How To Examine A Patient

A POCKET GUIDE
TO
STUDENTS OF MEDICINE
KOTHARI BOOK DEPOT
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
Printed by V. D. Limaye at the India Printing Works, 9 Bakehouse

Lane, Fort, Bombay, and published by Mohanlal B. Kothari,
Kothari Book Depot, Acharya Donde Jilarg, Parel, Bombay 12.
PREFACE TO THE SECOND EDITION

The text has again undergone a thorough revision with
greater emphasis on How to Examine a Patient and to elicit
the necessary information from the Patient so as to arrive at a
correct clinical diagnosis.
The zeal of a Modern Physician to indulge in the aid of
electro-medical gadgets might discourage a young student to
sacrifice sufficient time to elicit signs and symptoms under the
mistaken impression that the ultimate diagnosis of some diseases
rests on mechanical gadgets. This pitfall must be avoided by
one who wishes to be a successful clinician.
Bearing this in mind this book has been revised fully. Some readjustment in the matter that has no bearing on the Examination
of a Patient has been deleted and new chapters on Locomotor
System and Skin and its Appendages have been added. The
size of the book, on the whole, has been reduced in- size so as
to enable the student to make it a bedside companion during
his clinical studies.
March 1970.
M . DE SOUZA

This book was written for the specific needs of a student who
launches his clinical career with no experience to support him.
I am happy to note that it has found favour with him and hope
that the present format will increase its usefulness.
The main change in this edition has been the rewriting of
the old chapters and adding new ones on Blood, Genito-Urinary
System, etc., with emphasis on Methods of Examination.
History taking is an art which must be acquired by experience.
No detail is unimportant, and the correct diagnosis often rests
upon a careful balancing of probabilities. A first class history
is a necessary prelude to an accurate diagnosis. In fact, a wellelaborated anamnesis practically establishes the diagnosis in
several cases. The converse is also truea history taken
hurriedly and aimlessly without any data or properly obtained
facts, is not only valueless, but often highly misleading.
Time spent in questioning the patient intelligently is never
lost, but the type of questions to ask needs experience. This is
best acquired by constant clinical examination, for which reading this book is only an accessory and not a substitute. Some
are endowed with a gift of extracting concise and accurate
history from a patient. Such students learn more readily than
others, but the gift can certainly be acquired by anyone who
possesses the necessary will to learn. This book is mainly
intended for those who are not gifted with this art and the
author hopes it will help them in their careers both as students
and after.
M . DE SOUZA

The title How TO EXAMINE A PATIENT probablv describes the
scope of this little book better than any other. The importance
of Methodical Examination of a Patient cannot be overestimated. It forms the ground-work of thorough study in all
Medical Subjects. This book aims at providing a synopsis of
the Method of Examining a Patient and to teach the student
how to obtain an accurate history of the illness and what he
should look for to arrive at a diagnosis in a logical manner.
I have endeavoured to include these points in a small space,
and hence, it is not at all my intention to replace similar books
dealing in greater details.
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
Dyspnoea 62; Praecordial Pain 62; Palpitation 63;
Syncope 63; Giddiness 63; Venous Congestion 63.
Surface Marking of the Heart
Examination of the Heart
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.
Examination of the Mouth and Throat

Mouth 132; Lips 133; Teeth 133; Gums 133; Tongue
134; Palate 135; Breath 135.
Anatomical Landmarks of the Abdomen
Examination of the Abdomen
Mensuration 143; Auscultation 143.
Examination of the Abdominal Viscera
Stomach 144; Liver 144; Gall-bladder 145; Spleen 146;
Kidneys 146.
Rectal Examination
Examination of Faeces
Examination of Gastric Juice
Gastric Acidity
Hyperchlorhydria 153; Hypochlorhydria 153;
Achlorhydria 154.
Examination of the Peritoneal Fluid
Abdominal Swelling
Ascites 161; Tumours 166.
Abdominal Rigidity
Abdominal Pain
Colicky Pain 172; Pain in Children 173.
Common Digestive Disturbances
Dysphagia 175; Vomiting 178; Haematemesis 180;
Constipation 182; Diarrhoea 184; Steatorrhoea 186;
Blood in Stool 188; Melaena 191.
Intestinal Obstruction .
Acute Obstruction 192; Chronic Obstruction 192.
Liver
Enlargement 193; Jaundice 195.
Gallbladder
Spleen
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
ness 209; Tremors 209; Unconsciousness 209; Diplopia

209; Tinnitus 210; Speech Defects 210; Ataxia 210.
Examination of the Nervous System
Intellectual Functions 210; Skull and Spine 211; Cranial
Nerves 214; Motor System 239; Sensory System 244;
Reflexes 246.
Anatomy of the Central Nervous System
Cerebral Circulation
Cerebro-Spinal Fluid
Common Neurological Disorders
Convulsions 265; Epilepsy 268; Headache 270; Coma 274;
Speech Defects 277; Tremors 282; Gaits 284; Ataxia 288.
Motor Tracts and their lesions
Monoplegia 290; Hemiplegia 292; Paraplegia 299.
Sensory Tracts and their Lesions
Extra-Pyramidal SystemBasal Ganglia Lesions . . . .
Cerebellum and its Disorders
Spinal Cord and its Lesions
Spinal Nerves and their Lesions
210
256
257
259
265
289
304
307
308
308
312
CHAPTER V I
GENITO-URINARY
SYSTEM
General Scheme
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
Albuminuria 335; Anuria 337; Dysuria 339; Frequency

of Micturition 339; Glycosuria 340; Haematuria 344;
Haemoglobinuria 347; Polyuria 348; Oliguria 349;
Melanuria 349; Pyuria 350; Uraemia 351.
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
Appendix A: Vitamins and their Deficiencies

Appendix B:
428
Endocrine Glands and their Dysfunctions 430
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.
VI. FAMILY HISTORY.

VII. GENERAL EXAMINATION.
VIII. EXAMINATION OF T H E VARIOUS SYSTEMS.
IX. LABORATORY INVESTIGATIONS.
X. SPECIAL INVESTIGATIONS:Fluoroscopy,
X-rays, E.C.G., etc.
XI. DIAGNOSTIC IMPRESSION.
XII. SUGGESTED F U R T H E R STUDY.
XIII. PROGRESS OF T H E PATIENT.
HOW TO EXAMINE A PATIENT
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
1. Briefly list presenting complaints and their duration.

2. Let the patient express the symptoms in his own words.
3. Do not ask leading questions, unless necessary.
4. Avoid negative answers, unless deemed relevant.
HISTORY
OF T H E PRESENT
ILLNESS
Give chronological story of the illness, beginning with the

exact date of onset, with special reference to the presenting
symptom, i.e. the symptom which troubles the patient more than
any other. Also determine when the patient was last well, when
he left work and when he took to bed.
Inquire into the symptoms with special reference to:
1. Their mode of onsetwhether gradual, sudden or in
series of attacks; their order of appearance; the exact
location; their course, duration and progress; their aftereffects, such as weakness, loss of weight, vomiting, loss of
appetite, nervousness, prostration, etc. Intervals of freedom, if any.
When indicated, define the symptoms in terms of
severity, radiation, continuity, etc.
2. Predisposing factorsoverwork, overplay,
miscarriage, child-birth, general illness, etc.
quality,
dissipation,
CASE
TAKING
3. Factors modifying the symptomsfood, deep breathing,

posture, exercise, change of weather, etc.
4. Associated symptoms such as pains in the body, jaundice,
fits, coma, etc.
5. Treatment the patient may have takenif so, in what
form and its effects.
6. Supposed cause according to the patient.
PREVIOUS DISEASES
Inquire into the following, with their time of occurrence,
duration and results:
1. Similar attacks previously with dates and results of treatment.
2. Diseases of childhood, especially eruptive fevers, intestinal
disorders, lung diseases, etc.
3. Important illnesses like prolonged fevers, pains, epistaxis,
haemoptysis, haematemesis, cough, venereal diseases,
infectious fevers, lung diseases, jaundice, joint swellings,
abdominal diseases, marked change in weight, diabetes,
nephritis, etc.
4. Accidents and injuries, with details and disabilities
incurred.
5. Operations with dates and results.
6. In women:
(a)
(b)
(c)
(d)
Menstrual history.
Miscarriages and still-births.
Difficulty during delivery.
Abnormality of the child or foetus.
If the diagnosis of the previous diseases is not clear, describe

them in terms of symptoms, signs and duration of the illness.
PERSONAL HISTORY
1. Marital history: Duration. Age and health of consort
and children, if living, or age and cause, if dead. Former
marriages. Degree of compatibility.
2. Occupation: Nature of work and its surroundings. If

agreeable to the patient. Previous occupations. Business
affairs.
3. Environment: Conditions at home and its surroundings.
Localities where he lived before. Domestic life. Sources
of worry.
4. Social history: Education.
of dependants.
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.
If disturbed, its cause.
(f) Bowels and micturition; their frequency during day

and night.
FAMILY
HISTORY
1. Of parents, brothers, sisters and childrentheir state of

health; if ill, the nature of ailment; if deceased, the cause
of death and age at death.
2. In hereditary and familial diseasesespecially diabetes,
cardio-vascular diseases, renal disorders, migraine, haemophilia, nervous and mental diseasesinquire into details
in more generations in the same family and of consanguinity in marriage.
GENERAL
I.
EXAMINATION
CONSCIOUSNESS AND INTELLIGENCE
Note the degree of co-operation; promptness or delay in

answering questions; appearance of apathy, lethargy or fatigue.
CASE
TAKING
Many nervous patients, particularly those suffering from Grave's disease,

are unusually alert. Psychoneurotic patients are emotionally unstable. A
depressed patient takes long to answer questions. A patient suffering from
myxoedema is dull and apathetic. A melancholic reveals lack of interest
during examination. A hysterical patient is over-enthusiastic in answering
questions.
II.
DECUBITUS
The posture a patient adopts, especially when lying in bed,

often gives a valuable diagnostic clue. He prefers to adopt an
attitude which he feels is most comfortable.
Patients suffering from severe pain
obtain relief.
often assume
unusual
attitude
to
In pleural effusion and pneumonia, patients prefer to lie o n the same

side as the lesion in order to provide free expansion to the normal lung.
In early pleurisy, however, when the pain is severe, they prefer to lie on
the same side as the lesion in order to restrict the movements which are the
cause of pain.
Patients, with a cavity in the lung prefer to lie on the diseased side in
order to avoid constant or distressing cough.
W h e n acutely ill, patients passively lie in supine posture without
effort being made to change the position.
any
In severe respiratory or cardiac embarrassment the patient finds some

relief in orthopnoeic position. So also a patient prefers to sit up in
conditions like ascites that raise the intra-abdominal pressure.
In pericardial effusion, the patient finds comfort when leaning his body
forward.
In acute abdominal diseases, the patient lies on his back with one or both
legs drawn up according as the inflammation is limited to one side or is
more general. In colics and in coronary disease, the patient is very restless.
In acute intestinal colic, the patient prefers to lie o n his stomach with a
pillow underneath.
In meningitis and tetanus, there is marked stiffness of the neck and often
opisthotonus.
In acute arthritis the affected limbs lie in a helpless position.
In hemiplegia, the movements of the limbs are limited on the affected
side. In paraplegia, the lower limbs are immobile.
III.
VOICE AND SPEECH
T h e character of the voice is often

diagnosis of a case. In infantilism,
in virilism, it has the tone of an adult
the voice may have a brassy quality.
helpful in arriving at the

the voice is high-pitched;
male. In aortic aneurysm,
In laryngeal diseases, the
voice is husky and in laryngeal paralysis, it is feeble. (For

disturbances of speech see under Central Nervous System.)
IV.
GENERAL DEVELOPMENT AND N U T R I T I O N
Under this heading the following are to be considered:

1. General Appearance.
2.
Body Configuration.
3.
Height and Weight.
4.
Examination of the Head, Neck and Face.

(a)
(b)
(c)
(d)
(e)
(f)
(g)
Configuration of the Skull and Face.

Facial Expression.
Examination of the Eyes.
Colour of the Face.
Examination of the Lips.
Examination of the Nose.
Examination of the Ears.
5.
Examination of the Skin, Hair and Nails.
6.
Examination of the Lymph Glands.
7.
Examination of the Genitalia and Breasts.
8.
Examination of Joints and Extremities.

1. General Appearance
Note the posture and attitude of the patient, especially the

poise of the head, the slant of the shoulders, the inclination of
the trunk to the pelvis, the position of the arms and hands, the
appearance of the lower limbs, the gait (see under Central
Nervous System) and the mode of dress.
2. Body Configuration
In general, a patient may be grouped under any of the following groups according to his body configuration:
A S T H E N I C T Y P E : T a l l with long neck and flat chest, protuberant
lower abdomen, hands slender and fingers long. Such people are neurotics.
S T H E N I C T Y P E : S h o r t , broad, with thick neck,
s t u m p y fingers. Such patients are often hyperpietics.
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-
3. Height and Weight

Relevant details may be necessary when there is rapid loss or
increase in weight in a patient.
If the patient is obese, inquire into the
(a)
(b)
(c)
(d)
(e)
(f)
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.
If the patient is under-nourished, find out if it is

(a)
(b)
(c)
(d)
Rapid or gradual in onset.

Continuous or interrupted by gain in weight.
If accompanied or preceded by illness.
Average weight previously.
If the stature of a patient is far above or below limits, he may be classified

as a giant or a dwarf. Endocrinc dysfunctions appear to produce the greatest
changes in the height and weight of a patient. Deficiency of testicular or
pituitary secretions in a male causes feminine characteristics with deposition
of fat at the breasts and around the hips, with scanty hair o n the face.
In suprarenal cortical overactivity in females, the body contour is masculine
in appearance associated with hirsutism. In some pituitary dysfunctions,
there is generalised obesity with genital atrophy; in overfunction, the patient
is over-developed and resembles a giant.
4. Examination of Head, Neck and Face

Specially note the configuration and abnormalities of the
skull. Examine the scalp for texture of the hair, alopecia and
scars; neck for glands, scars, thyroid, rigidity, torticollis, etc.
Press over the sinuses to elicit tenderness.
While examining the face the following parts must be carefully examined:
(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.
PUFFYrenal disease, anaemia, myxoedema.

(c) EXAMINATION
OF THE
EYES
Examination of the eyes also includes examination of the

cornea, sclera, conjunctiva, eye-lids, eye-lashes and eye-balls.
Carefully examine them for the following abnormalities:
EYE-LIDSfor puffiness ( n e p h r i t i s , anaemia,
whooping
cough); ptosis (paralysis of the 3rd
(stimulation
of the sympathetic
nerve).
angioneurotic
cranial nerve);
oedema,
retraction
EYE-BROWSif fallen or scantythyroid disorders.

FISSURESslanting in mongolism.
SCLERAyellow in jaundice, red in haemorrhages.
C O N J U N C T I V A E p a l e in anaemia; red in conjunctivitis, high blood
pressure, fracture of the skull, cerebral haemorrhage, sub-acute bacterial
endocarditis.
C O R N E A for scars, ulceration, arcus senilis, etc.
EYE-BALLS for tensionincreased
in glaucoma, diminished in diabetic
coma. If prominent,
suspect thyrotoxicosis, orbital tumours, thrombosis
of the lateral sinus. If there is enophthalmos,
suspect sympathetic nerve
paralysis and severe dehydration.
' VISION, PUPILS, D E V I A T I O N , E T C . E x a m i n e under Central
Nervous
System.
CASE
(d) COLOUR
OF THE
TAKING
FACE
T h e complexion of a patient is mainly dependent upon the

colour of the cheeks. These may take up any of the following
abnormal forms:
PALEanaemia, aortic regurgitation
(pallor).
FLUSHEDhectic fever, mitral stenosis.

CYANOSEDcongestive cardiac failure, congenital heart.
YELLOWjaundice.
L E M O N YELLOWpernicious anaemia.
MUDDYdyspepsia.
WAXYchronic parenchymatous nephritis.
P L E T H O R I C h i g h blood pressure, polycythaemia.
PIGMENTEDAddison's disease, cancer stomach, etc.
DEPIGMENTEDalbinism,
TELANGIECTASESchronic
(e) EXAMINATION
OF THE
leucoderma.
alcoholism, cirrhosis liver.
LIPS
The appearance of the lips may be of some importance to

judge the general condition of the patient. Look for:
(a) COLOURpale in anaemia, cyanosed in heart failure apd congenital
heart diseases, dusky-red in polycythaemia.
(b) SIZEthick in myxoedema and acromegaly, thin and pendulous in
myopathies, swollen in acute nephritis and angioneurotic oedema.
(c) DEFORMITIEShare-lip,
(d) HERPESmalaria,
etc.
pneumonia,
meningitis, virus
infections.
(e) DRYtoxaemia, h i g h fever.

(f) STRIATIONSriboflavin deficiency, syphilis.
(g) ULCERSsyphilis, epithelioma, nutritional disorders.
(h) PIGMENTEDAddison's disease, cancer stomach, etc.
(i) DEPIGMENTEDleucoplakia,
syphilis.
(j) FISSUREDangular cheilitis, riboflavin deficiency.

() EXAMINATION
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
and myxoedema; large and
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
Carefully examine the ears including the meatus and the

mastoid for the following:
SIZElarge in mongolism.
SHAPEill-developed in lunatics and sometimes in epilepsy.
C O L O U R b l u i s h in ochronosis.
T E X T U R E c o a r s e in cretinism and myxoedema.
PRESENCE OF T O P H I g o u t .
D I S C H A R G E FROM T H E MEATUSotitis media.
T E N D E R N E S S OVER T H E
(h) EXAMINATION
OF THE
MASTOIDmastoiditis.
MUCOUS
MEMBRANES
Examine the following:

(a) CONJUNCTIVAEyellow in jaundice, pale in anaemia, congested in
conjunctivitis.
(b) LIPSpale in anaemia, blue in cyanosis.
(c) T O N G U E f o r colour, evidence of glossitis, ulcers and fissures.
Chap. IV.)
(d) PALATEespecially
for perforation as occurs in
(e) GUMSfor bleeding,

poisoning, etc.
retraction,
pigmentation,
(See
syphilis.
blue
line
of
lead
5. Examination of the Skin, Hair and Nails

(see Chapter IX)
6. Lymph Glands
Note their site, shape, size, consistency, mobility and tenderness. Look for them especially in the neck, axilla, supratrochlear and inguinal regions. (See Chapter VII.)
7. Genitalia and Breasts
These must be examined in every patient where there is suspicion of endocrine dysfunction. Note the following:
CASE
TAKING
11
(a) Their development.

(b) Pubic and axillary hair.
(c) Voice.
(d) Look for discharge, ulcers, scars, tumours, etc.
8. Joints and Extremities
(see Chapter VIII)
V. PULSE, RESPIRATION, TEMPERATURE
Always end the General Examination of the patient by noting down the Pulse, Respiration and Temperature.
A
For pulse, see under Cardio Vascular System.

Since breathing is the most important function of the chest,
observations regarding its depth, type and comparison on the
two sides is best noted while examining the Respiratory System.
For practical purposes the rate is taken during the General
Examination by noting the movements of the chest for full one
minute.
Temperature
Temperature in a patient is best recorded with a mercurial
thermometer which should be kept in position for about a
minute.
T h e usual procedure to record temperature is in the axilla,
but in a patient who is perspiring profusely, it is advisable to
take it by mouth. In rare cases, rectal temperature may have to
be recorded, especially in cholera where the skin temperature is
subnormal and rectal temperature is high.
Normal temperature is 36.5 to 37.2C or 97.5 to 98.5F.
Subnormal is below 36C or 97F.
Febrile means above 37C or 99F.
Hyperpyrexia means 41.5C or 106F.
Hypothermia means below 35C or 95F.
12
If a patient is febrile, inquire into the following:

1. Day of onset of fever.
2.
Mode of onsetwhether sudden or insidious.
3.
If associated with rigors, vomiting, headache, coryza,

body-ache, diarrhoea, etc.
4.
If continuous, remittent, intermittent or periodic.
5.
Whether it comes down by crisis or lysis.
6. Whether the patient is drowsy, delirious or comatose.

7.
If the patient perspires when the fever falls.
The common types of fevers may be grouped under the following headings:
A.
CONTINUOUSthe fever does not fluctuate more than about a

degree in 24 hours. Common example is lobar pneumonia.
B.
REMITTENTthe daily fluctuations in the temperature exceed a

degree or two, but does not touch normal. Typhoid fever is typically
remittent in type.
C.
INTERMITTENTthe fever touches normal for some hours during

the day. When the intermittence occurs daily, the type is quotidian;
when on alternate days, tertian; when two days intervene between
the attacks, the fever is known as quartan.
All these three types are
typically seen in malaria.
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
Intermittent Fever. Case of Malaria.
1.8
FIG. IV
Fever dropping by Lysis. Case o Broncho-Pneumonia.
By the time the History and General Examination of

the patient has been carefully gone into, the examiner
will be in a position to judge which system in the body
is mainly affected. Examine this System first and then
proceed to examine the other Systems.
Systems in which there are no revealing features of
involvement need not be described in detail.
CHAPTER
RESPIRATORY
II
SYSTEM
A.
INTERROGATION.
B.
COMMON SYMPTOMS AND SIGNS.
C.
EXAMINATION OF T H E UPPER AIR PASSAGES.
D.
EXAMINATION OF T H E CHEST.
I.
Inspection.
II.
Palpation.
III.
Percussion.
IV.
Auscultation.
E.
EXAMINATION OF SPUTUM.
F.
EXAMINATION OF PLEURAL FLUIDS.
1.8
H O W TO EXAMINE A PATIENT
A.
INTERROGATION
Particularly inquire into the family history of bronchitis,

asthma, tuberculosis and pleurisy. Also the previous history of
lung and pleural diseases, haemoptysis, glands in the neck, loss
of weight, etc. Occupation of the patient must be inquired
into to exclude industrial diseases.
In General Examination, particularly note the decubitus, the
condition of the eyes, the state and colour of the skin and lips,
the presence of emaciation and asthenia.
B.
COMMON
SYMPTOMS AND
SIGNS
COUGH (see page 43).

Inquire into the following:
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
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.
DYSPNOEA; ORTHOPNOEA (see page 53).

1. Its descriptionif paroxysmal or coming on effort.
2. Mode of onsetif sudden or gradual.
3. Exciting or aggravating factorsworry, anger, excitement, exercise.
4. Associated symptomscough, palpitation, pain, sweating,
collapse.
5. Evidence of any cardiac or respiratory diseases.
RESPIRATORY
SYSTEM
17
PAIN IN T H E CHEST (see page 45}.

Describe in detail:
1. Its positionwhether localised or spreading.
2. Its characterstitching, stabbing, etc.
3. Its durationif constant or intermittent.
4.
Its relation to breathing, coughing, sneezing, posture,

movements.
5.
Relieving and aggravating factors.
HAEMOPTYSIS (see page 48).

1. If preceded or accompanied by cough.
2.
Colour.
3. Amount on first occasion and subsequently.

4.
If mixed with froth and sputum.
5.
Symptoms of lung or heart diseases.
HOARSENESS OF VOICE (see page 50).

Inquire as to the following:
1.
Duration.
2.
If associated with sore throat.
3.
If progressive or improving.
4.
History of tuberculosis.
5.
Habits of smoking.
6.
Occupation.
HICCOUGH
1. History of gastric disturbanceseructation,
abdominal discomfort, etc.
2.
2
vomiting,
Chest disturbancessubsternal pain, praecordial pain or

discomfort.
1.8
3.
Nervous disturbancesneurosis, hysteria, emotion, meningitis, encephalitis, hydrocephalus, etc.
4.
Renal disorderschronic nephritis, uraemia.
COMMON SIGNS
1. Cyanosis. Examine the lips, cheeks, ears, nose and nails
particularly (see page 51).
2.
Clubbing of the fingers (see Chapter IX).
3.
Glands in the neck (see Chapter VII).
4.
Engorged veins, especially in the neck and chest.
5.
Oedema (see page 102).

SURFACE
MARKINGS
OF T H E
LUNGS
Before starting the examination of the Respiratory System it is necessary

to have some idea of the surface markings of the lungs and other important
structures.
T h e trachea, which begins at the level of the cricoid cartilage, bifurcates
at Ludwig's anglea prominence at the junction of manubrium and the
body of the sternum. T h e bifurcation corresponds with the level of the
2nd rib in front and the 4th D.V. behind.
T h e apices are situated about an inch above the clavicles corresponding
with the neck of the 1st rib in front and 7th cervical spine behind, the
right apex being a little higher than the left. From this point, the inner
margins of the lungs slant towards the sternum meeting each other in the
m i d d l e line at the angle of Louis. On the right side the margin of the
lung continues down as far as the 6th costal cartilage where it turns outwards to meet the mid-clavicular line at the 6th rib, the mid-axillary line
at the 8th rib, the scapular line at the 10th rib and the paravertebral line
at the spine of the 10th dorsal vertebra. On the left side the landmarks are
the same, with the exception that the lung border turns away from the
sternum at the 4th costal cartilage and then arches outwards and downwards
to reach the 6th rib, a little outside the parasternal line.
- At the apices and along the inner margins of the lungs the
so close to the lungs so as to follow the same surface markings,
lower border of the lungs the pleura extends further, lying 4
below the lung borders anteriorly and posteriorly, and over 6
in the axilla.
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.
Three central regions anteriorly.

1.
Suprasternalfrom cricoid to superior border of the manubrium.
2.
3.
Superior sternalfrom manubrium to Srd sterno-costal junction.

Inferior sternalfrom 3rd sterno-costal junction to the end of
sternum.
Five antero-Iateral regions.

1.
Supraclaviculararea above the clavicle.
2.
Clavicularover the clavicle.
3.
Infraclaviculararea below the clavicle up to the ,?rd sternocostal

junction.
4.
Mammarybounded by the 3rd sterno-costal junction above and

the 6th sterno-costal junction below.
5.
Inframammarybelow the 6th rib to the costal arch.
1.8
III.
IV.
T w o Iaternal regions.
1.
Axillary
2.
Infra-axillary
}
)
meet each other at 6th rib.
Four regions in the back.

1.
Suprascapularabove the scapulae.
2.
Scapularoverlying the scapulae.

(a) Supraspinousabove the scapular spine.
(b) Infraspinousbelow the scapular spine.
3.
Infrascapularbelow the scapulae.
4.
Interscapular, left and rightbetween the scapulae and the spine.
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.
C. EXAMINATION OF T H E AIR PASSAGES

1. NOSE. Look for the movements of the ala nasae.
Examine the nostrils for rhinitis, polypi, septal defects,
epistaxis and presence of foreign bodies. Examine the
sinuses for tenderness by pressing gently over them.
2.
3.
NECK. Look for enlarged glands, scars, oedema, venous

engorgement. Examine the thyroid gland.
LARYNX. Examine the vocal cords and look for evidence of inflammation, ulcers, etc. Use spatula and do
laryngoscopic examination whenever indicated.
4.
EXAMINE T H E TENDONS OF STERNOMASTOIDS.

In mediastinal shift the tendon is often prominent on the
side of the shift.
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
the mediastinum has been altered by diseases of the

pleura, such as effusion and pneumothorax pushing
the mediastinum away from the affected side, or of
the lungs, such as fibrosis or collapse drawing it towards the affected side.
(b) Tracheal tug. Extend the neck of the patient and
pull the larynx gently upwards. When there is an
aneurysmal dilatation, the pulsation of the aorta will
be distinctly felt transmitted at each systole of the
heart.
D.
EXAMINATION OF T H E CHEST
I.
INSPECTION
This reveals the configuration of the chest, the degree of

movements on the two sides, the type and rate of respirations.
Examine the front, back and sides of the chest by standing by
the side of the patient and, if necessary, from the foot of the
bed. T h e back is best examined by letting the patient sit up,
if possible. Special attention should be paid to the lower intercostal spaces; for, normally, the soft tissues are sucked in slightly
during inspiration though the ribs themselves become more
widely separated. This sucking in is diminished or abolished
in effusion and pneumothorax; whereas it is exaggerated in
fibrosis of the lungs and very much so in pulmonary collapse due
to bronchial obstruction.
Note the following during breathing:
1. Rate of Respiration.
2. Type of Breathing.
3. .Rhythm.
4. Form of Chest.
5. Movements of Chest.
6. Presence of Veins.
1.8

1.
R A T E OF R E S P I R A T I O N
T h e normal rate in an adult is 16-20 respirations per minute.

It bears a definite ratio to the pulse rate of about 1 to 4. An
increase in the rate of breathing is called tachypnoea and slowing is known as bradypnoea.
1.
Increased rate occurs in:

Exertion.
Nervous excitement.
Feversin pneumonia the rate may even be as high as
the pulse.
Anoxaemiacardiac, pulmonary, bronchial, laryngeal.
Alteration in the oxygen-carrying power of the blood
anaemias, poisoning, diabetes mellitus, chronic nephritis.
Pain while breathingpleurisy, peritonitis.
2.
Slowing of breathing occurs in:

Brain tumours.
Obstruction to the bronchi.
Narcotic drugsin opium poisoning the respiratory rate
may be as low as 5 to 6 per minute.
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.
Thoracic breathing occurs in paralysis of the diaphragm,

peritonitis and severe ascites.
2.
Abdominal breathing occurs in pleurisy,

and lung collapse.
3.
pleurodynia
RHYTHM
T h e normal breathing is rhythmical, with inspiration longer

than expiration. Changes in the rhythm may occur as follows:
P R O L O N G E D INSPIRATIONlaryngeal or tracheal obstruction especially laryngeal diphtheria in children and mediastinal growths in older
individuals.
RESPIRATORY
SYSTEM
PROLONGED EXPIRATIONbronchial
and renal asthma.
23
or pulmonary diseases, cardiac
DYSPNOEAlaboured breathing as occurs in congestive cardiac failure

and several other conditions. (See page 53.)
O R T H O P N O E A e x a g g e r a t e d form of dyspnoea, where the patient
it difficult to lie in bed.
finds
KUSSMAUL'S B R E A T H I N G t h i s occurs in ketosis, especially in diabetes

mellitus. T h e breathing is deep and perhaps a little more rapid
(air-hunger).
S T E R T O R O U S B R E A T H I N G o c c u r s in apoplexy.
HISSING E X P I R A T I O N m a y be present in uraemia.
CHEYNE-STOKE'S B R E A T H I N G t h i s consists of rhythmical waxing
and waning of respirationsalternations of hyperpnoea and apnoea. Anything that causes anoxaemia of the respiratory centre results in CheyneStoke's breathing; anoxaemia lowers its sensitivity and so abolishes
spontaneous rhythmical activity of breathing. T h e consequent apnoea
results in the accumulation of C 0 2 in the body, thereby reawakening the
centre and causing hyperventilation, which in turn removes the excess of
C 0 2 , whereupon the centre "goes to sleep again".
Causes of Cheyne-Stoke's breathing

(a) Left ventricular failure.
Essential hypertension.
Hypertension due to renal diseases.
Phaeochromocytoma.
Coronary
disease.
Vascular diseasesaortic regurgitation, patent ductus, coarctation of

the aorta.
(b) Lesions of the braincause increase in the intracranial pressure.
Meningitis.
Cerebral abscess.
Tumours.
Cerebral haemorrhage.
Cerebro-medullary degeneration. In such cases, Cheyne-Stoke's breathing is the main symptom sometimes.
(c) Poisons and toxins.
Opium, barbiturates, sulphonal,
chloral.
Uraemia.
4.
FORM OF C H E S T
A healthy chest is bilaterally symmetrical. Its contours are

smooth; it has no hollows and at most shows a slight recession
below the clavicles. It is ellipsoidal in shape with the longer
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
(a) Alar chest. There is protrusion of the vertebral borders of the

scapulae, drooping of the shoulders, long thorax, long neck and
very acute epigastric angle.
(b) Flat chest. Ribs are placed very obliquely, the subcostal angle
is very acute, the antero-posterior diameter shorter.
Generally
associated with "alar-chest".
2. Indicating past diseases

(a) Rachitic chest. T h e r e is depression on either side of the sternum;
in children, often associated with "rickety rosary"bead-like
enlargement at the costochondral junction. Result of old rickets.
(b) Pigeon breast.
Sternum unduly prominent; cross section
triangular. Result of obstruction to the upper air passages
childhood. Generally associated with rickets.
is
in
FIG. V I
Cross Section of
Rachitic Chest
Cross Section of
Pigeon Breast
(c) Harrison's sulcus. T h i s is a transverse groove passing outwards

from xiphisternum as far as mid-axillary line sometimes, occurring
along the line of diaphragmatic attachment.
Often associated
with a "pigeon breast" or rachitic chest.
(d) Funnel .chest. A depression found in the lower part of the
sternum. May b e congenital, as a result of rickets in childhood,
or an occupational deformity as found in cobblers.
(e) Kyphosis. Commonest cause of chest deformity, not due to
diseases of thoracic viscera, is kyphosisforward curvature of the
spine with dorsal prominence.
RESPIRATORY
SYSTEM 39
3. Indicating present disease

(a) Barrel-shaped chest. Ribs less oblique; Louis's angle very prominent; subcostal angle wider; anteroposterior diameter increased.
Occurs in emphysema.
(b) Distorted or phthisical chest. Wasting of interspaces; ribs unduly
prominent. Occurs in fibrosis of the lungs, generally tubercular.
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
(c) Scoliosis. T h e commonest cause of unilateral chest deformity, not

due to diseases of the thoracic viscera, is scoliosislateral curvature of the spine.
5.
M O V E M E N T S OF T H E
CHEST
1. Note carefully for deficiency of movements, bulging or

indrawing of the interspaces.
Ordinarily the chest moves uniformly on either side; hence,
while examining, note carefully whether there is equality of
expansion on the two sides. Note if there is any deficiency of
movements, bulging or indrawing of the interspaces. Note if
the accessory muscles are working. When dyspnoea is present
the accessory muscles are called into play, and hence, one should
carefully observe the movements of the alae nasi and of sternomastoids.
COMMON
ABNORMAL
MOVEMENTS
OF THE
CHEST
Causes of unilateral defective movements

(a) Obstruction to a main bronchus by a foreign body or new growths
there is often indrawing of the intercostal interspaces on the affected
side during inspiration.
(b) Consolidation
growths.
of
the
lungs
by
pneumonia,
tuberculosis
or
new
(c) Fibrosis of the lungs and pleural adhesions. In early tuberculosis

the apex on the affected side may show a characteristic lagging.
(d) Air and fluid in the pleural cavity.
(e) Massive collapse.
1.8
Causes of bilateral restricted expansion of the chest

(a) Emphysemain severe cases there may be bulging over the apices
during inspiration.
(b) Fibrosis of both the lungs.
(c) Bilateral
consolidation.
(d) Bilateral pleural effusion o r pneumothorax.
2. Note if the accessory muscles are working. This occurs in

all conditions that cause embarrassment to respiration. Typically
present in lobar pneumonia.
3.
Note the depth of the lung movements.
These may alter as follows:

S T E R T O R O U S BREATHINGparalysis of the soft palate.
apoplexy and coma.
Occurs in
STRIDORhissing sound occurring in paralysis of the vocal cords or

obstruction in the upper air passages.
WHEEZINGobstruction in bronchi as occurs in bronchial asthma.
HISSINGuraemia.
A I R H U N G E R d i a b e t i c coma.
R A T T L I N G o e d e m a of the lungs.
4. Look for Litten's diaphragmatic sign by standing at the

foot of the bed. T h e patient has to lie in bed which is placed
towards a well lighted window. T h e phenomenon takes the
form of a wave motion which begins on both sides at approximately the height of the sixth intercostal space, travels downwards and forwards with maximum inspiration over several
intercostal spaces. It is best seen in thin subjects. It is due to
a pull on the chest-wall by the diaphragm when it descends during inspiration. T h e movements of the diaphragm are diminished or absent i.e. Litten's sign is absent in pleural effusion,
pneumothorax, pneumonia, subdiaphragmatic abscess, lesions of
the phrenic nerves, or pleural adhesions.
6.
PRESENCE OF VEINS
Normally the veins in the chest are hardly visible. If present

in young adults, suspect early tuberculosis (varicose zone of
alarm); if present in elderly people, suspect lung growth or
mediastinal tumours.
RESPIRATORY
II.
SYSTEM
27
PALPATION
This confirms the impressions of inspection, especially the

movements of the chest and abnormal appearance of the chest
wall.
While palpating, look for the following:
1.
Apex-beat.
2.
Tenderness.
3. Fluctuation.
4. Form of the Chest.
5.
Movements of the Chest.
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
Press gently where the patient complains of pain, or where

there is a swelling. Watch the expression of the patient so as
to avoid unnecessary pain.
Tenderness may be due to local injury, myositis, hepatitis,
pleural diseases, heart diseases, etc.
3.
FLUCTUATION
This may be present when there is an abscess in the chest wall

or in empyema necessitatis.
4.
FORM
OF T H E
CHEST
(a) Confirm the findings of inspection.

