterial endocarditis.
3. Thrombosis of the portal vein.
4. Thrombosis of the splenic vessels.
H O W TO EXAMINE A PATIENT
202
V. Deficiency diseasesrickets.
VI. Metabolic disordersamyloid disease; Gaucher's disease.
VII. Neoplasticcysts, angioma, lymphosarcoma.
VIII. Congenital.
VERY
IXG
GREAT
SPLEXIC
COXDITIOXS:
ENLARGEMENT
OCCURS
IX
THE
FOLLOIV-
Splenic anaemia.
3.
4.
Gaucher's disease.
5.
Haemochromatosis.
6. Polycythaemia vera.
DIEFEREXTIA
L DIA
GXOSIS.
ALIMENTARY
SYSTEM
203
is likely to be resonant in front. Anorexia, anaemia, leucocytosis, achlorhydria, and presence of occult blood in the stools
and gastric juice, are points in favour of cancer stomach.
5. Pancreatic tumours. These are usually situated between
the ensil'orm cartilage and the umbilicus in the median line
of the abdomen. No edge and no notch can be felt. A splenic
tumour is situated more to the left of the middle line and rarely
extends to its right unless very large and then it crosses at or
below the umbilicus; whereas a pancreatic cyst commonly
reaches across to the right of the middle line above the navel.
Jaundice, palpable gall-bladder, fatty diarrhoea and glycosuria
are familiar accompaniments.
6. Tubercular peritonitismay produce various forms of
abdominal tumours but these do not as a rule extend close up
to the ribs; hence, fingers can be placed between the mass and
the costal cartilage. There may be associated ascites.
7. Faecal accumulation in the splenic flexure may be mistaken for an enlarged spleen but the mass is generally irregular,
more or less cylindrical and the source of error is usually
removed when the patient is re-examined after an aperient or
high enema.
M E T H O D OF INVESTIGATION.
A.
B.
HISTORY:
1.
2.
3.
4.
PHYSICAL EXAMINATION:
1.
2.
infection,
acute
leukaemia,
acute
204
H O W TO EXAMINE A
PATIENT
C.
3.
blood
dyscrasias,
Hodgkin's
4.
Banti's
BLOOD EXAMINATION:
1.
2.
3.
4.
5.
Lymph-node biopsyconfirms
disease, tuberculosis.
lymphatic
leukaemia,
Hodgkin's
3.
Polycythaemia.
4.
Haemolytic Anaemias.
5. Cirrhosis Liver.
SPLENOMEGALY AND GLANDULAR
ENLARGEMENTS
Hodgkin's Disease.
3.
Lymphosarcoma.
4.
Sarcoidosis.
CHAPTER
INTERROGATION.
B.
COMMON SYMPTOMS.
C.
III.
Cranial Nerves.
IV.
Motor System.
V.
VI.
D.
Intellectual Functions.
Sensory System.
Reflexes.
206
HOW
TO EXAMINE A
PATIENT
CENTRAL N E R V O U S SYSTEM
207
drowsiness,
lachryma-
208
209
H O W TO EXAMINE A
210
PATIENT
INTELLECTUAL FUNCTIONS
CENTRAL N E R V O U S
SYSTEM
211
H O W T O EXAMINE A
212
PATIENT
CRANIAL
No.
I.
II.
Name
Foramen of Exit
Type
Olfactory.
Sensory.
Sensory.
Optic.
Optic foramen.
III.
Oculomotor.
Superior orbital
IV.
Trochlear.
Superior orbital
fissure.
Motor.
fissure.
Mixed.
V.
VI.
VII.
VIII.
IX.
X.
XI.
XII.
fissure.
Motor.
Trigeminal:
1st division.
Superior orbital
2nd division.
Foramen
3rd division.
Foramen ovale.
rotundum.
Abducent.
Superior orbital
fissure.
Motor.
Facial.
Mixed.
Auditory.
Sensory.
Glosso-pharyngeal.
Jugular foramen.
Mixed.
Vagus.
Jugular foramen.
Mixed.
Spinal-accessory.
Jugular foramen.
Motor.
Hypoglossal.
Hypoglossal canal.
Motor.
CENTRAL N E R V O U S
SYSTEM
213
NERVES
Distribution
Mucous membrane of
nose.
Functions
the
Smell.
Retina.
Sight.
Eye movements.
Mandibular movements.
Mastication & deglution.
Sensibility of the face and
mucous membrane of the
mouth.
Eye movements.
Facial expression.
Secretory to the glands of
the mouth.
Taste.
Cochlea.
Semicircular canals.
Hearing.
Equilibrium.
Pharyngeal 8c laryngeal
movements.
Taste.
Pharyngeal
&
laryngeal
muscles, Heart, lungs and
all the abdominal viscera.
Trapezius & sterno-mastoid.
HOW
214
TO EXAMINE A
III.
PATIENT
CRANIAL NERVES
SECOND OR O P T I C NERVE
T h e optic nerve is developed as a cerebral tract and retains something
of that character throughout life. T h e primary visual neurones are
situated entirely in the retina. From there the fibres of the optic nerve
pass back to the optic chiasma. Here, the fibres from the inner half of
each retina decussate, whilst those from the outer half remain on the
same side. Each optic tract, therefore, consists of fibres from the outer
half of the retina on the same side and the inner half of the retina on the
opposite side. (See Fig. XX.) Each tract passes back to the superior
corpus quadrigeminum, the lateral geniculate body and the pulvinar of the
thalamus of the same side. In these, which are known as the primary
optic centres, most of the fibres of the optic tracts terminate. But another
system of fibres, which is known as the optic radiation, takes origin in the
lateral geniculate-body and passes through the posterior limb of the internal
capsule and then backwards to the cortex around the calcarine fissure and
this represents the chief visual centre.
Acuity of Vision.
3.
Colour Sense.
2.
Field of Vision.
4.
Fundoscopy.
1. Acuity of Vision.
Exclude errors of refraction and corneal opacities before
testing for acuity of vision. Ask the patient to count the fingers
by placing your hand at varying distance. For slight degree
CENTRAL N E R V O U S SYSTEM
215
IN THE
FIELD
OF VISION
MAY
OCCUR
AS FOLLOWS:
216
H O W TO EXAMINE A
PATIENT
RIGHT TIT
FIG. XX
CENTRAL NERVOUS
3.
SYSTEM
217
Colour Vision.
Ophthalmoscopy.
THE
OPTIC
DISCS.
NOTE:
(a) SHAPEnormally this is circular.
appear oval.
at
THE
BLOOD-VESSELS.
HOW
218
3.
TO EXAMINE A
PATIENT
PERIPHERY.
OPHTHALMOSCOPIC
APPEARANCES.
PAPILLOEDEMA.
RETINAL HAEMORRHAGES.
OPTIC NEURITIS.
In this condition the veins are very full and haemorrhages often occur
in the discs or in the neighbouring retina. T h e disc is not raised as in
papilloedema though the swelling extends further into the surrounding
tissues. Optic neuritis may occur in syphilitic basal meningitis which
damages the interstitial tissue of the nerve leading to loss of peripheral
vision much earlier than the involvement of the central vision. Retrobulbar
neuritis often occurs in disseminated sclerosis, neuromyelitis optica and in
poisoning by nicotine, methyl alcohol, lead, arsenicals and quinine.
4.
OPTIC ATROPHY.
219
T H I R D , F O U R T H AND S I X T H NERVES
(Oculo-Motor Nerves)
T h e sixth n c n e supplies the external rectus and the fourth nerve, the
superior oblique muscle. All the other musclcs along with the sphincter
pupillac, the muscles of accommodation and the levator palpebrae superioris
are supplied by the third nerve.
Ocular movements.
2.
Ptosis.
3.
Diplopia.
4.
Nystagmus.
5.
Pupillary reflexes.
1.
OCULAR
MOVEMENTS.
How to test:
Fix the patient's chin or head with one hand and move the
forefinger of the other in various directions. Let the patient
follow the finger with his eyes without moving the head.
Lesions involving any of these nerves may lead to limitation
of movements of the eye-balls due to paresis of the 3rd, 4tli or
6th cranial nerves. Defective movements may also be due to
disturbance within the extra-ocular muscles themselves, as in
myasthenia gravis and exophthalmic goitre. It may also be
due to tumours or inflammation within the orbit and in cavernous sinus thrombosis involving 3rd, 4th and 6th nerves.
In 6th nerve involvement there is inability to move the eye
outward and there is diplopia on looking in that direction;
there is often an internal squint. In nuclear lesions there is loss
of power of conjugate deviation of both the eyes to the side of
the lesion. T h e nuclei of the 6th nerve may be involved in
syphilitic basal meningitis, tumours, aneurysm of the internal
carotid artery, cavernous sinus syndrome and all conditions that
cause increase in the intracranial tension.
220
H O W TO EXAMINE A
PATIENT
PTOSIS.
T h e posture of the eyelids depends upon the tone of the orbicularis palpebrea (supplied by the 7th cranial nerve) which
closes the eyes; of the levators (supplied by the 3rd nerve) and
unstriated muscles (supplied by cervical sympathetics)
which
open the eyes. In third nerve palsy the levator palpebrae are
affected and the eyelids droop. In sympathetic paralysis also
there is drooping, but in former, it is of greater degree. Loss
of tone with loss of power in the levator can cause partial ptosis
as in tabes. In this condition, so alsio in cervical sympathetic
paralysis, the eyelids can be raised on upward deviation of the
eyes as contraction of the levator is unimpaired. Irritation of
the cervical sympathetic nerves causes retraction of the upper
eyelids as occur in thyrotoxicosis.
CENTRAL N E R V O U S
SYSTEM
221
DIPLOPIA.
H O W TO EXAMINE A PATIENT
222
rectus muscle, the false image belongs to the affected eye, i.e.
homonymous. In paralysis of the internal rectus muscle the
false image that is produced in the affected eye is heteronymous,
i.e. it produces crossed diplopia.
CAUSES OF D I P L O P I A :
I.
Monocular diplopia.
1. Dislocation of the lens.
2. Incipient cataract.
.3. Astigmatism.
4. Corneal opacities.
5. Detachment of the retina.
6. Some gross cerebral lesions causing ocular paresis.
II.
Binocular diplopia.
1. Paralysis of the ocular muscles.
2. Infectionsencephalitis lethargica, diphtheria, syphilitic
meningitis, botulism.
3. Poisonslead encephalopathy, alcohol.
4. Endocrine disordersdiabetes, exophthalmic goitre.
5. Disseminated sclerosis.
6. Arterio-sclerosis.
7. Migraine
8. Tumours of the brain.
9. Displacement of one eyeorbital
haemorrhage, cavernous thrombosis.
4.
growths,
abscess,
NYSTAGMUS.
223
B.
ETIOLOGY:
I. Ocular nystagmus:
1. Railway nystagmusphysiological and occurs in a fast
moving train.
2. Miner's nystagmusinvariably associated with head tre"f mors, vertigo, and intolerance to light. It is due to
badly lit mines, where the miners have to continually
msove the eyes to avoid fatigue.
3. Congenitalalbinism, absence of iris, total colour blindness.
4. Blenorrhoea neonatorum.
5. Partly blind peoplecataract, central scotoma.
The whole group produces pendular
type of
nystagmus.
224
4. Friedreich's ataxia.
5. Pontine or mid-brain lesions.
6. Medullary lesions.
7. High cervical lesionssyringomyelia.
8. Drugscodeine, barbiturates, dilantin, alcohol.
The nystagmus in the cerebellar group may be jerky or pendular. Quick phase is towards the side of the lesion and slow
phase is away from the lesion.
5.
PUPILS.
Size.
B.
Shape.
C.
Position.
D.
Equality.
E.
Reactions.
CENTRAL NERVOUS
SYSTEM
225
Mydriasis
(dilatation).
CAUSES:
1.
Brain infection.
2.
3.
4.
nerveaortic
aneurysm,
mediastinal
5.
Concussion.
6.
Anaemias.
7.
8.
9.
II.
Myosis
(contraction).
CAUSES:
1.
Pontine lesions.
2.
Tabes dorsalis.
3.
4.
5.
B.
2.
15
HOW
226
C.
TO EXAMINE A
PATIENT
2.
3.
D.
CAUSES OF UNEQUALITY:
1.
2.
(May occur in
E.
1.
Reactions.
2.
chronic
3.
CENTRAL NERVOUS
SYSTEM
227
(e) Encephalitis.
(f) Syringomyelia.
(g) Intracranial tumours.
(h) Haemorrhage.
(i) Alcoholic neuritis,
(j) Diphtheria.
4.
F I F T H O R TRIGEMINAL NERVE
This is a sensory and motor nerve. It is divided into three
branchesophthalmic, maxillary and mandibular. The motor
portion joins the mandibular division of this nerve.
1.
Ophthalmic
branchsupplies
sensory fibres to the eye-brows, cornea,
conjunctiva, upper eye-lids, forehead, scalp and nose.
2.
Maxillary branchsupplies
sensory fibres to the upper lip, sides of
the nose, cheeks, lower eye-lids, upper part of the temple and upper
gums.
3.
Mandibular
branch, which is both motor and sensory, supplies sensations to the jaw, external ear, lower part of the temple, mucous
membranes of the cheeks, tongue and lower gums. T h e motor
portion supplies the temporals, masseters and pterygoids.
Senspry portion.
1. Corneal and conjunctival reflexes.
These are best elicited by touching the cornea or conjunctiva with the end of a kerchief which results in
contraction of the orbicularis palpebrae. It is also
elicited by blowing on one cornea which results in
blinking in both the eyes. The nerves concerned are
the 5th (afferent) and 7th (efferent). The centre is in
the pons. In both 5th and 7th nerve lesions the corneal
242
H O W TO EXAMINE A
PATIENT
CENTRAL N E R V O U S
B.
SYSTEM
229
Motor Portion:
1. Ask the patient to clench his teeth and feel for the
masseters and temporal muscles, which normally stand
out with equal prominence on either side.
2.
5.
Paralysis of the Ophthalmic branch results in loss of sensibility of the areas supplied by this branch,especially conjunctiva, upper eye-lids and the scalp.
Paralysis of the Maxillary branch leads to abolition of
sensibility of the lower eye-lids, side of the nose, upper lip and
loss of palate reflex.
Involvement of the
sensibility of the lower
of the tongue. It also
ing in deviation of the
mouth.
230
HOW
TO EXAMINE
PATIENT
round the nucleus of the 6th cranial nerve and finally emerge between
the olive and the restiform body. Passing into the internal auditory
meatus along with the 8th cranial nerve, the 7th nerve enters the facial
canal of the temporal bone and goes to the geniculate ganglion. Distal
to this ganglion, it gives off the chorda tympani nerve which carries taste
fibres from the anterior two-thirds of the tongue via the lingual nerve.
T h e facial nerve leaves the facial canal through the stylo mastoid foramen,
passes through the parotid gland and supplies the muscles of the face.
T h e nerve, when in the facial canal, issues a small branch to the stapedius
muscle.
CENTRAL NERVOUS
SYSTEM
231
SUPRANUCLEAR LESIONS:
T h e lesion occurs in the pyramidal fibres between the cortex and middle
of the pons. T h e lower half of the face on the opposite side is involved,
in addition to hemiplegia. T h e eye can be closed but the teeth cannot
be bared on the affected side. T h e emotional movements remain normal
despite the loss of purposive movements, as a smile often draws out the
angles of the mouth on both sides. In bilateral supranuclear lesions, the
upper as well as the loner part of the face on either side is affected; the
emotional movements are also lost. T h e common causes are all vascular
accidents.
FIG.
XXI
NUCLEAR LESIONS:
A lesion at the lower border of the pons involves the nucleus of the 7th
cranial nerve resulting in paralysis of the whole face on the side of the
232
H O W TO EXAMINE A
PATIENT
2.
3.
4.
5.
LESIONS IN T H E I N T E R N A L AUDITORY
and signs of Bell's palsy.
6.
MEATUS:Deafness
E I G H T H OR AUDITORY NERVE
This is a purely sensory nerve and consists of two partscochlear portion
concerned with hearing and the vestibular portion concerned with
equilibrium.
A.
Cochlear Division.
Test for the power of hearing by means of a watch and use tuning fork
for the following tests:
CENTRAL NERVOUS
SYSTEM
233
Vestibular Division.
CEREBRAL:
1.
Functionalhysteria, neurasthenia.
2.
3.
4.
5.
Infectionsencephalitis,
syphilis.
the vertigo
is transient
or
temporary.
234
H O W TO EXAMINE A
II.
PATIENT
CEREBELLAR DISORDERSabscess,
nated sclerosis.
In this group
signs.
III.
tumours, infarction,
nystagmus
and other
dissemicerebellar
AURAL.
Otitis media, vestibular nerve disorders, labyrinthine disorders,
Meniere's disease, sea and air sickness. In most of these conditions
the vertigo is usually induced or tends to be aggravated on altering
the posture of the head. In labyrinthine disorders there is often
nystagmus and in Meniere's disease the vertigo is often associated
with vomiting, prostration and tinnitus. In sea and air sickness the
vertigo is associated with vomiting.
IV.
OCULAR.
Paralysis of ocular muscles, eye-strain, errors of refraction.
V.
TOXIC.
1.
Specific fevers.
2.
3.
Constipation, sepsis.
B.
TINNITUS.
EXTRA-AURAL.
1.
3.
4.
5.
6.
anaesthetics.
arterio-sclerosis.
CENTRAL NERVOUS
II.
SYSTEM
235
Aural diseases:
1. Lesions of the external auditory meatuswax, polypi,
foreign body.
2. Middle ear diseasesinflammation, suppuration, indrawn
tympanic membrane.
3. Disorders of the internal earMeniere's disease, labyrinthine disorders, otosclerosis, acoustic nerve tumours,
specific fevers, syphilis.
N I N T H OR GLOSSOPHARYNGEAL NERVE
This is a mixed nervemotor, sensory and secretory.
How to test:
Note if there is dysphagia and, if present, whether it is for
fluids. T o swallow fluids, quick action of deglutition muscles
is required, which fails to occur in lesions of bulbar nerves.
1. Test for taste of the posterior-third of the tonguea
difficult technique and of not much clinical value.
2. Test the pharyngeal reflex by tickling the back of the
pharynx. This should produce normally contraction of
the pharyngeal muscles. In hysteria and in some
apparently healthy people this reflex may be absent.
T h e 9th nerve is rarely paralysed alone. It is generally
involved along with the 10th and 11th nerves. Syringomyelia,
posterior inferior cerebellar syndrome, bulbar paralysis, rabies,
infective polyneuritis, posterior fossa tumours and aneurysms
are the common causes that lead to damage to these nerves.
T E N T H OR VAGUS NERVE
This is a mixed nerve and supplies motor fibres to the soft
palate, pharynx and larynx, respiratory tract, oesophagus, and
visceral fibres to the lungs, heart and abdominal viscera.