(b) Feel for subcutaneous emphysema.
characteristic spongy feeling.
If present, it has a
1.8

5.
M O V E M E N T S OF CHEST
(a) Measure the chest at full inspiration and expiration just

below the nipples. There should be a difference of at
least two inches normally.
(b) Compare the movements by placing the hands on the
sides of the chest and making the radial borders of the
thumbs meet the mid-line in front of the chest. Note the
distance of departure of the thumbs when the patient
takes a deep breath. For the movements of the apices,
stand behind the patient, place the thumbs near the
vertebrae and fingers over the apices. Note the movements of the fingers. Finally put one hand in front of
the chest and the other over the epigastrium. In health
both the hands are raised on inspiration. In paralysis of
the diaphragm the epigastrium falls during inspiration.
ti.
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
in pitch, is fairly well conducted by the smaller lung and,

hence, the vocal fremitus is usually well heard in them.
Over the trachea and bigger bronchi the fremitus is
normally more intense. An unusually thick voice will
tend to diminish vocal fremitus; so also a feeble voice.
III.
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.
Incorrect, because the pleximeter finger is not making close

contact with the chest.
B.
Correct position for pleximeter finger.
C.
Correct position of the hand during percussion.
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.
2. Note the resonance and its degree.

Particularly note the state of the lungs so far as their elasticity and air content are concerned. Also note the position of
the lungs in relation to the chest wall and whether they are
separated by fluid, air or both, in the pleural cavity.
While listening to the resonance, the following points iritist
be borne in mind:
;
(a) T h e percussion note of the right apex is slightly dull as compared
to the left due to eparterial bronchus underneath.
(b) T h e area over the liver and heart are dull to percussion.
(c) T h e area over the stomach is hyper-resonant. T h i s is known as
Traube's space.
It is a roughly semilunar area bounded on the right
by the inferior border of the liver, above by the apex, o n the left
by the anterior border of the spleen and below by the left costal arch.
Tympanitic resonance can usually be heard over this area as stomach
is situated underneath. T h i s area is obliterated in left pleural
effusion, enlargement of the left lobe of the liver, pericardial effusion
and sometimes in enlargement of the spleen. It is increased when the
stomach is distended with gas.
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.
Test for myotatic irritability.
In wasting diseases and often in tuberculosis, the muscles in

front of the thorax are unduly irritable and a light tap over
the sternum or over the pectoral muscles produces localized
contractions.
RESONANCE
1.
OF
LUNGS
INCREASED RESONANCE occurs in emphysema, pneumothorax and

over a big cavity in the lungs; also over a normal lung when a
portion of it or the other lung is consolidated.
Special types of increased resonance

SKODAIC RESONANCEa clear high pitched note occurring above
the level of pleural effusion i.e. over the lung that is relaxed, but
still containing air.
TYMPANITICa hollow drum-like sound occurring when air from
the lungs finds its way into the pleural cavity; may also occur in
severe emphysema.
AMPHORIC RESONANCEa peculiar low pitched metallic sound
occasionally heard while percussing over a pneumothorax or large
cavity.
BELL-SOUND. When one percusses in front of the chest with a
' couple of silver coins, one being used as a plexor and the other
as a pleximeter, a bell-sound may be heard on the back of the
chest when the pleural cavity contains air in a sufficient quantity.
CRACKED-POT SOUNDa hollow note caused by sudden expulsion of air through a constricted orifice. Occurs where a cavity
communicates with a bronchus. It is best elicited by asking the
patient to keep his mouth open, while percussing. Occurs in healthy
children while crying. May occur in pneumothorax and above the
level of fluid in pleural effusion.
2.
DIMINISHED RESONANCE occurs in pneumonia, thickened pleura,

tuberculosis, fibroid lung, collapse of the lung, atelectasis.
In pleural effusion, the percusion note is stony dull and resistance
is felt by the pleximeter. In tumours, it is dull or often stony dull.
RESPIRATORY
IV.
33
SYSTEM
AUSCULTATION
Auscultation of the chest is the most important part of the

examination of the Respiratory System. It clearly gives a picture of the exact state of the underlying lung and the pleura.
Besides, auscultation is the only method to detect foreign
sounds which are often found in most of the diseased conditions
of the lungs. T h e vocal fremitus, which is felt by the hand,
may not be a valuable guide to determine the vibrations caused
by the larynx, as the examiner's hand may not be so sensitive.
Vocal resonance is definitely a more reliable method.
Auscultate to determine the following:
1.
Character of breath sounds.
2. Presence of foreign sounds.

3.
Vocal resonance.
Place the stethoscope firmly over the chest so as to prevent

sounds resulting from its movements.
Learn to discriminate heart sounds while auscultating the
lungs.
Compare identical points on the two sides of the chest.
The following practical
auscultating the chest.
points
are to be observed
while
Hair on the chest produces a crackling noise when it comes in

contact with the stethoscope and may be mistaken for adventitious sounds.
In nervous patients and those feeling cold, shivering will
produce sounds that may be mistaken for adventitious sounds
in the lungs.
1.
CHARACTER OF B R E A T H
SOUNDS
While breathing, note the intensity of both inspiratory and

expiratory phases and if there is any pause between the two
phases.
Breath sounds may be divided into two wide groups:those without a
pause, vesicular breathing
and its variants,
and those with a pause
bronchial breathing and its variants.
3
34
HOW
T O EXAMINE A
PATIENT
Vesicular breathing and its variants

(i) VESICULAR BREATHING. Normal breathing is known as vesicular. T h e inspiration is heard thrice the expiration; there is no
pause between the two phases; inspiratory phase is distinct and
rustling in character; the expiratory phase is short, soft and low
pitched.
(ii) BRONCHO-VESICULAR BREATHING. There is a very small
pause between the two phases and the expiration is slightly longer
than normal. Normally it is heard over the second right interspace
because of the eparterial bronchus underneath. In diseased condition, it is heard in partial consolidation or infiltration of the lungs.
(iii) PUERILE. Sounds are harsher than normal but of normal duration; heard in children because the elastic tissue of the lungs is not
well developed. Also heard in old people due to loss of elasticity
of the lung tissue.
(iv) HARSH. Expiration is nearly equal to or slightly longer than
inspiration and as clearly heard as inspiration. Indicates loss ol
elasticity of the lung tissue and may be an early evidence of tuberculosis of the lungs. May occur normally over the 2nd right interspace due to the presence of eparterial bronchus underneath.
(v) PROLONGED EXPIRATION. Expiration is very much longer than
inspiration. Occurs in asthma and chronic emphysema.
(vi) "COG-WHEEL"
BREATHING.
Jerky
interruptions
during
inspiration. May occur normally in nervous individuals or may
signify unequal loss of elasticity in the lung lobules. Often heard
in early tuberculosis of the lungs, in neurotics, and in fatigue.
(vii) GRANULAR BREATHING. Finer type of interruptions than those
of "cog-wheel" breathing. If localised, it is an important sign of
early pulmonary infiltration.
(viii) FEEBLE OR ABSENT. T h e sounds may not be clear in fat individuals or may indicate defective expansion, as in early pneumonia,
thickened pleura, effusion, pneumothorax, phrenic nerve paralysis
or atelectasis of the lungs.
Bronchial breathing and its variants

In all these there is a distinct pause between inspiration and expiration.
(a) T U B U L A R BREATHING.
High pitched breathing with a small
but distinct pause and with inspiration equal to expiration. Heard:
in lobar and broncho-pneumonia.
(b) BRONCHIAL BREATHING. Inspiration is equal to expiration; both
phases harsh in character with a distinct pause. May be normally
heard over the trachea. Typically heard in tuberculosis of the lungs
and in broncho-pneumonia. May also be heard in tumours close to a
large bronchus, lung collapse and infarction. In pleural effusion,
distant bronchial breathing may be heard over the fluid. In empyema,
especially in children, bronchial breathing is often present.
RESPIRATORY
SYSTEM
35
(c) CAVERNOUS BREATHING. Botli phases have a peculiar hollow

character. There is a wide pause between the two. Heard over
cavities in the lungs. Normally heard over the larynx especially while
auscultating from the back.
(d) AMPHORIC BREATHING. Intense form of cavernous breathing
having a metallic quality, best imitated by blowing across the mouth:
of a bottle. Occurs over a cavity communicating with a bronchus.
2.
FOREIGN SOUNDS
These sounds are normally not heard over the chest.

occur in the following forms:
(a)
They
Ralescrackling sounds produced in the bronchi or

alveoli by the passage of air through a fluid exudate.
These are of three varieties:

(i) Fine rales or crepitationsheard best at the end of
inspiration in conditions where the alveoli are
blocked as in pneumonia.
(ii) Medium ralesoccur in smaller bronchi and are
audible at the end of inspiration and the beginning
of expiration. Often present in phthisis and
broncho-pneumonia. They may also be heard in
ordinary bronchitis, but in such cases they disappear
on coughing.
(iii) Coarse ralesoccur in bigger bronchi and are heard
throughout the inspiration and expiration, as in extensive phthisis. Coarse bubbling rales are also
heard in resolving stages of pneumonia and oedema
of the lungs. Metallic rales are coarse rales of a
high pitch giving the impression of a shower of
drops falling into a metallic vessel; they are associated with amphoric breathing, and like it, suggests
a large cavity in the lungs.
(b) Rhonchi. These are dry sounds produced by the passage of air through thick mucus.
They are of two varieties:
(i) Sibilanthigh-pitched sound due to presence of
mucus in the smaller bronchi; heard best during the
36
H O W TO EXAMINE A
PATIENT
latter half of inspiration and beginning of expiration as in bronchitis,

(ii) Sonorouslow-pitched sound heard throughout inspiration and expiration due to presence of mucus in
the larger bronchi; typically present in bronchial
asthma.
(c) Friction sounds or pleural rub. These sounds are due to
rubbing of the two surfaces of pleura in early pleurisy.
They occur when the two inflamed surfaces rub against
each other during inspiration as well as during the corresponding period of expiration. They are unchanged
on coughing and may be intensified by pressure with
the stethoscope. They are best heard where areas of
pleurisy are more frequent, namely in the axillae and
beneath the nipples.
(d) Metallic tinkle. Over pneumothorax, all transmitted
sounds acquire a tinkling quality, because the air in the
pleural space acts as a resonating chamber. The spoken
and whispered voice, the auscultated cough and rales
acquire a musical and bell-like tinkle and such findings
are pathognomonic of air in the pleural cavity.
(e) Hippocratic succussion. This is a term applied to a
splashing sound heard when a patient, who has fluid and
gas in the pleural cavity, is gently shaken or moves suddenly.
,(f) Post-tussive suction. This is a term applied to a sucking
noise heard over a cavity immediately after the patient
has coughed. It is produced by air rushing into the
cavity during inspiration after the cough. When distinctly heard it is of considerable diagnostic value as it
can only occur when a cavity is present.
3.
VOCAL RESONANCE
Just as laryngeal vibrations are palpable on the chest wall as

-vocal fremitus, so also they are audible through the stethoscope,
as vocal resonance. T h e advantage of the latter over the
former is that even high pitched sounds are appreciated by the
stethoscope which are not easily palpable.
RESPIRATORY
SYSTEM
37
Method. Ask the patient to say some words with a nasal

twang like ninety-nine, while auscultating. Compare identical
points on the two sides. Normally, the vocal resonance is more
distinct in the second right interspace and nearer to the larger
bronchi.
T h e vocal resonance may be increased, diminished or absent
in diseased conditions of the lungs or pleura. It is diminished
or absent in pleural effusion because the lung underneath is
relaxed and hence, fails to conduct the vibrations, pneumothorax, thickened pleura, emphysema, lung atelectasis, tumours
sometimes, and when a bronchus is blocked by a foreign body.
When exaggerated, it may be heard in the following forms:
(a) Bronchophony. T h e vocal vibrations are distinctly
heard. Occurs in consolidation of lungs, phthisis,
tumours adjacent to a bronchus, large infarctions, and
in a collapsed lung in intimate contact with a bronchus.
If bronchophony is present, ask the patient to whisper in
order to exclude a cavity, which also gives rise to bronchophony,
as it is surrounded by fibrous tissue.
(b) Pectorioloquy. Articulate voice sounds are clearly
heard; best elicited by asking the patient to whisper.
Characteristic of a cavity.
(c) Aegophony. Sound of a bleating character heard best
near the lower angle of the scapula in pleural effusion
of a moderate size i.e. at the upper limit of a pleural
effusion.
(d) Amphoric resonance. A peculiar metallic resonance
heard in cases of pneumothorax. T h e metallic resonance
is imparted to the breath sounds also.
E.
E X A M I N A T I O N O F SPUTUM
Physical Examination
Note the following:

A.
Quantity.
Note the amount passed in 24 hours and inquire whether

change of posture produces larger quantity as occurs in bron-
HOW
38
T O EXAMINE A
PATIENT
chiectasis. Measuring the quantity periodically is useful to

determine the progress in tuberculosis of the lungs and suppurative lung diseases.
A moderate amount of sputum, about two ounces daily,
usually mucopurulent, is expectorated daily in acute bronchitis;
a little larger amount is passed in chronic bronchitis, resolving
pneumonia and bronchogenic carcinoma. Larger amounts, i.e.
over ten ounces per day are passed in bronchiectasis, lung abscess
or when an empyema ruptures into a bronchus. Copious frothy
sputum is often expectorated in acute pulmonary congestion.
The sudden passing of several ounces of purulent sputum is
almost pathognomonic of a lung abscess, empyema or subphrenic abscess bursting into a bronchus. Rupture of a pulmonary hydatid cyst is characterised by sudden production of
clear, watery, salt-tasting fluid.
B.
Quality and colour.
MUCOIDclear, tough, jelly-like. T h e amount is generally not great.

Characteristically present in early bronchitis. T h e sputum is jelly-like
and sticky.
SEROUSthin,
Jungs.
watery,
FROTHYcopious,
nary oedema.
often blood-stained.
Indicates oedema
frothy, often blood-stained.
Also indicates
of
the
pulmo-
FIBRINOUSclear, tough and sticky and may be "rusty" in colour.

Occurs in lobar pneumonia.
PURULENTcontains pus and, hence, offensive in smell. Occurs in
abscess, gangrene, and when an empyema ruptures into the air-passages.
T h e sputum is thick and yelloweven greenand not sticky.
MUCO-PURULENTcontains lumps of muco-pus, which are heavier
than the other constituents and, hence, sink to the bottom when collected
in a conical glass or settle in "nummular" form when spat on a flat surface. Such sputum is seen in bronchiectasis, abscess, gangrene, putrid
bronchitis and where an empyema ruptures into the air passages.
BLOOD-STAINED. When m excess, it is to be distinguished from blood
coming from the stomach which is darker in appearance and acid in
reaction, whereas blood coming from the lungs is bright red in colour
and alkaline.
RUSTYoccurs in pneumonia.
B R I G H T REDphthisis, mitral stenosis, leaking aneurysm, bronchiectasis.
PRUNE-JUICE COLOUREDpulmonary oedema, bronchogenic carcinoma, pneumonia in the aged.
RED-CURRANT JELLYneoplasm.
RESPIRATORY
SYSTEM
39
ANCHOVY-SAUCE COLOUREDamoebic liver abscess bursting into the

lungs. (An ordinary liver abscess, if ruptured into the lungs, gives a
greenish-yellow colour to the sputum).
BLACK-SPUTUM
miners.
(not
to be mistaken
for blood)common
in
coal-
GREEN-SPUTUMoccurs as a result of disintegration of leucocytes when

there is retention of purulent sputum as in bronchiectasis and lung
abscess, when the infected sputum is not easily expectorated.
C.
Consistency.
A sample of the sputum should be prepared on a black tray

and examined with the help of two teasing needles for the following:
BRONCHIAL CASTSthese are greyish-white, tree-like casts of bronchi
about half cm. in length, often present in the sputum in chronic
bronchitis.
DITTRICH'S
the size of a
chiectasis and
They consist
bacteria.
PLUGSthese are yellowish caseous masses, usually about

pin-head, sometimes a little bigger, characteristic of bronfoetid bronchitis. When crushed, they emit a foul odour.
of granular debris, fat globules, fatty acid crystals and
CURSCHMAN'S SPIRALSthese are whitish wavy threads, often coiled

into little balls, resembling sago beans. They are better appreciated
under the microscope, where they appear as mucous threads with a bright
colourless central line, around which arc wound many fine fibrils in
spiral form. They are often found in bronchial asthma and nearly always
associated with the presence of Charcot-Leyden crystals.
LUNG-STONES. Pneumoliths, consisting of calcium carbonate or calcium
phosphate may be found in the sputum. They are generally flat and
occasionally have small appendices. Often found in chronic tuberculosis.
LAYER FORMATION. Muco-purulcnt sputum as occurs in bronchiectasis, lung abscess, gangrene, putrid bronchitis and chronic tuberculosis
with profuse expectoration, when collected in a conical
glass,
gradually settles into three layers: the lowest yellowish layer containing purulent flecks of pus, blood and shreds of lung tissue; the middle
serous, watery layer of moderate opacity; and the uppermost nontransparent foamy layer consisting of loose purulent balls mixed with air
and mucus.
,
D.
Odour.
In ordinary bronchitis, the sputum has no smell or has a

stale smell. In tuberculosis, the smell of the sputum is unpleasant and more so in bronchiectasis. In gangrene and putrid bronchitis, the odour of the sputum is very offensive and
may be so in lung abscess as well.
H O W T O EXAMINE A
40
PATIENT
Microscopic Examination.
A.
CELLULAR STRUCTURES
PUS CELLS.
These are disintegrated leucocytes.
EPITHELIUM. In heart failure, when there is pulmonary congestion,

iron containing pigment may be seen in the alveolar epithelium, the
so-called heart failure cells.
RED CELLS. Presence of a few of these cells have not much significance.
Any violent cough may cause a little bleeding into the alveoli.
EOSINOPHIL CELLSoccur in bronchial asthma and eosinophilic lungs.
B.
ELASTIC FIBRES
Their presence indicates destruction of lung tissue as occurs in phthisis,

gangrene or abscess.
C.
ORGANISMS:
PARASITESespecially look for hooklets in hydatid disease; so also for

lung flukes and segments of ecchinocci.
TUBERCLE BACILLI. Fix the slide by heat and stain by Ziehl-Neelsen's
method. Cover the smear with carbol-fuchsin and warm the slide until
steam rises from the surface of the stain. Do not boil. Decolourise with
20% sulphuric acid till all the visible colour is washed out. Wash with
distilled water. Countcrstain with dilute methylene blue for about 20
seconds. Wash, dry and examine under oil immersion lens for mycobacteria tuberculosis, which are stained red.
COCCI A N D BACILLI. Fix the slide by heat and stain by Gram's
method as follows: Stain the smear with oxalated gentian violet for 1
to 3 minutes. Drain off the stain and without washing pour Gram's
iodine on the slide. Keep it for one minute. Wash with water. Decolourise with rectified spirit, by allowing it to fall drop by drop on a
horizontally held slide and allowing it to flow over the stained area before
falling off the end of the slide. Decolourising agent should not be allowed
to act for more than two minutes. Wash well with water, counterstain
with one per cent saffranin for 20 seconds. Wash with water and dry
before examining for micro-organisms.
D. CURSCHMAN'S SPIRALSseen as bright colourless central lines
around which are wound tiny fibrils in spiral form. Commonly found in
bronchial asthma.
E. CHARCOT-LEYDEN CRYSTALSvisible under the microscope as
octahedral or spindle-shaped crystals of slightly yellowish tinge. Often
seen in bronchial asthma and parasitic infestation of the lungs.
F.
NEOPLASTIC CELLSmay be seen in bronchia] carcinoma.
G. ASBESTOSISgolden yellow bodies having bulbous enlargement at

the extremities resembling dumbells are characteristically seen in asbestosis.
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
There are inflammatory

changes in the pleura.
Following disease elsewhere.
2.
Brownish-yellow.
Pale yellow.
3.
Sp. gr. above 1015.
Sp. gr. below 1015.
4.
Protein content 3 to 5%.
Protein content 0.5 to 1.5%.
5.
Clots on standing.
Does not clot.
6.
Lymphocytes present.
Cells nil, or few endothelial cells.
1.
Malignancy
Sub-diaphragmatic
abscess. Pressure by glands
Actinomycosis
Hodgkin's malignancy
Pneumothorax
Pulmonary infarction
Pneumonia (secondary)
Malignancy
Tuberculosis
Chylous
(chyliform)
Pressnre on thoracic duct
Tuberculosis
Filariasis
(chyle)
Haemothorax
Renalacute nephritis, Tuberculosis

Lung infarction
nephrosis
New growths Blood dyscrasias
Livercirrhosis.
Infected pneumothorax Haemorrhagic small-pox
Malnutrition
Secondary to subphrenic
Severe anaemias
abscess
(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
MANIFESTATIONS OF COMMON RESPIRATORY

SYMPTOMS
COUGH
Coughing is a defensive reflex which helps to clear the lower
air passages and protect them against the entry of foreign
matter and prevents stagnation of secretion in the passages
themselves. It begins with inspirationthe deeper the inspiration the more air in the lungs and more effective the cough.
T h e glottis closes, the soft palate is raised, and all the accessory,
in addition to the ordinary muscles are tensed for a forced
expiration. T h e pressure in the respiratory tract rises as is
shown by congestion in the face and neck. Then the glottis
relaxes and the contents are expelled from the mouth.
Classification of Cough
Cough may be due to infections of the lungs, mechanical
irritation of the air passages and reflex conditions.
A.
Infections
COMMON COLDcough is short
paroxysmal till the mucus is cleared.
and
dry
at
first
and
later
PHARYNGITIScough is troublesome, and persistentgenerally dry.

LARYNGITIScough is noisy, sometimes husky and stridulous.
TRACHEITIScough is intensely irritating and may be paroxysmal;
even wheezing may be present.
BRONCHITIScough may be free or paroxysmal, but always productive.
PNEUMONIAcough is dry on the first day, followed by passage of
rusty sputum on the next day and frothy later on.
TUBERCULOSIScough is frequent, short and sharp and may be
dry in the early stages; later on it is persistent with copious purulent
expectoration.
PLEURISYsolitary, dry, hacking cough, suppressed by the patient
as much as possible to avoid pain.
BRONCHIECTASISconstant cough with copious expectoration of
unpleasant smell, more marked on waking in the morning or change
of posture.
LUNG ABSCESS AND GANGRENEthe cough is free, of offensive
sputum and often blood-stained. T h e expectoration may be affected
by change of posture.
HOW
44
T O EXAMINE A
PATIENT
PERTUSSISthere is a long drawn stridulous inspiration, followed

by series of short, sharp, expiratory coughs. T h e face becomes red,
the veins become prominent, and after the coughing ends, there is a
long drawn-out inspiration. T h e cough may be accompanied by
vomiting.
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.
Features of some characteristic coughs

SUDDEN COUGHrespiratory diseasestracheitis, bronchitis, bronchopneumonia.
COUGH W I T H PAINpneumonia, pleurisy.
COUGH ON LYING DOWNenlarged uvula, enlarged heart.
COUGH W I T H VOMITINGwhooping cough.
DRY COUGHphthisis, laryngitis, neurosis.
LOOSE COUGHbronchitis, phthisis, bronchiectasis.
SUDDEN PAROXYSM IN A CHILDsuspect foreign body and, if with
fever, laryngeal diphtheria.
SHORT A N D SUPPRESSEDdry pleurisy.
IRRITABLEearly phthisis, pharyngitis.
PAROXYSMALasthma, bronchitis, pertussis.
EXPLOSIVEphthisis, laryngitis, neurosis.
"BRASSY"aneurysm, mediastinal growths.
"BOVINE"prolonged with wheezing. Occurs in involvement of the
recurrent laryngeal nerve.
HACKINGphthisis, laryngitis, pharyngitis.
STRIDORpersistent thymus, laryngeal diphtheria.
BARKINGhysteria.
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:
46
TRACHEITISretrosternal pain which is o a sore, scratchy character,

made worse by coughing but not by deep breathing.
ANGINA PECTORISretrosternal pain of momentary duration characterised by a sense of impending death.
CORONARY DISEASEretrosternal pain of severe nature persisting for
hours or days and shooting along the left arm with accompanying collapse.
PERICARDITISsubsternal pain of prolonged duration, aggravated by
breathing, coughing, swallowing or bending. T h e apex is felt inside the
outermost border of the cardiac dullness; there is often pulsus
paradoxus.
STOMACH CONDITIONSdilated stomach often presses upon the heart
and causes mild retrosternal pain. The patient is generally about 20
years old and too young to have coronary disease. Hiatus hernia may give
rise to central pain and is often mistaken for heart diseases. X-ray of the
stomach is very necessary to arrive at a diagnosis.
MEDIASTINAL CONDITIONScause continuous boring
the sternum and later, pain on the side of the chest.
pain
behind
Causes of pain in the sides of the chest

1.
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.
HEART CONDITIONS. In coronary disease, although the pain is

central, is often referred to the side of the chest or along the left arm.
4.
MEDIASTINAL CONDITIONSboring pain felt under the sternum

rather than to the side of the chest.
5.
LIVER CONDITIONS. Hepatitis, liver abscess and congestion in the

liver, invariably give rise to pain in the right side of the chest.
EPISTAXIS
Bleeding from the nose may be due to local or general causes.
It often occurs spontaneously without any obvious cause.
A.
Local causes
Injury to the noseblow, fracture, foreign body, violent nose

blowing.
RESPIRATORY
SYSTEM
47
Ulcerationtraumatic, syphilis, malignancy, tuberculosis or

leprosy.
New growthsadenoids, polypi, fibromas, angioma.
Varicose veinshereditary telangiectasis.
Acute infectionssevere catarrh, diphtheria, scarlet fever,
influenza, whooping cough.
B.
General causes
High blood pressurehyperpiesia, nephritis, arterio-sclerosis.

High venous pressure as in severe bronchitis, emphysema,
after violent exercise in young.
Venous congestionmitral stenosis.
Cirrhosis of the liver.
Altered condition of the bloodhaemophilia, pernicious
anaemia, purpura, scurvy, leukaemia, obstructive jaundice.
Vitamin deficiencyscurvy.
Severe generalised infectionsenteric, scarlet fever, influenza,
small-pox and measles.
Tumours in the thorax.
Altered atmospheric pressuremountaineering, diving, flying.
C. Of obscure origin. May occur in childhood; and in
young girls as vicarious menstruation.
INVESTIGATION:
1. Inquire if the blood comes from both or one nostril. In
majority of cases if the causes are local, it comes from
one side.
2. Exclude trauma.
3. Examine the nares carefully to seek the bleeding spot,
and exclude ulceration, growths and foreign bodies.
4. Look for naevi on the face, to exclude hereditary
telangiectasis.
5. Take the blood pressure to exclude hyperpiesia.
6. Examine the blood to exclude blood dyscrasias.
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
Tuberculosishistory of cough, low fever, loss of weight and

signs in the chest.
Pneumoniahigh fever, cyanosis, rusty sputum, signs of
consolidation in the chest.
Lung abscesspatient passes large quantity of blood-stained
sputum; low fever and localised signs in the chest.
Bronchiectasiscough, purulent and offensive sputum, clubbing of the fingers, wasting of the chest.
Bronchial carcinomacough with prune juice coloured sputum; patient generally middle-aged; bronchoscopy essential.
Putrid bronchitisoffensive smell of the sputum which is
large in quantity; teeth often septic.
Parasitic diseaseshydatid disease and lung flukes can cause
bleeding. Blood reveals eosinophilia. Sputum examination
essential for diagnosis.
Traumatichistory helpful.
B.
CARDIO VASCULAR CONDITIONS
Mitral stenosis(due to venous congestion in the lungs)

thrill felt over the apex, presystolic murmur at the mitral area,
accentuation of the second pulmonary sound, congestion in the
liver and lungs.
Pulmonary infarctionsudden, severe pain in the chest with
fever and haemoptysis. May occur in mitral stenosis, congestive failure and in patients immobilised in bed for a long
period.
Aortic aneurysmmay leak or rupture into the lungs, the
latter-being immediately fatal.
RESPIRATORY
49
SYSTEM
Cardiac asthma. T h e haemoptysis is due to pulmonary

venous congestion. Patient gets paroxysmal attacks of dyspnoea
generally in the nights.
C. BLOOD DISEASESgenerally these do not give rise to
haemoptysis; they more often cause epistaxis and bleeding in the
gums. Purpura, scurvy, leukaemia and haemophilia are the
most important.
D. LIVER ABSCESS BURSTING I N T O T H E LUNGS
amoebic abscess especially gives rise to anchovy-sauce coloured
sputum.
E. SEVERE HAEMORRHAGIC INFECTIONSsmall-pox,
scarlet fever, etc.
F. VICARIOUS MENSTRUATIONmay occur in young
girls, although not common.
The commonest cause of haemoptysis is tuberculosis of the
lungs, and next in order, mitral stenosis and bronchogenic carcinoma. If an adult coughs blood, one should think of tuberculosis first and after forty, of cancer. On the whole the patient
should be regarded as suffering from tuberculosis, until the
contrary is proved. Bronchiectasis also may give rise to haemoptysis.
Haemoptysis is often mistaken for haematemesis
The following are the points of differentiation between the
two.
Haemoptysis
Haematemesis
1.
T h e blood is coughed up.
2.
Preceded
nausea.
by
cough;
T h e blood is vomited.
no
Preceded by nausea.
3.
Colour bright red.
Usually dark.
4.
Mixed with froth and sputurn.
Mixed with food particles.

Acid in reaction.
5.
Alkaline in reaction.
6.
History of
diseases.
7.
Stools contain no blood, unless blood is swallowed.
Stools may be even tarry.
8.
Episode lasts for days and

stains sputum for some time.
Episode is usually brief and stops

abruptly.
lung
or
heart
History of stomach trouble.
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
X-ray the chest, do bronchography, etc.

HOARSENESS OF VOICE
Hoarseness is due to lack of normal movements of the vocal

cords. It may be due to local conditions, which are the commonest causes, or due to organic paralysis.
A.
LOCAL CAUSES
Over-working of the vocal cordsshouting, singing, etc.
General weaknessdebility, convalescence, myasthenia gravis,

myxoedema.
Infections of the larynxlaryngitis.
Constant irritationalcohol, tobacco.
Ulceration of the larynxtuberculosis especially.
New growthspapilloma chiefly.
B.
ORGANIC PARALYSIS
Paralysis of the vocal cordsaortic aneurysm, mediastinal

growths, bronchial neoplasms.
Lesions at the base of the skullgrowths, thrombosis of the
lateral sinus.
Lesions in the bulbincluding thrombosis of the posterior
inferior cerebellar artery.
RESPIRATORY
51
SYSTEM
In lesions of the bulb and in lesions of the base of the skull,

other muscles are also affected, e.g., the soft palate, the pharynx
and the tongue.
In every case of chronic hoarseness examine the larynx with
a laryngoscope. Carefully inquire into the past history of
tuberculosis of the lungs and also syphilis. The commonest
cause of transient hoarseness is acute laryngitis and of chronic
sore throat, laryngeal tuberculosis. In hoarseness of long duration, also bear in mind syphilitic ulceration, tobacco excess,
myxoedema, paralysis of vocal cords, growth of the vocal cords
and myasthenia gravis. Growths of the vocal cords are easily
excluded by laryngoscopic examination, which must be performed in all cases of hoarseness of the voice.
CYANOSIS
By cyanosis is meant blue colouration of the skin
membranes. It is most noticeable in the lips, nose,
hands and feet. It depends upon the amount
haemoglobin present in the blood and not due to
C 0 2 as was once thought to be.
and mucous
cheeks, ears,
of reduced
an excess of
The factors that determine the degree of cyanosis are:

1. Insufficient oxygenation in the lungs due to failure of the
blood to reach them as in pulmonary stenosis, or to an alveolar
barrier as in pulmonary oedema, collapse, or consolidation.
2. Increased de-oxygenation in the capillaries due to stasis
from moderate cold, or to increased venous pressure as in heart
failure.
3. The degree of dilatation of the capillaries so as to make
cyanosis visible. The less the oxygen saturation and more dilated the capillaries, the more the cyanosis.
4. T h e amount of haemoglobin present. If it is excessive as
in polycythaemia, the cyanosis becomes more marked because of
the higher content of the reduced haemoglobin than when there
is less haemoglobin as in anaemia. T h e minimum amount of
reduced haemoglobin that causes cyanosis is 5 Gm. of Hb. per
HOW
52
TO EXAMINE A
PATIENT
100 c.c. of blood; hence, in severe anaemias where Hb. falls

below 5 Gm., cyanosis does not occur.
5. Pathological venous-arterial shunt of over one-third of
the cardiac output as in congenital heart diseases.
CAUSES OF CYANOSIS:
1. Local. Slowing of the blood flow as in cold weather or
vasomotor stimulation. The slowing allows greater dissociation of oxygen. If the cold weather is intense, dissociation of oxygen stops and although the circulation is
very slow the skin is coloured red.
2.
Obstruction to the return of blood to the heart:

(a) Right ventricular failure, tricuspid stenosis, pericardial effusion and constrictive pericarditis.
(b) Local obstructionpressure on the veins by tumours, venous thrombosis, or incompetent venous
valves.
In all the above conditions there is slowing of the current and

more oxygen dissociation plus greater capillary dilatation.
3. Lung Disorders:
(a) Congestion in the lungs. Mitral stenosis and left
ventricular failure cause some blood to pass through
the middle of the dilated capillaries and, hence, out
of contact with the alveolar air. If one-third of such
unoxygenated blood is shunted from the veins to the
arterial system, cyanosis results. Often, in such cases,
there is slowing of the return of blood to the heart
and, hence, two factors contribute to the appearance
of cyanosis.
(b) Diseases of the lungs. These may be acute or chronic. In pneumonia or infarction the blood is shunted back without being oxygenated and more so,
when there is moisture in the alveoli (early pneumonia and severe influenza) than in consolidation. In
lung destruction and emphysema there are enough
alveoli at the surface for oxygenation and, hence,
RESPIRATORY
SYSTEM
53
there is no cyanosis. However, in chronic emphysema

and acute bronchial asthma, the patient may not be
able to breathe enough air, resulting in cyanosis.
In pulmonary endarteritis (Ayerza's disease) there is
no blood reaching the lungs and, hence, cyanosis.
In acute infarction and sudden pneumothorax there
is embarrassment to respiration because of the severe
pain; hence, cyanosis.
4. Shunting of the venous blood directly into the systemic
circulation. In congenital disorders like single ventricle, dextraposed aorta, transposition of the great vessels and less commonly
in patent interventricular or interauricular septal defects, patent
ductus, Fallot's tetralogy and pulmonary stenosis, cyanosis can
occur if one-third of the blood is shunted from the veins. In
all such cases there is also capillary dilatation in order to help
the tissues to take up as much oxygen as possible resulting in
more cyanosis.
5. Tracheal or bronchial obstruction. This may reduce the
amount of inspired air to cause oxygenation of blood. Laryngeal
diphtheria, foreign bodies, Ludwig's angina, oedema of glottis,
pressure from mediastinal tumours are common examples.
6. High altitudes. There is oxygen lack and theoretically
cyanosis should occur. Actually it does not do so, but it tends
to exaggerate other types of cyanosis.
7. Blood conditions. Polycythaemia can produce cyanosis
due to higher content of reduced haemoglobin present in the
circulation.
Cyanosis must be differentiated from methaemoglobinaemia
due to poisoning with aniline compounds, potassium chlorate
and coal-tar derivatives; and from sulphaemoglobinaemia
due to sulphonamide poisoning. T h e cyanosis in these conditions is of a leaden hue.
*
DYSPNOEA
Although dyspnoea is a very important symptom of respiratory
and cardio-vascular diseases, alone it must not be taken as an
evidence of diseases of any of the above systems, unless the other
54
HOW
T O EXAMINE A
PATIENT
causes of dyspnoea have been excluded. A genuine dyspnoea is

characterised by more rapid and deeper breathing than normal,
and must be distinguished from the sighing and desire for deep
breath so often manifested by neurotic patients.
In cardiac conditions dyspnoea may occur only on effortan
early indication of cardiac decompensation. T o judge the capacity of the heart the grade of dyspnoea is a valuable guide. It is
very desirable to know how the patient's breathing responds to
physical tasks to which he has been accustomed then to compare
his response to some special tests with that of a healthy man.
Orthopnoea is a condition where the patient is breathless
continuously and finds it difficult even to lie down in bed. Such
a patient seeks comfort in adopting a semi-sitting posture even
during sleep.
CAUSES OF DYSPNOEA:
1. Mechanical obstruction to the air passages
(a) Obstruction to
laryngeal diphtheria,
or tumours pressing
cause inspiratory type
ly prolonged.
the upper air passagesnasal conditions,

foreign body, aneurysm, persistent thymus
upon the trachea. All these conditions
of dyspnoea, i.e. the inspiration is marked-
(b) Obstruction to lower air passagesbronchial asthma,

pleural effusion, pneumothorax, pneumonia, fibrosis, emphysema, pulmonary embolism, increased intra-abdominal pressure
(growths, fluids, etc.) These conditions produce expiratory type
of dyspnoea, i.e. the expiratory phase is markedly prolonged.
2.
Cardiac conditions
(a) In left ventricular failure, there is congestion in the lungs,

which becomes more evident when the patient is lying down,
resulting in cardiac asthma.
(b) I n right-sided failure, the chief factors that cause dyspnoea
is excess of CO, in the blood and increased B.M.R. in addition to
pulmonary congestion.
RESPIRATORY SYSTEM
3.
55
Upsetting of the acid-base equilibrium of the blood
(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.
5. Increased basal metabolism

(a) Exophthalmic goitrethe dyspnoea is moderate
occurs when the patient is doing some work.
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.
(e) Specific aortitis.

(f) Aortic stenosis and regurgitation.
In most of these cases, there is severe strain thrown on the
left ventricle. T h e attacks commonly come on at nights. T h e
patient wakes up with a sense of oppression or suffocation and
sits up with the windows thrown open to seek relief. T h e
breathing is laboured with inspiration a little longer than
expiration and in severe cases the distress is so great that the
patient sweats profusely and looks as if he is on the verge of
collapse.
3. Renal asthma. In such cases there is history of chronic
renal disease with polyuria, hyperpiesia, presence of albumin
and casts in the urine. T h e patient gets asthmatic attacks
which are not very severe and do not last long.
4.
Obstruction to the upper air passages
(a) Persistent thymus. The dyspnoea is of inspiratory type

and X-ray of the chest reveals the enlarged gland.
(b) Laryngeal diphtheria. Common in children, starts suddenly with inspiratory stridor and low fever.
(c) Foreign body in the trachea may also cause inspiratory
type of dyspnoea.
INVESTIGATION
In sudden acute dyspnoea, especially in a child, suspect laryngeal diphtheria, foreign body, laryngeal spasm due to tetany
associated with rickets. In all these conditions the patient gets
inspiratory type of dyspnoea with cyanosis and stridor.
Bronchial asthma is another cause of acute dyspnoea in a
child, but here the dyspnoea is of expiratory type with cooing
rhonchi and slow laboured respiration.
RESPIRATORY
SYSTEM
In adults the causes of acute dyspnoea are varied.

lowing are the common conditions:
57
T h e fol-
1. Bronchial asthma (see page 58).

2.
Cardiac asthma (see page 58).
Sometimes it is difficult to distinguish bronchial asthma from

cardiac asthma and test for circulation time may have to be
performed. T h e patient is injected 4 c.c. of 20% calcium gluconate intravenously and the time noted when the warm sensation reaches the pharynx. It takes 15 seconds in cases of
bronchial asthma and may even take 30 seconds in cardiac
asthma.
3. Renal asthma. History of chronic kidney disease and
presence of albumin and casts in the urine will help in the
diagnosis.
4.
Sudden catastrophy in the lung.
(a) Pulmonary infarctionsevere pain, dyspnoea, haemoptysis.

(b) Spontaneous pneumothoraxacute pain, dyspnoea, mediastinal shift, weak breath sounds on the affected side.
(c) Sudden massive collapse of the lungpain in the chest,
mediastinal displacement, absence of air entry.
(d) Massive pneumoniahigh fever, toxaemia, cyanosis, rusty
sputum, absence of air entry.
Age
Time of onset
Mode of onset
Symptoms
Expectoration
Duration
Associated symptoms .
2.
3.
4.
5.
6.
7.
8.
Renal Asthma
Midnight.
Sweating not severe.
May lastlonger.
the whole day or
Small sticky pellets.
cough comes later.
Starts with dyspnoea;
immediately
fol
No sweating.
Lasts for about half-an-hour.
Hardly any expectoration.
Dyspnoea only.
Nothing particular.
Late in the night.
Sweating profuse.
Lasts for 1-3 hours.
History of chronic nephritis.
After fifty generally.
Mucoid or rusty sputum.
lowed by cough.
Dyspnoea,
May be precipitated by May start after exertion

allergy.
Early morning.
After forty.
Family history; history of

History of left ventricular
previous attacks; history of
failure, hypertension, aortic
allergy.
or coronary disease.
Any age; often from youth.
History
1.
Bronchial Asthma Cardiac Asthma
DIFFERENTIATION BETWEEN THE THREE COMMON TYPES OF ASTHMA
58
Condition of the heart
Pulse
Blood pressure
Blood
Urine
11.
12.
13.
14.
15.
in
the
Generally clear;
Eosinophilia.
there may
veins.
Left ventricular enlarge ment.
and
presence of casts.
No eosinophilia.
Definite albuminuria
be mild albuminuria.
No eosinophilia.
High.
Full.
Left
ventricular
enlargement; gallop rhythm.
Full and bounding.

High.
No engorged
Respiration generally slow;

Rate of breathing may be
expiration twice the inspirafaster than normal; expiration; rales heard at the
tion slightly longer than
bases.
inspiration; few rales heard
at the base.
Engorged veins.
Nothing particular; borders

may not be percussed due to
emphysema.
May be low.
Clear.
veins
Respiration
slow
and
laboured; expiration thrice
the
inspiration;
rhonchi
heard all over the chest.
engorged
neck.
Feeble and rapid.
Signs in the chest
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.
EXERCISE TOLERANCE TESTS.
HOW
62
A.
T O EXAMINE A
PATIENT
INTERROGATION
Particularly inquire into the family history of rheumatism,

angina, apoplexy and heart disease.
In personal history, inquire into the previous diseases especially of rheumatism, chorea, scarlet fever, diphtheria, syphilis,
sore throat (tonsils) and "growing pains".
In general examination, particularly look for the build of the
patient, general appearance, the colour of the skin and mucous
membranes.
B.
COMMON SYMPTOMS AND SIGNS
DYSPNOEA; ORTHOPNOEA; DYSPNOEA ON EXERTION

(see page 53).
Note the following:
1. Its time of occurrence.
2. What type of effort causes the samewalking, climbing.
3.
Mode of onsetwhether sudden or gradual.
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.
Charactervice-like, burning, boring.
3.
Radiationleft arm, both arms, neck.
4.
Duration and frequencyseconds, minutes, days.
5.
Exciting causeexposure to cold, full stomach, excitement, effort, etc.

6. Aggravating and relieving factors.
CARDIOVASCULAR
SYSTEM
63
7. Associated phenomenasense of constriction, sense of impending death, dyspnoea, fainting, syncope.

PALPITATION (see page 99).
1. Whether it comes in attacks; if so, mode of onset
whether sudden or gradual.
2.
If conscious of any irregularity of the heart beat; if there

is an occasional thump.
3. If there is any relation to food, emotion, exertion, or
posture.
4. If any drugs are being used and with what results.
5. Aggravating and relieving factors.
SYNCOPE (FAINTING) (see page 100).
1. Description by the patient.
2.
If he fell during the attack.
3. If he was unconscious.
4. Associated symptomsdizziness, sweating, pallor, pain,
diarrhoea, fever, haemorrhage.
5.
Any history of taking drugs or food mixed with drugs.
6.
Previous health; any collapse before.
GIDDINESS (see Chapter V).

1. Inquire when it comes.
2.
If associated with headache.
3. Sleepif good or poor; dreams, delusions, hallucinations.

4.
If there is exhaustion after mental or physical work.
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.
Cyanosisif it increases on effort.
3. Engorgement of veins in the neck.

4.
Respiratory symptoms and signs:

(a) Cough.
(b) Haemoptysis.
(c) Epistaxis.
(d) Congestion in the lungs.
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.
Urinary symptomsif the quantity of urine is decreased

and high coloured.
7. Loss of weightespecially in children.

SURFACE
MARKING
OF THE
HEART
UPPER BORDER2nd left costal cartilage to 3rd right chondrosternal

junction reaching about an inch outside the sternum. This border is
mainly formed by the left auricle.
RIGHT BORDERfrom 3rd to 6th right chondro sternal junction about
an inch from the median plane. This is formed by the right auricle.
INFERIOR BORDERfrom the 6th sterno costal junction to the apex in
the 5th space about half-an-inch inside the left mid-clavicular line. This
border is mainly formed by the right ventricle and to a very slight extent by
the apical portion of the left ventricle.
LEFT BORDERa curved line from the apex to the 2nd left interspace
just inside the parasternal line. This line is almost wholly formed by the
left ventricle.
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.
Mitral valve lies behind the 4th left costal cartilage.
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
This enables the examiner to see the position and extent of

the apex beat, its force and rhythm, and the presence of abnormal pulsations over the praecordium, neck and epigastrium.
Examine the patient sitting and also in recumbent position.
Note the following:
1. Shape of the praecordium
If bulgingsuspect pericardial effusion, enlarged
mediastinal tumours, pleural effusion, scoliosis.
heart,
If flattenedmay be congenital deformity, old pericarditis,

fibrosis of lungs.
2. Pulsations and movements
IN T H E PRAECORDIUM:
(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:
(a) In the thorax (outside the praecordium)may be due to

pulsating tumours, aneurysms, pulsating arteries in coarctation of the aorta, pulsating empyema.
(b) Root of the neck.
(i) Suprasternal notchmay be due to pulsating thyroid
gland, abnormal thyroidea ima artery, aorta in hypertension, aneurysm, coarctation of the aorta.
(ii) Sides: Carotids (better felt than seen)may pulsate
on exertion, mental excitement, exophthalmic goitre,
aortic regurgitation, hypertension and aneurysm of
the carotid artery.
Jugulars (better seen than felt and often
visible in congestive cardiac failure.
(c) Epigastric pulsations.
following conditions:
double)
These may be due to any of the
(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
the nails of the fingers; there will be alternate blushing

and blanching of the tissues underneath. Capillary pulsation is easily felt over the lobules of the ears or tips of
the fingers, especially in aortic regurgitation.
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
This confirms what is noted on inspection.

2.
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
(iii) Coarctation of aorta sometimes.

(iv) May be in auricular septal defect.
Scoliosis is a common cause of outward displacement of the apex.
In dextrocardia the apex lies on the right side.
In cardiac enlargement the apex is mainly displaced downward; in dilatation, outwards: and in hypertrophy and dilatation, down and out.
In right ventricular hypertrophy the impulse is diffuse and mainly felt
to the left, but not appreciably downward as in left ventricular hypertrophy
in which condition the impulse of the apex is generally felt downwards rather
than outwards.
In pronounced abdominal distension the apex-beat may be displaced upwards and to the left. .
(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
FORCIBLE A N D HEAVINGleft ventricular hypertrophy.

WEAKmyocardial weakness, emphysema,
myxoedema.
SHARP A N D SLAPPINGmitral stenosis.

DIFFUSE A N D FAIRLY FORCIBLEanxiety, exertion, nervousness and
hyperthyroidism.
DIFFUSE A N D WEAKdilated
sometimes, pericardial effusion.
heart,
right
ventricular
hypertrophy
(b) Base of the heart. In aneurysm of the aorta pulsation

may be felt in the second right interspace. In left auricular
hypertrophy and right ventricular hypertrophy as occurs in
mitral stenosis, pulsation is often felt in the second and third
left interspaces.
(c) Over the praecordium. Diffuse pulsation over the praecordium suggests right ventricular hypertrophy, anxiety, hyperthyroidism, shunt from left-to-right as occurs in auricular septal
defect and other congenital disorders of the heart.
HOW
70
TO EXAMINE A
PATIENT
(d) Epigastric and abdominal pulsations. T h e two important

causes of abdominal pulsations are: transmitted impulse from
the aorta arid aneurysmal dilatation. They can be easily differentiated from one another by "flag test". Use two match
sticks with a bit of paper attached to their top ends, and allow
them to stand, parallel to each other over the pulsating area.
In transmitted pulsation both the stick's move up, and in expansile pulsation their upper ends move outwards.
(e) Other pulsationsneck, brachials, fermorals, temporals
and capillaries.
(f) Tracheal tugoccurs in aortic aneurysm due to transmission of the pulsation to the trachea. In order to elicit it, stand
behind the patient, place the tips of the index fingers beneath
the cricoid cartilage and lift the larynx up. A distinct tug is
felt with every beat of the heart if there is aortic aneurysm.
4.
THRILLS.
A thrill is an analogue of a murmur and the cause of its

production is the passage of blood from a smaller cavity into a
greater one. A thrill is intensified if the chest wall is thin, if
the blood flow is rapid, and if the site of production is near the
surface of the chest. T h e presence of a thrill is a more certain
evidence of an organic disease of the heart than the presence
of a murmur. It is best felt with the flat of the hand. If
present, it is perceived like the sensation of purring a cat makes
when stroked with the hand.
WHEN A T H R I L L IS FELT, N O T E :
(a) Its timingwhether it is felt before or after the systole

of the heart i.e. whether systolic or diastolic in time. A
pre systolic thrill is also a diastolic thrill and is felt just
before systole.
(b) Its positionlocate the exact place where the thrill is best
felt so as to fix the position of the damage to the valve.
A thrill is invariably present in all stenotic
generally absent in cases of regurgitation.
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
Percussion is mainly intended to determine the boundaries of

the heart. It often gives fallacious results because the greater
part of the heart is surrounded by the resonant lung; and the
roots of the great vessels at the base of the heart produce a note
ivhich cannot be distinguished from that caused by the heart.
In fat people and in emphysema it may be impossible to outline
the heart. Hence, percussion of the cardiac dullness has its
limitations. However, it is useful to detect the presence of pericardial effusion and aortic aneurysms, rather than to study the
changes in the size of the heart. The size and shape of the
heart is more accurately determined by radiological methods.
The technical details of percussion, are the same as described
in the Respiratory System. T h e percussion should not be too
light or too heavy.
The data obtained by percussion of the heart may be interpreted in terms of:
1. The position of the heart.
2.
T h e size of the heart or of the individual chambers.
3. T h e size of the great vessels at the base of the heart.

4.
The size of a distended pericardial sac, if present.
The borders of the heart are normally situated as follows:
H O W TO EXAMINE A
72
PATIENT
(a) Left borderhalf an inch inside the left mid-clavicular

line in the 5th interspace or three and half inches from the midsternal line. Percuss from the resonant area towards the border
of the heart, by standing to the left of the patient and keeping
the pleximeter parallel to the sternum or by standing to the
right of the patient and keeping the pleximeter at the right
angles to the border of the heart in the fifth interspace.
(b) Upper border3rd rib or upper border of the 3rd space
in the left parasternal line. Percuss rib by rib, and then space
by space. T h e dull area corresponds with the upper border.
(c) Right borderjust to the right of the right lateral sternal
line, at the level of the 4th interspace. It is difficult to define
this border as sternum comes in the way. Always locate the
upper border of the liver first, and then percuss a space above
with the pleximeter placed at right angles to the border of the
heart.
T h e position of the apex beat can be defined better by palpation than by percussion.
CARDIAC
DULLNESS.
T h e dullness in the heart-area is invariably modified as follows:

In enlarged left ventricle and cardiac dilatation, the dullness extends more
to the
left.
If the dullness extends to the right of the sternum in absence of lung

disease, pleurisy or pericardial effusionsuspect right ventricular hypertrophy.
In aneurysm of the ascending aorta, there is dullness in the 2nd right
interspace and the sternal percussion is absolutely dull.
In aneurysm of the descending aorta in the thorax there is often dullness
in the 2nd left interspace.
In enlargement of the pulmonary artery and left auricular enlargement
(mitral stenosis), there is dullness in the 2nd left interspace.
In pericardial effusion, there is generally pear-shaped dullness with
broader end downwards and with increased dullness both to the right
and to the left to the sternum; the apex-beat is felt inside the dullness
of the left side; and the cardio-hepatic angle becomes obtuse. In adhesive
pericarditis the heart is markedly enlarged and the dullness is increased
both to the left and to the right.
T h e cardiac dullness is lost in well-established emphysema.
In ascites, abdominal tumours and later months of pregnancy the diaphragm is pushed up causing the heart to lie more horizontally thereby
increasing the area of cardiac dullness.
CARDIOVASCULAR
IV.
SYSTEM
73
AUSCULTATION
Auscultation is of great value in the detection of valvular

defects of the heart. It is also of some importance in diseases
of the myocardium and of bigger blood vessels.
Although the sounds produced in the heart have a common
origin, their component elements may be heard with different
intensity over different parts of the cardiac areas. Hence, listen
to the mitral valve over the apex; to the aortic valve at the 2nd
right interspace in the parasternal line; to the pulmonary valve
at the 3rd left interspace; to the tricuspid valve at the lower end
of the sternum and follow that order.
Auscultation determines,
A.
Character of the heart sounds.
B. Rhythm of the sounds.

C. Adventitious sounds.
D.
A.
State of the blood vessels sometimes.
CHARACTER OF T H E H E A R T SOUNDS.
Generally two sounds are heard in a normal heart. T h e first

sound mainly depends upon the closure of the mitral and tricuspid valves and ventricular contraction. It is loud and prolonged and best heard at the apex. It is identified by its
association with the apex thrust and/or with the cartoid pulse.
The 2nd sound, synchronous with the closure of the aortic and
the pulmonary valves, is short and sharp and is better heard at
the base of the heart. Normally the 2nd aortic sound is more
distinct than the 2nd pulmonary sound in adults. In children
and young adults it is just the reverse. A 3rd sound may be
normally heard, especially in children and young adults. It is
probably due to vibration of the A-V valve cusps caused by inrush of blood during diastole and hence, often mistaken for a
mitral diastolic murmur.
While auscultating, pay greater attention to the first sound
at the mitral area and to the second sound over the aortic and
pulmonary areas.
Always listen to one sound or murmur at a time.
H O W TO EXAMINE A
74
The character
conditions:
1. At
PATIENT
of the heart sounds
may
vary
in
several
the apex
(a) 1st sound may be accentuated in hypertrophy (dull and

prolonged), mitral stenosis (short and sharp), fevers, emotion, neurasthenia, hyperthyroidism and in such other disorders which increase the excitability of the heart.
(b) 1st sound may be weak in acute illness, cardiac infarction,
prolonged fever, myocardial diseases, cardiac failure, peripheral failure, anaemias, pericardial effusion and in lung
conditions like emphysema and pneumothorax.
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.
Ordinarily two rhythmical sounds are heard over the heart

and is represented as lub . . . dup. In childrien three sounds
may be heard,} the 3rd sound being physiological and may be
represented as lub . . . dup-dup.
Changes in the rhythm may occur in the following conditions:
1. Reduplication of the 1st sound. Gallop rhythm is a
common condition in which three sounds are heard at the apex
indicating a serious myocardial disease. It is mainly due to
failure of the right and left ventricles to contract synchronously.
Gallop rhythm is of two varieties: presystolic gallop
rhythm
the commoner of the two and in which the extra sound is
related to auricular contraction and, hence, precedes the systole
of the heart and is represented by lub, lub . . . dup. It is often
present in left ventricular failure, chronic myocardial disease,
aortic regurgitation, hypertension and cardiac infarction. T h e
2nd variety is known as protodiastolic gallop rhythm in which
H O W TO EXAMINE A
76
PATIENT
the extra sound appears in early diastole; this may be easily

mistaken for physiological 3rd sound as this extra sound is also
heard in early diastole, and is represented by lub . . . lub., dup.
This type of rhythm is found in right ventricular failure, mitral
stenosis, congenital heart diseases, cardiac infarction, bundlebranch block, constrictive pericarditis and emphysema.
Physiological triple rhythm is often mistaken for gallop
rhythm; however, the best criterion for distinguishing between
the two is to note the state of cardiac function.
1 2
'
Normal Sounds
Reduplication of First Sound
Reduplication of Second Sound

FIG. X
Diagram of normal heart sounds & certain variations.

DIFFERENTIATION
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
Reduplication at the apex may also be due to an asynchronous

closure of the mitral and tricuspid valves, and this gives rise
to a protodiastolic gallop rhythm in which condition the prognosis is definitely better than in those conditions where there is
presystolic gallop rhythm.
2. Reduplication of the 2nd sound. This is best heard in
the pulmonary area and occurs commonly in mitral stenosis
when there is marked increase in the pulmonary pressure and,
sometimes, in chronic lung diseases. T h e split sounds are of
equal intensity and duration. Reduplication is often heard in
atrial septal defect.
3. Triple rhythm. This is more often physiological than
pathological and is often heard in mitral area in young adults.
It follows the 2nd aortic sound and is believed to be due to
rapid ventricular filling. It is often mistaken for protodiastolic
gallop rhythm.
4. "Tic-tac rhythm". When the action of the heart is
weakened and the diastolic pause shortened, the heart sounds
become evenly spaced resembling the ticking of a dock.
C.
ADVENTITIOUS SOUNDS.
Adventitious sounds include murmurs and friction sounds

heard over the cardiac area.
CARDIAC
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.
When murmurs are heard, determine:

1. Their time of occurrence.
2. Their point of maximum intensity.
3- Their character.
{high
H O W TO EXAMINE A
78
PATIENT
4.
Their direction o propagation.
5.
Their relation to respiration, posture and exercise.
1. Endocardial murmurs may be systolic or diastolic in time.

T h e murmurs that are heard between the 1st and 2nd sound or
replacing the 1st sound are systolic in time. Those that are
heard between the 2nd sound and the 1st sound or replacing
the 2nd sound are diastolic. T h e murmur that is long enough
to replace the systolic sound is generally known as pansystolic.
T h e diastolic murmurs are divided into three; early, mid and
late (presystolic). Presence of diastolic murmurs nearly always
indicate valvular diseases; not so the systolic murmurs.
2. T h e maximum intensity of the murmurs generally occurs
at the valve that is damaged; hence, even if a murmur is heard
all over the praecordium, it is very necessary to find where it is
best heard in order to locate the site of the lesion.
3. T h e character of a murmur is either harsh and grating or
soft and blowing. Obstructive murmurs are usually harsh and
regurgitant murmurs are apt to be soft. Functional and haemic
murmurs are soft in character. Presystolic murmurs of mitral
stenosis are crescendo in character. Systolic murmurs in mitral
disease are diminuendo in character.
4. T h e direction of propagation is selective to certain types
of murmurs and especially, when one hears a systolic murmur
at the apex one should not conclude that it is due to organic
disease of the heart unless there is propagation of the m u r m u r
towards the axilla. Conduction of a murmur is an indication
of its organic nature. In general, a mitral stenotic murmur is
strictly localised at the apex, a mitral regurgitant murmur is
conducted towards the axilla, an aortic stenotic murmur is conducted towards the neck vessels and an aortic regurgitant murmur is conducted down the sternum.
5. T h e stroke output of the right heart increases during
inspiration while that of the left heart increases during expiration. Hence, in general the murmurs that increase on inspiration can be attributed to the right heart and those that increase
on expiration, to the left heart.
CARDIOVASCULAR
SYSTEM
Mitral Regurgitant
Murmur.
Aortic Stenotic
Murmur.
79
Mitral Stenotic
Murmur.
Aortic Regurgitant
Murmur.
FIG. X I
Conduction of Murmurs.
Many functional murmurs are modified or even disappear on

inspiration. Organic murmurs often become more audible
during expiration. Pleuro-pericardial friction is often not heard
when the patient stops breathing.
Aortic diastolic murmurs and venous hum are best heard on
erect posture. Mitral diastolic murmurs are best heard on
recumbent position or when the patient lies on the left side.
Functional murmurs in the pulmonary area are best heard in
recumbent posture.
Exercise intensifies presystolic murmurs and even other organic murmurs.
D.
AUSCULTATION OF BLOOD VESSELS.
Auscultation over a great vessel may be necessary, especially

in the following conditions:
1. Aneurysma systolic m u r m u r is heard over the dilated
sac.
2.
Femoral arterya diastolic sound is often heard in aortic

regurgitation (Durozier's sound).
H O W TO EXAMINE A
80
PATIENT
3. Brachial arterya "pistol shot" sound is often heard in

aortic regurgitation, hypertension and anaemias.
4.
Neck veinsvenous hum may be heard in congestive

heart failure.
D.
PULSE
Ordinarily the pulse is felt over the radial artery. In certain

cases, especially in hemiplegias, the carotid artery may have to
be palpated; and in diseases of the aorta, like coarctation of the
aorta, the dorsalis pedis artery must be palpated.
T o feel the pulse, place three fingers of the right hand on the
patient's radial artery at the wrist.
Note the following:
1. Rate. Count the beats for at least half-a-minute if not
one minute. T h e average is 70 to 80 per minute. It is slightly
more in children and may be less in old age. A rate of 100 per
minute may be considered the upper limit of normal. In Auricular Fibrillation one may have to count the rate of the heart
beat by auscultation.
2. Rhythm. Note whether the pulse is regular or irregular;
if irregular, whether it is completely irregular or regularly irregular. If it is regularly irregular, decide whether the beats are
unequal in volume. If irregular or unequal, note the effect of
exercise on the rhythm.
3. Force. Place three fingers on the artery; the one nearest
the wrist is pressed firmly to prevent any pulse from the ulnar
artery reaching the finger through the palmar arch. T h e middle finger notes the beat. T h e proximal finger is used to compress the artery and to note the pressure necessary to obliterate
the pulse. The force of the pulse-beat gives an idea of the
systolic blood pressure. Therefore, the force of the pulse will
be increased in conditions that raise the blood pressure and
diminished in cases that lead to low blood pressure.
4. Volume. By pulse volume is meant the amplitude of
expansile movement of the vessel-wall during the passage of the
pulse wave. Apply just sufficient pressure to flatten the vessel
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
(a) THORACIC ANEURYSMthe pulse is delayed on one side. In

innominate aneurysm the light pulse is smaller than the left; in lesions
of the arch of the aorta near the left subclavian artery, the left pulse is
smaller and delayed.
(b) MEDIASTINAL GROWTHSmay compress the innominate or left
subclavian artery leading to delay in the pulse on that side.
(c) ACCESSORY CERVICAL RIBSmight kink the subclavian artery, if
unilateral. This abnormality is generally bilateral and hence, there is no
change in the pulse. Parasthaesias are more common.
(d) EMBOLISM OF ONE RADIAL ARTERYmay occur in septic endocarditis resulting in absent pulse rather than delay in the pulse.
(e) ATHEROMA OF T H E BRACHIAL OR SUBCLAVIAN ARTERY ON
ONE SIDEx-rays are confirmatory.
(f) HEMIPLEGIAespecially
picture.
when
local
atheroma
complicates
the
(g) POLIOMYELITISmay retard the growth of a limb and so produce

a small pulse.
(h) T R A U M A OF T H E RADIAL OR AXILLARY ARTERYmay cause
an arterio-venous aneurysm leading to a small pulse.
(i) COARCTATION OF T H E AORTAwhen immediately distal to the
origin of the left subclavian artery, may reduce the left radial pulsation.
PULSE AND ITS ABNORMALITIES

T h e normal rate ranges between 60 to 80 per minute. During sleep it is slower. The rate increases in standing position,
during exercise, emotional stress, anxiety, after eating, severe
anaemias, after haemorrhages, hyperthyroidism, paroxysmal
tachycardia, cardiac failure and in most of the febrile diseases.
Its increase in fevers is about 10 beats for every degree rise of
temperature and hence, when the fever is about 100F. the
pulse rate is about 100 beats per minute and when 101F. the
pulse rate is 110 and so on. Tachycardia or pulse above 100
occurs in sinus tachycardia, paroxysmal tachycardia, auricular
flutter and auricular fibrillation.
T h e pulse is slow in heart block, increased intracranial pressure, jaundice, post-febrile periods, hypothyroidism and during
digitalis administration. It is also slow in certain infections
like influenza and typhoid in which conditions the pulse is not
raised in proportion to the fever. Bradycardia or pulse below
60 occurs in sinus bradycardia and auriculo-ventricular block.
When the patient is at complete rest, say in sleep, the rate is
about 70 per minute. T h e alert rate i.e. when the patient is
CARDIOVASCULAR
SYSTEM
83
active, may be even 30 beats more than sleep-rate. If the

difference is less than 10, it is suspicious of heart disease.
T h e sleep-rate is taken normally when the patient has no
fever, no dreams, no restlessness, no over-heating in the room,
no meal for six hours previously, and between the fifth and
sixth hour of sleep.
(a) If the sleep-rate is above 90 it is always pathological; if
it is between 80 and 90, it is suspicious of involvement
of the heart.
(b) If there is no difference between alert-rate and sleep-rate
there is definite myocardial weakness especially when the
rate is above normal.
(c) In Grave's disease, the sleep-rate is always above 80 and
the difference between this and the alert-rate is small; if
there is high difference, it is because of the associated
emotional factors.
In conditions like auricular fibrillation, the pulse rate as
counted at the wrist may not indicate the true rate of ventricular contractions. In all such cases, the rate of the heart-beat
should be counted by auscultation at the apex and the difference
between this rate and the pulse rate at the wrist should be
recorded. This difference is referred to as the "pulse deficit".
FEATURES OF AN ABNORMAL PULSE
1. Thready pulse. T h e rate is rapid, the pulse wave is
small and disappears quickly. This is found in cases of severe
myocardial disease and peripheral circulatory failure.
2. Bounding pulse (high tension pulse)the pulse is wellsustained. Typically present in hyperkinetic circulatory states.
3. Collapsing pulse. T h e wave swings sharply upward and
disappears quickly. There is so much accentuation of the
dicrotic wave that it gives the impression of a double pulse at
the wrist. Occurs in severe febrile states, thyrotoxicosis, emotional disturbances and other disorders causing peripheral vasodilatation. An extreme form is the Corrigan pulse seen in
aortic regurgitation and sometimes in arterio-venous aneurysm
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
VARIATIONS IN T H E R A T E OF STIMULUS PRODUCTION

SINO-AURICULAR NODE:
85
IN
(a) Sinus arrhythmiathe pulse quickens on inspiration and

slows with expiration. This type of irregularity is of
vagal origin. Inspiration depresses the vagus producing
a momentary increase in the pulse rate. This is a normal
phenomenon in children, but may occur in nervous individuals during convalescence and acute illness. Its presence does not signify an organic disease of the heart.
(b) Pulsus paradoxusthe pulse decreases or is even absent
during inspiration and occurs in pericardial effusion.
2.
INTERFERENCE W I T H T H E SPREAD OF T H E STIMULUS:
(a) Sino-auricular blockcan occur in digitalis poisioning.