Note if there is regurgitation of fluids through the nose.
Test the palate as follows:
(a) Use a tongue depressor and ask the patient to say 'Ah'
and note whether both sides of the palate arch upwards.
HOW
236
TO EXAMINE
PATIENT
This occurs in
(c) Ask the patient to pronounce words which require complete closure of the naso-pharynx. In bilateral paralysis
of the vocal cords, words like "egg" sound like "eng".
In unilateral paralysis these symptoms are not observed.
In acute unilateral lesions, however, there may be "nasal"
quality to the speech.
Test the oculo-cardiac reflex by pressing on the eyeballs.
Normally the heart-rate is slowed by about 5 beats. The rate
increases in vagotonics and decreases in sympatheticotonics.
The rate remains the same in vagus paralysis.
The causes of lesions of the 10th nerve are the same as those
described under the 9th cranial nerve. The additional causes
are lesions in the thoraxaneurysms, mediastinal growth, etc.
ELEVENTH OR ACCESSORY NERVE
(Spinal-accessory)
Correctly speaking this nerve can no longer be considered as a cranial
nerve since it originates in the upper cervical spinal cord. From its origin
it runs upwards through the foramen magnum and then runs downwards
through the jugular foramen, where it receives a few fibres from the vagus.
It is apparently a motor nerve and supplies the Trapezius and the Sterno
Mastoid muscles, the rotators of the head. This nerve, since it enters the
cranium from outside, may therefore be considered a secondary cranial
nerve.
How to test:
1. Ask the patient to shrug shoulders against resistance.
The patient is unable to do so on the paralysed side.
2. Ask the patient to abduct the arms against resistance.
If there is paralysis of the Serratus Magnus such action
intensifies the winging of the scapulae. In isolated
Trapezius palsy, with the shoulder girdle at rest, the
scapula is displaced downwards and laterally, and is
rotated so that its superior angle is further from the spine
than the inferior angle; the vertebral border, particularly, at the inferior angle is flared; these changes are
accentuated when the arm is abducted from the side
CENTRAL NERVOUS
SYSTEM
237
238
H O W TO EXAMINE A
PATIENT
SYMPATHETIC NERVES
These nerves enter the eye-ball via the ophthalmic division
of the 5th cranial nerve and supply dilator fibres to the pupils.
Its stimulation results in the following:
1. Exophthalmos (see page 238).
2. Retraction of the upper eye-lids.
3. Widening of the pupils.
4. Excessive sweating on the affected side of the face sometimes.
Its paralysis results in the following:
1. Enophthalmos (see page 239).
2. Drooping of the upper eye-lid.
3. Contraction of the pupil with absence of dilatation on
shading the eye or on instillation of cocaine.
4. Loss of cilio-spinal reflex.
5. Absence of sweating.
EXOPHTHALMOS
Exophthalmos may be bilateral or unilateral.
Bilateral Exophthalmos:
CAUSES:
1.
Endocrine disorders:
(a) Grave's diseaseexophthalmos is almost always present. T h e
thyroid is enlarged and pulsatile; there is associated tachycardia
and tremors.
(b) Pituitary disordersmay cause exophthalmos; not
tumours,
especially
common.
2.
Neoplastic conditionsorbital
often bilateral.
lymphomas
are
3.
Vascular lesionsthrombosis of the cavernous sinus causes exophthalmos on one side and invariably spreads to the other side. There
is marked proptosis, the eyelids are engorged and the eye movements
limited.
4.
5.
Congenitaloxycephalus can cause exophthalmos in addition to difficulty of closing the eyes during sleep. T h e skull is elongated.
CENTRAL NERVOUS
SYSTEM
239
Unilateral Exophthalmos:
CAUSES:
1.
2.
Thrombosis of the cavernous sinusa very painful condition associated with involvement of the 3rd, 4th and 5th cranial nerves.
3.
4.
5.
6.
Arterio venous aneurysmnearly always produces pulsating exophthalmos. T h e blood-vessels of the retina and conjunctiva are dilated.
There is also loud blowing murmur over the eye.
7.
8.
exophthalmos.
EXOPHTHALMOS.
CAUSES:
1.
2.
3.
4.
5.
IV.
M O T O R SYSTEM
HOW TO EXAMINE A
240
PATIENT
Upper Limb.
THE
FINGERS:Ask
the
patient
to
squeeze
the
against
CENTRAL NERVOUS
SYSTEM
241
II.
Test for rigidity of the neck by placing a hand under the head of the
patient lying in supine position. Normally it should flex over the trunk.
In meningitis, tetanus and fracture-dislocations at the base of the skull
the neck is rigid.
III.
Trunk Muscles:
IV.
16
242
HOW
TO EXAMINE A
PATIENT
2.
Nutrition.
Muscular Tone.
CENTRAL NERVOUS
SYSTEM
243
Co-ordination.
Abnormal Movements.
H O W TO EXAMINE A
244
PATIENT
Gait.
SENSATIONS
Pain:
CENTRAL NERVOUS
SYSTEM
245
246
HOW
TO EXAMINE A
VI.
PATIENT
REFLEXES
Afferent Nerve.
Cranial V
Radial
Median
Femoral
Tibial
Pons
Musculocutaneous
C6-7
C6-8
L2_4
Si_2
S4.5
Cranial V
C5-6
Cranial VII
Cranial X
Efferent Nerve.
DM0
M10-12
Li
S^
Pons
Medulla
Centre.
Light
Cranial II
Midbrain
Cranial III
Accomodation
Cranial II
Occipital Cortex. Cranial III
Oculocardiac
Cranial V
Medulla
Cranial X
Bladder
N. Erigentes
S2_4
Rectal
Pudendal
S4-5
Visceral Reflexes.
Jaw
Biceps
Triceps
Supinator
Knee
Ankle
Deep Reflexes.
Corneal
Cranial V
Pharyngeal
Cranial IX
Upper abdominal
D 7 _i 0
Lower abdominal
D]0-i2
Cremasteric
Femoral
Plantar
Tibial
Anal
Pudendal
Superficial Reflexes.
Reflexes.
Pudendal
Radial
Median
Femoral
Tibial
Pudendal
Musculocutaneous
D7-10
L>io-i2
Genitofemoral
Tibial
Pudendal
248
H O W TO EXAMINE A
PATIENT
Fig. XXII
Flexor plantar
response.
Extensor plantar
response.
CENTRAL NERVOUS
2.
SYSTEM
249
DEEP REFLEXES
(a) Jaw jerk. T a p the chin with the mouth half-open and
the jaw relaxed. The jaw closes when the jerk is exaggerated. It is generally absent in health. It is increased
in upper neurone lesions above the 5th cranial nerve
nuclei. The afferent impulses are carried through the
sensory portion of the 5th cranial nerve and the efferent
impulses through its motor portion. T h e centre is in
the pons.
(b) Biceps. T h e arm is held in relaxed position with the
forearm midway between flexion and extension and
slightly pronated. The examiner places the thumb over
the biceps tendon of the patient and lets his forearm rest
on the examiner's hand. T h e thumb is then tapped with
a knee-jerk hammer and contraction of the biceps noted
or felt by the thumb. (See Fig. XXIII.)
(c) Triceps. T h e arm is held midway between flexion and
extension. T h e triceps tendon just above its insertion
on the olecranon process of the ulna is then tapped. T h e
response is extension of the forearm. (See Fig. XXIV.)
FIG. XXIII
FIG. XXIV
Biceps-Jerk.
Triceps-Jerk.
(d) Supinator jerk. Place the forearm in a semi-flexed position and slightly pronated and strike over the styloid
process of the radius. This produces supination of the
forearm and flexion at the elbow; there may be associated
250
H O W TO EXAMINE A
PATIENT
flexion of the wrist and fingers with abduction of the forearm. In lesions of the 5th and 6th cervical segments)
there may be contraction of the flexors of the hand and
fingers without flexion and supination of the forearm.
This is called inversion of the radial reflex. (See Fig. XXV.)
(e) Knee-jerk. This is best elicited with the patient seated
in a chair and with the testing limb crossing over the
other. If the patient is lying in bed the examiner lifts
both the knees by placing one hand beneath them. T h e
patellar tendons are then tapped and the response noted,
which consists of extension of the leg at the knee. If
the reflex is not easily elicited, reinforcement may be
carried out by asking the patient to hook together the
flexed fingers of the two hands and pull them apart just
at the time of taking the reflex, thereby diverting his
attention for a moment. (See Fig. XXVI.)
Fig. XXV
Fig. XXVI
Supinator Jerk.
Knee Jerk.
ABNORMALITIES
OF KNEE
JERK
Intoxicationbenzidrine, strychnine.
Infectionstetanus, meningitis.
5.
251
B.
TEMPORARY:
1.
2
Shock.
3.
Spinal shock.
4.
5.
Cerebral haemorrhage.
6.
Severe infections.
7.
Diabetic ketosis.
8.
Uraemia.
9.
OF LONGER D U R A T I O N .
ence in the reflex arc.
tensionmeningitis,
hydro-
1.
2.
3.
4.
252
H O W TO EXAMINE A PATIENT
(See
FIG. XXVII
Ankle-Jerk.
CENTRAL NERVOUS
SYSTEM
253
FIG. XXVIIl
Ankle-Clonus.
3.
I.
Micturition:
H O W TO EXAMINE A PATIENT
254
2.
Defaecation:
Deglutition:
Mass reflex:
T O N I C REFLEXES
CENTRAL NERVOUS
SYSTEM
255
Fig. XXIX
Kernig's-Sign.
3.
Brudzinski's signs:
The
4. Bickele's sign:With the arm raised and slightly backwards, extend the elbow. Resistance is offered in meningitis
and brachial plexus neuritis.
5. Grasp reflex:This reflex is normally present in infants,
but later it is suppressed by cerebral cortex. It is elicited by a
firm stroke across the palms in the radialward direction. All
the fingers flex and grasp the object and the thumb is fully
extended. In lesions of the opposite frontal lobe of the brain,
it is often present. In stuporose patients, with increased intracranial pressure, it may be present on both sides.
H O W T O EXAMINE A
256
PATIENT
T H E BRAIN.
1.
Cerebrum.
Fig. X X X
Lateral outline of the Brain.
ARegio Frontalis.
BRegio Centralis.
CRegio Parietalis
DRegio Temporalis.
ERegio Occipitalis.
FCerebellum.
GPons.
HMedulla Oblongata
aCerebral
Peduncles
b, e, dSuperior, Middle and Inferior Cerebellar Peduncles.
CENTRAL NERVOUS
SYSTEM
257
2.
3.
Mid-brain.
This is a short portion of the brain between the cerebrum above and
the pons below. It contains the four corpora quadrigemina and the two
cerebral peduncles. Nearly all the cranial nerve nuclei concerned with
vision and ocular movements are situated in this part of the brain.
4.
Brain-stem.
5.
Hind-brainCerebellum mainly.
B.
MOTOR SYSTEM.
C.
SENSORY SYSTEM.
D.
SPINAL CORD.
E.
PERIPHERAL NERVES.
CEREBRAL CIRCULATION
Next to liver, brain is the most highly vascularised organ in the body.
Further, there is marked plasticity in its compensatory regulating
mechanism. This is marked not only between the brain and other organs
in the body but within the brain itself, where different areas (speech,
auditory, etc.) are thrown into use at different times. T h e smaller cerebral
vessels are very elastic, and hence, easily overfill leading to congestion, or
contract leading to fainting. Some of them are also liable to rupture, especially the lenticulo-striate branch of the middle cerebral artery and other
vessels with congenital anomalies around the circle of Willis.
The avenue of blood intake into the brain are through the two internal
carotid arteries which enter the brain through foramen lacerum; and the
two vertebrals which enter the skull through the foramen magnum and
unite to form the basillar artery. The latter bifurcates into two large
posterior cerebral arteries and supply 2/5ths of the braintemporo-occipital
lobes, corpora quadrigemina, crura and parts of optic thalamus, whereas
the internal carotids supply 3 / 5ths of the brainfrontal and parietal lobes,
the cerebral peduncles and the internal capsule.
This arterial system, which constitutes the Circle of Willis, (see Fig. XXXI)
issues several branches to the various parts of the brain, of which the most
16
258
H O W T O EXAMINE A PATIENT
CEREBRAL
CIRCULATION
(Circle of Willis)
FIG. X X X I
important, from clinical point of view, are the middle cerebral artery, a
branch of the internal carotid which is often thrombosed leading to hemiplegia on the opposite side, and the posterior inferior cerebellar, a branch
of the vertebral artery, whose blocking causes acute giddiness and involvement of the lower cranial nerves.
The chief cerebral
arterial
disorders
arise from
the following:
1.
2.
3.
Sclerotic changesarteriosclerosis.
4.
5.
Thrombosis.
6.
Embolism.
259
CEREBROSPINAL FLUID
T h e cerebro-spinal fluid is formed in the choroid plexus by
a process of secretion and filtration. It is partly dependent
upon the osmotic tension of the blood.
From the lateral ventricles the spinal fluid passes through
the foramen of Munro into the third ventricle and thence by
the aqueduct of Sylvius to the fourth ventricle. It leaves the
fourth ventricle by way of three aperturesthe middle foramen of Magendie and the two lateral foramina of Luschka, and
reach the subarachnoid spacehere expanded into the cisterna
magna.
From there it passes downwards in the spinal subarachnoid
space and forwards and upwards about the base of the brain
to reach the surface of the hemispheres. Over these, it passes
in an upward direction to the vertex, the greater part naturally
travelling where the channel is deepestthat is, over the main
cerebral sulci.
The absorption occurs through the arachnoid villi- which are
projections of the subarachnoid space through the dura mater,
into the dural venous sinuses by filtration and osmosis. Some
may be absorbed by spinal veins.
COMPOSITION OF CEREBRO-SPINAL FLUID.
Quantity
Colour
Specific Gravity
Reaction
Pressure
Total solids
Proteins
Chlorides
Sugar
Urea
Calcium
Total cells per field
Alkaline; p H 7.35.
100-130 mm. of H.O.
1 Gm. per cent.
20 to 40 mgm. per cent.
700 mgm. per cent.
70 mgm. per cent.
10 to 20 mgm. per cent.
5 mgm. per cent.
5 lymphocytes.
260
H O W T O EXAMINE A PATIENT
TO PERFORM
LUMBAR
PUNCTURE:
Pressure
yellow
normal
low
normal or
slightly+
slightly+
Poliomyelitis
Acute
polyneuritis
Spinal-cord
tumours
Cauda equina
tumours
normal or
turbid
may be
turbid
normal
xanthochromic
increased
Abscess
300 c.c.
200 c.c.
increased
increased
meningitic
Sugar
normal
leSS
normal
slightly +
40-100 mgm.
normal
normal
very high
300 c.c.
10-300 polys and
later lymphos.
normal
slightly-f-
normal
normal
normal
normal
normal
normal
normal
normal
slightly-)10-100 polys.
normal
normal
normal
200 c.c. 50 lymphos. 50 mgm.
paretic 600 mgm.
normal
normal
0TOO lymphos.
normal or
normal
normal
slightly+
may be+
100 polys.
40 mgm.
normal
normal
meningitic
500 mgm. 40 mgm.
meningitic
700 mgm. 50 mgm.
normal
normal
normal
normal
50-100 mgm.
1000 polys.
700 c.c.
20 mgm.
Cells
5 lymplios.
Appearance Quantity
Disease
HOW
262
T O EXAMINE A
PATIENT
T o relieve pressure.
3.
4.
PHYSICAL EXAMINATION.
fluid over
meningitis,
CENTRAL NERVOUS
SYSTEM
263
MICROSCOPIC
EXAMINATION.
264
H O W T O EXAMINE A
III.
CHEMICAL
PATIENT
EXAMINATION.
brain; it is
encephalitis.
in tubercular
they are not
uraemia.
CENTRAL NERVOUS
SYSTEM
265
BIOLOGICAL TEST.
BACTERIOLOGICAL TEST.
DISEASES OF T H E BRAIN.
1. Idiopathic epilepsy.
encephalitis,
syphilis,
tuber-
266
H O W TO EXAMINE A PATIENT
5. Growthstumours, abscesses.
6. Defective development of the grey matterhydrocephalus, microcephalus, agenesis of the grey matter.
7. Functional.
B.
1. Stoke-Adam's syndrome.
2. Arteriosclerosis.
3. Hyperpiesia.
C.
ALIMENTARY DISORDERS
ENDOCRINE DISORDERS.
1. Hyperadrenalism.
2. Hyperinsulinism.
3. Hypoparathyroidism.
E.
METABOLIC DISORDERS.
1. Rickets.
2. Tetany.
3. Alkalaemia.
4. Cyanosis.
F.
EXTRANEOUS POISONS
1. Eclampsia.
2. Pneumonia, enteritis, etc. (especially in children).
3. Tetanus.
4. Cerebral malaria.
5. Uraemia.
6. Pregnancy toxaemia.
7. Heat stroke.
H.
REFLEX CAUSES
267
CONVULSIONS IN CHILDREN
Convulsions are common in early life because the central
nervous system is unstable and hence, responsive to small
stimuli.
AETIOLOGY:
I.
A.
General causes.
1. Infections:
(a) Acute specific fevers.
(b) Congenital syphilis.
2. Intoxicants:
(a) Strychnine, alcohol, lead.
(b) Intraneous poisonsuraemia.
3. Reflexdentition,
pyelitis.
worms,
phimosis,
otitis,
enteritis,
HOW
268
B.
T O EXAMINE A PATIENT
Cerebral conditions.
1. Epilepsy.
2. Inflammationsmeningitis, encephalitis.
S. Vascular.
(a) Aneurysm.
(b) Whooping cough.
4. Brain defectsidiocy, hydrocephalus, porencephalus.
5. Growthstumours, abscesses, cysts.
EPILEPSY
SYMPTOMATIC.
1.
2.
Nocturnal generally.
Occurs
at any time.
3.
Pattern stereotyped.
Mixed pattern.
4.
N o mental changes.
5.
Fits generalised.
Generally Jacksonian.
Grand mal.
Petit mal.
Jacksonian epilepsy.
Psychomotor epilepsy.
Myoclonic epilepsy.
CENTRAL NERVOUS
I.
SYSTEM
269
EPILEPSY MAJOR.
II.
P E T I T MAL.
JACK.SONIAN EPILEPSY.
PSYCHOMOTOR EPILEPSY.
H O W T O EXAMINE A PATIENT
270
MYOCLONIC EPILEPSY.
This type often runs in families. The movements are generally clonic and jerky and the patient just drops on the floor,
if erect. The fits often come on before unconsciousness; in fact,
in most cases there is no loss of consciousness.
INVESTIGATION
OF A CASE OF FITS:
1.
Think of epilepsy first in every case of fits. Inquire into the family
history, previous attacks and aura. Note the type of movements, their
distribution and if localised or generalised. Note if there is froth in
the mouth and if it is blood-tinged. Note the behaviour of the
patient after the fit.