There may be occasional dropping of beats.
(b) Auricular flutterauricles beat about 300 times per
minute and the ventricles about half that rate, with occasional missing of beats; in some cases only a quarter of
the beats reach the ventricles in which case there is
regular pulse of 75 per minute.
(c) Auricular fibrillationthe auricle ceases to contract as a
whole and individual fibres contract independently of
each other. The result is that the pulse becomes irregularly irregular and the rate above 100 per minute.
This is a common complication of mitral stenosis, thyrotoxicosis and coronary diseases. If the auriculo-ventricular conducting tissue is also damaged, many of the
auricular impulses are blocked and the ventricles beat at
about the normal rate, but the rhythm is still irregular.
(d) Partial heart-blocksome of the impulses fail to pass
from the auricle to the ventricles and reveal themselves,
while feeling the pulse, as a dropping of beats. A gap,
equivalent in length to two whole pulse-beats is felt over
the radial artery. A similar gap is often felt in extrasystoles, but sounds produced by the extra-systoles are
heard over the apex; not so in partial heart-block. Heartblock may occur in diphtheria, rheumatism, cardiosclerosis, gumma, neoplasm, etc.
86
3.
H O W TO EXAMINE A
PATIENT
STIMULUS ARISING FROM O T H E R AREAS RATHER T H A N T H E

SINUS N O D E :
(a) Extra-systolescommon in nervous individuals or senile

cardiac sclerosis. The pulse may be regularly irregular.
The finger fails to recognise the small pulse beat due to
premature contraction. T h e patient generally feels the
missing of the beat. The observer feels a small beat over
the radial pulse before its time followed by a more forcible one than normal after a compensatory pause, so that
the length of the two pauses equals the duration of two
normal beats. This irregularity disappears on exercise.
(b) Paroxysmal tachycardiaoccurs in paroxysms. Generally
the cardiac action is regular and the rate is often over
180 per minute in contrast to auricular flutter where the
rate rarely exceeds 150.
(c) Complete heart blockthe rate is very slow.
regular but in few cases may be irregular.
4.
Generally
T H E STIMULUS ARISES FROM T H E NORMAL PLACE, B U T T H E

RESPONSE IS VARIABLE IN A M P L I T U D E :
Pulsus alternansthis signifies that the ventricles are

exhausted and hence a condition of serious import. Even
beats are equal to one another but weaker than the odd beats.
E. BLOOD PRESSURE
Use mercurial sphygmomanometer for taking blood pressure
with the patient sitting or lying at ease with the forearm supported at heart level. See that he is not agitated. Auditory
method is more reliable. After fixing the armlet of the apparatus just above the elbow raise the pressure of the mercury
to about 30 mm. above the suspected systolic pressure. Place
the chest piece of the stethoscope over the radial artery just
below the armlet. Open the valve of the apparatus so as to
reduce the compression gradually. T h e first faint tapping
sound heard corresponds to systolic pressure and when the
sound just becomes nearly inaudible, the diastolic pressure.
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.
Heartstrength of contraction of the left ventricle.

causes increased pressure and vice-versa.
Increased force
2.
Volume of blood entering the aorta at each systole. In haemorrhages

and in other conditions where there is impediment to the flow of
blood, the blood pressure is lower.
3.
Condition of the arteries, especially elasticity. In old age the arteries

tend to lose their elasticity and the blood pressure rises.
4.
Increased peripheral resistancesvasoconstriction

pressure and vasodilatation lowers it.
5.
Condition of the bloodviscosity and volume. Increased viscosity as

occurs in polycythaemia raises the blood pressure.
raises
the
blood
Generally the systolic blood pressure of a grown-up is100

plus his age or half his age; and the ratio between the systolic,
diastolic and pulse pressure is 3 : 2 : 1. In females the blood
pressure is less than in males by about 10 points. The normal
B.P. is 110140 systolic and 7085 diastolic.
Ordinarily a high diastolic pressure should receive more
attention than high systolic pressure because the latter is
affected by such factors as exertion, emotion, stress and pain.
Conversely, a low systolic pressure has more significance than a
low diastolic pressure, since the former reflects the strength and
stroke-volume of the left ventricle.
A diastolic pressure of 100 mm. Hg. or above is considered as
above normal; over 130 is considered as serious. Systolic pressure under 100 mm. Hg. may be considered as low blood pressure and below 90 as serious.
Note the following points while taking the B.P.
(a) In a nervous patient, the first reading is often too high
and should be rejected; the second reading will more
closely represent the true pressure.
(b) It is advisable not to take the reading more than once or
twice, as compression of a limb induces a rise in blood
H O W TO EXAMINE A
88
PATIENT
pressure. T o reduce this source of error, when successive

estimations are made, the air pressure in the armlet should
always be allowed to fall to zero as soon as each reading
has been taken.
(c) In gross oedema of the arm or if the muscles are held
contracted, the readings are inaccurate.
(d) In auricular fibrillation the blood pressure is not reliable.
(e) In certain conditions, especially in aortic regurgitation,
the blood pressure in the leg may have to be recorded.
The patient lies face downwards and the cuff is applied
above the knee and auscultation carried out over the
popliteal artery. In health the systolic pressure in the
arm is slightly lower than in the leg when the patient is
in horizontal position. In aortic regurgitation the systolic pressure in the leg is much higher than in the arm;
in coarctation of the aorta the systolic blood pressure is
very low in the leg.
H I G H BLOOD PRESSURE
AETIOLOGY:
1.
HEREDITARY DIATHESIS (ESSENTIAL
HYPERTENSION).
(a) Benign Hypertension. This is common in both sexes

after the age of 50. May be symptomless or produce
symptoms like headache, giddiness, anginal attacks, palpitation, etc. There is thickening of the radial arteries,
left ventricular enlargement and blood pressure of about
180/90.
(b) Malignant Hypertension. This is more common in males
at the age of 40 to 45. Headache and papilloedema are
the two early and constant features of the disease. The
blood pressure may go up to even 300/150. Albuminuria,
retinal haemorrhages, cerebro-vascular accidents and uraemia complicate the picture. T h e heart is markedly enlarged to the left and gallop rhythm may set in when the
heart begins to fail.
CARDIOVASCULAR
SYSTEM
89
ARTERIAL DISEASES.
(a) Arteriosclerosis. This occurs after the age of 60. If the

smaller vessels are affected, they are visibly thickened
and tortuous; the blood pressure may be over 180/100.
However, if the great vessels are involved the blood pressure may be within normal limits for the age of the
patient. The heart is not much enlarged.
(b) Periarteritis Nodosa. This is not a common condition
and will probably reveal itself by fever, leucocytosis,
eosinophilia, etc.
RENAL 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.
(a) Aortic Regurgitation. This causes high systolic pressure

and low diastolic pressure resulting in high pulse pressure. The heart is markedly enlarged and a diastolic
murmur is heard over the aortic area.
(b) Complete A-V block. In this condition the systolic pressure is high but the diastolic pressure is within normal
limits.
(c) Coarctation of the Aorta. In this condition
is high in the arms only. There may be
collateral circulation in the scapular area.
pulse may be delayed on the left side and
pulsation is feeble or absent.
<j.
the pressure
well-marked
The radial
the femoral
ENDOCRINE DISORDERS.
(a) Thyroid. In Grave's disease the systolic pressure is

moderately high but the pulse pressure is raised due to
enormous amount of blood shunting into the enlarged
vascular thyroid.
(b) Phaeochromocytoma. In such conditions the hypertension
is paroxysmal in character. The tumour may be felt in
the loin. Regitine test is positive.
(c) Cushing's Syndrome. The patient is obese with tapering
limbs and small buttocks, purplish striae and polycythaemia.
(d) Ovarian Dysfunction. Menopause often leads to high
blood pressure.
7.
METABOLIC DISORDERS.
(a) Obesity. This

hypertension.
is generally
associated with
moderate
(b) Diabetes Mellitus. Long standing cases often lead to

high blood pressure due to thickening of the vessel walls.
(c) Gout. This is invariably associated with high blood
pressure.
CARDIOVASCULAR
8.
SYSTEM
91
BLOOD DISEASES.
Polycythaemia may cause a rise in the blood pressure. The

appearance of the patient is florid with blood-shot eyes, splenomegaly, cardiac hypertrophy, raised haemoglobin content and
increase in red cells.
9.
NEUROLOGICAL DISORDERS.
Increased intracranial tension, post-encephalitis, bulbar

poliomyelitis and lead encephalopathy often give rise to hypertension.
Of the various conditions that cause hypertension, essential
hypertension is the most important. Of this, the benign type
which appears in the 6tli decade is not so serious and may be
symptomless for many years.
In malignant hypertension, which occurs in the 4th or 5th
decade the prognosis is infinitely worse. The progress of the
disease is fairly rapid and the patient does not survive beyond
three years once the diagnosis is made. The presenting symptoms are paroxysmal headache, nocturnal dyspnoea and polyuria. Haematuria, blurring of vision and attacks of hypertensive encephalopathy are almost always present. Presence of
exudates or haemorrhages in the fundi are characteristic of the
disease. Paresis is fairly common and cerebral haemorrhage
very often puts an end to the distressing disease.
INVESTIGATIONS
A.
NECESSARY
IN A CASE OF
HYPERTENSION.
History:
1. Family history of high blood pressure.
2.
History of kidney diseases, diabetes, toxaemia of pregnancy.
3. Age. At 20 suspect unilateral cystic kidney; at 45

malignant hypertension, at 60 arteriosclerosis.
4.
Sexmalignant hypertension is more common in

males; arteriosclerosis is equally common in both sexes;
in females at the age of 45, the most likely cause of
hypertension is menopause.
5.
Occupationespecially to exclude industrial poisons.
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.
Central nervous system for neurosis, brain conditions

and funduscopy for arterial changes.
C.
Examination of urinefor sp. gr., albumin, casts and red

cells.
D.
E.C.G.
E.
Blood examination to exclude polycythaemia.
F.
X-ray of the heart and the genito-urinary tract.

LOW BLOOD PRESSURE
In adults a systolic blood pressure of 100 may be regarded as

the lower limit of normal, though age, sex, race and environment must be considered in the evaluation of this sign. However, a systolic pressure below 80 needs serious consideration
and may need immediate attention, especially in cases of acute
onset.
It is common for hypotensive patients to lack energy, with
symptoms such as headache, dizziness, exhaustion, etc. Yet,
these symptoms, when they occur, are an expression of an
inferior constitution rather than due to hypotension itself.
Hence, the importance of not regarding hypotension as a
disease like the opposite conditionshypertension, which carries
an infinitely more serious prognosis.
Persistent hypotension occurs in the following conditions:
1. Postural. An adult who is perfectly well feels giddy on
rising abruptly and may even faint. It is due to sluggish vasomotor control and is not fatal. This may also occur during
convalescence and in diseases of the central nervous system such
as encephalitis, syringomyelia or tabes dorsalis due to impairment of the vasomotor reflexes.
2. Chronic wasting diseasestuberculosis, anaemia, cancer,
etc., are generally associated with low blood pressure.
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.
5. Functional. In anorexia nervosa, the patient, who is

generally a female suffers from loss of appetite, anaemia and
wasting, in addition to low blood pressure.
Acute hypotension occurs in the following:
1. Vaso-vagal attacksthe pulse also falls to about twothirds of the normal.
2.
Peripheral circulatory failuredue to serious injuries,

extensive burns and haemorrhages.
3. Acute cardiac failurecoronary attacks, pulmonary embolism and severe toxaemias.

4. Stoke-Adam's syndrome.
5.
Rapidly developing pericardial effusion.

F.
EXERCISE TOLERANCE TEST
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.
The pain is situated behind the sternum. It is continuous

and gripping in character and generally radiates in different
directions especially towards the left arm. It is often provoked
by exertion. Not uncommonly the patient refers to it as
"indigestion". In fact when a patient above 50 complains of
stomach discomfort, one should always bear in mind heart
disease.
The common cardiac conditions that give rise to pain are:
1. When blood supply is deficient in coronary circulation:
(a) Angina pectorissudden pain lasting for a minute or
so accompanied by a sense of impending death. The
cause of pain is coronary spasm.
(b) Coronary diseasesevere pain, persisting for hours or
days with collapse. The pain generally radiates along
the left arm.
(c) In healthy personswhen an excessive demand of
work is put upon the heart, as running to catch a bus.
Such pain generally lasts for a minute or so. If it
lasts longer, it is suggestive of early coronary insufficiency.
CARDIOVASCULAR
2.
SYSTEM
95
When the diastolic pressure in the aorta is very low, as

in aortic regurgitation in which condition the coronary
vessels do not get sufficient blood during the diastolic
interval.
3. When the quality of blood is impoverishedanaemias,

diabetes mellitus.
4.
Abnormal heart rhythmparoxysmal tachycardia and

auricular fibrillation. In both, palpitation is more evident than pain.
5. Acute infection of the heart and pericardium:

(a) Acute rheumatic carditiscardiac pain may be present especially in children during the acute stage of
the illness. It is not affected by breathing as occurs
in pericarditis.
(b) Pericarditisin majority of cases, there is vague dull
praecordial oppression rather than pain; but when
parietal pericardium, especially next to pleura is
involved, there is stabbing pain, often made worse by
breathing or coughing.
6.
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.

KXTRA CARDIAC CONDITIONS.
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
(e) Acute intestinal obstructionpain is severe and more

marked in the abdomen associated with vomiting.
5.
Referred painPott's disease or spinal cord tumours may

give rise to pain in the cardiac area which becomes worse
on turning, coughing or stretching the arms. Localised
tenderness over the spine may be elicited.
6.
Superficial painsherpes, neuralgia, myositis and fibrositis

may cause pain in the heart area.
M E T H O D OF INVESTIGATION.
1. Age. At 20 suspect cardiospasm; at 40 to 50, coronary

disease; after 50, angina.
2.
Sex. Coronary disease is more common in males; pseudoangina in females.
3.
Family historyespecially of angina, coronary disease,

arteriosclerosis and high blood pressure.
4.
Character and site of pain.

Dullmyalgia, neuralgia.
Boringaneurysm eroding the bones.
Stitchingpericarditis, pleurisy.
Pain and palpitationextra-systoles, paroxysmal tachycardia.
Pain in relation to foodpeptic ulcer.
Discomfort rather than paingaseous disturbances in the
stomach.
Severe pain shooting along the armcoronary disease.
Vice-like pain with sense of impending deathangina
pectoris.
5.
Relation to exercise, food and coughing.

Anginal pain occurs after exercise.
Peptic ulcer pain has definite relation to food.
In spinal lesions the pain worsens on coughing.
Onset.
Attitude. Immobile.
Duration.
Radiation.
Shock.
Sweating.
Dyspnoea.
Vomiting.
Pulse. Unchanged.
Temperature. Normal.
B.P.
Heart sounds. Normal.
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.
Distant; gallop rhythm; pericardial rub
Falls.
Fever follows.
Small, often rapid.
Often present.
Sternum, often lower third.
Generally to the left arm.

Profuse.
Present.
Hours or days.
Restive.
Sternum, often mid-sternum.
Often at rest.
40-50 years.
Coronary Thrombosis.
Nil or diffuse to both arms and neck.
Rare.
Absent.
Slight.
Absent.
Minutes.
Site of pain.
3.
4.
During exertion.
Age of occurrence. 50-60 years.
1.
2.
Angina Pectoris.
DIFFERENTIATION BETWEEN ANGINA PECTORIS AND CORONARY THROMBOSIS.
98
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.
Increased rate, force or irregular action of the heart.
Palpitation generally does not imply heart disease but rather

some general disturbance of a nervous or debilitating character.
When heart disease is present, palpitation if at all is complained
of, is a minor symptom overshadowed by shortening of breath
or anginal pain.
T h e causes may be:
I.
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.
Aortic regurgitationthe patient feels throbbing

sensation over the heart and sometimes in the head.
H O W TO EXAMINE A
100
PATIENT
II.
Non-cardiacindigestion, toxaemias, hyperthyroidism

phaeochromocytoma, anaemias, pressure on the heart as
in pleurisy, ascites, etc.
III.
Functionalexercise, excess of tea, coffee, smoke or

alcohol, neurosis, effort syndrome, during menstruation,
menopause, pregnancy and during convalescence.
SYNCOPE (FAINTING)
Syncope is due to vasodilatation of cerebral vessels resulting

in vaso-vagal effects, i.e., slowing of the heart to 40-50 beats,
feeble action of the heart, pallor of the face, and slight convulsive movements of the head and neck. Syncope generally
occurs when the patient is standing. T h e patient will complain
of giddiness, often nausea and profuse sweating. He may even
fall down and lose consciousness for a few seconds.
Factors that contribute to fainting are:
(a) Upright posture leading to venous pooling below the heart.
(b) Instability of vasomotor control leading to vasodilatation.
(c) Hot and stuffy atmosphere, which increases peripheral dilatation.
(d) Ill-health, psychic factors, emotion, fright, etc.
Common causes of fainting:

1.
Functional.
1. Foul ventilation, unpleasant sight or smell.
2.
Exposure to grief, bereavement or any sudden emotion.
3. Anxiety, fear, etc., in nervous individuals.

4.
Exhaustion, fatigue as after strenuous work or in

excessive heat.
5. Convalescence, starvation.
6.
Orthostatichypotensive persons, especially during convalescence, starvation, long illness, prolonged

standing, lack of sleep, etc., may feel giddy on
change of posture such as standing suddenly from
recumbent posture.
CARDIOVASCULAR
SYSTEM
101
II.
Severe painrenal or biliary colic, coronary thrombosis,

pulmonary embolism, sudden visceral disorders like perforation, rupture, strangulation, etc.
III.
Loss of blood or plasmainjuries, burns, wounds, etc.
IV.
Chemical agentshistamine, nitrites, acetylcholine, anaesthetics, hypnotics.
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.
Syncope of cardiac origin may occur even when the patient

is lying down. There is no sweating and there is no vasodilatation.
It is primarily due to failure of the ventricular
output.
SHOCK
Shock is a disturbance of circulation resulting in insufficient
supply of blood to vital tissues, especially the brain resulting in
subnormal temperature, profuse sweating, intense thirst, low
blood pressure, rapid breathing, feeble pulse, cold and moist
skin and low urinary output.
Etiology:
A.
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.
Delayed haemorrhage from trauma, ruptured

spleen or kidney.
3.
Profuse diarrhoea and vomiting.
4.
Sudden severe emotion.
5.
Exposure to extremes of temperature.
6.
Blast and crush injuries.
liver,
7. Post-anaesthesia and post-operative shock.

8.
Overdose of hypnotics.
9.
Food poisoning and poisoning by irritants.
10. Specific fevers.

OEDEMA
It is convenient to discuss oedema under Cardio-Vascular
System. Although the causes are several, only one of them is
directly connected with Circulatory disturbances.
Oedema means an abnormal accumulation of fluid in the
tissue spaces or serous cavities. When in former form, there
is pitting on pressure and in latter conditions the fluid may
shift from one place to another. It is only when 5 to 6 litres
of fluid has collected in the water depots that oedema becomes
evident; and pitting is produced when the circumference of a
limb goes up by ten per cent.
Oedema of all forms is the result of water and salt retention
in the tissuesmainly retention of salts.
Factors governing transudate of fluid into the subcutaneous
tissues:
1. PERMEABILITY OF CAPILLARY ENDOTHELIUM. Normally this
is freely permeable to water and crystalloids, but impermeable to proteins.
Hence, when damaged, the permeability to proteins is increased as occurs
in inflammations, urticaria, histamine poisoning, snake-bites, etc.
2. CAPILLARY PRESSURE. Normally the capillary pressure at the
arterial end is 32 mm. Hg. and at the venous end, 12 mm. Hg. When the
venous pressure rises as in cardiac weakness, fluid enters into the tissues
resulting in oedema.
CARDIOVASCULAR
SYSTEM
103
3. COLLOID C O N T E N T OF T H E BLOOD. This is mainly maintained

by albumin and globulin. These tend to retain fluid in the blood-vessels
or actually help absorption of fluid from the surrounding tissues by action
of their osmotic pressure. T h e total plasma proteins are about 7 to 7.5
Gm. per 100 c.c. blood, of which albumin is 60% and globulin, 40%.
If the total quantity of proteins fall to 5.5 Gm. per cent or plasma albumin
to 2.5 Gm. per cent, oedema appears. Reduction in proteins occurs in
malnutrition, haemorrhage, massive ascitcs, and chronic nephritis with
severe albuminuria. Reduction in plasma albumin alone occurs in nephrosis;
the albumin molecule, which is one-fourth of the weight of globulin
molecule, diffuses more readily through the glomeruli in cases o nephrosis,
resulting in massive oedema.
4. CRYSTALLOID C O N T E N T OF T H E BLOOD. Retention of salts as
occurs in acute nephritis, helps retention of fluid in the tissues resulting in
oedema.
5. W A T E R C O N T E N T OF T H E BLOOD. Water retention is not
accepted as a general factor in the causation of oedema, but may be a
minor factor in acute oedematous nephritis.
6. CHANGES IN TISSUE CELLS. It is now believed that tissue cells
in nephritis have increased affinity for water due to excess of Na-ions in
them and this is considered one of the factors in the production of oedema
in kidney diseases.
7. CONDITION OF T H E KIDNEYS.
retention of crystalloids (acute nephritis) or
through the glomeruli (nephroses), resulting
cannot excrete salts freely. Hence, repeated
"pickled baby".
These, when damaged, cause

allow free passage of albumin
in oedema. In infants, kidneys
use o normal sali.ne may cause
8. NERVOUS CONTROL BY T H E HYPOTHALAMUS. This is not

an important factor in the causation of oedema, but plays an important
part in the retention of fluid in certain pituitary dysfunctions like Frolich's
syndrome.
Transudation or exudation of fluids into the tissues occurs

as a result of a number of causes. It is best recognised by the
characteristic "pitting" on pressure and should be distinguished
by the more solid swelling of lymphatic obstruction or myxoedematous conditions of hypothyroidism and which does not pit
on pressure.
CAUSES
A.
OF OEDEMA
IN
GENERAL:
CARDIAC CONDITIONS:
1. Congestive heart failure. Cardiac oedema is a gravity

oedema and appears first in the most dependent parts of
the body. The right ventricle fails to pass all the blood
it receives from the veins. The capillary walls are also
stretched and become more permeable to fluids.
104
IIOW T O E X A M I N E A
PATIENT
2. Pulmonary oedema. This is a cardiac variety of oedema

and is due to fluid passing from the distended capillaries
into the alveoli of the lungs. This is common in left
ventricular failure and the oedema is confined to the
lungs for a long time, before it appears elsewhere in the
body.
3. Pericardial diseases. In pericardial effusion and in
adherent pericardium especially, there is obstruction to
the flow of blood into the right auricle. This causes
oedema of the body; but, as the heart is able to p u m p
the little blood it receives into the lungs and into the
general circulation, oedema of the lungs may be absent.
B.
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:
In these conditions the face looks puffy and a small amount

of oedema may appear in the more dependent parts of the body
and abdomen. The total proteins of the plasma should fall
below 5.5 Gm. per cent or the albumen to 2.5 Gm. per cent to
produce oedema.
1. Anaemias.
pallor.
There is puffiness of the face in addition to
CARDIOVASCULAR
SYSTEM
105
2. Protein deficiency. There is generalised wasting of the

body and mild swelling. Starvation, diabetes, chronic
diarrhoeas and pregnancy are common examples.
3.
D.
Cachexia. Any wasting disease, sooner or later causes

decrease in the amount of plasma proteins leading to
oedema.
PORTAL O B S T R U C T I O N :
In cirrhosis of the liver the swelling appears in the abdomen

first. The chief factor perhaps is low protein diet followed by
compression of the hepatic branches of the portal veins. Excess
of fluid into the peritoneal cavity leads to pressure in the venous
circulation in the lower limbs leading to oedema of the legs.
Besides, liver disease interferes with the synthesis of proteins
leading to hypoproteinaemia and thus contributes to further
development of oedema.
E.
VITAMIN DEFICIENCY:
Beri-beri often gives rise to swelling in the various parts of

the body. The factors that contribute to it are faulty proteins
in the diet, decreased plasma proteins, cardiac failure and
secondary renal insufficiency.
F.
CIRCULATORY O B S T R U C T I O N :
1. Pressure on the veins by tumours, scars, pregnancy, etc.

causes swelling distal to the point of pressure.
2. Venous thrombosis, due to inflammation or stasis as in
femoral thrombosis, a painless pitting oedema develops
distal to the point of obstruction.
3. Local inflammation. The oedema of acute inflammation
is a localised swelling with evidence of inflammation;
slightly pits on pressure, especially around the inflamed
area.
G.
EPIDEMIC DROPSY:
In this condition several people in the locality develop

oedema of the legs in epidemic form. The cause of oedema is
vasodilatation of the capillaries.
106
H.

ALLERGIC CONDITIONS
1. Allergy. In this condition there is temporary change in

the capillary endothelium so that it becomes more permeable, resulting in localised oedema.
2. Angioneurotic oedema. This is also a localised oedema
of transient nature and may be intensely itching.
I.
HEREDITARY CONDITIONS:
Milroy's disease is a condition in which there is oedema of

the lower limbs affecting one or both the legs.
J.
LYMPHATIC OBSTRUCTION:
The swelling in such conditions is hard and does not pit on

pressure.
K.
SCLERODERMA:
T h e oedema in these conditions is due to local circulatory

changes and is confined to some parts of the body. T h e swelling is rather hard and tense to the feel.
CAUSES OF LOCALIZED
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
(b) Pressure by glands, tumours, etc.

5.
Local effects of irritants:
Mustard, gas, carbolic acid, etc.
6.
Congenital and hereditary disorders:

(a) Arterio-venous aneurysm.
(b) Milroy's disease.
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
Factors involved in cardiac failure:

(a) FALL IN CARDIAC O U T P U T . T h e normal is 4-5 litres per
minute. In gross failure it falls to even 50% of the normal, especially
in diseases primarily of the heart, such as valvular disorders, hypertension, coronary thrombosis, myocarditis and congenital heart
diseases. T h e cardiac output may remain high in conditions of heart
failure primarily due to non-cardiac diseases like severe anaemia,
thyrotoxicosis, patent ductus, arteriovenous fistula, Paget's disease,
emphysema and beriberi.
(b) RISE IN VENOUS PRESSURE. This begins to rise near the heart
when it begins to fail and is more so in right ventricular failure.
Normal venous pressure is 50-140 mm., H 2 0 . In right ventricular
failure it goes up to 280-380. At 220 mm., the liver begins to enlarge
and at 250 mm., oedema sets in.
(c) INCREASE IN BLOOD VOLUME. Normal is 3.55 litres. Volume
rises when there is inability on the part of the kidney to excrete salts.
'(d) INCREASE IX T H E CIRCULATORY RATE. Normal rate from arm
to tongue is 10 16 sec. In heart diseases without failure it is slightlyslow; in cardiac failure it is much slowed.
108
I.
CARDIAC FAILURE (Central)
This may beA.

A.
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.
7.
Severe acute myocarditis.
T h e main cause of acute failure in all the latter conditions is

lack of blood supply to the myocardium either directly due to
damage to the coronary vessels or impediment to the blood flow
in those vessels.
CONGESTIVE H E A R T FAILURE
This may be defined as a state in which the heart fails to
maintain an adequate circulation for the needs of the body,
resulting in congestion in the various parts of the body, especially in the lungs, liver and subcutaneous tissues (oedema).
From clinical point of view, congestive failure is divided into
two types, although both may be associated together.
I.
II.
Right ventricular failure.

Left ventricular failure.
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.
Secondary to chronic left ventricular failure.
4.
Primarily non-cardiac diseases. Diphtheria, toxic myocarditis, thyrotoxicosis, beri beri, severe anaemia, etc.
In rare cases right ventricular failure may occur in:

5.
Acute form as a result of massive pulmonary embolism.
6.
Sub-acute form due to repeated attacks of minor pulmonary embolism by clots or malignant cells.
II.
LEFT VENTRICULAR FAILURE.
This occurs in conditions in which the reserve of the left

ventricle is exhausted and with the appearance of one single
symptom of paroxysmal dyspnoea long before other symptoms
appear. This symptom generally appears at night because in
lying position the blood flow into the heart is more than in
upright position when a large quantity of blood is in the lower
part of the body. When the patient lies down in bed, more
blood goes into the lungs and hence, more chances for the lungs
to engorge.
Pulmonary oedema constitutes a more severe and acute stage
of left ventricular failure.
Causes:
1. Hypertension of any type.
2.
Aortic valvular diseasesaortic regurgitation, aortic stenosis.
3.
Coronary diseases.
110
II.
PATIENT
PERIPHERAL CIRCULATORY FAILURE
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,
2. Vasogenicspinal anaesthesia, anaphylactic shock, adrenal insufficiency.

3.
Toxaemias and infections.
Acute tuberculosis, severe pneumonia and diphtheria are the

most important causes.
4. Loss of fluids.
Haemorrhages, extensive burns and dehydration due
vomiting, diarrhoea, diabetes, acidosis and heat-stroke.
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.
1. Hypertrophy of the ventricles.

2.
Dilatation of the heart cavities.
3.
Combination of both.
CARDIOVASCULAR
The most important
SYSTEM
signs of enlargement
111
of the heart are:
(a) Displacement of the cardiac impulse.