2.
3.
4.
5.
6.
7.
8.
9.
HEADACHE
In majority of cases headache is of minor significance, but it
may be the first and only symptom of a grave disease, especially
of the brain.
COMMON
A.
CAUSES.
FUNCTIONAL:
CENTRAL NERVOUS
SYSTEM
271
1. Traumatic:
(a) Concussionmay produce headache even a week
after injury. Lumbar puncture often relieves the
headache.
(b) Contusionheadache is often paroxysmal, aggravated by sneezing or coughing and relieved by rest
and recumbency.
2. Inflammationsmeningitis, encephalitis, syphilis, abscess,
cysticercosis, disseminated sclerosis.
3. Tumoursaneurysmal, pituitary, cystic, new. growths,
hydrocephalus.
4. Vascular disorderscerebral haemorrhage, thrombosis,
embolism, subarachnoid haemorrhage, migraine.
5. Drugsnitrites, adrenaline, histamine.
LESIONS OF T H E CRANIAL NERVES
1. Injuries.
2. Infectionsperiostitis.
3. Dental diseases.
HOW
272
F.
TO EXAMINE A PATIENT
TOXIC CAUSES:
1. Exogenous.
(a) Foul air, CO-poisoning, CO2 poisoning.
(b) Drugsquinine, salicylates, alcohol, lead, tobacco.
(c) Infectionsmalaria, typhoid, etc.
2. Endogenous toxinsuraemia, cholaemia, diabetes, gout,
constipation.
G.
1. Those resulting in increase in the cerebrospinal pressurevenous congestion, suppressed menses, heart
failure, hypertension, arteriosclerosis.
2. Those leading to lowering of the cerebro-spinal pressure
after lumbar puncture, anaemias. Addison's disease,
injection of hypertonic saline, hypotension.
3. Inflammation of the arteriestemporal arteritis.
INVESTIGATIONS
OF A CASE OF
HEADACHE:
migraine,
2.
3.
Situation:
(a) If frontalsuspect uraemia, sinusitis, after a bout of malaria.
(b) If verticalconstipation or biliousness.
(c) If occipitalcerebellar
diseases,
subarachnoid
meningitis, posterior fossa tumours.
haemorrhage,
CENTRAL NERVOUS
SYSTEM
273
H O W T O EXAMINE A
274
PATIENT
OF COMA:
CEREBRAL CAUSES.
1. Traumatic.
CENTRAL NERVOUS
275
SYSTEM
2. Infective.
(a) Encephalitis, meningitis, abscess.
(b) Cerebral malaria.
(c) G.P.I.
3. Extraneous
pathy.
poisonarsenic,
alcohol,
lead
encephalo-
EXTRACEREBRAL CAUSES.
1. Cardio-vascular:
(a) Stoke-Adam's syndrome.
(b) Vaso-vagal attacks.
(c) Shock.
2. Extraneous poisonsalcohol, opium, barbiturates, carbon
monoxide, datura.
3. Intraneous poisonsuraemia, cholaemia, hyperglycaemia,
hypoglycaemia, Addison's disease.
4. Severe infectionsmalaria, typhoid, small-pox, etc.
5. Excessive heatheat, stroke, heat exhaustion.
METHOD
A.
B.
OF INVESTIGATION:
HISTORY.
1.
2.
3.
Localitypresence
place.
PHYSICAL
of
fumes,
extremes of
temperature,
drinking
EXAMINATION.
276
HOW
TO EXAMINE A
PATIENT
1.
2.
3.
4.
5.
EARSotitis, mastoiditis.
6.
7.
8.
RESPIRATIONair-hunger, (diabetes),
stertorous (apoplexy),
slow
rate (opium poisoning), Cheyne-Stoke's (high intracranial
tension).
9.
(shock),
poison-
10.
TEMPERATLTREhigh (cerebral
the brain).
11.
12.
13.
14.
15.
16.
malaria,
in
in
in
infections
LABORATORY INVESTIGATIONS:
(a) Urinefor sugar, acetone, albumin and casts.
(b) Bloodfor malarial parasites, urea, and sugar.
(c) C.S.F.for tension, proteins, red and white blood cells.
(d) Gastric lavagefor evidence of poison.
17.
of
SPECIAL INVESTIGATIONS:
(a) X-rays for evidence of fracture skull, brain tumours, etc.
(b) E.C.G. for detecting the condition of the heart.
(c) E.E.G. to exclude epilepsy and brain tumours.
CENTRAL NERVOUS
FEATURES
COMA : -
OF SOME
COMMON
SYSTEM
CONDITIONS
Opium poisoningpin-point
slow pulse.
THAT
277
GIVE RISE
TO
of
exposure,
scarlet
lips,
flushed
Cerebral haemorrhagehemiplegia, deepening coma, hypertension, stertorous breathing, slow and bounding pulse, C.S.F.
under pressure and tinged with blood.
Subdural haematomahistory of injury, temporary coma
followed by lucid interval, and some time later, further unconsciousness with slow pulse, unequal pupils, localised neurological signs and xanthochromia.
Post-epilepsyhistory of the disease, fits, tongue-biting, incontinence of urine, spontaneous recovery.
SPEECH DEFECTS
Speech is a cortical function; articulation is mainly bulbar.
For speech to be carried out normally, therefore, not only the
HOW
278
T O EXAMINE A
PATIENT
higher centres of the brain must be intact but also the motor
mechanism which controls the muscles of articulation, i.e. the
bulbar function must be perfect. Articulation is mainly
controlled by the muscles of the larynxpalate, tongue and
lipsall these being innervated by bulbar nerves. These
represent bilaterally in the brain. Hence, there must be
bilateral lesions of the pyramidal system to cause dysarthria,
but unilateral peripheral lesions, including those of the bulb
invariably cause dysarthria.
Abnormalities of speech may be grouped under two wide
headings:
A.
DEFECT IN A R T I C U L A T I O N
B.
A.
(DYSARTHRIA).
THE
DYSARTHRIA
FUNCTIONAL.
BRAIN LESIONS.
CENTRAL NERVOUS
SYSTEM
279
and
often
indistinct
280
H O W T O EXAMINE A
PATIENT
APHASIA
CENTRAL NERVOUS
SYSTEM
281
M O T O R APHASIA.
SENSORY APHASIA.
HOW
282
TO EXAMINE A PATIENT
FINE TREMORS.
These are best observed when the patient stretches his arms
in front of him. They are best felt when the stretched hands
are rested on the examiner's palm. They are usually toxic or
psychogenic in origin.
CAUSES:
1. Functional-hysteria, anxiety, emotion, fright, neurasthenia, convalescence and shivering due to cold.
2. Senile.
3. InfectionsG.P.I.
4. Intoxicationsalcohol, nicotine, tea, coffee, lead, mercury, morphia, cocaine, chloral, uraemia, and toxaemias
in general.
5. Endocrine disordershyperthyroidism, hyperinsulinism.
CENTRAL NERVOUS
II.
SYSTEM
2 8 3
COARSE TREMORS.
1. Disorders of the basal gangliaparalysis agitans (pinrolling), Parkinsonism (coarse. but may be orderly).
2. Hereditary ataxiasdiffuse cerebellar diseases. Tremors
appear when the muscles are brought into action; not
intensified towards the termination of the movement.
3. Chronic hemiplegiatremors may occur in the paralysed
limbs.
4. Exaggeration of fine tremors.
III.
CHOREIFORM MOVEMENTS:
INTENTIONAL
TREMORS.
TICS.
H O W T O EXAMINE A
284
PATIENT
CASE
OF
TREMORS
NOTE
THE
Mechanical defects in the lower limbs and pelvis, dislocation of hips, ankylosis of the joints, deformities of feet,
etc.
B.
CHARACTERISTIC
A.
GAITS
OF NEUROLOGICAL
IMPORTANCE
U N I L A T E R A L DEFECTS
SYSTEM
285
nerveunilateral
CENTRAL NERVOUS
BILATERAL DEFECTS
CEREBRAL LESIONS.
There
E X T R A PYRAMIDAL DISEASES.
CEREBELLAR DISORDERS.
286
H O W T O EXAMINE A
PATIENT
CENTRAL NERVOUS
SYSTEM
287
PERIPHERAL NERVES.
MUSCULAR DISORDERS.
T h e gait is
IX.
waddling.
FUNCTIONAL.
H O W T O EXAMINE A PATIENT
288
ATAXIA
Ataxia means lack of co-ordination while executing a movement which involves a group of muscles.
It may be due to muscular weakness, spasticity, involuntary
movements, sensory loss and cerebellar diseases, but in clinical
practice the term ataxia is restricted to inco-ordination resulting
from affections of the sensory and the cerebellar systems.
A.
SENSORY
ATAXIA
DISEASES T H A T
ATAXIA
CEREBELLAR ATAXIA
CENTRAL N E R V O U S
SYSTEM
289
I. Disseminated sclerosis.
2.
3. Cerebellar abscess.
4. Tuberculoma.
5. New growths.
RARE CAUSES:
1. Encephalitis.
2.
Schilder's disease.
TOXIC ATAXIAS:
1. Alcohol, barbiturates.
2. Hypoglycaemia due to overdose of insulin.
III.
HYSTERIA.
T H E M O T O R T R A C T S AND T H E I R LESIONS
ANATOMY OF T H E MOTOR TRACTS OR PYRAMIDAL SYSTEM.
Motor fibres start from the precentral gyrus, pass through the corona
radiata and coalesce to form the pyramidal tract, which Occupies the genu
and anterior 2/3rd of the posterior limb of the internal capsule. T h e now
compact pyramidal tract enters the cerebral peduncle, goes down the pons
and forms the anterior pyramid of medulla. In the lower medullary
region, 90% of the fibres cross and enter the spinal cord as crossed pyramidal tract, and 10% remain uncrossed and enter the spinal cord as direct
19
290
H O W T O EXAMINE A PATIENT
pyramidal tract, which also ultimately cross and end in the anterior horns.
There are very few fibres that remain uncrossed and supply the muscles
that have to work bilaterally, like diaphragm and intercostals.
LESIONS OF T H E M O T O R TRACTS PRODUCE T H E
FEATURES:
FOLLOWING
ETIOLOGY:
A.
WITHOUT
ATROPHY.
1. Pyramidal lesions:
(a) Vascular causesthrombosis, embolism, haemorrhage,
hypertensive encephalopathy.
(b) Infectionsabscess, encephalitis, meningitis.
(c) Disseminated sclerosis.
(d) Tumours.
(e) Trauma.
2. Extra-pyramidal lesionschorea, paralysis agitans.
3. Functional disorders.
B.
W I T H ATROPHY.
CENTRAL N E R V O U S
SYSTEM
291
W I T H O U T ATROPHY.
W I T H ATROPHY.
H O W T O EXAMINE A
292
PATIENT
RAPID ONSET.
1. Embolism.
(a) Blood clot as in mitral stenosis from the left auricle,
aneurysm, atheroma, coronary disease ( f r o m the left
ventricle),
femoral thrombosis (via the vertebral
veins).
(b) Vegetationsseptic
carditis,
and
subacute
bacterial
endo-
CENTRAL N E R V O U S
SYSTEM
293
arteriosclerosiscommon
after the
age
SLOW
ONSET.
1. Inflammations.
(a) Meningitis, encephalitis.
(b) G.P.I.
(c) Disseminated sclerosis.
(d) Sinus thrombosis.
H O W T O EXAMINE A
294
PATIENT
2. Trauma.
(a) Head injuries.
(b) Birth injuries.
3. Tumoursgrowths, abscesses, cysts.
4. Vascular disorderschronic subdural haemorrhage.
5. Congenital defectscerebral agenesis, porencephaly.
LOCALIZATION
OF THE LESION:
295
RIGHT
LEFT
EFFECTS OF LESIOM
COM TRALAT6R.L
MONOPLEGIA
GRUS
CONTRALATERAL,
HEMIPLEGIA
AON 5
MEDULLA
DORSAL
SPINAL
CORP.
IP&IAATEMI
MOMOPIE.CIA
(browhsequard's
STOCK OMfc)
FiC. XXXII
Motor Tract & its Lesions.
H O W TO EXAMINE A PATIENT
296
6. Pons:
(a) In the body of ponsprofound unconsciousness, pinpoint pupils, hyperpyrexia. Chief causes are pontine haemorrhage and encephalitis.
(b) Lower border of ponshemiplegia on the opposite
side and involvement of the 6 th cranial nerve on the
same side (Foville's syndrome)
or 6th and 7th
nerves (Millard's syndrome).
Common causes are
syphilis or growths at that level.
7. In the medulla:Hemiplegia on one side and paralysis
of the 9th, 10th, 11th and 12th cranial nerves on the
affected side. T h e damage, however, is rarely confined
to the pyramidal tracts and frequently extends to the
sensory tracts and even on the opposite side resulting in
quadriplegia.
8. In the upper cervical cord:The hemiplegia is on the
same side as the lesion. (Brown-Sequard's syndrome.)
Cranial nerves are not involved.
FEATURES
OF SOME COMMON
Cerebral Thrombosis.
HEMIPLEGIAS.
Lenticulo-striate artery is generally affected. Cerebral haemorrhage is common at about the age of 45-55. In 20 per cent
cases there has been a previous cerebro-vascular accident
generally an attack of hypertensive encephalopathy. Occipital
headache and vertigo are generally present before the attack.
There is deep coma, stertorous breathing, loss of corneal
reflexes, flaccidity of the affected limbs, high blood pressure, and
CENTRAL N E R V O U S
SYSTEM
297
OF INVESTIGATION:
298
HOW
TO EXAMINE A
PATIENT
CENTRAL N E R V O U S
SYSTEM
299
4. If the patient is unconscious determine the side of hemiplegia by the following observations:
(a) Eyes are deviated away from the paralysed side.
(b) Checks bulge during inspiration on the paralysed
side.
(c) Naso-labial fold is obliterated on the paralysed side.
(d) Limbs fall limply on the paralysed side.
(e) Corneal reflex is more diminished on the affected
side.
IV.
PARALYSIS OF B O T H T H E LEGS
(PARAPLEGIA)
A.
UPPER N E U R O N E TYPE.
Causes:
1. Compression paraplegiaPott's disease, turnouts, cysts,
aneurysms, gumma, leukaemia, Hodgkin's disease, spondylitis, Paget's disease, prolapsed disc.
2. Degenerationsdisseminated
sclerosis,
amyotrophic
lateral sclerosis, syringomyelia, Friedreich's ataxia,
motor neurone disease.
3. Inflammatory conditionscervical meningitis, syphilitic
myelitis, actinomycosis, pyaemia, virus infections and
spread of exanthematous fevers.
4. Deficiency diseasessubacute combined degeneration.
5. Vascular disordershaematomyelia,
anterior spinal artery.
thrombosis of
the
300
H O W TO EXAMINE A
PATIENT
LOWER NEURONE
TYPE.
Causes:
1. Lesions of the anterior hornspoliomyelitis.
2. Lesions of the posterior rootstabes dorsalis.
3. Lesions of the peripheral nervesneuritis.
4. Lesions of the myoneural junctionmyasthenia gravis.
5. Lesions of the musclesmyopathies.
6. Tumours and compressions of the lumbo-sacral plexus.
7. Tumours and injuries of the cauda equina.
DIFFERENTIATION
BETWEEN
UPPER
NEURONE
LESIONS.
AND
LOWER
1.
Paralysis.
Individual muscles or
groups of muscles
affected.
2.
Tone.
Spastic.
Flaccid.
3.
Wasting.
Rapid
4.
Sensory changes.
Absent.
Present generally
5.
Superficial
reflexes.
Not affected.
6.
Deep reflexes.
Exaggerated.
Absent.
7.
Trophic changes.
None.
8.
Associated
movements.
Present sometimes.
Not present.
9.
Electrical
reactions.
Absent.
Reaction of
degeneration.
PARAPLEGIA IN CHILDREN
Causes:
A.
LESIONS IN T H E BRAIN.
1. Congenital:
(a) Little's diseaseprobable cause is agenesis of the
grey matter. The patient is underdeveloped. The
CENTRAL N E R V O U S
301
SYSTEM
and encephalitisprevious
than
history
is
1. Congenital:
(a) Meningocoele and spina bifidacan produce paraplegic symptoms; there will be deformity in the
spine.
(b) Progressive spinal atrophyheredofamilial disease.
There is wasting of the glutei, flaccidity of the legs,
loss of deep reflexes and fasciculations; no pyramidal
signs.
(c) Hereditary spastic paralysisspasticity, "scissor" type
of gait, starting at about the age of 2 years.
HOW
302
TO EXAMINE A PATIENT
LESIONS OF T H E NERVES.
LESIONS OF T H E MUSCLES.
OF INVESTIGATION
OF A CASE OF
PARAPLEGIA.
B.
DETERMINE IF T H E LESION
N E U R O N E TYPE. (See page 300.)
1.
MODE OF ONSET:
If of upper
neurone
type,
IS
OF
UPPER
OR
LOWER
Pott's
disease,
degeneration,
G.P.I.,
syringo-
AGE OF T H E
303
PATIENT.
com-
3.
4.
E X A M I N E T H E SPINE A N D T H E V E R T E B R A L COLUMN F O R
EVIDENCE OF DEFORMITIESquite c o m m o n in Pott's disease a n d
syringomyelia.
5.
the
is of flaccid type,
the possibilities
are:
304
touch,
B.
sense,
All these sensations start from the skin and are regrouped into three tracts
before they enter the spinal cord to reach the brain.
To various parts of
Precentral gyrus
FIG. X X X I I I
Diagram of Sensory System.
ANucleus Cuneatus.
2 Column of Burdach.
BNucleus Gracilis.
3Spino tectal tract.
1Column of Goll.
4Spino thalamic tract.
CENTRAL NERVOUS
1.
SYSTEM
305
2.
3.
In the thalamus, the 3rd relay of all the sensory fibres starts, enter the
posterior third of the posterior limb of the internal capsule, pass through
the corona radiata and end in the sensory cortex i n the post-central gyrus.
LESIONS OF T H E SENSORY T R A C T
Disorders of the sensory system give rise to sensory phenomena, such as paraesthesias, loss of deep sensibility and loss of
tendon reflexes.
1. Peripheral nerve disordersthere is sensory loss, loss of
power and absent deep reflexes. T h e commonest cause is
peripheral neuritis. (See page 312.)
2. Posterior root lesionsall forms of sensations are lost and
also deep reflexes. There is ataxia and positive Romberg's sign. Tabes dorsalis is perhaps, the only cause.
3. Posterior column lesionsall deep sensations are lost and
the rest of the features are as in posterior root lesions.
The commonest cause is subacute combined degeneration.
There is often extensor response, since lateral columns
are often involved in this disease.
4. Lesions in the antero-lateral columnsthere is involvement of pain and temperature sensibility. Touch is not
affected as it has an alternative pathway in the posterior
columns. There is also wasting and fasciculations of the
20
306
HOW
affected muscles.
these columns.
TO EXAMINE A
PATIENT
Fig. XXXIV
BASAL GANGLIA.
CNCaudate Nucleus. PPutamen. GPGlobus Pallidus.
OTOptic Thalamus. ICInternal Capsule.
CENTRAL N E R V O U S
SYSTEM
307
HOW
308
TO EXAMINE A
PATIENT
cranial
nervesnystagmus,
slurring
CENTRAL N E R V O U S
SYSTEM
309
ivith the medulla oblongata at its rostral end. Its distal end, conus medullaris, extends as filum terminale as far as the 1st segment of the coccyx.
T h e spinal cord is symmetrically divided partly by the anterior median
fissure and posterior median sulcus. Each half may be divided into three
columnsanterior, lateral and posterior.
A.
THE
ANTERIOR
TRACTS:
1.
COLUMNS
CONTAIN
THE
FOLLOWING
DESCENDING TRACTS:
(a) Direct pyramidal tractvoluntary motion.
(b) Vestibulo spinal tractpostural reflexes.
(c) Tecto spinal tractvisual and auditory reflexes.
(d) Ponto-spinal tracthigher centre reflexes.
2.
ASCENDING TRACTS:
(a) Ventral spinothalamic tractlight touch.
(b) Spino-olivary tractreflex proprioception.
B.
LATERAL COLUMNS:
1.
DESCENDING TRACTS:
(a) Crossed pyramidal tractsvoluntary motion.
Descending Tracts
Ascending Tracts
Fig. X X X V
Tr; Section of the Spinal Cord.
1. Direct pyramidal tract; 2. Vestibulo-spinal tract; 3. Tecto spinal tract;
4. Crossed pyramidal tract; 5. Rubro-spinal tract; 6. Olivo-spinal tract;
7. Comma tract; 8. Septo-marginal tract;
9. Tract of Goll; 10. Tract of Burdach; II. Dorsal spino-cerebellar tract;
12. Ventral spino-cerebellar tract; 13. Lateral spino-thalamic tract; 14. Spinoolivary tract. 15. Ventral spino thalamic tract.
310
H O W TO EXAMINE A
PATIENT
ASCENDING T R A C T S :
(a) Dorsal spino cerebellar tractreflex proprioception.
(b) Ventral spino-cerebellar tractreflex proprioception.
(c) Lateral spino-thalamic tractpain and temperature.
(d) Lateral spino tectal tractlight touch.
C.
POSTERIOR COLUMNS:
1.
DESCENDING TRACTS:
(a) Comma tractassociation and integration.
(b) Septomarginal fasciculusassociation and integration.
2.
ASCENDING T R A C T S :
(a) Tracts of Golldeep pressure, vibration, etc. (lower limb).
(b) Tracts of Burdachdeep pressure, vibration, etc. (upper limb).
Li & L2 segments.
L 3 & I.4 segments.
L5.
the sacral & coccygeal segments.
Cauda equina.
3rd 8c 4th.
Sacral region.
1st & 2nd.
IV.
V.
Lumbar area.
1st.
2nd-4th.
8th-10th.
10th-12th.
5th 8c 6th.
Dorsal.
1st & 2nd.
7th 8c 8th.
Cervical.
3rd & 4th.
III.
II.
I.
Segment.
Cremasterics lost.
Knees lost.
No paresis.
Paresis.
Paraplegia.
Paraplegia.
Features.
H O W TO EXAMINE A
312
PATIENT
SPINAL NERVES
T h e spinal nerves consist of 31 pairs, each derived from the
spinal cord by two routesa sensory (dorsal) root and a motor
(ventral) root. They comprise as follows:
8 pairs of cervical nerves, 12 thoracic pairs, 5 lumbar pairs,
5 sacral pairs and 1 coccygeal pair. Functionally, each
nerve contains several kinds of fibres, but mainly motor and
sensory. Hence, any damage to them produce both motor
and sensory disturbances.
LESIONS OF T H E P E R I P H E R A L NERVES
Neuritis may be caused by several conditions of which the
following cover u p the most important ones:
1. Extraneous poisons.
(a) Metalslead, arsenic, bismuth, copper.
(b) Organic substancesalcohol, aniline, sulpha, COpoisoning.
2. Infections.
(a) After infective fevers like influenza, malaria, typhoid,
dysentery.
(b) Infections liberating toxins like diphtheria, tetanus,
botulism.
(c) Virus diseasesrabies, epidemic polyneuritis, acute
ascending polyneuritis.
(d) Sepsis, especially focal.
(e) Leprosy.
3. Metabolicdiabetes, gout, senile degenerations, starvation, hypertrophic interstitial neuritis, haematoporphyrinuria.
4. Blood disorderspernicious anaemia, leukaemia, Hodgkin's disease.
5. Vitamin deficiencyberi beri, pellagra.
313
GENERAL.
1.
Radiating pains.
2.
3.
Subjective sensationstingling,
4.
5.
6.
Hypotonia.
7.
Ataxia.
numbness,
etc.
8.
Objective sensationshypoaesthesia,
9.
anaesthesia.
10.
11.
12.
13.
NEUROMUSCULAR DISEASES
(See under Locomotor System, Chapter VIII)
nerve
CHAPTER VI
GENITOURINARY
SYSTEM
A.
INTERROGATION.
B.
C.
GENERAL EXAMINATION.
D.
E.
EXAMINATION OF T H E URINE.
F.
H O W TO EXAMINE A PATIENT
316
A.
INTERROGATION
SYMPTOMS
GENITO URINARY
DYSURIA.
SYSTEM
317
GENERAL E X A M I N A T I O N
Particularly look for puffiness of the face, anaemia and wasting. If there is general anasarca, inquire whether it started on
the face first. Examine especially the cardio-vascular system for
evidence of enlargement of the heart, left ventricular failure,
arterio-sclerotic changes and high blood pressure; and the fundi
H O W TO EXAMINE A PATIENT
318
E X A M I N A T I O N OF T H E GENITO-URINARY
SYSTEM
KIDNEYS.
T H E BLADDER
T H E E X T E R N A L GENITALIA.
G E N I T O URINARY
SYSTEM
319
OF A
URINE ANALYSIS
SAMPLE-.
PHYSICAL EXAMINATION
IN THE
COLOUR
OF
URINE.
chronic
OR
BROWNISHpresence
of
blood,
haemoglobin,
320
HOW
TO EXAMINE A
PATIENT
or
administration
of
carbolic
acid
or
other
coaltar
321
II.
CHEMICAL E X A M I N A T I O N
Inorganic constituents.
1.
2.
3.
4.
5.
6.
7.
8.
B.
20 Gms.
Chlorides
Phosphates
Sulphates
Oxalates
Sodium
Potassium
Calcium
Other minerals
10-12 Gms.
2- 3 Gms.
1.5- 2 Gms.
0.015 Gm.
4 Gms.
2 Gms.
0.2 Gm.
in traces.
Organic constituents.
30
Gms.
1.
2.
3.
4.
5.
25
1
0.5
1.5
1-2
Gms.
Gm.
Gm.
Gms.
Gms.
Urea
Ammonia
Uric acid
Creatinine
Purine bodies
I.
INORGANIC CONSTITUENTS
OF T H E
URINE
322
ORGANIC CONSTITUENTS
OF T H E
URINE
GENITO-URINARY
SYSTEM
323
Sugar.
1. Fehling's Test. Mix equal parts (3 c.c. of each) of
Fehling's A and B solutions and boil to make sure that the
Rochelle salt in B is not decomposed. If no reduction occurs,
boil 6 c.c. of urine in a separate test tube. Mix the boiled
urine with the boiled reagents and boil again. A red or yellow
precipitate will indicate the presence of sugar.
T h i s test is not very reliable as Fehling's solution is reduced by several
other substances, besides glucose, such as:
324
pentose.
GENITO-URINARY
SYSTEM
325
Blood.
1. Guaiacum Test. Mix 2 c.c. of 10 per cent acetic acid,
5 c.c. of urine (previously boiled to destroy oxidase enzymes and
cooled) and 5 c.c. of ether. In the second test tube place 5
c.c. of alcohol, 2 c.c. of H2O2 and a pinch of guaiacum powder.
Pour the latter solution slowly down the side of the first tube.
Blue colour appears at the junction of the two fluids.
2. Benzidine Test. Saturate 2 c.c. of glacial acetic acid
with benzidine in a test tube and shake for about a minute.
Add an equal volume of H2O2 and 2 c.c. of urine. Blue colour
appears immediately. (If the colour develops before the addition of urine, the glassware is not clean).
Bile Pigments.
H O W TO EXAMINE A PATIENT
326
MICROSCOPIC EXAMINATION
GENITO-URINARY
TYPES OF CASTS.
SYSTEM
327
(See Fig. X X X V I . )
corpuscles.
L
FIG. X X X V I
Microscopic appearance of organised urinary deposits.
A. Red blood cells. B. Leucocytes. C. Epithelial cells. D. Hyaline casts.
E. Granular casts. F. Epithelial casts. G. Fatty casts. H . W a x y casts.
I. Red blood casts. J. Leucocyte casts. K. Cylindroids. L. Air bubbles 8c
Oil globules.
328
H O W TO EXAMINE A PATIENT
BACTERIA.
6.
OVA A N D PARASITES.
7.
CRYSTALS.
ifM
ACID
A
C
X A Li
1 IKir
fA!
\ L r\M
NL.
E
I
Fic.
XXXVII
GENITO-URINARY
SYSTEM
329
ALTERED
URINE.
PHYSIOLOGICAL B A L A N C E B E T W E E N
BLOOD
AND
B.
1.
2.
E L I M I N A T I N G P O W E R OF T H E
KIDNEYS.
UREA CONCENTRATION
TEST.
2.
WATER CONCENTRATION
TEST.
but
330
TEST.
N o food or fluid is allowed after 6 p.m. in the evening before the test
which begins at 8 a.m. the following morning. T h e patient empties the
bladder and drinks:
R x . Urea
15 gms.
Tinct. Auranti
Aqua ad.
1 cc.
100 cc.
TEST.
Restrict fluids after the mid-day meal o n the day previous to the test.
T h e evening meal should be dry and consist mainly of proteins. Collect
urine in the morning and note its specific gravity. T h e n give the patient
600 c.c. of water to drink. Collect urine after 1, 2, 3 and 4 hours and
note the amount and the specific gravity of each specimen.
N O R M A L READINGS:Specific gravity of morning urine before the
test is about 1025. T h e amount excreted i n four hours is 90% of the
amount of water taken. T h e specific gravity of the first specimen is not
above 1005 and gradually rises in the subsequent specimens.
A B N O R M A L R E A D I N G : A constant specific gravity of 1010-1012 suggests renal deficiency.
KIDNEY ENLARGEMENT
An enlargement of a kidney has the following characteristic
features:
1. The large intestine is in front of the organ; hence an
area of resonance can usually be obtained in front of
a renal swelling.
2. The area of dullness to percussion is continuous from
the lateral aspect of the swelling to the middle line posteriorly, i.e. there is no area of resonance between the mass
and the vertebral column as in a case of splenic tumour.
3. A renal tumour usually retains the shape of the kidney.
It is rounded at its borders and poles, and does not possess any edges or sharp margin as in the case of splenic
or hepatic swellings.
4. A renal tumour, in the process of enlargement, projects
forwards and downwards. It may fill up the natural
GENITO-URINARY
SYSTEM
331
hollow of the loin, but seldom causes prominence posteriorly as occurs in perinephric abscess.
5. A renal tumour may be movable downwards and inwards
and can be felt bimanually, and if movable, can be
pushed back into the loin.
6. In right-sided kidney tumours, there is usually a line of
resonance between the upper margin of the tumour and
hepatic dullness.
DIFFERENTIAL DIAGNOSIS.
A kidney swelling may be mistaken for the following:
(a) T U M O U R OF T H E GALL-BLADDERusually oval in outline,
situated immediately below the right costal margin just below the
tip of the ninth costal cartilage and freely movable with respiration.
T h e r e may be attacks of biliary colic. Cholecystography reveals n o
dye in the gall-bladder.
(b) LIVER E N L A R G E M E N T t h e dullness is continuous w i t h the hepatic
dullness in the chest; it is also freely movable on respiration. A
Riedel's lobe may cause difficulty but the latter is not so round as a
kidney.
(c) SPLENIC E N L A R G E M E N T t h e edge is generally well, defined Snd
often notched; grows downwards and obliquely forwards and no
fingers can be passed between the tumour and the costal arch.
(d) P E R I N E P H R I C ABSCESSthe swelling is ill-defined and the general
symptoms are more acute. T h e skin over the area in t h e loin may
be oedematous and the abscess may project from behind.
(e) PELVIC T U M O U R e s p e c i a l l y with a long pedicle may simulate
movable kidney; so also an uterine fibroid. T h e s e generally are
situated in the middle line of the body and P.V. examination will
be h e l p f u l in the diagnosis.
(f) S U P R A R E N A L
TUMOURSthese
are
extremely
difficult
to
distinguish from kidney tumours. Generalised wasting, anaemia and
haematuria are more in favour of suprarenal tumours.
(g) FAECAL A C C U M U L A T I O N m a y be of sufficient size to form a sort
of tumour. Constipation, flatulence and griping are the c o m m o n
symptoms. Administration of a large enema will clear the gut.
(h) A P P E N D I C U L A R ABSCESSmay be mistaken for a right-sided renal
tumour. Pain and swelling in the iliac fossa rather than in the loin,
are suggestive.
(i) MALIGNANCY OF T H E L A R G E INTESTINEespecially o the
ascending or descending colon may form a tumour closely resembling
a renal swelling because it can be grasped bimanually and is movable
in the same direction as a renal tumour. X-rays will reveal the
diagnosis.
332
ABNORMALITIES OF M I C T U R I T I O N
A person in health micturates about five times during the
24 hours, the total amount of urine passed being about 1500 c.c.
This varies according to the amount of fluid taken, the amount
lost by perspiration, vomiting, diarrhoea, etc.
T h e act of micturition is controlled by a nervous mechanisma stretch
reflex from the bladder starting an impulse w h i c h causes contraction of the
main detrusor muscle with reciprocal relaxation of the internal sphincter.
T h e tone of the detrusor keeps the bladder contracted down o n its contents, whether these are large or small in amount. But when the intravesical pressure reaches a certain height owing to accumulation of urine
within the bladder, rhythmic contraction of its walls develop thereby causing
relaxation of the internal sphincter, allowing escape of the urine into the
urethra. T h e special centre controlling the motor functions of the bladder
is situated in the spinal cord at the level of the third sacral region, but
the brain can control this centre to a great extent.
NON-NEUROLOGICAL CAUSES
Frequency.
(a) Diabetes mellitus, diabetes insipidus, chronic nephritis,
hypertension.
(b) Vesical irritabilitycystitis, prostatitis, calculus, cancer.
(c) Renal irritabilityrenal
kidney.
colic,
pyelitis,
tubercular
forcible).
333
forceless).
Difficulty of Micturition.
(a) Mechanical obstructionurethral stricture, prostatic
enlargement, impacted calculus in the urethra, phimosis,
uterine fibroids, retroverted uterus, etc.
(b) Retention of urinestricture, enlarged prostate, calculi
in the urethra, vesical papilloma and disorders of the
nervous system.
B.
NEUROLOGICAL CAUSES
1. Functional
disturbances
of micturition.
Emotion,
hysteria, enuresis, etc. cause frequency of micturition
sometimes.
2. Toxaemias. In the early stages there is inhibition of
the parasympathetics resulting in distension of the
bladder; later the sympathetics are also inhibited resulting in dribbling.
3. Paralysis of the sympathetics, i.e. hypogastric nerves.
There is initial frequency of micturition which is soon
controlled by will, as these nerves are not so important
in man for the purpose of micturition.
4. Injury to parasympathetics, i.e. pelvic nervesResults
in retention of urine first, but as the post-ganglionic
fibres are capable of independent reflex activity, retention is replaced by "automatic" bladder. T h e automatic
emptying, however, is not powerful enough to empty the
bladder completely, and, hence, there remains "residual"
urine in the bladder.
5. Injury to the cord, i.e. motor or somatic nerves.
(a) In acute lesions of the lumbar or sacral regions the
detrusor muscle at once become toneless and fails
to contract on the accumulated urine, and as the
internal sphincter remains contracted "retention"
334
H O W TO EXAMINE A PATIENT
results; when it cannot be further distended, "dribbling incontinence" occurs. As the external sphincter
is also paralysed, voluntary control of the bladder
too, is lost. T h e bladder so paralysed is in danger
of being infected. If the shock due to spinal injury
passes off, the detrusor regains its tone and adapts
itself to the bulk of its contents. Later, rhythmic
contractions similar to those which occur in normal
state appear and help relaxation of the internal
sphincter and permits escape of urine. This reflex
or automatic micturition is usually independent of
extrinsic stimuli, but may be excited by anything
which increases intravesical tension, as straining or
pressure on the abdomen.
(b) In lumbar or higher spinal lesions, the independence of vesical plexus and of the post-ganglionic
autonomic cells and fibres is not affected; hence,
although the bladder is not under voluntary control
its capacity is less than normal and as a rule does
not empty itself fully; its recovery of automatic
evacuation is more rapid and its response to distension is brisker.
(c) When sacral segments are destroyed the external
sphincter remains toneless and dribbling incontinence results. When sensory impulses from its walls
are not interrupted in the hypogastric nerves or in
the spinal cord, the discomfort due to overfilling of
the bladder induces voluntary efforts to empty it
by contraction of the abdominal wall.
6. Injury to afferent nerve supply. In tabes dorsalis the
excitability of the detrusor is reduced and allows excessive amount of urine to collect in the bladder. Micturition may occur if the patient wishes it; if not, dribbling
results due to overflow.
7. Injury to cortex and pyramidal tracts. In hemiplegia
the voluntary control may be affected resulting in difficulty in starting the flow. Precipitancy occurs in spastic
paresis as in disseminated sclerosis and other spinal
GENITO-URINARY SYSTEM
335
OF
pathological
globulin in
albumin is
more easily
ALBUMINURIA.
I N T H E KIDNEY:
A.
Primary.
336
H O W TO EXAMINE A PATIENT
is more pus in
the
tract
Secondary.
1. High fevers.
2. Congestive cardiac failure.
3. Hypertension, especially malignant.
4. Pregnancy toxaemia and other toxic states.
5. Renal infarctionsub-acute bacterial endocarditis.
6. Amyloidosisliver and the spleen may be enlarged.
7. Thrombosis of the inferior vena cava.
8. Subarachnoid haemorrhage:Albumin occurs during the
first 48 hours after the haemorrhage and may be accompanied by some glycosuria.