(b) An increase in the area of cardiac dullness.
When the left ventricle is enlarged the displacement of the
cardiac impulse is mostly downwards than outwards. When due
to enlargement of the right ventricle the impulse is more outward than downwards with marked pulsation in the epigastrium
and also dullness extending to the right.
Before cardiac
following:
enlargement
is
diagnosed,
exclude
the
(a) Mechanical displacement of the heart by fluid or air in

the right pleural cavity.
(b) Retraction of the left lung exposing the heart.
When the impulse of the apex is forceful and heaving, hypertrophy of the left ventricle is likely; and if diffuse, right ventricular enlargement.
If dullness is increased to the right, the cause is likely to be
right ventricular enlargement; if to the left, left ventricular
enlargement, and if increased in all directions, enlargement of
both the ventricles. Dullness in the second left interspace indicates enlargement of the left auricle or enlargement of the
pulmonary artery; in the 2nd right interspace, aneurysm of the
ascending aorta.
I.
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:
(a) Aortic Regurgitation. T h e greatest enlargement occurs

in aortic regurgitation. T h e heart is both hypertrophied
and dilated, it is easily diagnosed by the presence of a
diastolic murmur at the base of the heart conducted down
to the sternum, presence of water-hammer pulse and high
pulse pressure.
112
PATIENT
(b) Aortic Stenosis. There is hypertrophy mainly of the left

ventricle. The pulse is anacrotic and there is a systolic
murmur in the aortic area conducted to the neck vessels.
(c) Aneurysm of the ascending aorta. If this involves the
aortic ring rendering it incompetent although the cusps
are healthy, one gets symptoms of aortic regurgitation and
hence enlargement of the heart. There will be dullness
in the 2nd right interspace also.
2.
MITRAL
REGURGITATION:
T h e heart is both dilated and hypertrophied; there will be a

systolic murmur over the apex conducted towards the axilla.
3.
HYPERTENSIVE
HEART
DISEASE:
T h e degree of enlargement may not be proportional to the

height of the blood pressure nor to its duration. T h e heart is
hypertrophied and the apex is displaced more downwards than
outwards. The impulse is forcible and heaving in character.
T h e first sound at the apex is prolonged and the second aortic
sound accentuated.
II.
ENLARGEMENT OF T H E R I G H T VENTRICLE
Causes:
1.
DISEASES
OF THE LEFT SIDE OF THE HEART:
(a) Mitral Stenosis. The left auricle is first hypertrophied

and then dilated, passive congestion in the lungs follow
and the right ventricle is next enlarged. A diastolic
thrill, presystolic murmur and dullness in the 3rd left
interspace are characteristic features of the disease.
(b) All conditions which cause Left Ventricular Enlargement.
In course of time the left ventricle fails to maintain compensation; the right ventricle begins to overwork and
keeps on enlarging till it also fails leading to congestive
heart failure.
2.
DISEASES OF THE LUNGS
(COR PULMONALE):
Chronic bronchitis, fibroid lungs, chronic emphysema, etc.,

throw a strain on the right side of the heart resulting in its
CARDIOVASCULAR
113
SYSTEM
hypertrophy. The main symptoms will be cough of long

duration followed by evidence of cardiac failure.
3.
DISEASES OF THE RIGHT SIDE OF THE

MOSTLY CONGENITAL
DISEASES.
HEART,
(a) Pulmonary Stenosis. This is not a common disease by

itself. T h e patient is not disabled early; cyanosis and
clubbing of the fingers appear late. A rough systolic murmur and a thrill in the pulmonary area point to the
diagnosis.
(b) Fallot's Tetralogy. Consists of pulmonary stenosis, patent
interventricular septal defect, dextraposed aorta and enlarged right ventricle. The child is cyanosed in early life
and polycythaemia is present. The cardiac impulse is
displaced to the right and is diffuse in character.
(c) Eisenmenger's Complex. This consists of ventricular
septal defect, dextraposition of the aorta, right ventricular hypertrophy and dilated pulmonary artery. The
enlargement is mainly to the right.
(d) Auricular Septal Defect. This may be symptomless and
devoid of physical signs, but if the defect is large the
strain on the right ventricle may lead to failure. Cyanosis then appears. A systolic murmur may be heard in
the 2nd left interspace, though seldom as pronounced as
in pulmonary stenosis. T h e pulmonary artery may be
enlarged producing a familiar "hilar dance" noticed on
screening. The right ventricle is enlarged.
(e) Lutenbacher's Disease. This consists of'patent interauricular septal defect and mitral stenosis. Radiologically
the left auricle is much less enlarged than expected and
the right heart is very prominent.
(f) Patent Interventricular Septum. This may run a benign
course, but if the defect is great, both the ventricles get
enlarged and the main stress finally falls on the right
ventricle. There is a rough systolic murmur in the 4th
left interspace. There is no cyanosis.
(g) Patent Ductus Arteriosus. This may not show cardiac
enlargement in the beginning. Either of the two ventri8
114
PATIENT
cles may be enlarged first, but soon the right ventricular

enlargement dominates the picture. There is no cyanosis
and no clubbing, but the patient may be under-developed.
The pulse is large, especially after exercise. The characteristic "machinery murmur" is heard in the pulmonary
area.
In all these conditions which cause enlargement of the right
ventricle the anterior surface of the heart is formed almost
entirely by the right ventricle. There is systolic recession in
the epigastrium due to enlarged right ventricle. The apex beat
is diffuse in character and mainly formed by the right ventricle.
T h e cardiac dullness is broadened; venous pulsation in the neck
is well-marked and the pulmonary 2nd sound is accentuated.
III.
ENLARGEMENT OF T H E WHOLE H E A R T
Causes:
1. Myocardial
disease.
fibrosisoften
the
outcome
of
coronary
2. Myocarditisespecially after rheumatism.

3. Thyrotoxicosisthe heart may be moderately enlarged.
There is tachycardia, pulsating carotids, exophthalmos
and enlarged thyroid gland.
4.
Myxoedemathe heart is often enlarged. T h e patient's

appearance is coarse, skin dry, eye-brows scanty and pulse
slow.
5. Acromegalythe face is egg-shaped in appearance with

enlarged tongue and enlarged lower jaw.
6. Vitamin B deficiencyberi beri may cause considerable
enlargement. There may be associated neuritis and swelling of the calf muscles.
7. Chronic anaemiathe heart is mainly dilated and a
haemic murmur may be present in the pulmonary area.
8. Paget's disease, especially during the active stages the
.heart may be enlarged.
9. Familial megalocardiapresent from birth.
CARDIOVASCULAR
SYSTEM
115
10. Gaucher^ disease, Glycogen disease, Amyloidosis and

Haemochromatosis are rarer causes of heart enlargement
which require special investigation for their diagnosis.
IV.
CARDIAC DILATATION
Dilatation occurs when

1. Ventricle has to eject blood against an abnormal resistance. All conditions that give rise to hypertrophy finally
cause dilatation of the heart.
2.
When the contractile power of the ventricle is impoverished:

(a) Pericardial effusion.
(b) Myocarditisacute and chronic.
(c) Severe anaemias.
(d) Severe toxaemias.
(e) Thyrotoxicosis.
(f) Vitamin B deficiencyberi beri.
(g) Severe cardiac arrhythmias.
In most of these cases the apex is displaced outwards and

is diffuse in character. 1st sound is weak and often short and
sharp, resembling the 2nd sound. The heart sounds may give
the impression of "tick-tack" rhythm. T h e 2nd pulmonary
sound is accentuated. The pulse is rapid and the blood pressure is low.
MURMURS AND T H E I R SIGNIFICANCE
Murmurs may be grouped under four
cardial, myocardial, exocardial and vascular.
headingsendo-
ENDOCARDIAL MURMURS
I.
FUNCTIONAL
These are systolic in time, soft in character, best heard over

the pulmonary area and unassociated with any structural damage
to the heart. The murmurs often disappear on change of
116
PATIENT
posture and when the breath is held in inspiration. Such murmurs may be heard in fevers, anaemia, nervousness, tachycardia,
hyperthyroidism, etc.
II.
These may be acquired or

A.
ORGANIC
congenital.
ACQUIRED
MURMURS
These may be systolic or diastolic in time. They may be heard

in mitral, aortic, pulmonary or tricuspid area. T h e first three
areas must be examined in all suspected valvular diseases of the
heart.
MITRAL MURMURS
These may be systolic or diastolic in time.

1. Systolic Murmurs
T h e presence of such murmurs at the apex, unless harsh in

character has not much significance. They may occur due to
several other conditions which have no bearing to any heart
disease as such. Common conditions that give rise to systolic
murmurs at the apex are:
(a) Temporary or permanent dilatation of the heart without
any real organic heart or mitral valve disease. This is
the commonest cause.
(i) Physiological, as after exercise and in a rapidly growing child.
(ii) Anaemia, malnutrition, infections, fevers, tachycardia.
(b) Organic disease of the heart without deformity of the
mitral valve. This is the next common cause.
(i) Hypertension.
(ii) Grave's disease.
(Blood is ejected with a snap).
(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
(d) Aortic Stenosis. This murmur may be heard at the apex

in some cases. In such cases diminution of the 2nd aortic
sound is important to diagnose aortic stenosis.
(e) Congenital heart diseasespulmonary stenosis, patent
ductus, ventricular septal defect, atrial septal defect,
coarctation of the aorta. In nearly all these conditions
the murmur is best heard to the left of the sternum in
the 3rd and 4th interspaces.
(f) Pericardial rub. This may be mistaken for a systolic
murmur. This is a to-and-fro sound which changes on
pressure with the stethoscope.
(g) Tricuspid incompetence. The murmur may be heard at
the apex, but is usually louder at the lower end of the
sternum and intensified on deep inspiration.
Presystolic Murmur (Mitral Stenosis)
Presystolic & Systolic Murmurs (Mitral Stenosis

& Regurgitation)
Pansystolic Murmur
(Mitral Regurgitation)
Systolic Murmur
(Functional)
Fig.
XII
118
PATIENT
In assigning systolic murmurs their correct importance, much

reliance should be placed upon the history of rheumatic infection, size of the heart, presence of any other valvular murmur
especially a diastolic murmur at the apex. If the systolic murmur is conducted towards the axilla, in majority of cases, it
suggests mitral regurgitation. In all such cases a persistent
search must be made for a diastolic murmur of mitral stenosis,
which so commonly accompanies mitral disease.
2. Diastolic Murmurs
A diastolic murmur is invariably of organic origin and is

nearly always due to mitral stenosis. It may be mistaken for
splitting of the 1st sound, which is often present in health. In
cases of doubt put the patient on a moderate exercise and then
auscultate. T h e presystolic murmur becomes more prominent,
while splitting is unaltered or disappears. Common conditions
that give rise to diastolic murmurs at the apex are:
(a) Mitral stenosis. T h e murmur being strictly localised, the
patient must be carefully examined, if necessary, on
change of posture or after exercise.
(b) Relative mitral stenosis:
(i) Austin-Flint murmur of aortic regurgitation due to
considerable dilatation of the left ventricle resulting
in relative stenosis at the mitral valve.
(ii) Markedly dilated left ventricle due to severe rheumatic myocarditis.
(iii) High grades of anaemiaassociated with a systolic
murmur.
(c) Transmitted from aortic regurgitationin such cases the
presence of water-hammer pulse and high pulse pressure
will confirm the diagnosis.
T h e chief features of mitral stenotic murmur are:
(i) Harsh in charactercrescendo, if purely presystolic.
(ii) Appears after a definite interval of time after diastole.
(iii) Localised at the apex over a small area.
CARDIOVASCULAR
SYSTEM
119
(iv) Better heard with a bell-chest piece.

(v) Better heard when the patient bends forward and slightly
to the left.
(vi) Becomes more pronounced when the patient is put on
mild exercise.
In mild mitral stenosis the left atrium is able to empty fairly
rapidly through the narrowed valve and the resulting murmur
is mid-diastolic.
T h e 'opening snap' heard in mitral stenosis is a loud sound
heard just after the 2nd heart sound and is due to high leftatrial pressure which forces the mitral valve to open rapidly
when the ventricle relaxes. It is present as long as the damaged
mitral valve is not rigid or calcified.
AORTIC MURMURS
These may be systolic or diastolic in time.

1. Systolic Murmurs
These murmurs are fairly common in the aortic area in

elderly persons and are usually associated with dilatation of the
aorta. Common causes are:
(a) Dilatation of the aortachronic hypertension, dynamic
effect of aortic regurgitation, arterio sclerosis, syphilitic
aortitis. T h e murmur is soft in character.
(b) Aortic stenosis:
(i) Rheumatic or sclerotic in origin. T h e murmur is
harsh, mid-diastolic or crescendo-diminuendo 'diamond-shaped' in character and is accompanied by a
systolic thrill.
(ii) Congenital sub-aortic stenosisthe murmur is very
loud and can be even heard at a distance.
(c) Aortic aneurysmthe murmur is soft; there is dullness
over the swelling which is pulsatile.
(d) Coarctation of the aortathe systolic murmur is also
heard at the back. There is tortuosity of arteries, the
blood pressure in the upper limbs is high and in the lower
limbs low.
120
IIOW T O E X A M I N E A P A T I E N T
(e) Pulmonary murmursmay be transmitted to the aortic

area, but they are best heard to the left of the sternum.
These are always organic and indicate aortic incompetence.

They may be heard over the aortic or pulmonary area. T h e
characteristic water-hammer pulse helps to arrive at a diagnosis
of aortic regurgitation from pulmonary regurgitationthe
latter, a rare diseasewhen the murmur is heard over the pulmonary area.
Systolic "diamond-shaped"
(Aortic Stenosis)
Murmur
Diastolic Murmur
(Aortic Regurgitation)
Systolic & Diastolic Murmurs

(Aortic Stenosis & Regurgitation)
FIG. XIII
Common conditions that give rise to diastolic murmurs at the

aortic area:
(a) Aortic regurgitation. T h e characteristic features of this
murmur are:
(i) Soft and blowing diminuendoin character.
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)
Syphilis between 35 and 50 years.

Arteriosclerosis, at advanced age.
Rheumatism.
Subacute bacterial endocarditis.
(v) Traumaticmay be a factor if the aortic valve is

congenitally deformed.
(vi) Dilatation of the aortic ostium due to syphilitic
aortitis.
(vii) Chronic hypertensiondue to dilatation of the aortic
ring.
(viii) Dissecting aortic aneurysms.
(ix) Severe anaemia, in association with a haemic murmur.
(b) Pulmonary regurgitationa rare condition and the murmur is better heard over the pulmonary area rather than
over the aortic area.
PULMONARY MURMURS
These are generally systolic and on rare occasions diastolic in

time.
1.
Systolic Murmurs
Systolic murmurs over the pulmonary area are quite frequent

and may not be of much significance so as to help in the diagnosis of heart diseases. They are more commonly due to functional disorders and are common when there is increased flow of
122
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.
Diastolic murmurs in the pulmonary area are rare. T h e

commonest cause of such murmurs is aortic regurgitation and
the murmur is best heard in the 3rd or 4th interspace, whereas
a real pulmonary regurgitant murmur is best heard in the
2nd left interspace. Capillary pulsation and water-hammer
pulse is present in the former and not in the latter.
Causes:
(a) Graham-Steel murmur of mitral stenosis, due to relative
incompetence of the pulmonary valve as a result of dilatation of the pulmonary artery.
(b) Left ventricular failure with pulmonary congestion.
CARDIOVASCULAR
SYSTEM
123
(c) Chronic lung disease with pulmonary congestion.

(d) Chronic obliterating pulmonary endarteritis.
(e) Congenital defect of the pulmonary valve causing regurgitation.
(f) Wide patent ductus arteriosus.
(g) Acute or chronic endocarditis of the pulmonary valve.
B. CONGENITAL MURMURS
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.)
IIOW TO EXAMINE A PATIENT
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.
Acute cardiac failuresoft systolic murmur heard at the

due to stretching of the left ventricle.
Febrile diseasessame as in '2'.
Anaemias and fatty degenerationsame as in '2'.
EXOCARDIAL MURMURS
These murmurs are of two varieties:

1. Pericardial frictionthis is a to-and-fro murmur, best
heard over the area of the heart not covered by the lung. The
1st element which is more distinct, occurs in systole and the 2nd
element during diastole. It is heard so close to the ear as
though it is produced in the stethoscope itself. It is not affected
by breathing, may alter with the change of posture of the
patient and is modified by pressure with the stethoscope. T h e
murmur is due to rubbing of the two layers of the pericardium
against each other in the presence of an exudate.
2. Pleuro-pericardial rubbest heard where the pleura meets
the pericardium, especially just outside the apex beat. It occurs
during the cardiac systole and becomes more distinct during
inspiration, although deep inspiration and holding the breath
may render it faint.
VASCULAR AND HAEMIC MURMURS
Murmurs over the blood-vessels or due to their defect may be
heard in the following conditions:.
1. Anaemiassoft systolic murmur heard best in the 2nd or
3rd left interspace; becomes less distinct when the patient
assumes an erect posture. T h e murmur is due to an abnormally
CARDIOVASCULAR
SYSTEM
125
high flow of blood which is of low viscosity, through a normal

valve, but through a dilated pulmonary artery.
2.
sac.
Aneurysma systolic murmur is heard over the dilated
3. Aortic Regurgitationa loud, pistol-shot sound is heard

over the femoral arteries followed by a soft diastolic murmur
Duroziefs sound. May be heard in Patent Ductus and Arteriovenous Aneurysm.
4. Arterio-Venous Aneurysma rough continuous murmur
with a systolic accentuation is heard over the defect.
5. Coarctation of the Aortaa soft systolic murmur is heard
over the innominate, carotid or subclavian artery. T h e murmur
is often heard in the back at the angle of the left scapula.
6. Grave's diseasea systolic murmur may be heard over the
thyroid when it is enlarged.
7. In Hypertension, Anaemias, Thyrotoxicosis and Aortic
Regurgitation systolic thuds"pistol shot" soundsare often
heard over the brachial and other big arteries.
8. Jugular veinsa venous hum is often heard over the neck
veins in congestive cardiac failure when the patient is examined
in erect posture.
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.
EXAMINATION OF T H E ABDOMINAL VISCERA.
F.
RECTAL EXAMINATION.
G.
EXAMINATION OF FAECES.
H.
GASTRIC ANALYSIS.
I.
EXAMINATION OF PERITONEAL FLUIDS.
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
4. Whether preceded by pain; if it eases the pain.

5. Preceding nausea.
6. Tasteif sour, bitter or tasteless.
7. Character and quantity of the vomit according to the
patient.
INDIGESTION.
1. Exact definitionpain, flatulence, anorexia, sense of
fullness.
2. Relation to food and bowel movements.
3. Habits; addiction; diet.
4. General health.
SORE T O N G U E .
Note the following:
1. Duration.
2. If ulcerated.
3. Patchy or diffuse.
4. If particular type of food causes more discomfort.
5. Associated dyspepsia.
6. Associated
anaemia.
7. If taking any medicines.

DIARRHOEA (see page 184).
1. Duration.
2. Frequency.
3. If associated with fever or loss of weight.
4. If the stool is mixed with blood or mucus.
5. If more persons in the family are affected.
6. If there is abdominal pain.
7. If there is associated tenesmus.
8. If the patient is aware of the call.
9
130
IIOW
T O EXAMINE A PATIENT
9. Its relation to meals or special articles of food.

10. Colour and consistency of the stool.
CONSTIPATION (see page 182).
1. Duration.
2. Time interval between the passing of stools.
3. Habits as to food, smoke, tea, etc.
4. If partial or absolute.
5. Associated symptomspain, vomiting, anorexia.
6. Any alternating diarrhoea.
7. Any grooving or flattening of the stools.
HAEMATEMESIS (see page 180).
1. Amount of haemorrhage.
2. Appearance of the vomitif bright red, dark red or
'coffee-ground'.
3. History of stomach disorder.
4. Appearance of the stool (for melaena).
APPETITE.
1. If more or less.
2. If less, for what type of food. (Verify if the patient is
afraid to eat on account of subsequent pain.)
3. If more, if associated with thirst.
4. Duration, degree and progress.
5. If associated with any illness, especially gastric symptoms
like pain and vomiting, loss of weight, etc.
6. If taking any drugs for reducing (amphetamine, etc.).
THIRST
1. Inquire if he has polyuria.
2. Note if there is any high fever or toxaemia.
3. Note if there are any gastro-intestinal symptomsvomiting, diarrhoea.
ALIMENTARY SYSTEM
131
4. Inquire into the history of profuse bleeding.

5. Find out if the patient takes drugs, especially, belladona,
largactyl, antrenyl, etc.
DYSPHAGIA (see page 175).
Inquire:
1. If it is for solids, liquids or both.
2. If accompanied by pain.
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
SWELLING OF T H E ABDOMEN (see page 160).

2. Duration.
3. If it varies in size.
4. If the body weight is increasing.
5. History of heart or kidney disease or anaemia.
FLATULENCE.
1. Its relation to particular types of food.
2. If offensive.
3. If passing flatus or belching gases.
ERUCTATION.
1. If it produces any taste in the mouth.
2. Its relationship to meals.
3. If particular type of food causes the symptoms.
WATER-BRASH.
1. Its taste.
2. If excessive.
3. If accompanied by salivation.
HEART-BURN.
1. If continuous or in relation to food.
2. T h e exact location of the burning sensation.
3. If there is regurgitation of fluids.
EXAMINATION
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.
Hutchinson's teeththe two upper central permanent incisors arc

narrow at the free edge and have a semilunar notch at "the biting
edges. Characteristic of congenital syphilis.
b.
Moon's molarsthe molars are dome-shaped.

syphilis.
c.
Acromegalythe lower jaw is enlarged and, hence, there is spacing

of the teeth; often the lower teeth project outside the upper.
d.
Fluorosisthere is mottling of the front teeth.
Also occur in congenital
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.
congestive heart failure, congenital
heart
Strawberryscarlet fever.
PigmentedAddison's disease.
Depigmentedsyphilis,
leucoderma
sometimes.
"Geographical tongue"congenital heart, neurosis.

2.
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,
thyrotoxicosis, dementia paralytica, senility.

Twitchingsmotor neurone diseases.
9.
Deviationinvolvement of the 7th or 12th cranial nerves.
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
5. Uraemia (ammoniacal smell), diabetic coma

smell), severe liver disease (musty smell).
(acetone
6. Drugs like paraldehyde, creosote, turpentine,

ether, volatile oils, etc.
alcohol,
ANATOMICAL LANDMARKS OF T H E
ABDOMEN.
For the purpose of describing and localizing lesions, the abdomen is

divided into nine regions, by means of two vertical linesfrom the midpoint
of the inguinal ligament on each side; and two transverse lines(a) subcostal, drawn across at the level of the lowest points of the 10th costal
arches, and (b) intertubercular line, drawn across the most prominent parts
of each iliac crest. T h e regions in the middle row from above downwards
are known as epigastric, umbilical and hypogastric regions; and in each
lateral rowhypochondiac, lumbar and iliac regions. T h e umbilicus lies
opposite the 4th lumbar vertebra
above the iliac line. T h e aorta bifurcates about
below and slightly to the left of the umbilicus. T h e
transpyloric plance lies midway between the suprasternal notch and the
upper border of the symphysis pubis. It usually lies halfway between the
xiphisternum and the umbilicus and corresponds posteriorly with the 1st
lumbar vertebra.
FIG. XIV
Division of the abdomen
into regions.
Division of the abdomen

into quadrants.
RT. HYPOCHONDRIUM.
RT. LUMBAR REGION.
B.
C.
LEFT HYPOCHONDRUM.
E.
UMBILICAL REGION.
F.
LEFT LUMBAR REGION.
Part of right lobe of liver; whole of

Part of left lobe of liver (sometimes).
left lobe of liver.
Part of stomach.
Part of stomach, including its orifices.
Splenicflexureof colon.
1st and 2nd parts of duodenum. Tail of pancreas.
Pancreas.
Most of the spleen.
Upper end of spleen.
Parts of kidneys.
Suprarenals.
EPIGASTRIC REGION.
RT. ILIAC REGION.
End of ileum.
Caecum.
Vermiform appendix.
G.
HYPOGASTRIUM.
I.
LEFT ILIAC REGION.
Coils of ileum.
Coils of jejunum and ileum.
Upper part of rectum.
Sigmoid flexure.
Sigmoid loop.
Urinary bladder.
Gravid uterus.
H.
Part of right kidney.

Part of right and sometimes both Part of left kidney (sometimes).
Part of ileum (sometimes). kidneys.
Descending colon.
Most of transverse colon.
Part of jejunum.
3rd part of duodenum.
Coils of jejunum and ileum.
Parts of mesentery and great
omentum.
Part of stomach.
D.
Most of the right lobe o liver.

Hepaticflexureof colon.
Gall-bladder.
Part of the right kidney.
A.
THE NORMAL CONTENTS OF THE ABDOMINAL REGIONS.
ALIMENTARY SYSTEM
137
138
H O W TO EXAMINE A
PATIENT
EXAMINATION OF T H E ABDOMEN
1.
INSPECTION
Inspection reveals the condition of the abdominal wall, the

size of the abdomen and any irregularity in its contour as a
result of some swelling underneath. The examination must be
conducted with the patient lying flat on his back.
1. Look at the general contour of the abdomen. See if there
is any bulging or retraction. If there is any asymmetry,
note the exact location of the abnormality. Note the
shape and position of the umbilicus.
2. Pulsations. These may be visible over the abdomen in
the following conditions:
(a) Aortic pulsationsvisible in thin individuals, nervous people and in anaemic persons.
(b) Transmitted impulse from a tumour overlying the
aortacancer of the stomach is a common example.
(c) Dilatation of the right ventriclethe impulse corresponds with the apex.
(d) Aneurysmal pulsationexpansile in character.
(e) Congested liverpulsation is felt posteriorly also.
3. Movements of the abdominal walls. Normally the
abdominal wall bulges during inspiration and falls
during expiration.
In paralysis of the diaphragm, the abdomen bulges
during expiration.
In peritonitis, there is no movement of the abdomen.
In localised peritonitis, i.e., in acute cholecystitis,
appendicitis, etc., there is diminished movement over the
affected viscus.
4. Peristaltic waves. These are best elicited by a sharp tap
with the finger over the abdominal wall. This is a very
important sign to diagnose pyloric stenosis in infants
and chronic intestinal obstruction. Visible peristalsis of
ALIMENTARY
SYSTEM
139
the stomach, especially in an infant, indicates pyloric

obstruction.
5. Surface of the abdomen.
Examine the following:
(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
(c) Prominence of veins. Note the direction of the blood

flow. Commonly occurs in obstruction to the inferior
vena cava where the inferior epigastric veins are distended, and in portal obstruction where a number of
veins are seen distended radiating from the umbilicus
(icaput medusae).
(id) Pigmentation (see Chapter I X ) .
(e) Eruptions, nodules and scars.
(/) Position and shape of the umbilicusmay be stretched
or everted in ascites.
(g) Evidence of hernia. Ask the patient to cough and
look for distension in the inguinal area.
(h) Evidence of oedema.
II.
PALPATION
Palpation determines the presence of tenderness, rigidity, or

undue laxity of the abdominal wall. It is the principal method
of detecting an enlarged viscus and the presence of tumours.
Palpation in Abdominal Examination is as important as auscultation is in Cardio-Vascular Examination.
Let the patient lie on his back with the shoulders a little
raised and legs bent to relax the abdomen. He should keep
the mouth open and breathe quietly but deeply. In palpation
of the lower abdomen, it may be helpful to have the legs of the
patient fully extended. Use the flat of the hand to begin with
especially while feeling for a tumour and then use the finger
tips to locate its margins. For tenderness and rigidity, the pal-
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,
Uniform swelling of the abdomen may be caused by obesity, distension

of the abdomen, gas in the intestine or fluid in the peritoneal cavity. An
over-filled bladder, pregnant uterus or a large ovarian cyst causes swelling
of the abdomen which at a first glance may appear uniform, but on closer
examination is limited to the area of the viscus. In visceroptosis, the lower
abdomen bulges on standing.
Irregularities in the contour of the abdomen may be caused .by enlargement of viscera, such as liver, spleen, kidney, gall-bladder or by tumours
arising from the various organs in the abdomen. Distension of one part
of the alimentary tract may also produce irregularity in the contour of the
abdomen, e.g. gastric distension, producing a bulge in the epigastrium or
colonic distension causing bulging in the flanks.
III.
PERCUSSION
Percussion adds confirmatory information in the case of an

enlarged viscus or tumours. It is also very valuable to detect
the presence of free fluid in the peritoneal cavity.
Percuss lightly from the front to the flanks. Note if it is
tympanitic. If there is dullness, determine if it is continuous
with the solid organs. If fluid is suspected, percuss the abdomen with the patient lying down on his back and then lying
alternately on each side. If the fluid is free in the peritoneal
cavity, this movement will lead to a displacement of the fluid
(.shifting dullness). M a p out the boundaries before and after
changing the position of the patient.
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
Mensuration is valuable to note the progress of the patient,

especially when suffering from ascites.
T a k e the following measurements:
1. Circumference at the level of the umbilicus and at the
level of maximum distension.
2. From the umbilicus to symphysis pubis and to the
epigastric angle.
3. From the umbilicus to the anterior superior spines.
These measurements are very useful from prognostic point of
view and also to diagnose ovarian growths, which grow obliquely upwards and where the two measurements from the
umbilicus to anterior superior spines differ, the one towards the
growth being bigger.
V.
AUSCULTATION
This part of the examination is not so important. Auscultation

may be useful to distinguish between paralytic ileus and other
forms of intestinal obstruction. Normally numerous borborygmi are audible on auscultation over the abdomen. In peritonitis and paralytic ileus these sounds may be entirely absent.
In obstructive lesions of the intestinal tract they may be greatly
exaggerated.
In oesophageal obstruction, the patient is asked to hold fluid
in his mouth and the stethoscope is placed over the lower part
of the chest. While swallowing, two sounds are heardfirst as
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
Especially note for tenderness, evidence of growths and

splashing sounds. T o elicit "splashing", stand to the left of the
patient, place one hand over the left lower ribs behind and
with the other one over the stomach, make short, sudden dips.
Splashing will be partly heard and partly felt.
Splashing felt three hours after meals suggests dilatation of the stomach.
It often forms an oval swelling in the epigastrium and left hypochondrium.
Visible peristalsis of the stomach, especially in an infant, indicates pyloric
obstruction.
A tumour of the stomach may form a visible swelling in the left hypochondrium or epigastric region. It is movable with respiration. T h e commonest tumour in this region is carcinoma of the pylorus.
Tenderness over the stomach suggests neurosis or peptic ulcer. In gastric
ulcer there may be hyperaesthesia to the left of the middle line and in
duodenal ulcer to the right.
2.
LIVER (see page 192).
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
is hard and irregular. If the liver is enlarged, note the degree

of enlargement. In congestive heart failure the size of the
liver is roughly proportional to the degree of failure and its
shrinkage is a useful indication of the response to treatment.
Note if the upper border is displaced by percussing down
along three linesmid-clavicular, mid-axillary and scapular
after making sure that the right thoracic cavity is normal.
Feel the surface of the liver and note if it is tender to pressure. In cancer and gumma the surface is irregular. In alcoholic cirrhosis, the surface is finely irregular; in most other
forms of liver enlargement, e.g. chronic venous congestion,
hepatic abscess, amyloid disease, fatty liver and leukaemic infiltration, the surface of the organ is quite smooth. If the liver
is tender, one has to think of congested liver of heart failure,
a n d inflammatory lesions like hepatitis and liver abscess. Gross
enlargement of cancer, syphilis, amyloid disease and blood
dyscrasias remain quite painless for a long time.
See if the liver is pulsatile by placing one hand over the right
ribs behind and the other over the organ in front. In marked
venous congestion of heart failure, the liver is often pulsatile.
3.
GALL-BLADDER (see page 199).
Feel for tenderness, especially at the tip of the 9th right

costal cartilage with the patient sitting and leaning forward.
Next stand behind and to the right of the patient, tuck the
fingers under the costal margin of the patient just outside the
right rectus muscle. T h e patient is then told to take a deep
breath; as the liver descends, the gall-bladder is brought in
contact with the examining fingers and, if inflamed, the patient
experiences sharp pain and the inspiration is immediately
arrested. This is known as "Murphy's sign". A distended gallbladder in the presence of jaundice is due to some cause rather
than gall-stonesgenerally cancer of the head of the pancreas.
T h i s is known as "Courvoisier's law". It is explained by the
fact that gall-stones, if present for a long time, cause fibrosis of
the gall-bladder; thus, when a stone is later impacted in the
common bile-duct, jaundice results, but the gall-bladder is unable to expand.
10
146
H O W T O EXAMINE A
PATIENT
If the gall-bladder is enlarged it may be felt as an oval,

smooth, tense swelling moving downwards during inspiration.
4.
SPLEEN (see page 201).
Stand to the right of the patient, who is in recumbent posture

with the head slightly raised and knees drawn up. Put the left
hand behind and the other in front; with the posterior hand
tilt the spleen forwards while the patient takes a deep breath,
and palpate with the right hand from well down the right iliac
fossa to the left costal margin.
Feel for the edge, notch and consistency. T h e anterior border
of an enlarged spleen goes downwards and inwards. Fingers
cannot be put between the spleen and the costal arch.
T h e spleen may be felt firm in blood diseases and soft in
infections. T h e more chronic the enlargement as in malaria,
the more firm is its consistency.
KIDNEYS (see Chapter VI).
These organs, although strictly speaking come under the
Genito-Urinary System, are best examined along with the other
organs in the Abdomen.
Kidneys move slightly with respiration and a movable kidney
on the right side is apt to be mistaken for a distended gallbladder and vice versa. However, a distended gall-bladder can be
temporarily pushed back from the abdominal wall, b u t always
tends to spring forward again, whereas a movable kidney is not
felt easily when pushed back in its position. Another distinguishing feature is that a kidney can be pushed down towards
the pelvis and held there during even forcible expiration, while
the gall-bladder moves upwards during the expiratory phase.
An enlarged left kidney may be mistaken for the spleen.
T h e points of distinction are:
(a) Spleen has a sharp edge in which a notch can be felt,
whereas the edge of a kidney is rounded.
(b) Fingers can be passed between the upper end of the kidney and the costal arch, but not between the ribs and an
enlarged spleen.
ALIMENTARY
SYSTEM
147
(c) There may be intestinal resonance over a renal tumour

but not so in a case of splenic tumour.
(d) A renal tumour is bimanually palpable between the two
hands placed in front and posteriorly; not so in the case
of an enlarged spleen.
An enlarged kidney may be easily mistaken for perinephric
abscess. In addition to tenderness a perinephric abscess tends
to point backwards whereas an enlarged kidney tends to bulge
forward.
RECTAL EXAMINATION
Perform P.R. with the patient lying down on the left side
with the right leg drawn up, or in knee-elbow position. First
examine the anus for evidence of piles, fissures arid fistulae.
Then introduce the right index finger covered with a fingerstall well lubricated with vaseline into the rectum with a rotatory movement. Note for tenderness, tone of the anal sphincter,
presence of faecal masses, stricture, tumour or "ballooning" of
the rectum.
EXAMINATION OF FAECES
Obtain a specimen without
enemas. Use saline cathartic,
second stool. T h e specimen
barium and also from urine as
the use of oily purgatives or

if necessary, and examine the
should be entirely free from
far as possible.
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
BROWNin an average and well balanced diet

YELLOWmilk diet, intake of senna, rhubarb, santonin.
BROWNISH BLACKhigh meat diet.
LIGHT YELLOWhigh fatty diet, obstructive jaundice, steatorrhoeas.
GREENexcessive intestinal peristalsis; enteritis in children.
Bilirubin
in such cases has no sufficient time to convert into stercobilin.

BLACK OR TARRYmelaena, due to presence of blood.
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.
CLAY COLOUREDobstructive jaundice, biliary obstruction.

FROTHY AND WHITISHsteatorrhoeas.
RICE-WATERcholera.
I'EA-SOUPtyphoid.
B R I G H T REDbleeding
Meckel's diverticulum).
RED C U R R A N T
in
colon
or rectum
(piles,
cancer,
polypi,
JELLYintussusception.
STREAKS OF BLOOD
ulcerative colitis.
WITH
PLENTY
OF
MUCUS
AND
PUS
RED W I T H LITTLE MUCUSdysenteries.

FLAKES OF MUCUSmucus colitis.
C. Odour:The normal stool is not very disagreeable in

odour and is due to presence of indole and skatol. Absence of
bile favours putrefaction and, hence, the stool may be offensive.
In meat eaters, there is excess of hydrogen sulphide in the stool
and, hence, the stool is offensive. In vegetarians the stool is
not unpleasant to smell. In milk diet there is hardly any odour.
In cholera there is very little organic matter and, hence, the
stool is almost free from odour; so also in severe diarrhoea and
bacillary dysentery. Strongly foetid stool occurs when there are
ulcerative processes going on in the intestine or in carcinoma
of the rectum. Highly acid faeces smell sour. If the stool is
alkaline and of foul odour, one should suspect chronic enteritis.
.D. Consistency:Normal stool should be soft, but formed.
Children tend to have softer stools while old people may pass
hard faeces. The more the residue the softer the stool and
vice versa. In obstinate constipation the stool is dry and hard.
Slimy stool is due to excess of mucus. In hypoacidity the stool
is semi-liquid. If grooved, suspect rectal growths; if ribbonshaped, obstruction in sigmoid flexure; if pencil-like, spasm of
the anal sphincter.
ALIMENTARY
SYSTEM
149
Watery stools are found in all cases of diarrhoeas; In cholera

the stool is liquid, odourless and alkaline. Purulent stool is
found in dysenteries. Slimy stool indicates that the lesion is in
the large intestine. In muco-membraneous colic the stool contains mucoid casts of the bowel.
E. Reaction:Normally the reaction of a stool is same as
that of blood, i.e. slightly alkaline with p H 7.5. Heavy intake
of lactose produces acid reaction. So also excess of carbohydrate
food. Bacillary stool is alkaline. Amoebic stool is acidic. In
fermentative diarrhoea the stool is alkaline.
F.
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.
G. Parasites:Ascaris, ankylostomes, ' whipworms, thread

worms, segments of tapeworms are easily noticed in the stool,
if present.
CHEMICAL EXAMINATION
Make an emulsion of a small bit of faecal matter in 2.5 ex.
of water or normal saline. Particularly examine the stool for.
blood and urobilin and in special cases, for fat content and
other abnormal substances.
A. BLOOD:Perform benzidine test. Avoid giving the patient iron,
bismuth, meat and chlorophyll substances for 3 days before the test. T h e
patient should not use tooth brush for at least 48 hours before the test.
Test:Mix a small portion of faeces in water in a test tube. Boil the
.suspension to destroy enzymes and cool. In another test lube make a
saturated solution of benzidine in 2 c.c. of glacial acetic acid and add to
150
it 2 c.c. of H 3 OJ or ozonic ether. Add some of the emulsion to this mixture

b l u e colour develops if blood is present.
B. U R O B I L I N : W i t h mortar and pestle m i x a few grammes of fresh
facces with an equal quantity of 10% mercuric chloride solution. Let it
stand for 624 hours. Urobilin gives a red colour, while bile gives green
colour.
MICROSCOPIC EXAMINATION
A.
IS.
CELLS.
1.
Epithelial cellsindicate intestinal
2.
Red cellsindicate melaena, dysentery, blood dyscrasias, etc. Normal

stool contains n o blood.
irritation.
3.
White cellssmall number is normal. If large, it suggests intestinal

inflammation.
Macrophage cells may be seen in amoebiasis.
Eosinophil cells indicate allergy.
CRYSTALS.
1.
Calcium oxalate,
normally present.
fatty
acid
crystals
and
triple
phosphates
2.
Haematoidin crystalsyellowish needles occurring

often present in intestinal haemorrhage.
3.
Charcot-Leyden crystals may be present in amoebiasis.
in
groups
are
are
U N D I G E S T E D FOOD.
1.
Vegetable matter, especially fibres are often seen in a normal stool.
2.
Animal matter, especially fibrous tissue may be present in a normal

stool. Ordinarily, there should not be any muscle fibres.
3.
Undigested starch may be present in small quantity

Excess suggests disorder of carbohydrate metabolism.
4.
Ova a n d cysts are easily detected in infected persons.
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.
Technique for Gastric Analysis:

N o f o o d is to be given to the patient after 6 p . m . the evening before the
test, which should be started early the following morning.
In cases of
suspected obstruction to the gastric outflow a charcoal biscuit may be given
in the evening before the test.
W i t h the patient sitting up in bed or in a chair introduce into the
stomach a Ryle's tube u p t o '20' mark indicated o n the rubber tube and
then aspirate the gastric residue to note its volume and for the necessary
analysis. N o t e if it has fragments of the charcoal biscuit; if so, it suggests
obstruction. T h e patient is then given the test-meal. T h i s is prepared by
adding two tablespoonfuls of oatmeal to a pint of water and boiled till
it is reduced to about half the quantity. T h e meal is then strained through
a piece of muslin and sugar is added to taste. T h e patient is asked to
swallow the meal and about 10 c.c. of the gastric contents are withdrawn
every 15 minutes for two hours for testing.
H I S T A M I N E T E S T . T h i s test is performed w h e n n o HC1 is found in
the gastric juice as in cases of pernicious anaemia, gastric cancer, etc. as
this substance liberates the secretion of acid in the stomach. Histamine is
injected in doses of 0.5 mg. after the fasting juice is withdrawn. T h e
drug should b e avoided if the patient's blood pressure is below 100 as it
reduces t h e pressure. It should also be avoided in suspected cases of
phaeochromocytoma as it causes sudden drop of pressure. Samples are
aspirated as above.
Nearly half the cases which show no free HC1 in the gruel meal, secrete
acid after histamine injection.
EXAMINATION OF THE GASTRIC JUICE

A.
PHYSICAL
EXAMINATION.
1. V O L U M E : N o r m a l volume of fasting juice averages 50 c.c. If it is

above 100 c.c. suspect pyloric stenosis, hypersecretion and excessive regurgit a t i o n from d u o d e n u m .
- 2. C O L O U R : A few streaks of bright red blood in the gastric juice
are generally due to trauma and have no significance. Larger amounts
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
1. STARCH:Normal gastric juice does not contain starch or food

particles. Their presence indicates gastric retention and suggests pyloric
stenosis. If starch is present, addition of Lugol's iodine to the gastric juice
gives bluish colouration.
2. ; MUCUS:Normally very small amount of mucus is present in the
fasting juice. Excessive mucus suggests gastritis and may also occur in some
cases of gastric retention.
3. HYDROCHLORIC ACID:Normal quantity of HC1 varies from 0
to 30 ml. N / 1 0 HC1 per 100 ml. of gastric juice. T h e total acidity is
usually 10 ml. N / 1 0 HC1 and is greater in quantity than free acid. Absence
of free HC1 has no much significance, but absence of total acidity suggests
true achlorhydria: this, however, can be confirmed by determining the
response of gastric mucosa to histamine.
4. LACTIC A C I D : N o lactic acid is present in normal fasting juice.
It is found when there is gastric retention associated with hypochlorhydria
or achlorhydriaa combination likely to occur in gastric carcinoma and
pyloric stenosis.
C.
Use a centrifugalized deposit of the fasting stomach

for the following:
contents.
Look
1. FOOD PARTICLESstarch and muscle fibres. Normally they should

not be present.
2. YEAST CELLS AND SARCINAEtheir presence suggests fermentation
in the stomach.
3.
MALIGNANT CELLSmay be present in cancer of the stomach. .
4.
BOAS-OPPLER BACILLIsuggests cancer of the stomach.
16 7
ALIMENTARY
SYSTEM
GASTRIC ACIDITY
1.
HYPERCHLORHYDRIA
CAUSES:
1. Gastric and duodenal ulcers.

2. Gastric tabetic crises.
3. Reflex causes:
(a) Hyperstenic gastric diathesis.
(b) Appendicitis.
(c) Cholecystitis.
4. Gastric hypersecretion (Reichman's disease).
5. Chlorosis.
Hyperchlorhydria, if left untreated, may lead to peptic
ulcer in course of time.
2.
HYPOCHLORHYDRIA
CAUSES:
1. Gastriccancer, gastritis, atonic dyspepsia.

2. Blood diseasespernicious anaemia, severe secondary
anaemia, simple achlorhydric anaemia, nutritional anaemias.
3. Deficiency diseasespellagra.
4. Hyperthyroidism.
5. Diabetes mellitus.
6. Chronic cholecystitis.
SEQUELAE OF
HYPOCHLORHYDRIA
(a) Due to loss of defence mechanism bacteria enter the small

intestine and duodenum and cause duodenitis or enteritis.
(b) B.Coli ascend to the gall-bladder leading to cholecystitis
and later, stone-formation.
154
(c) Proclivity to colon-typhoid infections, cholera and amoebic dysentery.

(d) Toxaemias leading to rheumatoid arthritis, dermatitis,
asthma, allergy.
3.
ACHLORHYDRIA
This means complete absence of free and total acids in the

gastric juice. All the conditions that give rise to hypochlorliydria may give rise to complete achlorhydria.
CAUSES:
1. Gastriccancer, chronic
syphilis of the stomach.
gastritis,
atonic
dyspepsia,
2. Intestinalchronic appendicitis, chronic cholecystitis,

chronic pancreatitis, tubercular enteritis, sprue.
3. Blood diseasespernicious anaemia, severe
anaemias, simple hypochromic anaemia.
secondary
4. Deficiency diseasespellagra.
5. Endocrine disordersAddison's
myxoedema, diabetes mellitus.
disease,
thyrotoxicosis,
6. Allergic disordersbronchial asthma.

7. Skin conditionschronic eczema, psoriasis.
8. Infectionschronic sepsis, rheumatoid arthritis.
9. Constitutionaloften runs in families.
The two important diseases that invariably cause achlorhydria
Ore Pernicious Anaemia and Cancer of the Stomach.
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.
yCast; sarcinae. Nil.
Nil.
Present.
Food Particles. Nil.
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; stasis of food.
Cancer stomach.
Pyloric obstiuction.
Cancer, gastritis.
Duodenal ulcer.
Peptic ulcer, cancer, acute gastritis,
oesophageal varix, trauma by the
stomach lube.
Chronic gastritis, cancer.
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
Common.
Mid-epigastric.
Variable.
X-rays.
Gastric analysis.
Mclacna.
Haematemcsis.
obsessional.
"Crater" seen.
Rare.
Always hyperchlorhydria.
May occur.
Duodenal cap deformed.
Generally hyperchlorhydria.
'
Right of the middle line.
By food, alkalis.
Triplefood, comfort, pain.
By food, alkalis, vomiting.
comfort.
Rare.
line.
2-4 hours after food.
Slightly to the right of the middle
Left of the middle line.
Rare.
Common.
Tenderness & hyperesthesia
Relief of pain.
Anxious,
Robust.
Common in better classes.
After 40 years.
Much more in males.
1/2 to 2 hours after food.
Lean and lanky.
Common in poorer classes.
30-40 years.
Rhythm. Quadruplefood, comfort, pain.
Radiation.
Site.
Onset of pain.
Temperament.
General development.
Social condition.
Age.
Slightly more in males.
Sex.
Duodenal Ulcer.
Gastric Ulcer.
Features.
DIFFERENTIATION BETWEEN GASTRIC AND DUODENAL ULCER.
ALIMENTARY SYSTEM
157
30-45 years.
X-rays.
Gastric analysis.
Tumour.
Common.
Lost.
Almost always present
Not so.
"Crater" seen or duodenal cap

distorted.
Hyperchlorhydria.
Not felt.
STOMACH.
Ragged ulcer seen.
Achlorhydria.
May be palpable.
If present, disappears on diet. Always present.
May be present.
Occult blood in gastric juice.
Occult blood in stool.
Not too common.
Vomiting.
After food or alkalis.
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
16 7
ALIMENTARY
SYSTEM
EXAMINATION OF PERITONEAL FLUID

METHOD
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.
QUANTITY.Presence of excessive fluid suggests portal cirrhosis

and malignancy. If the fluid fills up rapidly after tapping, suspect
malignancy, even if it is not tinged with blood.
2.
COLOUR.In general the colour of ascitic fluid is light-yellow.

richer the colour, the greater is its protein content.
3.
The
a.
Light yellowtransudate or exudate.
b.
Faintish pinksuggests presence of red cells of about- 10,000 per

ml. and may be due to tubercular infection.
c.
Red colour suggests malignancy and less frequently, tuberculosis.
d.
Pyocyaneous infection imparts greenish colour to the fluid.
e.
Marked opacity suggests pseudo-chylemay be due to tuberculosis,

excess of leucocytes in an exudate, and in rare cases due to
presence of carcinomatous cells.
f.
Milky white suggests presence of chyle, commonly due to filiarasis.
SPECIFIC GRAVITY.In general, the sp. gr. is dependent

the protein contcnt of the fluid.
a.
upon
Cirrhotic and nephrotic fluids have sp. gr. of 1015 or less.
b.
In cardiac ascites the sp. gr. is 1015 to 1020.
c.
Tubercular fluid has sp. gr. of 1018.
d.
Infected fluid has sp. gr. of 1018 or more.
e.
Neoplastic fluid, if it contains too much blood, may have higher

sp. gr. than 1015.
4.
ODOUR.In almost every case, the ascitic fluid is odourless; in

Pyocyaneous infection the odour is offensive and in B. Coli infections
the odour is faecal.
5.
CLOT FORMATION.The higher the protein content, the more

likely and more rapid the clotting. In most cases the fluid has no
sufficient proteins to let the fluid clot on standing.
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.
Sp. gr. below 1005.
Sp. gr. above 1008.
3.
Colourlight yellow or very

slightly cloudy.
Clear or cloudy, purulent or

bloody.
4.
Few cells present.
500 to 40,000 cclls per cm.
5.
Odournil.
Odour nil or putrid, if purulent.
6.
Protein content less than

2.5 gms. per cent.
Protein content over 3 gms..

per cent.
7.
Does not clot.
May coagulate.
8.
Sero-mucin absent.
Sero-mucin present.
9.
Result of congestive heart

failure, obstruction to venous
flow or low blood proteins.
Result of inflammation or
malignancy.
COMMON DISORDERS OF T H E ABDOMEN

SWELLING OF T H E ABDOMEN
Swelling of the abdomen may be grouped under
headings:
A.
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.
Examine the patient for physical signs.
B.
Exclude simulating conditions.
C.
Determine the cause of ascites.
Inspection. T h e abdomen is distended uniformly. T h e skin

is tense and shiny and there may be lineae albicantes.
If the
fluid is moderate in quantity, bulging of the flanks will be wellmarked and when there is excessive fluid the lower ribs will
be pushed forward, the subcostal angle widened and the umbilicus everted. In cirrhosis of the liver the veins become prominent, especially around the umbilicus with the flow of blood
in upward direction. Respiratory movements are diminished
with mild dyspnoea and the apex beat shifted upwards and
slightly outwards.
Palpation. T h e abdomen may exhibit varying degrees of
tenseness. A fluid thrill may be obtained. "Dipping" sensation
is almost always present. In tubercular peritonitis a sausageshaped mass of the diseased omentum may be felt.
Percussion. Percussion note may be resonant in front and
dull in the flanks when the patient is in supine position. An
11
162(j
U shaped dullness is generally elicited when the fluid is free in

the peritoneal cavity. Shifting dullness is invariably elicited
when there is free fluid in the abdomen.
Mensuration. In ascites the navel is more towards the
symphysis pubis than to the ensiform cartilage and equidistant
from the anterior superior iliac spines; whereas in large ovarian
cysts the umbilicus is nearer to one anterior iliac spine than to
the other and the distance from the anterior superior iliac
spine to the umbilicus is greater on the side of the cyst.
B.
EXCLUDE SIMULATING
CONDITIONS.
1. TYMPANITIS. T h e outline of distended coils of the intestine may

be visible and peristaltic movements may be noticed. T h e percussion note
is resonant and there is no fluid thrill.
2. OVARIAN CYST. T h e umbilicus is nearer to the ensiform cartilage
than to the pubis and often displaced laterally. T h e pcrcussion note is
usually dull in front and resonant in flanks. T h e outline of the upper
border is convex and not concave as in the case of ascites. Mensuration
reveals the greater transverse circumference below the umbilicus whereas
in ascites it is at the level of umbilicus. Rectal examination may reveal
the uterus drawn outwards and its mobility impaired, whereas it is Iondown and movable in ascites.
FIG. XVIII
Distinction between an ovarian cyst (left) and ascites (right)
by percussion of the abdomen.
16 7
ALIMENTARY
SYSTEM
3. GRAVID UTERUS. There will be history of amenonhoea arul

characteristic condition of the breasts. There will be dullness in front of
the abdomen with a convex upper border and resonance in the Hanks.
P.V. examination reveals patulous cervix.
4. DISTENDED BLADDER. This is felt as a globular mass in the
middle line and tender to pressure if not due to nervous diseases. T h e
passage of a catheter clears all doubts.
5. GENERAL OBESITY. T h e umbilicus reveals as a deep pit.
may be transverse folds in the abdomen.
There
6. P H A N T O M T U M O U R . T h e abdomen may be tense but not dull

to percussion, and the note is uniform all over the abdomen.
7. CYSTIC SWELLINGS, especially of pancreas, hydronephrosis and
hydatid cysts may simulate ascites. They do not, as a rule, cause uniform
distension of the abdomen. They are more commonly mistaken for local
collection of fluid. Pancreatic cyst is found in the upper part of the
abdomen and is more or less circular in outline. In hydronephrosis, there
may be disappearance of the fluid-swelling after Dietl's crisis. In hydatid
cyst there is definite thrill and eosinophilia in the blood.
8. FIBROIDS. If big, they may be mistaken for ascites, but the mass
is solid on palpation and roundish in appearance.
9. IMPACTED FAECES, should not be mistaken for ascites as masses
that are felt are irregular and the bowel dears up with a high enema or
purgative.
C.
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
(d) Cancerousrarely occurs before 40 ancl the growth is

practically always secondary. Rapid emaciation and
cachexia are generally present. The ascitic fluid is
invariably blood-stained and fills rapidly after tapping.
2. Diseases of the liver.
(a) Cirrhosis of the liver. This is the commonest cause of
ascites. There may be history of alcoholism and possibly haematemesis, melaena or jaundice. Other features
are telangiectasis on the cheeks, furred tongue, morning
vomiting, loss of appetite and constipation. T h e liver
may be enlarged but more often shrunk. Abdominal
veins are distended and the spleen enlarged.
(b) Perihepatitis. This condition is difficult to diagnose in
early stages. When the patient with supposed cirrhosis
has to be tapped too often, the cause is more likely to be
perihepatitisa condition which is really a part of
chronic peritonitis. The capsule of the liver becomes
much thickened which retracts and distorts the organ
causing ascites. A patient with perihepatitis may survive for a long time, but a patient with cirrhosis of the
liver seldom survives a year after the need to tap the
abdomen arises.
(c) Growth in the liver. Progressive jaundice, cachexia and
anaemia are almost always present. Portal glands are
enlarged; liver is enlarged, hard and nodular to the feel.
The ascites develops rapidly and fills equally rapidly on
tapping.
3.
Obstruction to the Portal Vein

(a) This is most commonly due to enlargement of the portal
lymph glands by secondary deposits of malignant disease,
especially in cancer of the pancreas. The bile-ducts are
also obstructed simultaneously in most cases, and hence
jaundice often accompanies the ascites.
(b) Thrombosis of the portal vein. This is rare and may be
infected from inflamed piles or appendix giving rise to
fever and rapidly developing ascites.
16 7
ALIMENTARY
SYSTEM
4. Obstruction to the Inferior Vena-Cava.

may be due to extension from a thrombosed
It is associated with oedema of the lower back,
perhaps haematuria due to involvement of
followed by ascites.
This is rare and

vein in the leg.
albuminuria and
the renal veins,
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
cases, secondary deposits of malignant disease may obstruct the

thoracic duct and produce ascites.
M E T H O D OF INVESTIGATION
1.
Note if the swelling started in the abdomen first.
2.
Look for evidence

nutrition.
S.
Examine the fluid after puncture.
of
tuberculosis,
4.
Perform liver function tests.
5.
Perform biopsy of the liver.
heart
disease,
anaemia,
mal-
Note the following:

(a) If there is only ascites and hardly any swelling elsewhere, or the
ascites appeared first in cases where there is also oedema of the legs,
the probable cause is peritonitis, cirrhosis of the liver, thrombosis or
pressure on the portal veins, or obstruction to the lymphatic flow.
(b) If associated with general anasarca and especially, if the swelling has
started on the face first, the probable cause is nephritis.
(c) If swelling appears on the legs first, and then ascites appears, heart
failure should be thought of first and obstruction to the vena cava
and severe anaemia next.
(d) If jaundice accompanies ascites, it is suggestive of cirrhosis of the
liver and if severe, malignancy.
(e) If the liver is enlarged along with ascites, cancer should be thought
of first especially if jaundice is present; so also perihepatitis and
congestive heart failure if there is no jaundice.
(f) If there is ascites associated with multiple lumps, suspect tubercular
peritoneum.
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
tended bladder; other causes are pregnant uterus,

and enteroptosis.
16 7
fibroids,
ovarian cysts
A prominence in the right hypochondrium may be due to an enlarged

liver or gall-bladder; and in the left hypochondrium, cancer stomach,
enlarged spleen, tumour of the left kidney or adrenal and cancer of the
splenic flexure of the intestine.
A swelling in the right lumbar region may be due to an enlarged liver,
tumour of the right kidney or adrenal; and in the left region, the same
conditions as on the right side and an enlarged spleen.
A swelling in the right iliac fossa may be due to an appendicular abscess,
T.B. caecum or malignancy, ovarian cyst or fibroid, psoas or pelvic abscess,
T.B. peritonitis, intussusception, faecal accumulation. In the left iliac
region a swelling may be due to diverticulitis, volvulus and olher conditions
as in the right iliac fossa.
2. Size. T h e larger the tumour the more difficult it is to

determine its origin; however, certain tumours, like an ovarian
cyst, by its very large size gives a valuable clue as to its nature
and origin.
3. Consistency. A distended viscus like stomach, intestine
or urinary bladder are easily recognised by their soft consistency.
T h e consistency of organs like liver and spleen are generally
firm unless due to neoplastic infiltration when it is hard.
Cystic tumours, e.g. pancreatic or ovarian cysts have a jelly-like
consistency.
4. Shape. In the early stages a tumour may correspond in
shape with the viscus from which it is arising. This is especially
so in the case of kidneys and spleen. As the tumour grows
larger the characteristic shape is often lost.
5. Mobility. Tumours of the following organs move with
respiration:Stomach, liver, gall-bladder, spleen, transverse
colon and kidneys. Those of the pancreas and pelvic organs
do not.
6. Tenderness. Although a large number of abdominal
tumours are painless, the following are invariably tender to
palpation in the respective regions.
In the right hypochondrium, liver conditions like hepatitis, congestion,
abscess and gall-bladder disorders like cholecystitis and calculi generally
cause pain on pressure.
In the left hypochondrium, splenitis and infarction can produce pain
and enlargement of the organ.
168(j
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:
1. Stomach and Duodenumperforated ulcers.

2. Gall-bladderacute cholecystitis, rupture.
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
(c) Stretching of the capsule of a viscus, e.g. the liver, as

occurs in cardiac failure or in splenitis.
Tissues which appear to be relatively insensitive to pain
are:
(a) Gastric and intestinal mucosa. Intense gastritis or enteritis gives rise to discomfort rather than pain.
(b) Parenchyma of the liver, spleen and kidneys. Even large
growths in these organs may be painless.
ABDOMINAL PAIN IS OF T W O VARIETIES:
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.
In appendicitis the pain is of visceral type followed by peritoneal lypr.

In biliary colic the pain is of visceral type. In cholecystitis the pain is of
peritoneal type. In peptic ulcer the pain is probably of mixed type, but
more visceral. In perforation the pain is of peritoneal type. In pancreatitis
the pain is of visceral type and is due to distension of the pancreas; there
is no rigidity.
170(j
CAUSES OF ABDOMINAL PAIN.
A.
Acute abdominal painpain coming on suddenly:

I. With shock
1. Perforation of some organ or cystpeptic ulcer,
appendicular abscess, hydatid cyst, ovarian cyst, etc.
There is severe pain associated with shock, vomiting, collapse and evidence of toxaemia.
2. Internal haemorrhagerupture of ectopic gestation, spleen, liver, after injuries. Shock is more
marked than pain.
3. Acute intestinal obstructionstrangulated hernia,
intussusception. There is severe pain, vomiting
and rapid pulse.
4. Torsion of an organovarian cyst. Previous history
and acute, severe pain are suggestive.
5. Embolism of the mesenteric arteryhistory of subacute endocarditis, melaena, enlarged and tender
spleen and embolic phenomena elsewhere.
6. Acute pancreatitissudden acute pain, vomiting,
constipation, circulatory collapse, brownish discolouration around the umbilicus.
II. Without shock
1. Colicintestinal, biliary, renal. Pain is severe,
radiating in character with associated vomiting.
Temperature is normal generally.
2. Acute appendicitispain in the right iliac fossa,
vomiting at the onset, tenderness at the McBurney's
point, rigidity, constipation.
3. Pancreatic calculusparoxysmal pain, fatty stools,
glycosuria of mild type.
4. Splenic embolismsudden pain in the
region; history of endocarditis sometimes.
5. Referred painpulmonary embolism,
thrombosis, pneumonia in children.
splenic
coronary
16 7
ALIMENTARY
SYSTEM
6. Tabetic crisissevere pain in the abdomen with

vomiting.
7. Peritonitis.
(a) Acutethis may be localised at first; soon
becomes generalised, especially if there is perforation. The pulse is fast, the abdomen is
rigid and immobile, temperature raised, bowels
constipated with nausea and vomiting. Pressure over the abdomen increases the pain.
(b) Chronic peritonitisthere is a dull feeling of
heaviness rather than acute pain. The omentum may be rolled up. The commonest cause is
tuberculosis.
B.
Chronic abdominal pain

Causes:
I. Stomach conditions
1. Peptic ulcerpain has definite relation to food.
2. Hiatus herniapain comes on soon after eating.
3. Cancer in late stagesanorexia, anaemia, cachexia,
"coffee-ground" vomiting, invariably present.
4. Visceroptosisdull, dragging pain coming on soon
after eating; relieved on lying in bed. Liver and
kidneys may be displaced.
II. Intestinal conditions
1. Chronic appendicitispain in the right iliac fossa,
constipation, general malaise, sometimes nausea
and vomiting. X-rays confirm the diagnosis.
2. Chronic intestinal obstructionstrictures (simple
or malignant), pressure by a tumour. There is generalised intermittent pain gradually worsening; constipation, vomitingat first food and later faecal
matter.
3. Spastic colondyspepsia, constipation, with alternating diarrhoea. Pain along the colon which is
often felt as a tender tube.
172
IIOW TO EXAMINE A FATIENT
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:
1. Oesophageal colican intermittent, burning pain in the

centre of the lower chest. The pain is deeply situated and may
be quite severe.
2. Gastric colicaching or sharp in character, epigastric in
position, and tends to occur at a set time after meals.
3. Small-intestine colictypically occurs in the centre ol the
abdomen, severe, sharp in character, and gives rise to much
restlessness. T h e fluctuations in intensity of the pain are rapid
and violent. T h e abdomen may be distended. Pressure over
the abdomen relieves the pain.
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
4. Peritonitispain continuous, legs drawn up, decubitus

supine position. Movement is resented by the patient.
There is local rigidity in the area of the cause of the
trouble, vomiting and constipation.
174
FATIENT
5. Inguinal herniaeasily reducible and no operation is

necessary. If irreducible, operation must be performed.
6. Acute appendicitismay occur after the age of 2 years.
The pain is continuous or colicky, the child wriggles
or lies still. If the child is sleeping an hour after pain,
probably it is not acute surgical condition. If sleeping
after 24 hours of pain, wake the patient up to see if
surgical intervention is necessary. Always do P.R.
7. Meckel's diverticulumprevious history of melaena and
later peritonitis, is probably due to perforation of the
diverticulum.
B.
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-
2. Mumpsmay cause acute pancreatitis, with severe pain

in the abdomen and vomiting.
C. Referred pain:
1. Pneumonia, Pleurisy,both these conditions may give
rise to referred pain in the abdomen on the affected
side. Pneumonia especially, may be mistaken for acute
peritonitis. In pneumonia the patient likes to lie on
the affected side and in peritonitis on the back.
2. Pericarditisthe patient is breathless, prefers to lie
propped up in bed. Pulsus paradoxus may be present.
3. Pott's diseasemay give rise to referred pain in the
abdomen. Examination of the nervous system will
confirm the diagnosis.
D.
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
vomiting. In purpura vomiting comes first and then

pain. Bleeding from the gums and purpuric spots on
the skin excludes abdominal diseases.
INVESTIGATION OF ABDOMINAL PAIN:
1.
History:Inquire into previous diseases.
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.
Sex: In females suspect biliary colic, ovarian cyst, rupture of ectopic

gestation.
4.
Examine the abdomen for rigidity and tenderness.
5.
Examine the organs in the abdomen.
6.
Perform P.R. and P.V. examination.

NERVE MECHANISM OF ABDOMINAL PAIN
Site of stimulus.
Causative agent.
Location of pain.
1.
Cerebral cortex or
basal ganglia.
Nervousness, anticipation of pain,

cold
atmosphere.
Affects
the
whole
abdominal wall; varies
in intensity; abolished
easily.
2.
Lower 6 dorsal
nerves.
Pleurisy, pneumonia,
infection of the chest
wall.
Limited to the affected side; varies

in
extent and degree.
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.
Varies with the nature

of the irritant and
suddenness
of
the
stimulus.
COMMON DIGESTIVE DISTURBANCES

DYSPHAGIA
Dysphagia means difficulty in swallowing. It may be due to
mechanical obstruction, nerve dysfunction or due to pain while
swallowing.
176
IIOW
TO EXAMINE A
FATIENT
ETIOLOGY:
A.
MECHANICAL
OBSTRUCTION
IN THE
OESOPHAGUS.
In all these conditions the dysphagia is for solids and later

on for liquids also.
1. Strictures
(a) Cicatrical strictures by corrosives, etc. The site is generally high in the oesophagus near the pharynx.
(b) Peptic ulcer. T h e site is lower down near the stomach.
(c) Spasmodic stricturesoesophageal pouches.
2. Cancercommonest cause.
3. Foreign bodiesfish-bone, dentures.
1. Pressure from outside
(a) Aneurysmespecially of the transverse arch.
(b) Enlarged thyroid.
(c) Mediastinal growths.
(d) Diaphragmatic hernia.
(e) Cardiac conditionshypertrophy, pericardial effusion.
B.
MECHANICAL
PALATE
DEFECTS
OP THE
MOUTH,
TONGUE
AND
cleft palate, malignancy of the tongue, etc.