9. Drugs and poisonscantharides, mercury, gold, turpentine, hexamine, sulpha products and overdose of vitamin D.
10. Diabetic coma.
11. All blood dyscrasias due to presence of blood cells or
haemoglobin in the urine.
12. Scurvy.
In all these conditions the albuminuria
shadowed by the primary condition.
tends to be over-
GENITOURINARY
C.
SYSTEM
337
Orthostatic.
This is not common, but may occur in children and
young adults. It is thought to be due to partial obstruction of the renal veins in the erect posture, perhaps
associated with lordosis or with the presence of abnormal
vessels. T h e morning specimen does not contain albumin, but when the patient is up and about, urine reveals
albumin.
II.
C O N D I T I O N S I N T H E URETERSCalculi,
tumours.
III.
CONDITIONS
IN T H E
prostate, tumours, trauma.
BLADDERCalculi,
cystitis,
enlarged
IV.
C O N D I T I O N S I N T H E U R E T H R A C a l c u l i , tumours, trauma.
I.
Pre-renal:
Renal causes:
H O W TO EXAMINE A PATIENT
338
Post-renal:
the
GENITO-URINARY SYSTEM
339
DYSURIA
CAUSES
ARE-.
of the ex-
OF
MICTURITION
340
OF GLYCOSURIA
ENDOCRINE
DISTURBANCES.
to
R E N A L GLYCOSURIA:
GENITO-URINARY
C.
SYSTEM
341
CEREBRAL CONDITIONS:
DISEASES OF T H E L I V E R :
ALIMENTARY DISORDERS:
1. Alimentary glycosuriadue to excessive intake of carbohydrate food. This is probably a precursor of diabetes
mellitus. T h e glucose tolerance curve in alimentary
glycosuria is characteristic. (See Fig. XXXVIII.)
2. Hunger glycosuria:Such glycosuria becomes more evident when a starved patient is fed, and is due probably
to temporary overloading of the body with food to which
he was not accustomed.
3. Rapid emptying of the stomach especially after gastrectomy or gastro enterostomy; there is rapid absorption of
sugar from the upper part of the small intestine and
hence, post-prandial glycosuria.
F.
INFECTIONS:
CHEMICAL A G E N T S :
342
H.
CHRONIC
DEGENERATIONS:
TO INVESTIGATE
A CASE OF
GLYCOSURIA.
1.
Examine the urine for sugar with Benedict's solution. Repeat the
test to exclude emotional glycosuria. Note the colour of the urine
which, if darkened, may be alkaptonuria.
2.
T e s t for acetone.
3.
4.
5.
GLUCOSE
TOLERANCE
The
TEST.
Fast the patient for 12 hours. Perform the test in the early morning
and start by taking blood for fasting-sugar test. T h e patient then drinks
50 grammes of glucose dissolved in water and blood is collected every halfhour for the next two hours.
T h e usual curves noted are:(See Fig.
XXXVIII.)
1.
2.
3.
4.
S U G A R F O U N D IN T H E
1.
PENTOSE.
URINE.
GENITO URINARY
SYSTEM
343
SEVERE
DIABETES
MODERATE
DIABETES
MILD DIABETES
RENAL
THRESHOLD
ALIMENTARY
GLYCOSURIA
RENAL
GLYCOSURIA
HOURS
FIG. X X X V I I I
GLUCOSE T O L E R A N C E CURVE
( T h e shaded area represents the m a x i m u m and m i n i m u m normal
variations in the blood sugar-level.)
2.
LACTOSE.
logical.
physio-
3.
4.
344
5.
GLUCOSE.
method of detecting
calorimetry.
the correct
sugar
in the urine
is
HAEMATURIA
By haematuria is meant the appearance of blood in the urine.
This may be caused by diseases of or injury to any part of the
urogenital tract or adjacent organs. It may also occur in blood
dyscrasias and in some systemic diseases.
CHIEF
CAUSES:
A.
G E N I T O U R I N A R Y DISEASES.
I.
Renal disorders:
1. Nephritisacute and focal; malignant sclerotic kidneys.
History of the disease and urine examination will reveal
the real cause.
2. Tuberculosis of the kidney. There is pus in the urine
in addition to red cells; in most cases pyuria is more
predominant than haematuria. Common in young adults.
3. Hydronephrosis. Haematuria is not so well marked;
there is intermittent polyuria.
4. Malignancy;
Hypernephroma. Painless
intermittent
haematuria is characteristic of renal neoplasm in the
early stages; later on there is anaemia, weakness and
wasting.
5. Calculus. Colicky pains as a rule are present; the bleeding is seldom profuse and may increase after exercise;
there may be difficulty in starting micturition.
6. Infarctionsub-acute bacterial endocarditis. There will
be signs in the heart, clubbing of the fingers and embolic
phenomenon elsewhere.
7. Polycystic disease. History from birth; polyuria; kidneys
are enlarged; haematuria comes late.
8. Injury. The diagnosis will be obvious.
9. Poisons. Sulpha, mercury, hexamine, turpentine, cantharides, etc.
G E N I T O URINARY
II.
SYSTEM
345
Ureteric causes:
1. Calculus. There is always history of renal colic during
the descent of the stone; radiological examination is
diagnostic.
2. New growths.
turia.
III.
Vesical causes:
1. Acute cystitis. There is vesical tenesmus, suprapubic
tenderness and fever; pyuria is more marked than haematuria.
2. Bilharzia infection. Presence of ova in the urine confirms the diagnosis.
3. Calculus. Haematuria is slight and occurs in the terminal urine; frequency of micturition during the day is
quite common.
4. New growthspapilloma, carcinoma. In both these
conditions clotting of the blood in the bladder may cause
urgent desire to micturate.
5. Prostateadenoma, carcinoma. There is associated frequency of micturition. P.R. examination is very helpful.
6. Injuries and foreign bodies. History of the case, cystoscopy and radiological examination will reveal the cause.
IV.
Ureteral Causes.
1. Acute urethritis. Gonococcal infection very often causes
haematuria; presence of urethral discharge makes the
diagnosis evident.
2. Angioma. Although rare, may cause severe and recurrent haematuria; blood is passed spontaneously or while
passing urine.
3. New growthspapilloma or carcinoma. These growths,
can cause initial haematuria not necessarily associated
with micturition.
4. Injury.
History is evident.
346
B.
IIOW
TO EXAMINE A PATIENT
D U E T O DISEASES OF T H E N E I G H B O U R I N G
ORGANS.
1. Cancer uterus or rectummay involve the bladder resulting in vesical irritability and haematuria.
2. Acute appendicitisdue to direct spread of the inflammatory process to the vesical wall.
3. Acute salpingitismay involve the bladder by direct
spread of the inflammation.
4. Pelvic abscessmay inflame the bladder.
C.
G E N E R A L DISEASES.
B.
CASE
OF
HAEMATURIA
NOTE
THE
SYMPTOMS.
1.
2.
3.
E X A M I N A T I O N OF T H E U R I N E .
1.
2.
3.
G E N I T O URINARY
SYSTEM
347
if it comes in the initial stages, the blood comes from the ureter
or prostate; if evenly stained, it comes from the kidneys.
4.
C.
PHYSICAL E X A M I N A T I O N OF T H E
PATIENT.
1.
Carefully examine
swelling, etc.
especially
for
2.
3.
4.
5.
tenderness,
HAEMOGLOBINURIA
Haemoglobinuria indicates presence of haemoglobin in the
urine. The colour of the urine may be smoky, pink, red, brown
or black. On cent/rifuging, the colour of the supernatant fluid
does not change as occurs in much commoner conditions of
haematuria when the red cells fall to the bottom. Albumin is
always present in haemoglobinuria and may persist for several
days after the disappearance of the blood pigments.
ETIOLOGY.
A.
Extraneous poisons.
1. Drugssulpha, camaquin, quinine (especially while
being administered in cases of malaria), pot-chloras, turpentine, ca,rbolic acid, etc.
2. Snake venoms.
3. Serum injections.
4. Incompatible blood transfusions.
5. Toxic gasesCO, H2S, arseniuretted hydrogen.
B.
Infections.
1. Black-water fever and malaria.
2. Paroxysmal haemoglobinuriaas occurs in cases of
syphilis after exposure to cold, due to liberation of an
autohaemolysin which destroys the red cells.
348
IIOW
TO EXAMINE A PATIENT
D.
E.
F. Vasomotor
disease.
G.
disordersangio-neurotic
oedema;
Raynaud's
AnaphylaxisHenoch's disease.
POLYURIA
Polyuria means excessive secretion of urine.
CAUSES OF T R A N S I E N T P O L Y U R I A :
caffeine,
mercurials,
CAUSES OF C O N T I N U O U S P O L Y U R I A :
hypertension
G E N I T O URINARY SYSTEM
349
4. Hyperpiesiavery high blood pressure, markedly enlarged heart, presence of hyaline and granular casts in the
urine, sometimes haematuria; and changes in the fundi.
5. Amyloid kidneyevidence of chronic sepsis; liver and
spleen may be enlarged.
6. Cystic kidneysthere may be polyuria, increased blood
pressure; X-rays are revealing.
7. Diabetes insipidusintense polyuria, urine of low specific
gravity, headache and adiposity sometimes; urine examination is negative.
OLIGURIA
Oliguria means that the patient passes decreased quantity of
urine.
CAUSES:
350
renal
abscess,
tuber-
2. Uretericcalculus.
3. Vesicalcystitis, tuberculosis, calculus, tumours, bilharzia
infection.
4. Ureteralurethritis, prostatitis.
II.
GENITO URINARY
SYSTEM
351
TO
INVESTIGATE-.
(a) Carefully go into the history of the case and other symptoms.
(b) Cystoscopic examination reveals most of the cases of bladder involvement.
(c) Radiography is invaluable in detecting stones and several
of the kidneys that give rise to pyuria.
disorders
URAEMIA
This is a symptom-complex due to renal insufficiency or
failure resulting in retention of urea and N-products in the
body the end-products of protein metabolism. It appears there
are several other factors, besides azotaemia, i.e. rise in blood
urea, that contribute to this symptom-complex of which the
following are important:
(a) K-accumulation in the blood.
(b) Increase in the cholesterol content of the blood.
(c) Rise in the magnesium content of the blooda substance
that contributes to drowsiness and coma.
(d) Fall o calcium whose presence in adequate quantity
prevents an increase of magnesium in the blood thereby
preventing drowsiness.
Whatever the causative substance, it is handled by the body
as urea, which, due to defect in the glomerular filtration is not
adequately excreted in the urine and hence, retained in the
circulation.
TYPES OF URAEMIA
I.
E X T R A - R E N A L OR P R E RENAL
URAEMIA.
352
GENITOURINARY
SYSTEM
353
(heat
stroke)
L O W BLOOD PRESSURE.
ABNORMAL
METABOLISM.
354
RENAL
URAEMIA.
GENITO URINARY
SYSTEM
355
P O S T - R E N A L URAEMIA.
syndrome".
CAUSES:
III.
II.
I.
2. Malignant
1. Benign
Polyuria
Nephrosclerosis
Traces
2. Non-embolic
Nephrosis
,,
+ +
+ +
Hyaline
&
0
0
+ + +
+ +
+ +
granular
& fatty
+ + + +
+ + +
& fatty
++
0
0
N-R*ention
+ + + + + +
0
0
cdcma
+ + + +
+ +
+ + + +
Blood
Fatty, waxy
0
+ + + +
& hyaline
Hyaline,
Occasional
Hyaline
Granular
Casts
granular
Granular
Blood
+ + + +
+ + +
+ + + +
Polyuria
1. Embolic
D. Focal
C. Chronic , ,
turia
Urine
AlbumiHaemaV
+ + ++ + + +
"""a
-oliguria
+ + ++ + + + + +
++
B. Subacute nephritis
2. Type II
1. Type I
A. Acute nephritis
Inflammations
Urea
356
H O W T O EXAMINE A PATIENT
CHAPTER YII
HAEMOPOIETIC SYSTEM
INTERROGATION.
COMMON SYMPTOMS AND SIGNS.
EXAMINATION OF BLOOD.
1. Blood Cells.
2.
Haemoglobin Estimation.
3.
Examination of a Smear.
4.
Reticulocyte Estimation,
5.
Haematocritic Determination.
6.
7. Estimation of Platelets.
8.
Fragility Tests.
9. Sedimentation Rate.
10. Blood Coagulation.
11. Prothrombin Time.
EXAMINATION OF T H E BONE MARROW.
CHEMISTRY OF BLOOD.
BLOOD GROUPING.
358
HAEMOPOIETIC SYSTEM
Haemopoietic System mainly consists of blood-forming organs
in the body, the bone marrow being the chief of them. Spleen
and liver are examined under the Alimentary System and
lymph glands under General Examination.
INTERROGATION
Carefully inquire into the history of loss of blood, bleeding
piles, purpuric haemorrhages, bleeding tendencies, jaundice, etc.
In females, inquire into the history of excessive menstruation.
Elicit past history of malaria, kala-azar, etc., the possibility of
lead poisoning and malignancy. Dietetic history is also very
important to exclude nutritional disorders. Subjective sensations such as breathlessness, giddiness and sense of tiredness may
point to the affection of the blood. Puffiness of the face, swelling of the feet, colour of the face and of the mucous membranes
may reveal the true nature of the disease.
COMMON SYMPTOMS AND SIGNS
General weakness, sense of exhaustion, undue fatiguability,
symptoms of dyspnoea, palpitation, praecordial pain on exertion, fainting attacks, puffiness and pallor of the face, pale lips
and conjunctivae, glossitis, dysphagia, koilonychia, rapid pulse,
low blood pressure, weak heart and haemic murmurs may be
the presenting symptoms and signs of blood diseases.
EXAMINATION OF T H E BLOOD
NORMAL BLOOD ANALYSIS
A.
PHYSICAL PROPERTIES.
HAEMOPOIETIC SYSTEM
359
W H I T E B L O O D CELLS.
Average diameter8.15 u.
Differential Count
Polymorphonuclear cells
Lymphocytes
Monocytes
Eosinophils
Basophils
D.
60-70%
20-30%
2-5%
1-3%
o-i%
PLATELETS.
BLEEDING TIME1-5
minutes.
F.
C O A G U L A T I O N TIME5-10 minutes.
G.
P R O T H R O M B I N T I M E 1 2 seconds.
360
M E T H O D OF BLOOD E X A M I N A T I O N
Capillary blood is used for cell count, haemoglobin estimation.
and bleeding time.
Venous blood is used for serological tests, blood chemistry and
coagulation time.
I.
A.
E S T I M A T I O N OF T O T A L R E D B L O O D CELLS.
E S T I M A T I O N OF T O T A L W H I T E B L O O D CELLS.
Fill the pipette with blood upto "0.5" mark and dilute it
with a solution of 3% acetic acid upto "11" mark. Fill the
counting chamber and count the leucocytes in 16 large squares
i.e. 256 small squares. If there are " N " white cells in all the
squares there will be N/256 cells in each small square; multiply
this by 4000 as above and by the dilution i.e. 20 to get the
count of white cells in 1 c.mm. i.e. N / 6 4 x 4000 x 20.
II.
ESTIMATION OF HAEMOGLOBIN
CONTENT
HAEMOPOIETIC SYSTEM
361
EXAMINATION OF A SMEAR
staining
FOR D I F F E R E N T I A L
COUNT.
IV.
ESTIMATION OF RETICULOCYTES.
HAEMATOCRITIC DETERMINATION.
PACKED CELL V O L U M E .
(P.C.V.).
362
M E A N CORPUSCULAR V O L U M E .
(M.C.V.).
V O L U M E INDEX.
(V.I.).
COLOUR INDEX.
This means the amount of haemoglobin present in an individual red cell. It is calculated as the ratio between the percentage of Hb. to the percentage of red cells. The Hb. percentage
is obtained directly by the reading of the haemoglobinometer,
while that of red cells (taking 5 millions per c.mm. as 100%)
is obtained by multiplying the red cell count by 2 and striking
of the last five digits, e.g. a count of 3,400,000 red cells per
c.mm. =68%. If the Hb. as available in grammes the C.I. is
calculated as follows:
Gm. of Hb. found
Normal Hb. (15 Gms.)
No of R.B.C. found
Normal no. of R.B.C. (5)
The normal C.I. is 1. It is increased in megalocytic anaemias
and diminished in microcytic anaemias.
llAEMOPOIETIC SYSTEM
SATURATION
363
INDEX.
E S T I M A T I O N OF PLATELETS.
FRAGILITY TEST.
Set up 9 small test tubes each containing 1 c.c. of NaCl solution, varying from 0.80% to 0.25%. Draw 5 c.c. of blood in a
syringe and add a drop to each tube and record the concentration of saline at which haemolysis occurs. Normally haemolysis
takes place in 0.44% of NaCl solution or below; no haemolysis
occurs in solution at 0.45% and above. Ordinarily, arterial
blood is less fragile than venous. C 0 2 saturated blood is very
fragile. In haemolytic jaundice there may be increased fragility
in solution upto 0.60% NaCl. In chronic obstructive jaundice,
pernicious anaemia, sickle-cell anaemia and haemolytic anaemia,
the red cells are less fragile.
IX.
SEDIMENTATION RATE.
T h e rate of sedimentation depends upon the increased fibrinogen and globulin, and decreased albumin in the blood. A normal sedimentation rate does not exclude diseases; but an increased rate is suggestive and excludes functional diseases.
Sedimentation rate is also useful to judge the prognosis, especially in tubercular infections.
364
METHOD
OF ESTIMATION:
CONDITIONS
ARE:
WHERE
THE
SEDIMENTATION
RATE
2. Degenerations.
Nephrosis and cirrhosis of the liverin both due to loss of albumin
in the blood.
3. Heart diseases.
(a) Acute rheumatic carditis.
(b) Syphilitic aortitis.
(c) Infarctionheart or pulmonary.
(d) Infective endocarditis.
4. Brain lesions.
Abscess, tuberculoma, subdural haematoma, malignancy,
metastasis.
5. Abdominal conditions.
Increased in all inflammations; in appendicitis it is normal in the
first 24 hours but increased later; in peptic ulcer it is nearly always
normal unless inflamed or perforated.
6. Joint conditions.
(a) Acute rheumatismuseful to detect activity.
(b) Rheumatoid arthritis.
(Normal in osteoarthritis.)
llAEMOPOIETIC SYSTEM
365
SEDIMENTATION
IS FOUND
IN:
1. New-born infants.
2. Congestive heart failure.
3. Polycythaemia.
4. Sicklecell anaemia.
5. Allergy.
X.
A.
BLOOD COAGULATION.
BLEEDING T I M E .
C O A G U L A T I O N OR C L O T T I N G
TIME.
Method. Draw 5 c.c. of blood and eject 1.5 c.c. into 3 test
tubes (8 x 70 mm. in size) placed in a rack. After one minute
tilt the first test tube to see if the blood is clotted and then tilt
the same every 15 or 30 seconds to verify if the blood is clotted.
Agitation interferes with coagulation so the end point is determined in tubes 2 and 3.
Average clotting time is 5-10 minutes.
It is increased in:
366
PROTHROMBIN TIME.
Draw blood into an oxalate solution to remove free Calciumions and centrifuge. To the plasma thus produced add thromboplastin to provide an excess of thrombokinase. T o this add
CaCl2 and note the time taken for the plasma to clot. Normally
it is 12 to 25 seconds. This is reduced when insufficient Vit. K
is absorbed from the intestine as in liver diseases, melaena
neonatorum and during administration of anticoagulants.
EXAMINATION OF THE BONE MARROW
The aspiration and study of smears of bone marrow is often
necessary in the study of blood dyscrasias, especially in multiple
myeloma, aleukaemic leukaemia and aplastic anaemia. It is
also useful in the confirmation of diagnosis of all leukaemias,
pernicious anaemia, thrombocytopaenia, leishmaniasis and disseminated lupus erythematosus.
Technique:Sternal puncture is generally performed with
an 18 gauge lumbar puncture needle. Smear is made immediately after the aspirated marrow is oxalated, and stained with
Wright's or Giemsa's stain. Count 1,000 leucocyte cells, plus
the nucleated red cells seen, while classifying the leucocytes.
llAEMOPOIETICSYSTEM
USUAL
PICTURE
IS AS FOLLOWS:
367
TYPES OF CELLS
MARROW
PERIPH
BLOOD
2.5%
0%
6%
0%
15%
17.5%
0%
0%
12.5%
1-2%
27%
50%
Myeloblasts
Promyelocytes
Neutrophile series:
Myelocytes (have round or oval nuclei)
4%
1-3%
Basophils
1%
0-1%
Lymphocytes
Monocytes
13%
20-30%
1.5%
4-8%
0.2%
0%
2.0%
0%
Pronormoblasts
4-5%
0%
15%
0%
Normoblasts
368
H O W T O EXAMINE A PATIENT
BLOOD CHEMISTRY
Blood may have to be examined especially for sugar, proteins,
urea, calcium and cholesterol. Either whole blood, plasma or
serum may have to be examined by special techniques which are
outside the scope of this book.
BLOOD CHEMISTRY
Normal Constituents in 100 ml. of Blood.
Acetone
Ascorbic acid
Bicarbonates
Bilirubin
Calcium
Chlorides (total)
Glucose
Iron
Lipoids
Cholesterol
Fatty acids
Phospholipids
N-Compounds
Non-protein nitrogen
Urea
Creatinine
Uric Acid
Phosphatase
Acid phosphatase
Alkaline phosphatase
Phosphorus
Potassium
Proteins (plasma)
Albumin
Globulin
Fibrinogen
Sodium
1-5 mg.
0.5-1.5 mg.
26-32 mg.
0.1-0.4 mg.
9-11 mg.
570-620 mg.
80-120 mg.
80-175 mg.
130-200 mg.
300-450 mg.
60-200 mg.
20-40 mg.
15-30 mg.
1-2 mg.
2-4 mg.
0.5-2 unit
1.5-4 unit
2.5-4.5 mg.
15-20 mg.
4-5 gm.
1.5-2 gm.
0.2 gm.
300-350 mg.
HAEMOPOIETIC SYSTEM
VARIATIONS
IN
1.
GLUCOSE:
NORMAL
BLOOD
369
VALVES.
hyperthyroidism,
hyper-
TOTAL
CHLORIDES-.570-620
Increased in the f o l l o w i n g :
(a) Nephritis i n general.
(b) Congestive heart failure.
(c) Pituitary cachexia.
(d) Excessive salt intake.
Decreased in the following:
(a) Severe diarrhoea.
(b) Severe vomiting.
(c) Excessive sweating.
(d) Addison's disease.
(e) Meningitis sometimes.
(f) Decreased salt intakestarvation.
(g) Mercurial diuresis.
3.
N-COMPOUNDS.
24
370
in the
above
arthritis.
hydronephrosis.
dyscrasiasmyeloma,
leukaemia,
remission
of
pernicious
anaemia.
4.
PLASMA
PROTEINS:
divided as follows:
6-7.5 gm.
per
They
are
A l b u m i n : 4 . 5 gm.
G l o b u l i n : 1 . 8 gm.
Fibrinogen:0.2 gm.
Hyperproteinaemia occurs in the following conditions:
(a) Acute diarrhoea, especially in children.
(b) Severe vomiting, especially in children.
(c) Extensive burns.
Hypoproteinaemia occurs in the following conditions:
(a) Kidney diseasesnephrosis,
nephritis.
CHOLESTEROL:
130-200 mgm.
arteriosclerosis.
obstruction
llAEMOPOIETICSYSTEM
371
cirrhosis.
anaemia, haemolytic
anaemias.
A.
obstruction.
SALTS.
vomiting.
nephritis.
B.
as
in
(b) Endocrine
disordersCushing's
syndrome,
tumours, overdosage of corticosteroids.
pyloric
stenosis,
adreno cortical
(c) Acidosis.
(d) Overdosage of sodium or Na-PAS; also mercurial diuretics.
(e) Post-operative conditions giving rise to paralytic ileus.
(f) In certain familial myopathies.
C.
372
D.
BLOOD GROUPING
Blood compatibility must be determined before blood transfusion is undertaken. Individuals are divided into four groups
according to the interaction of the sera of the one and the red
corpuscles of the other. The four groups assume existence of
two corpuscular agglutinogens A and B and two corresponding
serum agglutinins a and b. An agglutinogen e.g. A and the
corresponding serum agglutinin a cannot be present in the same
blood as autohaemolysis will take place.
R E L A T I O N B E T W E E N T H E SERUM A N D R E D CELLS.
Serum of groups.
Red
cells of
groups.
AB
A, i.e. agglutinin b
B, i.e. agglutinin a
-)-
ft
-f
llAEMOPOIETICSYSTEM
373
374
BLOOD
llAEMOPOIETIC SYSTEM
375
PROTEINS.
B.
C.
VITAMINS:
1.
2.
Vitamin C.
3.
D.
I N T E R N A L SECRETIONSThyroxine,
E.
I N T R I N S I C F A C T O R I n the stomach.
F.
PIGMENTS.
A.
PROTEINS.
ACTH,
cortisone.
MINERALS.
A person weighing 70 kgm. has about 5 gm. of iron in his body, over
half (60-70%) of which is in the form of haemoglobin, about 5% as myohaemoglobin and the rest in several other forms.
T h e supply of iron must compensate the daily excretion of about o n e
mgm. in adult males and a little extra in females for the additional
menstrual loss, burden of pregnancy and lactation. An ordinary diet will
supply an ample amount of Fe if its iron content exceeds 5 mgm. per day,
376
the
utilization
of
iron by
converting
it
into
VITAMINS.
Vitamin B12 and folic acid are marrow stimulants. T h e i r absence cause
megalocytic anaemias. Vitamin B 12 appears to be the extrinsic factor of
Castle. This, along with the intrinsic factor present in the stomach, acts
at proerythroblastic stage, so that if it is absent the maturation is deflected
t o the megalocytic series of cells instead of forming normoblasts.
Vitamin C is also a marrow stimulant and its deficiency causes anaemia
of normocytic type.
Vitamin B-complex have certain components whose absence cause megalocytic anaemia as in pellagra. T h e chief components are riboflavin, nicotinic
acid and pyridoxine.
D.
INTERNAL
SECRETIONS.
INTRINSIC FACTOR IN T H E
STOMACH.
Its
PIGMENTS.
which
ANISOCYTOSIS.
(Change in size):
llAEMOPOIETICSYSTEM
377
POIKILOCYTOSIS.
(Change in shape):
POLYCHROMATOPHILIA.
(Irregularity in staining):
This indicates an increase of young red cells in the circulation and occurs in the following forms:
1. Normoblastsnucleated red cells. Indicates activity of
the bone marrow. Commonly seen in severe anaemias.
2. Patchy staining of the cellsindicates immature red cells.
Occurs in pernicious anaemia and most of the blood
dyscrasias.
3. Punctate basophiliathere is stippling of some of the
red cells. Occurs in plumbism. May also occur in severe
anaemia, leukaemia and chronic malaria.
378
Basophilia
Reticulocytes
Nornioblasu
Fig. X X X I X
Alteration in appearance o red cells.
4. Reticulocytosisoccurs in acute bleeding, and in pernicious anaemia when the patient is being treated with liver
extract thereby indicating bone marrow activity.
ANAEMIAS
Anaemia means lack of haemoglobin in the blood generally
associated with reduction in the number of red cells.
AETIOLOGICAL CLASSIFICATION OF ANAEMIAS.
A.
D U E T O LOSS OF B L O O D .
I.
II.
B.
Haemorrhagic diseases.
D U E T O DEFECT IN T H E FORMATION
I.
OF B L O O D .
II.
HAEMOPOIETIC SYSTEM
PATHOLOGICAL
CLASSIFICATION
OF
379
ANAEMIAS.
MACROCYTIC ANAEMIAS
The red cells are bigger than normal and the colour index
above one. The mean corpuscular value is more than 94 c.u.
CAUSES:
NORMOCYTIC ANAEMIAS
The red cells are more or less of the same size as that of
normal cells. The colour index is less than one, and the mean
corpuscular volume is 78-94 c.u.
Causes:
1. Acute haemorrhages.
2. Blood destructionmetals, bacteria, protozoa, haemolysis.
3. Blood dyscrasiasleukaemia, Hodgkin's disease, Gaucher's, Banti's etc.
4. Deficiency diseasesmyxoedema, scurvy.
5. Aplastic anaemias in general.
6. Infections.
380
H O W TO EXAMINE A PATIENT
III.
MICROCYTIC
ANAEMIAS
The size of the red cells are smaller than normal and the
colour index less than one. The mean corpuscular volume is
less than 78 c.u.
Causes:
1. Chronic haemorrhagespeptic
ankylostomiasis, etc.
ulcer,
bleeding
piles,
Personal history.
(a) Diet to exclude nutritional
anaemias.
3.
4.
5.
Examine carefully for evidence of jaundice, subacute combined degeneration, Plummer-Vinson syndrome, etc.
6.
7.
8.
etc.
POLYCYTHAEMIA.
Polycythaemia denotes a significant increase in the red cells
above normal, generally above 6 millions per c.mm. of blood.
THE
I.
COMMON
CAUSES
ARE:
R E L A T I V E POLYCYTHAEMIA D U E T O :
llAEMOPOIETIC SYSTEM
381
SECONDARY
POLYCYTHAEMIA.
derivatives,
phenacetin,
POLYCYTHAEMIA VERA.
This is not a common disease. It starts insidiously with dizziness, tinnitus and headache. The appearance of the patient is
dusky red with blood-shot eyes. The spleen is enlarged, the
heart is enlarged and there is marked polycythaemia.
W H I T E BLOOD CELLS.
THESE
1.
CONSIST
GRANULAR
OF THREE
VARIETIES.
SERIES.
15%.
Five-lobed, 2%.
Myelobjasl
(has nucleoli)
Granular monocyte
with indented
nucleus
Nongranular
monocyte with
round nucleus
Neutrophilic
meiamyelocyte
Eoiinophilic
metamyelocyte
Nongranulat
monocyte with
indented nucleus
Band metamyelocyte
Granular monocyte
with round nucleus
Neutrophilic
Eosinophilic
Basophilic
(polymorphonuclear leukocytes)
Fig. X L
Development of
Granular Leucocytes
Development of
Monocytes
llAEMOPOIETICSYSTEM
383
T H E L Y M P H O C Y T E SERIES.
iBrffi lymphocyte
Lymphoblastic
plasma cell
Granular
small lymphocyte
Granular
large lymphocyte
Fig.
XLI
Development of Lymphocytes.
3.
T H E MONOCYTES SERIES.
384
The primary function of the white blood cells is defence of body against
infection by phagocytosis and probably by the production of antibodies.
1. Physiological.
(a) After exercise, exposure
digestion.
to sunlight
and
during
llAEMOPOIETIC SYSTEM
385
LEUCOPENIA.
In such conditions the white cell count is below 5,000 and is
almost always due to diminution of polymorpho nuclear cells.
CAUSES-.
386
1. Physiologicalin infancy.
2. Infections.
(a) Acute bacillary dysentery, whooping cough, glandular
fever, measles, small-pox and mumps.
(b) Chronictuberculosis, syphilisespecially congenital,
chronic empyema and chronic appendicitis.
3. Chronic lymphatic leukaemia.
4. Inconstant in hyperthyroidism, hypothyroidism, diabetes
mellitus, Banti's disease and in exposure to ultra-violet
rays.
5. In infants and young children suffering from rickets and
malnutrition.
Lymphocytes may be diminished in the acute stage of an infection, conditions of exhaustion, after abdominal catastrophes,
after burns, in heart failure, after excessive irradiation, and in
terminal phases of uraemia.
llAEMOPOIETIC SYSTEM
387
MONOCYTOSIS.
CAUSES:
1. Glandular fever.
2. Protozoal infectionsmalaria, kala-azar.
3. Monocytic leukaemia.
4. Endocarditis lenta.
5. Hodgkin's disease.
6. Tuberculosis.
7. Sarcoidosis.
8. Sympathetic ophthalmia as a result of damage to one eye.
9. Tetrachlorethane poisoning.
EOSINOPHILIA.
This denotes an increase in the number of eosinophil cells
in the blood. The upper limit is about 4%. Above 5% may
be considered as pathological.
CAUSES:
388
H O W T O EXAMINE A PATIENT
1. Myeloid leukaemia.
2. Cirrhosis liver.
3. Folycythaemia vera.
4. May be increased in early stages of Hodgkin's disease.
5. May be increased in early stages of small-pox and chickenpox.
PLATELETS OF THE BLOOD
Normal platelet count in the blood is 200,000 to 400,000 per
c.c. Their presence is essential for proper coagulation of blood.
When diminished the patient shows tendency to bleed on
slightest trauma. Their excess favours thrombosis as occurs after
operations or splenectomy. Post-operative platelet increase is
due to absorption of tissue products and the increase is proportional to the amount of tissue damaged. This applies to wounds
and injuries also.
LESS
PLATELETS
IN
THE
FOLLOWING
CONDITIONS:
I.
DIMINISHED PRODUCTION
CIRCULATION
IN T H E BONE
OCCURS
DUE
TO
MARROW.
llAEMOPOIETIC SYSTEM
389
D E S T R U C T I O N BY T H E SPLEEN
U T I L I Z A T I O N OF P L A T E L E T S F O R T H E P U R P O S E O F :
ARE
INCREASED
IN:
BLOOD DYSCRASIAS.
weakness,
390
H O W TO EXAMINE A PATIENT
B.
INFECTIONS.
ENLARGEMENTS
llAEMOPOIETIC SYSTEM
391
CHAPTER VIII
LOCOMOTOR SYSTEM
A.
INTERROGATION.
B.
GENERAL EXAMINATION.
I.
II.
Muscles.
Bones.
1.
2. Vertebral Column.
3.
Long BonesExtremities.
4.
III.
Joints.
IV.
Gaits
H O W TO EXAMINE A PATIENT
394
A.
INTERROGATION.
EXAMINATION OF MUSCLES.
Inquire into the family history of similar diseases, the milestones in the life of the child, personal history and occupation.
Test the muscles for weakness, tone and movements. Note if
there are tremors, fasciculations, etc.
M U S C U L A R DISORDERS.
D U E T O LESIORS OF T H E NERVOUS
T h e most important of these are:
SYSTEMMYELOPATHIES.
D U E T O LESIONS IN T H E MUSCLESMYOPATHIES.
important of these are:
T h e most
LOCOMOTOR SYSTEM
395
EXAMINATION OF BONES.
1.
SKULLHEAD A N D NECK.
Note the skull for its shape, size, areas of tenderness, swelling,
bulging, and also the physiognomy of the face.
Common Cranial and Facial Deformities.
A.
DEVELOPMENTAL
DEFECTS:
396
H O W TO EXAMINE A PATIENT
Fig.
Cretin
XLII
Mongol
E N D O C R I N E DISEASES:
1. Pituitary Disorders.
(a) ACROMEGALYwell-marked supra-orbital ridges, face larger than
normal, large and protruding jaw, enlarged and fissured tongue.
T h e whole face is egg-shaped with narrower end upwards.
(b) CUSHING'S SYNDROMEuniformly puffy face ( m o o n
face).
Common in anterior pituitary dysfunction due to hypersecretion of
basophil cells. O f t e n results during corticosteroid therapy.
2. Thyroid Disorders.
(a) C R E T I N I S M : T h e face
flat nose, thick lips, large
tongue, m o u t h half open,
growth and 'pot-belly'.
(b) MYXOEDEMA:Coarse and dry skin, puffy and pale face, scanty
hair especially at the eye-brows, dull and apathetic look. (See
Fig. XLIII.)
LOCOMOTOR SYSTEM
397
(t) T H Y R O T O X I C O S I S : P r o m i n e n t eye-balls, retracted eye-lids staring eyes, dilated pupils, diminished blinking and lack of convergence. (See Jig. XLIII.)
Fig. XLIII
Myxoedema
Grave's Disease
CHRONIC INFECTIONS.
(a) C O N G E N I T A L SYPHILIS: Frontal bosses, overhanging forehead,
depressed nasal bridge, striations o n the lips, Hutchinson's teeth
and keratitis.
(b) L E P R O S Y : W r i n k l i n g of the forehead, cheeks, chin and ears d u e
to subcutaneous infiltration by lepra nodules (leonine
appearance).
(See Fig. XLIV.)
(c) T A B E S DORSALISptosis w i t h wrinkles on the forehead due to
overaction of the frontalis to keep the eyes open. Pupils narrow.
D.
NERVOUS DISORDERS.
(a) BELL'S P A L S Y : O n the affected side the eye is half open, w i t h
loss of furrows o n the forehead and the nasolabial fold. (See
Fig. XLIV.)
(b) M Y A S T H E N I A G R A V I S : D r o o p i n g
head, "a sneer for a smile".
eye-lids,
drooping
of
with
the
a
H O W TO EXAMINE A PATIENT
398
Fig. XLIV
Bell's Palsy
E.
Leprosy
DEFICIENCY DISEASES.
OF THE
HEAD.
CAUSES:
I.
II.
FUNCTIONAL.
1.
Hysteria.
2.
Spasmodic torticollis.
INFECTIONS OF T H E
1.
III.
IV.
BRAIN.
Meningitis.
2.
Encephalitis.
3.
4.
Tetanus.
2.
Strychnine poisoning.
3.
Hydrophobia.
NEOPLASTIC.
1.
2.
LOCOMOTOR SYSTEM
V.
GENERAL
399
INFECTIONS.
1.
2.
Laryngeal
3.
obstruction
2.