C.
PAINFUL
SWELLING.
1. Inflammation of the tongue, mouth, pharynx.

2. Plummer-Vinson syndrome.
deficiency anaemia.)
D.
NERVE
(Inflammation due to Fe-
DYSFUNCTIONS.
In most of these cases if not all, there is dysphagia for liquids.

T o swallow liquids quick action of the swallowing muscles is
necessary and this is lacking in bulbar or nerve dysfunctions;
invariably there is also nasal regurgitation of fluids while
swallowing.
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
(b) Mode of onset:

If acutesuspect foreign body in the oesophagus, encephalitis and
thrombosis of posterior inferior cerebellar artery.
If gradual in onsetsuspect malignancy and strictures.
(c) History of swallowing corrosivessuggests cicatrization.
(d) Dysphagiafor solids, suggests
liquids, nerve dysfunction.
mechanical
obstruction;
and
for
(e) Nasal regurgitationsuggests 9th cranial nerve paralysis.

(f) Haematcmesissuggests malignancy.
2.
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.
Vomiting centre situated in the medulla.
2.
Efferent fibres in the vagus supplying the stomach, phrenic : i m c s

of the diaphragm and spinal nerves of the abdominal muscles.
Afferent fibres in the vagus and from other paths via
nerves.
4.
the spinal
Muscular wall of the stomach, diaphragm and abdominal muscles.
Tn all cases of vomiting exclude regurgitation of food before further

investigations to detect the cause of vomiting are carried out. In certain
diseases of the oesophagus the food that is swallowed is regurgitated alter
a varying interval of lime. These conditions are:
(a) Stricture of oesophagusfibrous or malignant.
(b) Spasm of the oesophagus.
(c) Pressure from withoutaneurysm, mediastinal conditions.
(d) Achalasia cardia.
(e) Diverticular pouches.
In all these conditions the regurgitated matter is undigested food, alkaline
or neutral in reaction and generally diluted with mucus. X-ray with barium
confirms the diagnosis.
Vomiting due to alimentary and toxic disorders is usually preceded by
nausea. Vomiting without antecedent nausea, particularly if sudden in
onset and projcctile in character, suggests a lesion in the brain. Vomiting
that produces relief of pain is likely due to an organic obstruction and
peptic ulcer. Repealed vomiting unattended by loss of weight is psychogenic
in origin.
CAUSES OF
A.
VOMITING.
ALIMENTARY T R A C T :
1. Gastricindiscretion in diet, hunger, gastritis, venous

congestion, ulcers, cancer, pyloric spasm, poisons and
emetics.
2. Extra-gastricappendicitis, intestinal
bladder disturbances, pancreatitis.
B.
obstruction,
gall-
NERVOUS CONDITIONS:
1. Hysteria, fear, disgust, shock, unpleasant smell or taste

or sight.
Al I M E N T A R Y S Y S T E M
179
2, Increased intracranial tension-tumours, meningitis,

hydrocephalus, etc.
3. Migraine, Meniere's disease.
1. Disorders of semicircular canals, including air and sea
sickness.
5. Cyclic vomitingcommon in children.
6. Drugsapomorphine, ipecac, anaesthetics, tobacco, alcohol.
7. Tabetic crisis.
C.
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.
180
FATIENT
(b) After mealsgastric ulcer, acute gastritis, dyspepsia,

neurosis.
(c) No relation to fooddilated stomach, cerebral diseases, gastric crises of tabes.
4. Vomiting in childrenmay not be of any significance;
indiscretion in diet, diarrhoea, overfeeding, acute fevers,
acute gastritis, gastro-enteritis, acute abdominal diseases,
acidosis, pyloric stenosis, cyclical vomiting are the common causes.
INVESTIGATIONS.
Note the following:

1. Q U A N T I T Y : I t is large in pyloric obstruction, especially when this
is due to pyloric cancer. Undigested matter is often found in vomit when
there is pyloric obstruction. Copious vomit containing bile indicates
obstruction below the ampulla of Vater.
2. ODOUR:Most vomits possess a characteristic penetrating odour due
to the acid present. Offensiveness indicates serious disease. Faecal odour
may occur in intestinal obstruction. Unpleasant odour may occur when
fermentation goes on in the stomach as in gastric carcinoma.
3.
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.
May be neutral in gastric carcinoma
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:
1. Epitheliomadysphagia is more common than haematemesis. In fact, bleeding is rare.

2. Ruptured aneurysminvariably fatal.
3. Ruptured oesophageal veinscirrhosis liver.
be ascites.
There will
4. Foreign body perforating the oesophagus.

B.
FROM T H E STOMACH:
1. Acute gastritisgenerally due to eating irritating food.

There will be tenderness over the stomach, nausea and
vomiting in addition to pain soon after eating.
2. Toxic gastritisgenerally due to infections and sepsis.
3. Corrosive poisonsstrong acids or alkalis destroy the
mucous membrane of the upper alimentary tract and
cause severe pain in the mouth, throat and stomach. If
due to arsenic, there will be severe vomiting and diarrhoea also.
4. Ulcersgastric ulcer is more prone to haematemesis than
duodenal ulcer. The patient gives history of pain with
definite relation to food.
5. Cancerthe patient gets "coffee-ground" vomiting;
nausea, anorexia, anaemia and wasting are chief features.
Gastric juice shows absence of HC1 and presence of
occult blood.
6. Abdominal aneurysm bursting into the stomachsudden
severe haematemesis, invariably fatal.
7. Gastrostaxisvicarious menstruation; more common in
anaemic women.
8. Hereditary telangiectasisthere
rather than haematemesis.
is generally
epistaxis
9. Idiosyncrasyaspirin, etc., may cause bleeding in the

stomach.
IIOW TO EXAMINE A FATIENT
82
C.
DUODENUM :
1. Ulcersduodenal
liaematemesis.
ulcer
causes
melaena
rather
than
2. Cancervery rare in this region.

3. Gall-stones ulcerating into the duodenummay sometimes cause liaematemesis. There will be history of colics
and jaundice.
O.
LIVER DISORDERS ( P O R T A L O B S T R U C T I O N ) :
1. Cirrhosis liverthere will be ascites, enlarged or

shrunken liver, and enlarged spleen. T h e bleeding
occurs due to varicosity of the oesophageal veins.
2. Prolonged jaundicebleeding occurs due to deficiency
of prothrombin.
3. Splenic anaemiafrequently gives rise to haematemesis.
T h e spleen is enlarged, later the liver, followed by ascites.
it
ACUTE INFECTIONS :
Haemorrhagic small-pox, yellow fever, scarlet fever, acute

yellow atrophy, malaria, septicaemia.
F.
BLOOI) DISORDERS:
Splenic anaemia, purpura, leukaemia, polycythaemia, scurvy,

haemophilia.
T h e commonest causes of profuse haematemesis are gastric
ulcer, cirrhosis liver and splenic anaemiaCONSTIPATION
Constipation is defined as a condition where the patient does
not feel sense of relief after evacuation. Normally the residue
of a meal reaches the pelvic colon in 16 hours and is excreted
within 24 hours although in some cases it may pass after 48
hours. Hence, an individual may be regarded as constipated
if his bowels are not open at least once in 48 hours.
ETIOLOGICAL CLASSIFICATION:
A.
Colonicpassage through the colon is delayed.
ALIMENTARY SYSTEM
I.
183
Deficient motor activity:

1. Due to direct action on the intestinelead poisoning, excessive smoking, abuse of tea.
2. Due to lack of central stimulusshock, worry, depression.
3. Reflex causespainful abdomen, pelvic
gall-bladder disorders, appendicitis.
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.
Deficient reflex activity:

1. Less or improper foodlack of mechanical stimulus.
2. Myxoedemalack of chemical stimulus.
3. Abuse of purgatives and enemas.
4. Depression of nervous systeminsanity, neurasthenia, hypochondria, psychological conviction that
bowels do not move without aperients or enematas.
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.
Insufficient formation of faeces

J. "Greedy colon".
2. Less residue reaching the colonanorexia, oesophageal
or pyloric obstruction.
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.
Severe secondary anaemia.
5. Nutritional anaemia.
6.
Pellagra.
7. After gastrectomy or gastroenterostomy.

B. Enterogenous: T h e origin is in the small intestine. In
diarrhoeas of this type a mechanical stimulant produces an
exaggerated reflex resulting in more frequency.
Al I M E N T A R Y
COMMON
SYSTEM
185
CAUSES:
1. Dieteticunbalanced diet,
tion in diet, idiosyncrasy.
indigestible
food,
indiscre-
2. Drugspurgatives and poisons of medico-legal importance.

3. Infections
(a) General infectionsinfluenza.
(b) Bacillary infectionscholera, enteric.
(c) Tuberculosis of the intestine.
(d) Protozoallamblia intestinalis, malaria.
(e) Food poisoning.
(f) Helminthictape-worms, ascaris, ankylostomiasis (all
rare causes of diarrhoea) .
(g) Ulcerative colitis.
4. Toxaemiasuraemia.
5. Endocrine disturbanceshyperthyroidism.
6. Steatorrhoeas (see page 186).
7. Congestion of the intestinecardiac failure, cirrhosis
liver.
8. Nervous
(a) Post-prandial.
(b) Fear, anxiety.
(c) Irritable bowel.
9. Wide variations in the temperature:
(a) Severe chill.
(b) Heat-stroke.
C.
Colonic diarrhoeas.
T h e origin is in the colon.
COMMON CAUSES:
(a) Infectionsbacillary, amoebic, balantidium coli.

(b) Cancer colon.
(c) Mucous colitis.
In colonic diarrhoea the patient passes loose stools with colic
and tenesmus. T h e stools are generally semi-formed, mucoid
and contain blood.
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:
1. Acute generalised infectionspneumonia, pyelitis, meningitis, otitis.

2. Teethingsupposed to cause diarrhoea.
IV.
STEATORRHOEAS:
1. Coeliac disease (see page 188).

2. Congenital fibrocystic disease of the pancreasusually
noticed in early infancy. The child passes large, bulky
stools, leading to wasting, abdominal distension and
rickets.
STEATORRHOEAS
This disorder is to be suspected when the stool is pale, bulky
and greasy in appearance. Faecal fat is present in the form of
neutral fat or fatty acids.
Al I M E N T A R Y
AETIOLOGY
I.
SYSTEM
187
PANCREATIC DISEASESdue to lack of lipase the fat

is not split up and neutral fat passes in the stool.
Common conditions are:

1. Chronic pancreatitisthe patient complains of abdominal pain and diarrhoea with or without jaundice.
2. Pancreatic calculithere may be colicky pains in the
epigastric area; often associated with diabetes.
3. Cancer pancreasjaundice is more prominent than
steatorrhoea; there are no diabetic manifestations.
4. Congenital fibrocystic diseaseusually noticed in early
infancy; causes steatorrhoea, wasting, abdominal distension and signs of latent rickets.
II.
ABSENCE OF BILE IN T H E STOOLthe fats are not

emulsified and hence, not absorbed. The patient passes
fatty acids in the stool.
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.
BLOCKAGE OF INTESTINAL LYMPHATICS

1. Intestinal tuberculosis may cause steatorrhoea.
fats are found in excess in the stool.
Split
2. Filariasis may cause blockage of lymphatics and hence,

steatorrhoea.
3. Malignancy in the abdomen may produce
condition.
IV.
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
2. Coeliac diseaseoccurs in children giving rise to

steatorrhoea, abdominal distension and rickets.
3. Idiopathic steatorrhoeaoccurs in adults and often
gives rise to lack of calcium in the blood and even
osteomalacia. The tongue is sore and there is macrocytic anaemia. Common in temperate zones.
4. Regional ileitisoften gives rise to bulky fatty stools.
5. Amyloid diseasemay give rise to steatorrhoea.
6. Hill diarrhoeathere is functional breakdown of the
gastro-intestinal function due to low barometric pressure and high humidity. Mainly affects Europeans in
tropical zones during rainy season. The stool is pale,
copious, fatty, occurring 5 to 6 times a day before midday.
V
GASTRO COLIC OR JEJUNO-COLIC FISTULAmay

interfere with the fat absorption; faeces will reveal neutral
fats.
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.
May not be present.
General features.
Dwarfism may occur.
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 :
1. Pilescommonest cause; blood falls in drops after the

stool which is constipated.
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 :
1. Dysenteriesespecially amoebic and bacillary.

2. Non-specific ulcerative colitismay cause bleeding; the
stool contains lot of mucus and pus with very little blood.
3. Diverticulitismay give rise to bleeding; the patient
generally cannot pass stool without an enema or aperient.
C.
LESIONS OF T H E SMALL I N T E S T I N E :
1. Intussusceptionthere is severe pain, vomiting, often

faecal, abdominal discomfort, visible peristalsis and prostration are the chief features.
2. Typhoid ulcerationremittent fever, slow pulse, coating
of the tongue, tympanitis. Haemorrhage occurs in the
second week.
3. Schistosome infectioncommon in Far East. Stool examination for ova reveals the diagnosis.
D.
BLOOD DYSCRASIAS:
Purpura, scurvy, agranulocytosis, leukaemia, splenic anaemia,

erythroblastosis.
Shallow.
Sharp.
Serpiginous.
Inflamed.
Red cells in clumps.

Red cells in rouleaux formation.
Lymphocytes & mononuclears
Polymorphs.
Macrophagesscanty.
Macrophagespresent.
E.Hystolitica.
Culture lor Bacilli positive.
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.
AMOKBIC DVSFNTL-RY. BACILLARY I)YSINTI.RY.
DIFFERENTIATION BETWEEN AMOEBIC A N D BACILLARY DYSENTERY.
190
IlOW TO EXAMINE A PATIENT
A1,1 MEN I ARY
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.
C.! [ISUS OF MELAENA :
STOMACH CONDITIONS:
1. Cancer stomachthe black colour is not so evident.

Occult blood test of faeces is almost always positive.
2. Gastric ulcerrarely causes melaena. Haematemesis is
more common.
3. Duodenal ulcerfairly common cause of melaena.
B.
SWALLOWED BLOODderived from haemoptysis or epistaxis.
C.
LIVER CONDITIONScirrhosis liver.
D.
INTESTINAL CONDITIONS:
1. Typhoid haemorrhagethe stool is more often bright red

than tarry.
2. Embolism of the superior mesenteric arterygenerally a
complication of infective endocarditis.
3. Thrombosis of the mesenteric veinsresult of abdominal
injury or intra-abdominal infection.
4. Contusion of the bowelas a result of direct injury to
the abdomen.
E.
BLOOD DISORDERS:
1. Blood dyscrasiaspurpura, haemolytic anaemias, leukaemias, splenic anaemia.

2. Melaena neonatorumdue to erythroblastosis foetalis or
some haemopoietic disturbances.
INTESTINAL OBSTRUCTION
CAUSES:
A.
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.
1. Strangulation by bands or adhesions.

2. Volvulus.
3. Paralytic ileus.
4. Pressure by tumours.
ACUTE INTESTINAL OBSTRUCTION
The common causes of acute intestinal obstruction
strangulation, intussusception and volvulus.
are
All these give rise to acute pain in the abdomen, bilious

vomiting followed by faecal, severe constipation and collapse.
The abdomen is distended, tympanitic with no peristalsis.
CHRONIC INTESTINAL OBSTRUCTION
The common causes of chronic intestinal obstruction are
tumours in the wall of the intestine, strictures, strangulation,
impacted faeces and round worms.
These conditions give rise to intermittent colicky pains,
occasional vomiting, and partial constipation. T h e abdomen is
distended with visible peristalsis and the cause of the trouble
may be felt as a palpable lump in the abdomen.
COMMON DISORDERS OF T H E ABDOMINAL ORGANS
LIVER
In adults the liver is about 1 / 36th of the body weight, but in infants
it is 1 /24th of the body weight so that it is relatively larger in children
than in adults. A normal liver, therefore, may be palpable in a child.
Ordinarily, in an adult, the organ is not palpable but in people with lax
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.
Proptosisthe liver is better felt on erect posture.

Alteration in the contour of the chesttightly lacing in females,
curvature of the spine, rickets.
Right-sided pleural effusion or pneumothorax.
Right-sided diaphragmatic abscess sometimes.
Cancer stomach.
Malignancy of the transverse colon.
Faecal impaction in the transverse colon.
Chronic peritonitis causing puckering of the greater omentum.
Riedel's lobe.
Enlarged gall-bladder.
3.
4.
5.
6.
7.
8.
9.
10.
All these
size of the
conditions
liver.
may give a false impression
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).
11. Without jaundice.

1. Regular.
(a) Cirrhosisbiliary,
diabetes.
13
alcoholic,
Banti's,
bronzed
194
PATIENT
(b) Congestive heart failureespecially mitral disease

and right sided failure.
(c) Blood dyscrasiasleukaemia,
splenic anaemia.
Hodgkin's
disease,
(d) Protozoal diseaseschronic malaria, Kala-azar.

(e) Lipoid dystrophiesGaucher's disease.
(f) Amyloid disease.
(g) Perihepatitis.
2. Irregular.
(a) Syphilis.
(b) Early secondaries.
B.
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.
Hepatitis, including abscess formation.
2.
Venous congestion of heart failure.
3.
Early cirrhosis.
4.
Actinomycosis.
5.
Visceroptosis.
6.
Catarrh of the bile-ducts.
7.
Later stages of carcinoma.
In nearly all these conditions
the liver is enlarged.
LIVER DULLNESS MAY BE DIMINISHED IN FOLLOWING

CONDITIONS:
1. Acute yellow atrophy.

2.
Terminal stages of portal cirrhosis.
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
sion of the boivels, the hepatic

diminished.
dullness
195
is
apparently
INVESTIGATION OF A CASE OF ENLARGED LIVER:

1.
Note the sizeslightly enlarged in hepatitis; moderately enlarged in

obstructive jaundice, congestive heart failure, early cirrhosis; very
large in malignancy, leukaemia, Hodgkin's disease.
2.
Shapeif irregular, suspect gumma or malignancy.
3.
Surfacesmooth in hepatitis and congestive heart failure; granular

in cirrhosis; nodular in malignancy and gumma.
4.
Tendernesspresent in hepatitis, liver abscess,

failure; not present in malignancy and cirrhosis.
5.
Jaundicepresent in infective hepatitis, malignancy, obstruction of

the bile duct.
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
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
Metabolism of bile pigments.
Jaundice, in general may be grouped under three headings,

obstructive, hepatogenous and haemolytic.
A.
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
3. Pressure from outsidegrowths, enlarged glands, pancreatic lesions.

B.
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.
In malescirrhosis, pancreatic disorders, cancer.

In femalesgall-stones and gall-bladder diseases.
198
PATIENT
3.
OCCUPATIONin sewer workers suspect Weil's disease; in industrial

workers, toxic hepatitis.
4.
RATE OF SPREAD OF JAUNDICEif rapid, suspect virus hepatitis;

if persistent, chronic pancreatitis; if persistent and progressive, cancer
liver and cancer of the head of pancreas.
5.
PROGRESSIVE LOSS OF WEIGHTcancer.
6.
ABDOMINAL PAINgall-stones, pancreatic disorders.
7.
CONDITION OF T H E LIVERif nodular, cancer; if smooth,

obstruction; if gall-bladder is enlarged, cancer of the head of pancreas;
if ascites is present, cirrhosis; ascites and severe jaundice, cancer.
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.
Delayed or biphasic reaction i.e. colour slight at first, becoming intense

after a few minuteshepatogenous jaundice.
In the second tube add
a little alcohol to precipitate proteins and then add the diazo solution
blue colour appears which may mean normal. If intense, it suggests
haemolytic
jaundice.
In practice the quantitative estimation of icteric
index is more reliable. T h e normal figure is 10-30. It may go up to
even 90 in jaundice.
2. THYMOL T U R B I D I T Y TEST. This test is based on the fact that
in liver diseases there is tendency for plasma-albumin to fall and the
globulin to rise. T h e albumin may fall to 3 gms. per 100 c.c. of plasma
or lower, and the globulin may be raised to 3 gms. per 100 c.c. T h e
albumin-globulin ratio which is normally 2 to 1 is disturbed and brought
nearer to 1.
TEST:
Add a little colloidal suspension of thymol to the plasma of the patient.
Normally there is no precipitation, the solution remaining clear. Plasma
from cases of jaundice has a precipitating effect.
READINGS:
Normal0.4 units of turbidity.
Obstructive jaundicenormal results or slightly increased but not above
5 units.
Al I M E N T A R Y
SYSTEM
199
In hepatitis and parenchymatous disease of the liver the turbidity is

greatly increased and is always above 5.
S. ALKALINE-PHOSPHATASE T E S T : This test is very reliable to
judge the efficiency of the liver as this organ plays an important part
in the metabolism of alkaline phosphates. Normal level is 5 to 15 KingAmstrong units. In obstructive jaundice it is 30 to 60, and in hepatitis,
rarely above 25 units. Unfortunately, alkaline phosphates are also increased
in bone diseases, such as rickets, Paget's disease and in bone secondaries
of cancer prostate.
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:
(a) Riedel's lobethis is symptomless; the lobe is generally

situated further to the right than is a gall-bladder and is
more apt to simulate a movable kidney.
(b) Secondariesgenerally more than one nodule is felt,
associated with jaundice and ascites. The lump is hard
to the feel.
(c) Gummanot so common nowadays. It is felt like a firm
and irregular mass. There will be history of syphilis and
W.R. will be positive.
(d) Liver abscessif single, may be mistaken for gall-bladder.
There is definite tenderness over the area, leucocytosis
and history of amoebic dysentery.
(e) Hydatid cystmore often it is embedded into the liver
substance and may be difficult to feel; if it projects from
its outer surface, it has an elastic feel. Blood examination
reveals eosinophilia.
2.
RENAL T U M O U R S :
The gall-bladder is more easily felt anteriorly than posteriorly

while the reverse is the case with the kidney. The kidney is
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:
New growths of pylorus, duodenum, transverse colon and

suprarenals may be big enough to simulate an enlarged gallbladder. But they seldom have the smooth oval outline that
the gall-bladder nearly always possesses. In addition, there may
be symptoms attributable to new growths such as dilatation of
the stomach, coffee-ground vomiting, secondaries in the liver,
etc. to indicate the diagnosis.
ENLARGEMENT OF T H E GALL-BLADDER
CAUSES:
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.
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-
1. Chronic myeloid leukaemia.

2.
Splenic anaemia.
3.
Tropical diseasesmalaria, kala-azar.
4.
Gaucher's disease.
5.
Haemochromatosis.
6. Polycythaemia vera.
DIEFEREXTIA
L DIA
GXOSIS.
1. Kidney tumours. A renal tumour is more deeply situated;

there is generally a tympanitic note over it due to intestine
intervening between the tumour and the anterior abdominal
wall. A renal tumour slopes away as it approaches the ribs and
hence, it is not difficult to slip the fingers between its upper
pole and the costal margin. Abnormalities in the urine may
afford additional evidence to support kidney tumours.
2. Suprarenal tumours. These may be mistaken for a
kidney or splenic tumour; in fact, it is nearly impossible to
distinguish a suprarenal tumourhypernephroma for example
from renal enlargement, unless there is cachexia and presence
of red cells in the urine.
3. Cancer of the splenic flexure. This is generally annular
to the feel, giving rise to no definite tumour but to distension
of the transverse colon, with symptoms of chronic, followed by
acute intestinal obstruction. The mass is generally resonant
to percussion and has no well-defined edge or notch.
4. Cancer of the stomach. When sufficiently well developed, cancerous growth in the stomach may be mistaken for
a splenic tumour. However, it has no well-defined edge and
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.
If there is feversuspect infection.
2.
If there is pallorsuspect pernicious anaemia, leukaemia, haemolytic

anaemia.
3.
If there are purpuric spotssuspect subacute bacterial endocarditis,

thrombocytopenia, leukaemia.
4.
If there is haematemesissuspect portal cirrhosis, splenic anaemia,

leukaemia.
PHYSICAL EXAMINATION:
1.
General appearancepale in anaemia and leukaemia; plethoric in

polycythaemia.
2.
Size of the spleen:

(a) Slight enlargementacute
haemolytic anaemia.
infection,
acute
leukaemia,
acute
(b) Moderate enlargementmalaria, kala-azar, Hodgkin's disease,

chronic leukaemia, polycythaemia, chronic haemolytic anaemia.
204
H O W TO EXAMINE A
PATIENT
(c) Big enlargementmalaria, kala-azar, splenic anaemia, Gaucher's

disease, lymphosarcoma.
C.
3.
Lymph-glandsif enlarged, suspect

disease, infective mononucleosis.
blood
dyscrasias,
Hodgkin's
4.
Liverif enlarged, suspect kala-azar, malaria, leukaemia,

syndrome.
Banti's
BLOOD EXAMINATION:
1.
Leucocytosisbacterial infection, leukaemia.
2.
Leucopeniatyphoid, malaria, kala-azar.
3.
Red cellsdiminished in all anaemias and in most of the blood

dyscrasias; increased in polycythaemia.
4.
Bone-marrow biopsyconfirms leukaemias, kala-azar, etc.
5.
Lymph-node biopsyconfirms
disease, tuberculosis.
lymphatic
leukaemia,
Hodgkin's
SPLENOMEGALY AND HEPATOMEGALY

These are generally associated in the following conditions:
1. Chronic Myeloid Leukaemia.
2.
Chronic Lymphoid Leukaemia.
3.
Polycythaemia.
4.
Haemolytic Anaemias.
5. Cirrhosis Liver.
SPLENOMEGALY AND GLANDULAR
ENLARGEMENTS
These are commonly present in the following diseases:

1. Lymphoid Leukaemia.
2.
Hodgkin's Disease.
3.
Lymphosarcoma.
4.
Sarcoidosis.
CHAPTER
CENTRAL NERVOUS SYSTEM

A.
INTERROGATION.
B.
COMMON SYMPTOMS.
C.
EXAMINATION OF T H E NERVOUS SYSTEM.

I.
II.
Examination of the Skull and Spine.
III.
Cranial Nerves.
IV.
Motor System.
V.
VI.
D.
Intellectual Functions.
Sensory System.
Reflexes.
EXAMINATION OF T H E CEREBROSPINAL FLUID.
206
HOW
TO EXAMINE A
PATIENT

In no department of medicine is a careful and expert
history-taking more important than in diseases of the Nervous
System. The same physical sign may have different significance
according to whether it has come on suddenly or gradually.
Hence, greater attention must be paid to minute details of each
and every symptom. Knowledge of anatomy and physiology of
the Nervous System is the basis on which the various symptomsi
and signs are to be interpreted.
INTERROGATION
Particularly inquire into the following:
1. Family history of mental diseases, chorea, migraine, fits
and paralysis.
2. Nature of patient's workif exposed to poisons like
lead, mercury, manganese, volatile oils, etc.
3. History of syphilis and trauma.
4. Addiction to alcohol and drugs.
COMMON SYMPTOMS
FITS (see page 265).
Inquire into the following very carefully:
1. Duration and frequency,
2. Any assigned cause.
3. Any history of trauma.
4. The time of occurrence.
5. Description of a fitif localised or generalised.
6. Intervals in betweenlongest and shortest.
7. If preceded by auraits character.
8. Any unconsciousnessits duration.
9. Whether the patient falls and injures himself; whether
he bites his tongue.
10. If there is froth in the mouth.
CENTRAL N E R V O U S SYSTEM
207
11. If visceral reflexes are affected.

12. After effectssleep, headache, automatism, paresis.
FAINTING (see page 99).
1. If consciousness is lostif completely.
2. Its; duration.
3. If the patient was aware that he was going to faint.
4. If accompanied by convulsions.
5. Colour of the patient during the attack.
6. Associated phenomenanausea, sweating, trembling.
7. Circumstances of the onsetemotion, pain, prolonged
standing, congested surroundings.
HEADACHE (see page 270).
1. Its situationlocalised or generalised.
2. Its frequency.
3. Character and severity.
4. Its duration.
5. If constant or paroxysmal.
6. Time of occurrence and when maximal.
7. If it disturbs the patient in the nights.
8. Aggravating factorssneezing, coughing, posture, worries, emotion, etc.
9. Relieving factorsrest, drugs, etc.
10. Associated symptomsvomiting,
tion, fits, diplopia.
drowsiness,
11. History of high or low blood pressure.

12. History of trauma.
13. History of aura before the attack.
lachryma-
208
DIZZINESS, VERTIGO (see page 233).

1. If continuous or paroxysmal.
2. If the patient tends to fall in any particular direction.
3. Its severity.
4. If variable with posture.
5. Associated phenomenavomiting, tinnitus, deafness.
6. History of blood pressure.
PARALYSIS (see page 290).
2. Part of the body involved.
3. Any premonitory symptomsheadache, giddiness, vomiting.
4. Any accompanying symptomsconvulsions, coma.
5. Previous similar attacks.
6. History of heart or kidney disease.
7. Its progresswhether maximum at the onset or increasing.
8. Other symptoms of nervous diseases.
NEURALGIC PAINS (see page 313).
Note the following:
1. Its siteexact distribution.
2. Charactermild, severe, burning, boring, tingling, numbness, "pins and needles", "lightning-like".
3. Radiation.
4. Duration.
5. If continuous or remittent.
6. Aggravating factorssneezing, coughing, etc.
7. Relieving factorschange of posture, etc.
8. Associated phenomena.
209
NUMBNESS AND TINGLING.

1. Its extent and distribution.
2. Whether sudden or gradual.
3. Whether periodic or continuous.
4. Its duration.
5. Effect of temperature.
TREMORS AND SPASMS (see page 282).
1. Part of the body affected.
2. Their description.
3. If present when sleeping.
4. If present on voluntary muscular action.
UNCONSCIOUSNESS (see page 274).
1. If the patient can be roused.
2. If any drugs were administered.
3. If any sensations preceded the attack.
4. Duration.
5. Any accompanying fits.
6. Progress of the attack, any accompanying fever.
7. Previous health.
8. History of accidentshead injury especially.
9. History of diabetes and renal diseases.
10. Possibility of poisoning.
DIPLOPIA (see page 221).
1. If the object is seen double with one eye open (monocular) or with both eyes (binocular).
2. If it increases on looking in particular direction.
3. Duration.
14
H O W TO EXAMINE A
210
PATIENT
4. Any accompanying symptoms, especially headache, giddiness, vomiting, tinnitus.

NOISES IN T H E EAR (TINNITUS) (see page 234).
1.
2.
3.
4.
Type of noisebuzzing, ringing, hearing voices, etc.

Their intensityif variable.
If persistent or occasional.
If associated with vertigo.
LOSS OR DEFECT OF SPEECH (see page 277).

1.
2.
3.
4.
5.
Mode of onsetif sudden or gradual.

If the patient understands simple commands.
If he understands written words.
If the patient speaksif so, if intelligible.
If he can write.
ATAXIA (see page 288).

1.
2.
3.
4.
5.
6.
7.
If continuous or coming on in attacks.

Its duration.
If worse in the dark.
If worse on closing the eyes.
Any associated symptomsvertigo, etc.
If there is any tendency to fall on one particular side.
Possibility of poisoningalcohol, hypnotics, narcotics.
EXAMINATION OF T H E NERVOUS SYSTEM
I.
INTELLECTUAL FUNCTIONS
It is important to judge the patient's intellectual state in the

early stages of the General Examination as it will give an indication that will help in the subsequent investigation of his
symptoms.
Note the following:
1. State of consciousnesscoma, semi-consciousness, state of
confusion, stupor.
CENTRAL N E R V O U S
SYSTEM
211
2. Appearance and behaviour.

3. Promptness of response to questionswhether talkative
or answers in monosyllables.
4. Right or left handed.
5. Memory for recent and past events.
6. Sleep, dreams, delusions, hallucinations, delirium.
7. Emotional statealso whether happy, depressed, euphoric, irritable.
8. Abnormal conductchange in temperament, change in
morality, business acumen, phobias, anxiety state,
negativism, etc.
9. Orientation in time and space.
10. Speech and articulation (see page 277).
II.
EXAMINATION OF SKULL AND SPINE
Careful examination of the head and spine may be necessary

as part of the neurological examination. In every case where
the brain is suspected to be the cause of the trouble, it is essential to examine the head carefully by inspection, palpation,
percussion and even auscultation. Shape of the head may reveal
early rickets, congenital syphilis, hydrocephalus, acromegaly,
Paget's disease, etc. Palpation may bring to light the state
of fontanelles, ridges of old fractures, areas of tenderness, etc.
Percussion may reveal tympanitic sound in internal hydrocephalus or craked-pot sound in children when the cranial
sutures have slightly separated by increased intracranial pressure. Auscultation, by placing the stethoscope over the mastoids,
may reveal bruits of intracranial aneurysms or vascular tumours.
Spine must be examined carefully for anatomical defects,
movements, abnormal curvatures, tenderness, presence of lumps,
evidence of spina bifida, etc.
ABNORMALITIES OF T H E SKULL AND SPINE
(See Chapter VIII)
H O W T O EXAMINE A
212
PATIENT
CRANIAL
No.
I.
II.
Name
Foramen of Exit
Type
Olfactory.
Cribriform of the ethmoid.
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.
Internal acoustic meatus.
Mixed.
Auditory.
Internal acoustic meatus.
Sensory.
Glosso-pharyngeal.
Jugular foramen.
Mixed.
Vagus.
Jugular foramen.
Mixed.
Spinal-accessory.
Jugular foramen.
Motor.
Hypoglossal.
Hypoglossal canal.
Motor.
SYSTEM
213
NERVES
Distribution
Mucous membrane of
nose.
Functions
the
Smell.
Retina.
Sight.
Sup., med., inf., recti and

oblique muscles of the eyeball.
Eye movements.
Superior oblique muscle of

the eye-ball.
Eye movements.
Muscles of mastication.
Skin of the face.
Mucous membrane of the
mouth.
Mandibular movements.
Mastication & deglution.
Sensibility of the face and
mucous membrane of the
mouth.
Lateral rectus of the eyeball.
Eye movements.
Muscles of the face.