(especially in
VERTEBRAL
diphtheria).
COLUMN.
OF THE
SPINE.
2.
(g) Functionalhysteria.
H O W TO EXAMINE A PATIENT
400
II.
ANGULAR.
(a) Pott's diseasecommonest
cause.
DIFFUSE
KYPHOSIS.
(muscular dystrophies,
congenital
spastic
Osteo-arthritis.
Myopathiespseudo-hypertrophic
2.
Secondary to h i p disease.
paralysis.
3.
4.
5.
Physiologicalpregnancy.
BACKACHE.
Although backache may be due to several causes other than
that of the vertebral column, the conditions that give rise to
the same are best considered here.
C O M M O N CAUSES:
1.
LESIONS OF T H E V E R T E B R A L C O L U M N :
(a) Prolapsed
disc, spondylosis,
osteo-arthritis
(all these start with
backache followed by pain along one or b o t h the sciatic nerves).
(b) Pott's Diseasecommonest
cause; leads to local rigidity and tenderness and later loss of normal curvature of the spine.
(c) Traumatichistory
(d) Tumoursextradural
tumours especially; p a i n worsens on jarring;
segmental root pains most conspicuous.
LOCOMOTOR SYSTEM
2.
401
LESIONS OF T H E MUSCLES.
(a) Lumbagogenerally
sure; back is stiff.
(b) Posturalmore
3.
4.
5.
F U N C T I O N A L c o m m o n in young w o m e n or at menopause.
3.
LONG
BONESEXTREMITIES.
26
402
All the local swellings of the bones produce pain and tenderness of the affected area.
4.
FINGERS.
Present
III.
EXAMINATION OF JOINTS.
LOCOMOTOR SYSTEM
403
404
ARTHRITIS.
Diseases of joints can be classified under two groupsacute and chronic.
A.
ACUTE ARTHRITIS.
Common causes:
1.
INFECTIONS.
(a) Infective
arthritismay
be of acute onset. Large joints are
involved, usually one, which is moderately swollen. If small
joints are affected, they are generally multiple.
(b) Gonorrhoeaacute
onset, very painful, generally the knee is
involved; may suppurate.
(c) Sequelae
of infective
diseasesin
typhoid, spine may be involved; in bacillary dysentery, the knee may be affected.
(d) Sepsis ans pyaemiaone
suppurate.
associated
with
COLLAGEN DISEASES.
Rheumatismacute
never suppurate.
3.
affected
METABOLIC DISEASES.
Goutsudden
onset in the middle of the night; metatarsophalangeal joint of the great toe is commonly affected.
4.
DEFICIENCY DISEASES.
Scurvyknees
chiefly involved associated with
rhages in the skin.
5.
petechial
haemor-
BLOOD DISEASES.
Haemophilia
often causes bleeding in the synovial membrane of
the joint, commonly the knee. T h e r e is pain on movement, tenderness and often
fluctuation.
6.
B.
T R A U M A T I C h i s t o r y of injury.
CHRONIC ARTHRITIS.
Common Causes:
1.
INFECTIONS.
(a) Infective
arthritismay
start as acute and go on into chronic
stage. Large or small joints are involved.
(b) Rheumatoid
arthritissmall
joints of the hands are generally
involved. T h e swellings are fusiform in shape. There may
be ulnar deviation of the fingers.
(c) Tuberculosiscommon
in children. Hip-joint is commonly
affected and vertebral column. Small joints may be involved
in adults.
LOCOMOTOR SYSTEM
405
(d) Syphilisone
big joint is generally involved which is moderately
tender. T h e pain is worse at nights. In tabes the knee may
be involved leading to its distorsion. T h e joint is painless,
although swollen.
(e) Pulmonary
ost.eo-arthropathythe
distal ends of the long
bones, especially of the hands, are symmetrically enlarged
along w i t h clubbing of the fingers. T h e cause is absorption
of septic matter from the lungs, intestine or the liver.
In congenital heart diseases, where the clubbing is
marked, the involvement of the long bones is minimal.
2.
COLLAGEN
well-
DISEASES.
(a) Polyarteritis
nodosapainful
swelling of acute onset, with fever
and nodular swellings on the superficial arteries.
(b) Disseminated
lupus erythematosuscommon
in young women,
starts with fever, eruption, polyarthritis, leading to nephritis,
myocarditis and leucopenia. L.E. cells are found in the blood.
3.
BLOOD
DISEASES.
Haemophiliamay
repeated trauma.
4.
DEGENERATIONS.
(a) Osteoarthritisshoulder
involved leading to marked restriction
of movements, muscular wasting and grating sensation. Small
joints of the hands may be involved leading to radial deviation
of the fingers and presence of Heberden's nodes. .
(b) Spondylitis
deformanslumbar
vertebrae are commonly involved
leading to rigidity of the back, restriction of movements and
sciatic pains.
5.
METABOLIC.
(a) Chronic goutmay be chronic from the beginning or the sequel
of successive attacks of acute gout. Big joints may be affected.
T o p h i are generally present.
(b) Still's diseasecommon
in children. Many joints are involved
associated with lymphadenopathy
and splenomegaly. T h e
disease ends with crippling deformity of the joints.
6.
NEUROPATHIES.
T a b e s and syringomyelia can give rise to arthropathies, which are
painless. T h e knees are mainly involved.
CHAPTER IX
SKIN AND ITS APPENDAGES
(Hair and Nails)
A.
INTERROGATION.
B.
HISTORY OF T H E ILLNESS.
C.
EXAMINATION OF T H E SKIN.
I.
Inspection.
II.
Palpation.
III.
Microscopic Examination.
D.
EXAMINATION OF T H E HAIR.
E.
EXAMINATION OF T H E NAILS.
408
A.
INTERROGATION.
EXAMINATION OF T H E SKIN.
I.
INSPECTION.
intake of
409
BRONZEDhaemochromatosis.
P I G M E N T E D d u e to melanin deposit in the skin (see below).
DEPIGMENTEDleucoderma, albinism, syphilis and some skin diseases.
is
full
of
melanin);
cancer
Eruptions.
If eruptions are present, note their extent, mode of spread,
distribution, colour, type, duration, and whether accompanied
by itching or burning. Also inquire if the patient took any
drugs.
Types of rashes:
M A C U L A R (not raised above the skin)Occur in syphilis, typhoid, scarlet
fever, purpura.
ROSEOLAR (a generalised eruption
syphilis and some skin diseases.
of
macules)occurs
in
typhus,
410
small-pox,
erysipelas.
Haemorrhages.
Haemorrhages under the skin may be classified into the following groups:
PETECHIAEtiny haemorrhages, less than one m m . in diameter.
P U R P U R I C SPOTS2 to 5 mm. in diameter.
ECCHYMOSESlarger than 5 mm. in diameter.
H A E M A T O M A t h e bleeding is large enough to produce an elevation
of the skin.
TELANGIECTASISsmall collections of dilated skin vessels.
Purpuric and petechial haemorrhages are often seen in purpura haemorrhagica, scurvy, vitamin K deficiency, cerebro-spinal fever, typhus, subacute
bacterial endocarditis, leukaemia, Hodgkin's disease, and aplastic anaemia;
less frequently it may be seen in nephritis, cancer, tuberculosis and cachexia.
Ecchymoses and haematomas are more due to local trauma than due to
medical diseases.
Ulcers.
If ulcers are present, note the following points: -
(i) D U R A T I O N . In case of venereal ulcers, inquire about the incubation period which is 3 to 4 days in soft chancre and 3 to 4 weeks
in syphilis.
(ii) MODE OF ONSETif it started after trauma, or with a lump in
the gland as in tuberculosis, or after dermatitis as in varicose ulcers.
(iii) ASSOCIATED PAIN. Inflamed ulcers are painful. Tubercular
ulcers are generally painful. Syphilitic, malignant and trophic
ulcers are painless.
(iv) SIZE A N D SHAPE. Tubercular ulcers are oval. Syphilitic ulcers
are circular. Carcinomatous ulcers are irregular in shape and size.
411
PALPATION.
Palpate the skin by passing the hand gently over the body
and note the following:
1. If dry or moist. If there is sweating, note if it is generalised or localised.
Dry skin is noticed in pneumonia, diarrhoea, polyuria and
myxoedema. Moist skin is seen in tuberculosis, rheumatism, crisis
of p n e u m o n i a , Grave's disease and neurasthenia. Profuse sweating occurs in shock, severe toxaemia and peripheral circulatory
failure.
H O W TO EXAMINE A PATIENT
412
Subcutaneous emphysemaif present, it is felt as a crackling sensation on palpation; may be felt in the chest-wall
when air escapes from the lungs.
III.
MICROSCOPIC
EXAMINATION.
EXAMINATION OF T H E HAIR.
SCANTYhypothyroidism.
EXCESSIVE G R O W T H O N T H E C H I N , F O R E A R M A N D LEGS
Cushing's syndrome and adrenocortical syndrome in females (virilism).
T H I C K , GREASY A N D
T H I N , SILKY A N D
ABUNDANTAcromegaly.
SOFThyperthyroidism.
HAIRinfantilism,
SIDEmyxoedema.
E.
EXAMINATION OF T H E NAILS.
413
Typically present
IRREGULARcongenital
RIDGED A N D BRITTLEsprue,
the
nailbeds
in
and
blood
syphilis.
hypoparathyroidism.
CHAPTER IX
EXAMINATION OF CHILDREN
Although in general, the examination of children is essentially
the same as examination of adults, yet their age and inability to
express symptoms present special problems.
The examiner may have to depend heavily on the mother
to get some facts, especially developmental history, difficulty
during labour, feeding and nursing.
The following observations will be of help as a preliminary
to the more detailed description.
1. Be patient, observant, accurate and gentle while examining children.
2.
FAMILY
HISTORY.
progresswhen
crawling,
sitting,
standing,
416
HISTORY
OF PRESENT
ILLNESS.
CLINICAL
1.
GENERAL
EXAMINATION.
EXAMINATION.
EXAMINATION O F CHILDREN
417
(d) Consciousness.
If the child is not fully conscious, decide if it is due to
delayed mental progress, infection or severe anaemia. A
conscious infant reacts readily to environment by smiling if
he is pleased, or by crying if frightened or annoyed.
(e) Vitality and playfulness.
Acute illness quickly lessens a child's normal vitality and
destroys his natural interest in play.
(f) Colour of the skin.
Look for pallor, cyanosis, jaundice, haemorrhages, etc.
(g) Voice.
Note if it is hoarse, weak or if the child cries too much.
(h) Facial expression.
(i) Skull.
Note the size of the skull, especially for hydrocephalus,
microcephalus, localised bulging, etc. Note the fontanelles
and sutures.
27
H O W TO EXAMINE A PATIENT
418
CHEST.
419
EXAMINATION OF CHILDREN
T H E C A R D I O VASCULAR SYSTEM.
80/60
90/65
110/70
420
gestive of rheumatic endocarditis even in the absence of rheumatic history (joint pains, growing pains, tonsillitis, chorea).
In a normal child the 2nd pulmonary sound is louder than the
2nd aortic sound.
4.
GASTRO I N T E S T I N A L SYSTEM.
Examine the mouth for stomatitis, septic teeth, herpes, angular stomatitis, etc. Smell of the breath is often unpleasant in
stomach disturbances. Note the tongue for atrophy, stomatitis,
ulceration, thrush, etc.; the inner surface of the cheeks for ulcers,
Koplik's spots of measles, etc.; the gums for sponginess (scurvy)
and throat for tonsils.
Teeth are cut at approximately the following time:
T E M P O R A R Y T E E T H (20 teeth)
Lower central incisors (2)
Upper central incisors (2)
7-9 months.
9-12 months.
12-18 months.
6-8 months.
18-20 months.
24-28 months.
TEETH
(32 teeth)
6 years.
7 years.
8 years.
9-10 years.
10-11 years.
12 years.
12-13 years.
17-25 years.
EXAMINATION OF CHILDREN
421
GENITO URINARY
SYSTEM.
N E R V O U S SYSTEM.
CHAPTER XI
EXAMINATION OF PSYCHIATRIC PATIENTS
The general scheme is the same as in general medicine with
special emphasis on the following points: A.
CHIEF COMPLAINT.
FAMILY HISTORY.
PERSONAL HISTORY.
Habits.
Social activities.
Career of the patient.
5.
6.
7.
424
D.
ILLNESS.
E X A M I N A T I O N OF T H E P A T I E N T .
425
convenient to include under this heading. Observe the constancy of the mood, the influence which changes it; the appropriateness of the patient's apparent emotional state to what he
says.
4. Delusions and Misinterpretations. What is the patient's
attitude to the various people and things in his environment?
Does he misinterpret what happens, give it special or false
meaning, or is he doubtful about it? Does he think anyone
pays special attention to him, treats him in a special way,
persecutes him or influences him, bodily or mentally, in ordinary
or scientific or pretenatural ways? Laughs at him? Shuns him?
Admires him? Tries to kill him? Harm or annoy him? Does
he depreciate himself in any regard, his morals, possessions,
health? Has he grandiose beliefs?
5. Hallucinations and other disorders of perception. These
may be auditory, visual, olfactory, gustatory, tactile, visceral.
The source, vividness, reality, manner of reception, content,
especially if auditory or visual must be reported in detail.
When do these experiences occurat night, when falling asleep,
when alone? Any peculiar bodily sensations? Feeling of deadness? Unreality?
6. Compulsive phenomena. These may be obsessional
thoughts, impulses, or acts. Are they felt to be from without,
or part of the patient's own mind? Does their insistence distress him? Does he recognise their inappropriateness? Does
he repeat acts, such as washing unnecessarily to reassure himself?
7. Orientation. Record the patient's answers to questions
about his own name and identity, the place where he is, the
time of day and the date. Does he find anything unusual about
the way in which time seems to pass?
8. Memory. This may be tested by comparing the patient's
account of his life with that given by others, or examining his
account for intrinsic evidence of gaps or inconsistencies. Information which he gives about his previous life, his personality,
sexual experiences, etc. should be confirmed from his closest
relations. Enquirie for recent events, such as those of his admission to hospital and happenings in the ward since. Note if
426
Appendices
Retards growth.
(c) B(;Pyridoxine.
2 mgm.
5 mgm.
Beri beri.
Anorexia, constipation.
4 to 5,000 units.
2 to 3 mgm.
(b) Axerophthol.
Hyperkeratosis, xerophthalmia,
night-blindness.
Deficiency lesions
EXAMINE
Vit. B-complex.
Fats, carrots.
Daily requirements
TO
(a) Carotene.
Principal sources
HOW
Vit. A
Name
About 20 vitamins are known of which 12 or so are needed for normal development. Vitamins A , D, E and K are
fat-soluble; the rest are water-soluble. The fat-soluble vitamins require lipids, bile, for their absorption from the intestine.
The water-soluble ones are diffusible and are easily absorbed from a normal intestine. Both, the water-soluble vitamins,
especially of the B-complex group and some of the fat-soluble ones like vitamin K, are synthesized by the intestinal flora.
VITAMINS
APPENDIX A
4 2 8
PATIENT
Vit. KNaphtoquinone.
! 3UU
..
f
j
J
unlts
1 to 3 meg.
5 mgm.
"]
Rickets, osteomalacia.
Teeth decay.
Scurvy.
Hypoprothrombinaemia.
"
Pellagra.
Capillary bleeding.
50 mgm.
Vit. B12Cyanocobalamin.
(c) D3Ergosterol.
Germinating seeds, wheat
germ oil.
(b) D2Calciferol.
V i l . ETocopherol.
50 mgm.
1 to 2 mgm.
1 to 3 mgm.
10 mgm.
(a) DiDehydrocholesterol.
Vit. D.
Citrus fruits.
(h) Biotin.
APPENDIX A
429
I.
A.
Stimulates thyroid.
Parathyroid influencing.
CHO influencingdiabetogenie.
Lipid influencingketogenic
6.
7.
8.
Stimulates parathormone.
Lactogenicprolactin.
5.
EXAMINE
Gonad influencing:
4.
Thyrotrophic hormone.
TO
Growth hormone.
ACTHcorticotrophic.
1.
Chief action.
HOW
2.
Important hormones.
Pituitary.
Glands.
I.
ENDOCRINE SYSTEM
APPENDIX B
4 3 0
PATIENT
Gonads.
VI.
3.
Progesterone.
1. 2.Corticosteroids.
Controls metabolismStimulates
of water and
salts.
Adrenalin; nor-adrenalin.
nerve-endings;
constricts
capillaries.
Oestrogens.
Testosterone.
Helps metabolism.
Controls Ca and P metabolism.
Insulin.
Parathormone.
Thyroxine.
animals.
Vasopressin (antidiuretin).
2.
Oxytocin (pitocin).
1.
Ovaries.
Adrenals.
V.
B.
Pancreas.
IV.
Testes.
Parathyroid.
III.
A.
Thyroid.
Pars intermedia.
C.
II.
Posterior pituitary.
B.
APPENDIX
B
4 3 1
I.
A.
Pathology
Anterior Pituitary
Pituitary.
Gland
Clinical Features
the
typeobesity,
retardation, re-
(c) Lawrence-Moon-Biedl
hypogonadism, mental
tinitis pigmentosa.
(a) Lorain typedwarfism, sexual infantalism, mentally normal, look young for
their age.
II.
432
H O W TO EXAMINE A PATIENT
K>
CC
Thyroid
Parathyroids
III.
Posterior Pituitary
II.
B.
achlor-
Hyposecretion.
Hypersecretion.
Osteitis
Hyposecretion.
Tetanycarpo-pedal
spasms, laryngismus
stridulus, sensitive peripheral nerves. Serum
Ca is below 5 mgm. per cent.
fibrosabone
pains,
weakness,
drowsiness, spontaneous fractures, Serum Ca
is above 15 mgm. per cent.
face, dry
hydria.
macrocytic anaemia,
Hypertension,
Hypersecretion.
Hyposecretion.
Hypersecretion.
APPENDIX B
433
V.
IV.
Medulla
B.
Pancreas
Cortex
Pathology
A.
Adrenals
Gland
Hyposecretion.
Hypersecretion.
Hyposecretion.
Hypersecretion.
Hyposecretion.
Hypersecretion.
Clinical Features
Phaeochromocytomaparoxysmal attacks of
diseaseasthenia, pigmentation,
hypotension.
Addison's
(i) Congenitalpseudohermaphroditism
in females and pubertas praecox in
males.
434
H O W TO EXAMINE A PATIENT
Hydatid disease.
Plague.
Typhus.
Dogs.
Fish.
Goats.
Fleas.
House-fly.
Lice.
Mites.
Typhus.
Bovine
tuberculosis.
Brucellosis.
Anthrax, T.saginata, Sleeping-sickness.
Undulant fever (abortus).
Cattle.
Bubonic
fever. Typhus.
Hydatid disease.
Tularaemia.
Rats.
Tsetse-fly.
Sand-fly.
Mosquitoes.
Trypanosomiasis.
Ticks.
Weil's
fever
disease. Rat-bite
Undulant
plague.
Trichiniasis, T. Solium.
(abortus).
Encephalitis.
Glanders.
Sheep.
Rodents.
Pigs.
Mice.
Cat-scratch fever.
Cats.
Horses.
Ornithosis. Psittacosis.
Birds.
INFECTIOUS DISEASES
APPENDIX C
APPENDIX C
435
10 to 14 days.
10 to 21 days.
10 to 14 days.
10 to 14 days.
Typhoid.
Typhus.
Varicella (Chicken-pox).
v
pSa!-'
1st day.
'
vesicular
'
Maculo-papular.
Papular.
papUlar
2nd week.
3rd day.
Small-pox.
2nd day.
Macular.
EXAMINE
2 to 4 days.
1st day.
^pHk's
litorm.
'
Morbi
Erythematous.
TO
Scarlet fever.
2nd day.y
4th da
7 to 14 days.
i
Measles.
Sp tS
IIOVV
2nd day.
2 to 5 days.
Erysipelas.
Roseolar.
Initial1st day.
Punctate.
Appearance of rash
2 to 6 days.
Terminal4th day.
Incubation period.
Denoue
"
Disease
436
PATIENT
f.
Ova.
Remarks.
of
the
anus
Ova, thin shelled and
contain
coiled embryos.
Wide spread.
T. Kcchinococcus.
slightly
ovoid
Man, sheep, dogs,
embryonal
arc intermediate
hosts,
Wide spread.
Megalocytic anaemia.
Brown coloured with
Cyclops are intera lid at one end.
mediate hosts,
Egg
with 6
hooklets.
Hydatid cyst.
No symptoms.
Only
females
are
Diarrhoea and urtiOva
thin
shelled.
Sexual cycle outside
found in the intestine
caria.
often notched at larthe human body.
1" long.
val stage.
Trichuris trichuria,
(whipworm).
Strongyloides
stercoralis.
Clinical features.
Males 6 in.
Nothing
particular,
Ova yellow, elliptical
World-wide distribulong,
and
females
may cause intestinal
with thick outer shell
tion;
common
12 in. long.
obstruction.
showing excrescences.
children.
Round.
Oxyuris vermicularis
(thread worms).
Ankylostoma
duodenale.
Ascaris.
Intestinal worms.
Name.
IV.
in
APPENDIX
C
4 3 7
Clinical features.
7-10
Trich. Spiralis.
Larvae ejaculated
from ulcer.
Animal host is
cyclops.
Haematuria, eosinophilia.
Urticaria, ulcer,
cellulitis.
Resemblefinecatgut;
Fever, painful
75-100 mm. long.
Guinea worm.
Remarks.
Ova.
Blood infestation.
l'ilaria.
If.
T. Solium.
T. Saginata.
Name.
438
H O W TO EXAMINE A PATIENT
INI) E X
Abdomen, 138
anatomical landmarks, 136
auscultation, 143
inspection, 138
mensuration, 143
palpation, 139
percussion, 141
Abdominal contents, 137
pain, 168, 128
pain in children, 173
reflexes, 246
rigidity, 168
swelling, 160, 132
tumours, 166
Abnormalities of micturition, 332
Abnormalities of skull, 395
Accessory nerve, 236
Accoucher hand, 402
Aceto-acetic acid, test, 324
Acetone, test, 324
Achlorhydria, 154
Achondroplasia, 395
Acidity, gastric, 153
Acromegaly, 396
Adie's pupils, 227
Adrenal gland, 434
Aegophony, 37
Aerophagy, 132
Agranulocytosis, 383
Alar chest, 24
Albumin, test, 323
Albuminuria, 335
Albumino-cytologic dissociation, 264
Alternans, pulsus, 86
Ammonia in urine, 322
Amoebic dysentery, 190
Amphoric breathing, 35
resonance, 32, 37
Amyotonia congenita, 287
Amyotrophic lateral sclerosis, 394
Anacrotic pulse, 84
Anaemias, 378
Anaemiascontd.
macrocytic, 379
microcytic, 380
normocytic, 379
Analysis, blood, 358
gastric, 151
urine, 319
Anasarca, 103
Anatomical landmarks, abdomen,
136
Anatomy of the brain, 256
Angina pectoris, 98
Anisocytosis, 361
Ankle-clonus, 251
Ankle-jerk, 251
Anorexia, 130
Anuria, 337
Aortic murmurs, 119
regurgitation, 120
stenosis, 119
Ape-hand, 402
Apex beat, 68
Aphasia, 280
Appearance, face, 8
Appetite, 130
Argyll-Robertson pupil, 226
Arteriosclerosis, 89
Arrhythmia, sinus, 85
Arthritis, 484
Ascending tracts, 309
Aschoff's nodes, 402
Ascites, 161
Asthma, bronchial, 55, 58
cardiac, 56, 58
renal, 56, 58
Ataxia, 288, 210
Ataxic gait, 286
Atrophy, optic, 218
peroneal muscular, 394
Auditory nerve, 232
Auricular fibrillation, 85, 99
flutter, 85, 99
septal defect, 113
439
440
Breathing, varieties, 34
Bright's disease, 356
Bronchial asthma, 55, 58
Bronchial breathing, 34
Bronchophony, 37
Broncho-vesicular breathing, 34
Brown Sequard's syndrome, 291
Brudzinski sign, 255
Calcium in blood, 371
Cancer, stomach, 158
Caput medusae, 139
Cardiac asthma, 56, 58
dilatation, 115
dullness, 72
enlargement, 114
failure, 108
murmurs, 115
pain, 94
sounds, 73
Cardiomegaly, 110
Casts, urinary, 327
Cavernous breathing, 35
Cerebellar disorders, 308
Cerebellum, 308
Cerebral circulation, 257
embolism, 292, 297
haemorrhage, 292, 296
thrombosis, 293, 296
Cerebro-spinal fluid, 259
Cerebrum, 288
Chaddock's sign, 248
Charcot-Leyden crystals, 40
Cheeks, examination, 9
Chemistry of blood, 368
Chest, deformities, 24
examination, 21
movements, 25
pain, 45, 17
Cheyne-Stoke's breathing, 23
Children, examination of, 415
Chlorides in blood, 369
in urine, 321
Cholesterol in blood, 370
Chorea, 308
Chyle, test, 326
Chylous effusion, 42
Cilio-spinal reflex, 246
INDEX
Circulation, cerebral, 257
Circulatory failure, 107
Circumduction gait, 284
Claw-hand, 402
Clonus, ankle, 251
patellar, 252
Clot retraction time, 366
Clotting time of blood, 365
Coagulation time, 365
Coarctation of the aorta, 90
Clubbing of fingers, 412
Cochlear nerve, 219
Coeliac disease, 188
Cog-wheel breathing, 34
Colics, abdominal, 72
Colour of the face, 9
Colour index of blood, 362
Colour vision, 217
Co-ordination of muscles, 243
Coma, 274, 209
Congenital heart diseases, 113. 123
murmurs, 123
syphilis, 397
Congestive heart failure, 108
Conjugate deviation of eyes, 220
Conjunctival reflex, 227
Constipation, 182, 130
Convulsions, 265
in children, 267
Corneal reflex, 227
Coronary disease, 94, 98
thrombosis, 98
Corpus luteum, 431
Corpus striatum, 307
Corrigan's pulse, 85
Cough, 43, 16
Courvoisier's law, 145
Cracked-pot sound, 32
Cranial nerves, 212, 213, 214
abducent, 219
accessory, 236
auditory, 232
cochlear, 232
facial, 229
glosso-pharyngeal, 235
hypoglossal, 237
oculo motor, 219
olfactory, 214
Cranial nervescontd
optic, 214
trigeminal, 227
trochlear, 219
vagus, 235
vestibular, 233
Creatinine in urine, 322
Cremasteric reflex, 246
Crepitations in the lungs, 35
Cretinism, 396
Crystals, urinary, 328
Curshman's spirals, 39, 40
Curvature of the spine, 299
Cushing's syndrome, 432
Cyanosis, 51
Cyto-albuminal dissociation, 264
Decubitus, 5
Defaecation reflex, 254
Defects of vision, 214
Deficiency anaemias, 378, 379
Deformities of the chest, 24
Deglutition reflex, 254
Descending tracts, 309, 310
Deviation, conjugate, 2Q7
Diaphragmatic sign, Litten's 26
Diarrhoea, 184, 129
in infants, 186
Diastolic murmurs, 118, 120
Dicrotic pulse, 84
Diplopia, 221, 208
Disseminated sclerosis, 299
Dittrich's plugs, 39
Dizziness, 233, 208
Ductless glands, 430
Ductus arteriosus, patent, 113
Dullness, cardiac, 72
Duodenal ulcer, 157
Durozier's sound, 79, 125
Dysarthria, 278
Dysentery, amoebic, 190
bacillary, 190
Dysphagia, 175, 131
Dyspnoea, 53, 16, 63
paroxysmal, 55
Dystrophia myotonica, 287
Dvsuria, 339, 319
441
442
Ears, examination, 10
Ecchymosis, 410
Efficiency tests for kidney, 329
Effusion, pleural, 42
Eisenmenger's reflex, 113
Embolism, cerebral, 297
Empyema, 42
Encephalitis, hypertensive, 297
Endocardial murmurs, 115
Endocrine dysfunctions, 432
Endoc.-ine glands, 430
Enlargement of the gall-bladder, 200
of the heart, 110
of the kidneys, 330
of the liver, 195
of the l y m p h glands, 389
of the spleen, 201
Enophthalmos, 239
Enteritis, 185, 186
Eosinophilia, 387
Epilepsy, 268
Jacksonian, 269
Major, 269
minor, 269
myoclonic, 270
psychomotor, 269
Epistaxis, 46
Erb's type of paralysis, 394
Eructation, 132
Eruptions, 409
Eruptive fevers, 436
Erythematous rash, 409
Exercise tolerance test, 93
Exocardial murmurs, 124
Exophthalmos, 238
Expression, facial, 8
Extra-pyramidal system, 307
Extra-systoles, 86, 99
Eyes, appearance of, 8
Face, examination, 7
Facial expression, 9
Facial nerve, 229
Faeces, examination, 147
Failure, cardiac, 108
circulatory, 107
congestive, 108
left ventricular, 109
Failure cardiaccontd.
peripheral, 110
right ventricular, 109
Fainting, 100, 63, 207
Fallot's tetralogy, 113
Fatty casts, urinary, 328
Fehling's test, 323
Festinating gait, 285
Fevers, 12
Fibrillation, auricular, 99
Fits, 265, 206
Flatulence, 132
Flutter, auricular, 99
Fragility test, 369
Fremitus, rhonchal, 28
tactile vocal, 20
Frequency of micturition, 339, 317
Friction sounds in the chest, 36
Frohlich's syndrome, 432
Froin's syndrome, 264
Fundus examination, 217
Funnel-shaped chest, 24
Gait abnormalities, 284
Gall-bladder, 199, 145
Gallop-rhythm, 75
Gastric acidity, 153
analysis, 151
ulcer. 157
Gerhard's test, 324
Giddiness, 233, 208
Glands, lymph, 389
Glosso-pharyngeal nerve, 235
Glucose in blood, 369
tolerance test, 342
in urine, test, 323
Glycosuria, 340
alimentary, 341
pancreatic, 340
renal, 340
Gmelin's test, 325
Gonads. 431
Gordon's sign, 248
Graham-Steel murmur, 122
Granular casts, 327
Granulocytosis, 381
Grasp reflex, 255
Grave's disease, 397, 433
INDEX
Guaiacum test, 325
Gums, examination, 133
Hypogonadism, 397
Hypotension, 92
360
paroxysmal, 347
Haemoptysis, 48, 17
Haemorrhage, cerebral, 296
subarachnoid, 297
Haemorrhages in the skin, 410
Hair, 412
Harrison's sulcus, 24
Harsh breathing, 34
Headache, 270, 207
Head retraction, 398
Heart-block, 85, 86, 99
Heart-burn, 132
Heart, congenital, 113, 123
enlargement, 110
failure, 108
murmurs, 115
sounds, 73
surface marking, 64
Heberden's nodes, 402
Hemianopia, 215, 216
Hemiplegia, 292
Hcpato-jugular reflex, 67
Hiccough, 17
H i g h blood pressure, 88
Hippocratic succussion, 36
Hoarseness of voice, 50, 17
Horner's syndrome, 239
Hutchinson's teeth, 133
Hyaline casts in urine, 327
Hydatid cyst, 194
Hydrocephalus, 395
Hvperchlorhydria, 153
Hvperglycaemia, 369
Hypertension, benign, 88
malignant, 88
Hypertensive encephalitis,
Hypochlorhydria, 153
Hypoglycaemia, 369
Hypoglossal nerve, 237
297
443
444
Murmurscontd.
pansystolic, 116
pulmonary, 121
systolic, 116, 119, 121
vascular, 124
Murphy's sign, 145
Muscular atrophy, 394
diseases, 394
dystrophies, 394
Myasthenia gravis, 395, 397
Mydriasis, 225
Myelitis, transverse, 299
Myelopathy, 394
Myocardial murmurs, 124
Myoclonic epilepsy, 270
Myopathy, 394
Myosis, 225
Myotonia atrophica, 287
congenita, 287
Myxoedema, 396, 433
Nails, examination, 412
clubbing, 412
koilonychia, 413
onychia, 413
N-compounds in blood, 369
Nephritis, 356
Nephrosclerosis, 356
Nephrosis, 356
Nerves, cranial, 212, 213, 214
peripheral, 312
sympathetic, 238
Neuralgic pains, 313, 208
Neuritis, 312
Optic, 218
peripheral, 313
Neuro muscular disorders, 394
Nodes, Aschoff's, 402
Heberden's, 402
Osier's, 402
Noises in the ear, 234, 210
Normoblasts, 377
Normocytic anaemias, 378
Nose, examination, 9
Numbness, 209
Nystagmus, 222
INDEX
Obstruction, bronchia), 54
intestinal, 192
laryngeal, 56
tracheal, 56
Ocular movements, 219
Oculo motor nerves, 219
Oedema, 102
Olfactory nerve, 214
Oliguria, 349, 316
Onychia, 413
Ophthalmoscopy, 217
Oppenheim's sign, 247
Optic atrophy, 218
nerve, 214
neuritis, 218
thalamus, 307
Organic reflexes, 255
Orthopnoca, 56, 16
Orthostatic albuminuria, 337
Osier's nodes, 402
Osteogenesis imperfecta, 395
Ovalocytosis, 377
Ovaries, 431
Ovarian cyst, 162
Oxalates in urine, 322
Oxaluria, 322
Oxycephalus, 396
445
Paralysiscontd.
Erb-Duchenne's, 394
pseudo-hypertrophic, 394
Paraplegia, 299
in children, 300
Parathyroid, 433
Paretic curve, 265
Parkinson's disease, 307
syndrome, 307
Paroxysmal haemoglobinuria, 347
tachycardia, 99
Patellar clonus, 252
Patent ductus arteriosus, 113
interventricular septum, 113
Pectorioloquy, 37
Periarteritis nodosa, 89
Pericarditis, 72
constrictive, 72
Perihepatitis, 164
Peroneal type of atrophy, 394
Peripheral circulatory failure, 110
neuritis, 312
Peritoneal fluid, 159
Peritonitis, 168, 172
Pernicious anaemia, 379
Peroneal muscular atrophy, 302, 394
Petechiae, 410
Petit Mai, 269
Phosphates in urine, 322
Phosphaturia, 322
Phosphorus in blood, 372
Pigmentation of skin, 409
Pigeon-breast, chest, 24
Pituitary gland, 430
tumours, 432
Plantar reflex, 246
Plasma proteins, 370
Platelets in blood, 388, 359
estimation, 363
Pleural effusion, 42
fluids, 41
Poikilocytosis, 361, 377
Poliomyelitis, 302
Polychromatophilia, 361, 377
Polycythaemia, 380
Polyneuritis, 312, 313
Polyserositis, 163
Polyuria. 348, 316
446
INDEX
Rigidity, abdomen, 168
neck, 398
Rinne's test, 232
Romberg's sign, 288
Rothera's test, 324
Salivary glands, 135
Saturation index, blood, 363
Schaefer's sign, 247
Sclerosis, amyotrophic lateral, 394
disseminated, 299
Sclerotic kidneys, 256
Scoliosis, 399
Scotoma, 215
Sedimentation rate, blood, 363
Sensations, tests for, 244
Sensory tracts, 305
Septal defects, auricular, 113
ventricular, 113
Shock, 101
Sickle-cells, 307
Sinus arrhythmia, 85
bradycardia, 99
tachycardia, 99
Skew deviation, 299
Skin, examination, 408
pigmentation, 409
Skodaic resonance, 32
Skull, abnormalities, 395
examination, 211
Sodium in blood, 371
Sore tongue, 129
Spasms, muscular, 209, 282
Speech defects, 277, 210
Spherocytes, 377
Spinal cord, 308
curvature, 399
lesions, 310
nerves, 312
tracts, 309
Spine, examination, 399
Spleen, 201, 146
Splenic enlargement, 201
Sprue, 187
Sputum, 37
Squint, 219
Steatorrheas, 186
447
448
Thirst, 130
Thrills, cardiac, 70
Thrombocytopaenia, 389
Thrombosis, cerebral, 296
coronary, 98
Thyroid, 433
Thyrotoxicosis, 396, 433
Tics, 282
Tic-tac rhythm, heart, 77
T i n g l i n g , 209
Tinnitus, 234, 210
T o n e , muscular, 242
T o n g u e , examination, 134
soreness, 129
ulcers, 135
T o n i c reflexes, 254
T o p h i , 402
Trachea, 20
Tracheal tug, 70
Tracts, ascending, 309
descending, 309
Transfusion of blood, 373
Transverse myelitis, 310, 299
Traube's space, 31
Tremors, 282, 209
Triceps jerk, 249
Trident hand, 482
Trigeminal nerve, 227
T r i p l e rhythm, 76
T u b u l a r breathing, 34
T u m o u r s of abdomen, 166
Tympanitis, 162
Ulcers, duodenal, 157
gastric, 157
skin, 410
tongue, 135
Unconsciousness, 274, 209
Uraemia, 351
263
Ziehl-Neelsen's stain, 40
MBBS
V.
(BOMBAY):
D.
(OBST)
CHAPHEKAR
DGO
(DUBLIN):
R.C.O.G.
LM
(ROTUNDA):
(LONDON)
ESSENTIALS OF H U M A N EMBRYOLOGY
By
B I I A T N A G A R AND
KOTHARI
*
*
CORONARY H E A R T DISEASE
Epidemiology and Prevention
By
N.
P.
SAHETA
RONALD
BODLEY
Physician to H . M .
The
SCOTT
Queen