Glands of the mouth.
ant. -frd of the tongue.
Facial expression.
Secretory to the glands of
the mouth.
Taste.
Cochlea.
Semicircular canals.
Hearing.
Equilibrium.
Pharyngeal & laryngeal

muscles.
poterior Jrd of the tongue.
Pharyngeal 8c laryngeal
movements.
Taste.
Levator palati muscles.
Movement of the soft

palate.
Deglution.
Pharyngeal
&
laryngeal
muscles, Heart, lungs and
all the abdominal viscera.
Trapezius & sterno-mastoid.
Movements of the head 8c

shoulder.
Muscles of the tongue.
Movements of the tongue.
HOW
214
TO EXAMINE A
III.
PATIENT
CRANIAL NERVES
FIRST O R OLFACTORY NERVE

For testing this nerve, use substances with mild aroma like
clove oil, peppermint oil or tincture of asafoetida and not
ammonia or glacial acetic acid as these substances irritate the
5th cranial nerve. Test each nostril separately after excluding
obstructive nasal conditions.
See if there is any anosmia (loss of smell), parosmia (perverted
smell), or hyperosmia (excessive smell).
Damage to the first nerve often causes anosmia and is likely to be due
to tumours projecting from the lower surface of the frontal lobe or by
fracture involving the anterior fossa causing damage to the olfactory tracts.
In lesions of the uncinate gyrus hallucinations of smell are commonly
encountered with. Hyperosmia and parosmia are more likely due to functional disturbances and psychoneurosis. Hyperosmia may also occur as an
aura of epilepsy.
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.
Test the nerve for the following:

1.
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
of impairment of vision Snellen's chart, which consists of letters

of different sizes is more useful.
Defect in vision may occur as follows:
Amblyopiadefect in visual acuity leading to weak eyesight.
Amaurosiscomplete blindness.
Nyctalopianight blindness generally due to vitamin A
deficiency.
2. Field of Vision.
For rough estimation of the field of vision the following
method is fairly satisfactory: Seat yourself opposite to the
patient at a distance of about two feet. If the right eye is to be
tested ask him to close his left eye and let him look fixedly at
your left eye which should be at the same level as that of the
patient. Hold a pencil between his face and your own and
keep moving it from outside towards the eye and note when
the patient and you can see the movement of the pencil. Test
the field in all directions. When found abnormal, accurate
charts should be prepared by perimetry.
Field defects. (See Fig. XX.)
CHANGES
IN THE
FIELD
OF VISION
MAY
OCCUR
AS FOLLOWS:
(a) C O N C E N T R I C D I M I N U T I O N , i.e. the vision is contracted all round

its periphery. Occurs in hysteria, papilloedema, some forms of optic
atrophy, bilateral lesions of the anterior part of the cortical visual
ccntres and various affections of the retina.
(b) C E N T R A L SCOTOMA, i.e. loss of vision confined to the centre of
the field. Occurs in local diseases of the choroid or of retina in
the neighbourhood of the macula; in such cases the defect may occur
only in one eye. Unilateral central scotoma is also produced by
optic or retrobulbar neuritis and is quite common in disseminated
sclerosis. It may also occur due to toxic causes or vitamin deficiency
when it is generally bilateral. It may also result from pressure o n
the optic nerve or in lesions of the posterior part of the cortical
visual centres.
(c) HEMIAXOPIA, i.e. loss of sight in one half of the visual field.
Occurs as follows:
(i) Homonymousblindness occurs in one half of both sides of the
eyes due to lesions behind the optic chiasma on one side.
(ii) Superior or inferior hemianopiameans loss of upper or lower
halves of the visual fields respectively. These types are rare.
216
H O W TO EXAMINE A
PATIENT
(iii) Quadrantic hemianopiainvolves one quadrant of the field.

Occurs in lesions of the optic radiations or occipital lobes. T h e
loss of vision is confined to about quarter of the normal field.
(iv) Bi temporal hemianopialoss of vision in the temporal halves
of both the fields. Can occur in involvement of the nasal half
of the optic nerves and the commonest cause is tumour of the
pituitary body. It may also occur due to inflammatory or
traumatic lesions of the optic chiasma.
(v) Bi-nasal hemianopialoss of nasal fields on both sides. It can
only be produced by bilateral lesions confined to the uncrossed
optic fibres, on each side of the chiasma. Hence, it is rare.
Nasal hemianopia is usually unilateral and may result from
lesions in the optic radiation.
Lut tft
RIGHT TIT
FIG. XX
(The Optic Nerve (showing visual defects).

A. Blindness of the left eye. B. Bi-temporal hemianopia. Q . Left nasal
hemianopia. C2. Right nasal hemianopia. QC*. Bi-nasal hemianopia.
D. Right homonymous hemianopia with loss of light reflex. E. Right
homonymous upper quadrantic hemianopia. F. Right homonymous lower
quadrantic hemianopia. G. Right homonymous hemianopia with no
pupillary changes. H. Right homonymous central hemi-scotoroa.
CENTRAL NERVOUS
3.
SYSTEM
217
Colour Vision.
T h e material used for testing colour sense are coloured

skeins. Common types of colour blindness are red-green; they
select blue skeins to match purple. T h e other types are yellowblue who select red or orange to match purple.
Testing for colour sense is more of academic interest than of
any clinical importance. However, in certain occupations like
train-driving, testing for colour sense is necessary.
4.
Ophthalmoscopy.
Ophthalmoscopic examination is essential in every patient

who is suffering from cardio vascular disease or disorders of
the nervous system.
Examine the fundi in a dark room, if possible and note the
following:
1.
THE
OPTIC
DISCS.
NOTE:
(a) SHAPEnormally this is circular.
appear oval.
If there is astigmatism, it may
(b) COLOURnormally it is of a rosy tint but distinctly paler than

the rest of the fundus. T h e nasal side is generally redder than the
other side. In optic atrophy the disc becomes very pale and even
greyish white. In active hyperaemia its colour approaches to that
of the rest of the fundus as occurs sometimes in hypermetropia.
(c) PHYSIOLOGICAL CUPthis is the palest area seen in the fundus
and should not be mistaken for optic atrophy.
(d) EDGEit should be clear and well-defined normallyespecially
its outer side.
at
(e) S U R R O U N D I N G S OF T H E DISCS. Always examine this area for

haemorrhages or miliary tubercles as both these are more o f t e n seen
i n the immediate neighbourhood of the discs.
2.
THE
BLOOD-VESSELS.
Normally the arteries look thinner and lighter in colour as compared

to veins. Generally, they do not pulsate but may do so in cases of aortic
regurgitation and in increased intraocular tension. T h e veins sometimes
pulsate, even in normal eyes.
Note the point where an artery crosses a vein. Normally it is possible
to see the vein walls through the artery without any break in the calibre
of the vein. In hypertension with arterio-sclerosis the veins may be compressed at the point of arterial crossing.
HOW
218
3.
TO EXAMINE A
PATIENT
PERIPHERY.
Examine the retina carefully, especially for diabetic retinopathy which

gives rise to tiny haemorrhages in the retina.
CHARACTERISTIC
1.
OPHTHALMOSCOPIC
APPEARANCES.
PAPILLOEDEMA.
This arises as a result of pressure and not due to inflammation. It is

usually bilateral. In early stages the veins are fuller than normal; the
optic discs are blurred. Later, the oedema increases and the disc gets
swollen; the veins become tortuous and the arteries look smaller than
normal; the edge of the disc is no longer clear, and there may be small
haemorrhages near the discs. In cases of severe increase in the intracranial
pressure there may be intense oedema of the discs resulting in "choked
discs". T h e commonest condition that causes papilloedema is increased
intracranial tension as in cerebral tumours. In milder form it may occur
in subarachnoid haemorrhage, cerebral abscess, sub-dural haematoma and
in subacute or chronic forms of meningitis. Papilloedema does not occur
in cerebral haemorrhage. Swelling of the disc is often seen in chronic
nephritis and in malignant hypertension. Unilateral atrophy due to direct
pressure on the optic nerve and papilloedema on the opposite side is
typically present in frontal lobe tumours (Foster-Kennedy syndrome).
2.
RETINAL HAEMORRHAGES.
Retinal haemorrhages may be seen in hypertension, chronic nephritis,

diabetic retinopathy, aplastic anaemia, thrombocytopaenia, purpura and
embolism of the retinal artery. They appear as elongated streaks with
flame-shaped edges.
3.
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.
Optic atrophy is associated with decreased visual acuity and a change

in colour of the optic disc to light pink, grey or white.
Primary atrophy is produced by processes which involve the optic nerve
without producing papilloedema; these include retrobulbar neuritis, neurosyphilis, growths pressing on the optic nerve, degenerative diseases and
toxic substances.
True secondary optic atrophy results from degeneration of the ganglion
cells of the retina as in retinitis pigmentosa and as a sequel to papilloedema.
In secondary atrophy the disc is pale, its edge ill-defined and the lamina
cribrosa blocked with organised exudateremnants of the previous oedema
of the nerve-head. In primary type, the disc is dead-white in colour with
sharply defined margins like a "full-moon in a retinal sky". T h e lamina
219
cribrosa is well-marked and the absence of small vessels on the disc is

notable.
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.
Examine the nerves for the following:

1.
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
In 4th nerve paralysis there is impairment of downward

movement such as difficulty in going down the steps. This nerve
is rarely affected alone. It may be involved in meningitis.
In 3rd nerve paralysis there is ptosis, failure of movement of
the eye-ball inwards, dilatation of the pupils, loss of pupillary
reactions and may be external squint and diplopia. This nerve
is often involved in meningitis, gumma, aneurysms, tumours,
and cavernous sinus thrombosis.
Conjugate deviation of the eyes. Such condition is often
observed in supra-nuclear lesions. T h e supra-nuclear centres
for conjugate movements of the eyes are located in the frontal
and occipital lobes. A lesion that damages either one of these
centres interrupt their connections with the brain-stem and
cause weakness or paralysis of movements of both the eyes in
one or both directions. In hemiplegia, where the lesion is in
the cerebral hemisphere (supra-nuclear) the patient may not be
able to look on either side; generally the patient looks away
from the side of the lesion in the acute (irritative) stage. In
pontine lesions this role is just reversed.
Skew deviation of the eyesi.e. one directed upwards and
the other downwardsoccurs in certain lesions of the labyrinth,
8th nerve lesions and in cerebellar disorders.
2.
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.
SYSTEM
221
In order to estimate the degree of ptosis, one must eliminate

the action of occipito-frontalis muscle. This is done by pushing down the latter muscle so that the eye-brows are kept at
level and then asking the patient to look up.
In 3rd nerve paralysis, in addition to ptosis there may be
dilated pupils and external strabismus. When all the muscles
supplied by the 3rd nerve are involved, it is considered probable that the lesion has affected the nerve itself in its peripheral
course; when a single muscle is involved the lesion is
more likely to be in the region of the nucleus; small infarcts
often cause nuclear palsies. Aneurysm of the internal carotid
system, tumours and inflammations in the region of the sella
and pressure from herniation of the uncinate gyrus in expanding lesions of the cerebral hemisphere, are the most common
cau^fes of peripheral oculo-motor palsies.
Besides lesions of the 3rd cranial nerve, ptosis can occur in
the following other conditions:
1. Paralysis of the cervical sympathetic nerves (Horner's
syndrome).
2. Myasthenia gravisthe drooping is due to muscular
weakness.
3. Tabesthe drooping is due to hypotonia of the eye-lids.
4. Congenitaloften associated with defect in vision.
3.
DIPLOPIA.
Diplopia may be either monocular or binocular, i.e. an object

is seen double with one eye, or single with each eye separately
and only double when both eyes are open. T o distinguish between these two conditions it is necessary that each eye is closed
in turn while testing.
Diplopia may be present in all positions of the eye but
increases when an attempt is made to move the eye in that
direction towards which the paralysed muscle would normally
move it.
Diplopia may be homonymous
or uncrossed and heteronymous or crossed. In diplopia, due to paralysis of the external
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.
Nystagmus means involuntary rhythmic oscillations of the

eyes independent of their normal movements. The oscillations
are generally horizontal, but may be vertical or even rotatory.
T o examine for nystagmus, ask the patient to look straight
in front of him. Place your finger before his eyes and ask
him to follow it. The finger should be moved from one direction to another in quick succession both horizontally and from
223
above downwards. Normally, the patient can freely move the

eye-balls. When nystagmus is present the eye-balls oscillate.
T h e horizontal nystagmus, which is the commonest, is of two
varieties:
A.
Pendular, where movements are equal on both sides.
B.
Jerky, consisting of a quick phase and a slow phase, the

slower jerk being towards the voluntary movement.
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.
II. Labyrinthine nystagmus:

1. Experimentallasts not more than 2 minutes after the
stimulation has ceased.
2. Labyrinthine disordersconsists of a slow phase when
the eyes are directed away from the side of the disease.
3. Lesions of the vestibular apparatus (Meniere's disease)
the slow phase is towards the lesion and the quick phase
on the opposite side.
III. Cerebellar nystagmusthe damage is invariably in the
region of the 4th ventricle.
2. Encephalitis.
3. Cerebellar disorders.
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.
T h e size of the pupil is influenced by many factors, chief of

which is intensity of light falling on the retina. T h e afferent
pathway for the light reflex is the optic nerveoptic chiasma
optic tractsuperior colliculus. From here, another set of
neurones continue the pathway to the oculo-motor nuclei, from
which the efferent pathways arise via the 3rd nerve. T h e pathway for accommodation appears to differ in the sense that the
centre lies in the occipital area.
Test the pupils for the following:
A.
Size.
B.
Shape.
C.
Position.
D.
Equality.
E.
Reactions.
In testing for reaction to light, throw a beam of light from

an electric torch held on the side and not in front of the eye
so as to avoid the patient accommodating the pupil while seeing
the torch. Test each eye separately.
In testing for reaction to accommodation the patient is told
to look at a distance. T h e observer's fingers are then suddenly
held about 6" in front of the patient's nose and he is told to
look at it. T h e pupils should contract as he accommodates the
eyes to look at the finger and dilate as the finger is moved away.
Testing for convergence of the eyes is the same as testing for
accommodation. T h e observer should keep the fingers at a
CENTRAL NERVOUS
SYSTEM
225
distance and gradually move towards the patient who is told

to converge his eyes at the finger. Convergence test can be
elicited even in blind people by asking the patient to look at
a distance and then to ask him to imagine that he is looking at
his own finger in front of his face.
T o test for consensual
on one eye reacts upon
some of the optic fibres)
the other and the effect
be observed.
A.
I.
Mydriasis
reflex of the pupils (i.e. light thrown

the other eye due to decussation of
one eye must be shaded while testing
on the pupil of the shaded eye is to
Size of the Pupils.
(dilatation).
CAUSES:
1.
Brain infection.
2.
Drugsatropine, hyoscine, cocaine, alcohol.
3.
Irritation of the sympathetic

growths, Pancoast's syndrome.
4.
Paralysis of sphincter pupillae3rd nerve lesion or of its ganglion.
nerveaortic
aneurysm,
mediastinal
5.
Concussion.
6.
Anaemias.
7.
Sympathetic overactivityneurasthenia, fear, anxiety, hyperthyroidism.
8.
Certain mental states such as epilepsy, acute mania, catalepsy.
9.
When optic atrophy has caused blindness.
II.
Myosis
(contraction).
CAUSES:
1.
Pontine lesions.
2.
Tabes dorsalis.
3.
Sympathetic nerve paralysissyringomyelia, aneurysms, Horner's and

Pancoast's syndromes.
4.
Drugsopium, pilocarpine, eserine.
5.
Acute encephalitis or intracranial abscess irritating the 3rd cranial

nerve. (There is dilatation later.)
B.
Shape of the Pupils.
It is distorted in the following conditions:

1.
Old iritis, injuries, iridectomy, corneal perforations.
2.
Tabes, G.P.I, or in syphilis with lesion in the short ciliary nerves or

in the ciliary ganglion.
15
HOW
226
C.
TO EXAMINE A
PATIENT
Position of the Pupils.
Eccentricity occurs in the following:

1.
Syphilis of the nervous system.
2.
Lesions of the mid-brain.
3.
Lesions of the foremost part of the 3rd nerve nucleus.
D.
Comparison of the Pupils.
CAUSES OF UNEQUALITY:
1.
Iridectomy, glaucoma, corneal perforation, iritis on one side.
2.
(a) Tabes, G.P.I.

(b) Paralysis or stimulation of one cervical sympathetic (common in
Horner's syndrome).
(c) Paralysis or stimulation of one 3rd cranial nerve.
carotid aneurysm or intracranial growths.)
(May occur in
(d) Trigeminal neuralgia.

(e) Concussion and cerebral irritation.
(f) Optic atrophy.
E.
1.
Reactions.
Light reaction is lost in the following:

(a) Argyll-Robertson pupil in Tabes and G.P.I.there is lack of
response to light and preservation of the response to accommodation. Argyll-Robertson pupils have the following characteristics
narrow, moist pupils, not reacting to light, reacting promptly to
accommodation. T h e site of the lesion is probably superior
colliculus.
(b) Optic atrophy with blindness.
(c) 3rd nerve paralysis and degeneration of the ciliary ganglion (there
is consensual reflex in the opposite eye).
(d) Cerebral haemorrhage, thrombosis, tumours, meningitis,
alcoholismthe pupils are large.
2.
chronic
Reaction to accommodation may be lost in:

(a) Diphtheria.
(b) Epidemic encephalitis.
(c) Basal meningitis.
(d) Tumours of corpora quaclrigemina.
3.
Loss or reduction to light and accommodation reflexes may occur in

the following:
(a) 3rd nucleus paralysis.
(b) Syphilis.
(c) Injuries to the eye.
(d) Diabetes.
CENTRAL NERVOUS
SYSTEM
227
(e) Encephalitis.
(f) Syringomyelia.
(g) Intracranial tumours.
(h) Haemorrhage.
(i) Alcoholic neuritis,
(j) Diphtheria.
4.
Other peculiar pupilary reactions:

(a) Myotonic pupil (Adie's pupil)the affected pupil is larger and
does not react to light. Contracts slowly on convergence and
slowly relaxes again. T h e abnormality is generally unilateral.
Its presence has no significance.
(b) Paradoxical reactionpupil dilates to light; may occur in tabes.
(c) Hippusalternate contraction and dilatation of the pupils which
sometimes goes on rhythmically; may occur in disseminated
sclerosis, brain tumours and alcoholics. More often seen where
there is central scotoma. May be of no significance at all.
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.
Test the nerve as follows:

A.
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
reflex is lost. In 5th nerve lesions stimulation of the

cornea on the affected side will produce no blinking
in the opposite eye but stimulation on the normal side
produces consensual response. If the 7th nerve is
paralysed, its stimulation still produces blinking in the
opposite eye.
Corneal reflex may be bilaterally abolished in com a of
any type.
The conjunctival reflex is often absent in normal individuals who have a high threshold for pain, and often
in hysteria.
Sensations of the whole of the face, but the angles of
the jaw.
Use cotton wool and pin to test for sensations.
Sensations of the anterior two-thirds of the tongue.
It has been definitely proved that the chorda tympani
nerve that supplies gustatory sensations to the anterior
two-thirds of the tongue is a branch of the facial nerve
and correctly speaking, the taste sensations should be
tested under the facial nerve; but, as the ordinary
sensations of the mouth are supplied by the fifth nerve,
it is advisable to test the tongue sensations under the
fifth nerve. For testing the sense of taste use concentrated solutions of sugar, salt and quinine. Let the
patient protrude the tongue and keep in that position till the test is over. Dry the tongue with cottonwool and then use the solutions. Use quinine solution
last, as this substance leaves after-taste. Ask the
patient to shake his head according to whether he feels
the taste or not. These solutions are best applied to
the tongue with a glass rod.
Sensation of the inside of the mouth.
For testing the inside of the mouth ask the patient to
drink from a tumbler. If the nerve is affected, he
wTill feel as if the tumbler is broken.
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.
Ask the patient to open the mouth. If the nerve is

affected the jaw deviates towards the paralysed side,
being pushed over by the healthy external pterygoid
muscles.
3. Ask the patient to move his jaw from side to side

against resistance. In paralysis of one side, the patient
is able to move the jaw towards the paralysed side but
not to the non-paralysed side.
4.
^
Test the jaw-jerk with the mouth slightly open and

placing a tongue depressor over the lower incisors and
tapping the protruding end. The normal response is
almost imperceptible. It is absent in peripheral lesions
and active in supranuclear lesions.
5.
Look for wasting of the masseters. If they are wasted,

concavities will be noticed above and below the zygoma
and sometimes fasciculations in the involved muscles.
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.
Mandibular division results in loss of

part of the face and anterior two-thirds
affects the muscles of mastication resultjaw on the affected side on opening the
SEVENTH OR FACIAL NERVE

T h e facial nerve is a mixed nerve, being motor to the muscles of facial
expression and platvsma, and sensory, supplying taste fibres to the anterior
two-thirds of the tongue via the chorda tympani nerves. The nucleus of
the nerve lies deep in the pons. On leaving the nucleus, the fibres wind
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.
Test the nerve as follows:

1. Ask the patient to shut the eyes and then try to open
them. If the orbicularis is weak the affected eye opens
out easily. In lower motor neurone lesions the affected
eye does not close fully.
2. Ask the patient to raise the eye-brows. No wrinkling of
the forehead occurs on the paralysed side.
3. Ask the patient to frown. In lower neurone lesions no
wrinkling occurs on the affected side.
4. Ask the patient to whistle. T h e patient is unable to do
so if the nerve is paralysed.
5. Ask him to smile or show his teeth. T h e corner of the
mouth on the affected side is not drawn backwards.
6. Ask him to inflate his mouth with air and blow out the
cheeks. T a p with the finger in turn on each inflated
cheek. Air escapes from the mouth more easily on the
weak side.
7. Ask the patient to open his mouth against resistance and
see if the platysma muscle contracts. It fails to do so
on the paralysed side in cases of hemiplegia. (Babinski's
platysma sign.)
Note the following:
1. Lachrymation or excessive salivation.
2. Naso labial folds. They are obliterated on the paralysed
side.
3. Apparent deviation of the jaw when the patient is asked
to open the mouth.
4. Redness of the eyeoften occurs on the paralysed side.
CENTRAL NERVOUS
SYSTEM
231
LESIONS OF T H E FACIAL NERVE

A.
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
Seventh Cranial Nerve.

Lesions:1. Outside the stylomastoid foramen; 2. 8c 3. Fallopian canal;
4. Geniculate ganglion; 5. Int. auditory meatus; 6. Lower border
of Pons.
B.
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
lesion and contralateral hemiplegia. There are no changes in taste or

hearing. T h e nucleus o the 6th cranial nerve may be involved resulting
in internal strabismus on the same side as the lesion. T h e commonest
cause is syphilitic basal meningitis.
C.
INTRANUCLEAR LESIONS:(See Fig. XXI.)

These comprise 75% of all facial nerve lesions.
1.
PERIPHERAL LESIONS (outside the stylomastoid foramen):

Results in drooping of the mouth on the affected side, difficulty in
closing the eyes and whistling; food collects between the cheeks and
gums; forehead cannot be wrinkled; lachrymation; false deviation
of the tongue on the paralysed side. T h e commonest cause is exposure
to draft; may also be due to injuries, operation, forceps at birth and
parotid tumours. This condition is known as Bell's palsy.
2.
LESION IN T H E FALLOPIAN CANAL: This involves the chorda

tympani nerve and results in loss of taste to anterior two-thirds of
the tongue, in addition to the above features. Commonest cause is
otitis media.
3.
LESIONS HIGHER IN T H E CANAL:Involves the nerve to

stapedius muscle resulting in features of 1 and 2 and hyperacusis.
4.
LESIONS INVOLVING T H E GENICULATE GANGLION:Onset is

acute with pain in the ear; herpes may precede the palsy.
5.
LESIONS IN T H E I N T E R N A L AUDITORY
and signs of Bell's palsy.
6.
LESIONS A T T H E EMERGENCE OF T H E FACIAL NERVE FROM

T H E PONS:5th, 6th and at times 11th and 12th nerves are involved
along with the 7th nerve.
MEATUS:Deafness
Note: Certain muscular disorders like myasthenia gravis,

heredofamilial
dystrophies
and myotonia dystrophica
can cause bilateral facial
weakness.
The face looks flat and expressionless with loss of naso-labial folds.
Such
muscular disorders should not be mistaken for nerve lesions.
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:
1. Rinne's test:Hold over the mastoid of the patient a

vibrating tuning fork; as soon as he ceases to hear it,
put it in front of the ear. Normally aerial conduction
is better than bone conduction, i.e. Rinne's test is
positive. In middle ear diseases the opposite occurs,
CENTRAL NERVOUS
SYSTEM
233
i.e. Rinne's test is negative. In nerve deafness both air

and bone conduction are diminished but retain their
normal relationship, i.e. Rinne's test is still positive.
2. Weber's test:Place the vibrating fork on the centre of
the patient's forehead. In middle ear diseases the
vibrations are louder on the diseased side, i.e. Weber's
test is positive. In nerve deafness, the tuning-fork is not
heard on the affected side, i.e. Weber's test is negative.
B.
Vestibular Division.
Note if there is any vertigo, unsteady gait and nausea.

Caloric and rotational tests are employed to produce change
in the endolymph current in the semicircular canals. It results
in nausea, dizziness and horizontal nystagmus when the vestibular apparatus is normal. When the vestibular nerve function is lost there is no dizziness nor nystagmus. With incomplete interruption of the nerve function the usual responses
will be decreased on the involved side.
Abnormal auditory sensations like tinnitus, hyperacusis and
hallucinations of sounds may be present in cases where the 8th
nerve is normal, chiefly in mental diseases.
Common disorders of the Auditory Nerve:
VERTIGO.
T h e terra "vertigo" or dizziness signifies a subjective sensation of movement through space usually felt as a rotation or sensation as if the external
objects are moving.
Etiological Classification.
I.
CEREBRAL:
1.
Functionalhysteria, neurasthenia.
2.
Irregular blood supply to the brainfainting, loss of blood, anaemia,

cardiac feebleness, high blood pressure, low blood pressure, StokeAdam's syndrome, aortic regurgitation, arterial diseases, sudden
change in posture.
3.
Aura in epilepsy and migraine.
4.
Increased intracranial tensiontumours.
5.
Infectionsencephalitis,
syphilis.
In almost all these conditions
the vertigo
is transient
or
temporary.
234
H O W TO EXAMINE A
II.
PATIENT
CEREBELLAR DISORDERSabscess,
nated sclerosis.
In this group
signs.
III.
there is also associated
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.
Tobacco, alcohol, anaesthetics, opium.
3.
Constipation, sepsis.
B.
TINNITUS.
Tinnitus means subjective sensations of ringing, etc. in the ears. It does

not include hallucination of hearing voices, which usually indicates mental
trouble.
ETIOLOGY:
I.
EXTRA-AURAL.
1.
Variations in the blood pressure.

(a) High B.P.
T h e tinnitus is not affected by posture.
(b) Severe anaemias.
T h e noises are relieved on lying down.
(c) Increased venous pressurebruit de diable in venous congestion.

T h e noises are aggravated on lying down.
2.
Intra cranial lesions:

(a) Arterio-venous aneurysmthe sounds are synchronous with the
pulse.
(b) Pressure on the 8th nerve trunk e.g. in tumours in the cerebellopontine angle.
3.
Cardiac diseasesaortic regurgitation.
4.
Functionalmigraine, neurasthenia, hysteria, aura in epilepsy.
5.
Drugsquinine, salicylates, antipyrin, tobacco,
6.
Chronic diseasesgout, chronic nephritis,
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
(b) See if the voice of the patient is hoarse.

bilateral paralysis of the vocal cords.
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
against resistance; on forward elevation of the arm,

however, the flaring of the inferior angle virtually disappears. These features are important to distinguish
Trapezius palsy (11th cranial nerve) from Serratus Anterior palsy (C 5, 6 if 7), which produces an equally characteristic winging of the scapulae, but in which the movement of the arms in these two planes has the opposite
effect.
In Serratus Anterior palsy there is comparatively little
change in the appearance of the shoulder-girdle at rest;
there is however, slight winging of the inferior angle of
the scapula and slight shift medially towards the spine.
When the outstretched arm is thrust forward, the entire
scapula, particularly, its inferior angle shifts backwards
away from the thorax, producing the characteristic wing
effect. Abduction of the arm laterally, however, produces
comparatively little winging.
3. There may be difficulty in rotating the chin on the
opposite side due to paralysis of the Sternomastoid.
T W E L F T H O R HYPOGLOSSAL NERVE
This is a motor nerve to the tongue.
1. Ask the patient to protrude the tongue. It is deviated
to the paralysed side due to unopposed action of the
Geniohyoglossus muscle in lower neurone lesion, and
apparent deviation away from the lesion in supranuclear
lesions (hemiplegia).
2. Ask him to move the tongue from side to side. T h e
patient cannot move it freely on the paralysed side.
3. Look for wasting and fibrillary twitchings, which are
evident on the paralysed side in nuclear or infranuclear
lesions.
4. Note if there is any dysarthria. This occuris in 12th
nerve lesion due to wasting of the tongue on the affected
side. This nerve is generally affected in all bulbar
lesions.
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.
Bone diseasesleontiasis osseum, due to overgrowth of the skull bones

can cause protrusion of the eye-balls and terrible disfigurement of
the face.
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.
Orbital cellulitisthere is evidence of inflammation, fever, oedema

of the lids and chemosis.
2.
Thrombosis of the cavernous sinusa very painful condition associated with involvement of the 3rd, 4th and 5th cranial nerves.
3.
Orbital periostitis in chronic casesdifficult to diagnose; X-rays reveal

increased density in the affected bone.
4.
Intra-orbital tumoursosteoma, tubercular abscess, and gumma of the

optic nerve sheath can cause protrusion of the eye-ball. T h e eye
may be displaced up or down or to the side and cannot be pressed
back. There is often associated diplopia.
5.
Meningocoeleoften causes exophthalmos, which may pulsate and is

reducible by pressure with fingers.
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.
Varicosity of the orbital veinscauses intermittent

T h e veins around are prominent.
8.
Traumaorbital haemorrhage or empyema can cause protrusion of

the eye-ball, often accompanied by diplopia.
exophthalmos.
EXOPHTHALMOS.
CAUSES:
1.
Fracture of orbital wall especially of the nasal wallin the earlier

stages there may be transient exophthalmos due to emphysema.
2.
Paralysis of the sympathetic nerveHorner's syndrome.
3.
Shrinking of orbital tissueafter suppuration in the orbit.
4.
After surgical operation in the orbitshrinking of the orbital tissue

may occur.
5.
Loss of fat in the orbitsold age, emaciation, dehydration, etc.
IV.
M O T O R SYSTEM
Under Motor System test the following functions of the

muscles:
1. Power.
2. Nutrition.
3. Tone.
4. Co-ordination.
5. Abnormal movements.
6. Gait.
HOW TO EXAMINE A
240
PATIENT
1. Power of the Muscles.

Test the various muscles in the body against resistance. Note
if there is any foot-drop or wrist-drop or any other muscular
defect. Determine whether the patient is capable of performing gross muscular movements, such as walking, sitting up in
bed or moving each of the limbs as a whole. Next, test the
power of the individual or groups of muscles by asking the
patient to throw into action the particular muscle or muscles
which one wishes to test.
TEST AS FOLLOWS:
I.
Upper Limb.
A B D U C T O R POLLICIS BREVIS:Ask the patient to abduct his thumb

in a plane at right angles to the index finger.
OPPONENS POLLICIS:Ask the patient to touch the tip of his little
finger with the point of his thumb.
A D D U C T O R OF T H E T H U M B : Ask the patient to grasp a book with
the forefinger and thumb.
INTEROSSEI AND LUMBRICALS: Ask the patient to flex the
metacarpo-phalangeal joints and to extend the distal phalanges. T h e
interossei also abduct and adduct the fingers. In claw-hand or main-engriffe these muscles are paralysed resulting in over extension of the first
phalangeal joints and flexion of the distal two.
FLEXORS OF
examiner's hand.
THE
FINGERS:Ask
the
patient
to
squeeze
the
FLEXORS OF T H E W R I S T : W i t h hand in supine position, ask the

patient to bring fingers towards the forearm.
EXTENSORS OF T H E W R I S T : W i t h hand in prone position grasp
the wrist of the patient and then ask him to bend the hand upwards.
T h e fingers must be held fixed as the wrist can be extended by long
extensors of the fingers. Note if there is wrist drop which generally occurs
in radial nerve palsy.
BRACHIO-RADIALIS: Ask the patient to bend the forearm placed
midway between pronation and supination against resistance. A healthy
muscle stands out prominently at its upper part.
BICEPS:Ask the patient to bend the forearm at the elbow
resistance. A healthy biceps stands out prominently.
against
TRICEPS:Ask the patient to extend the forearm which the examiner

holds in a flexed position.
SUPRASPINATUS A N D DELTOID:Ask the patient to lift his arm
straight at right angles to his side. T h e first 30 of this movement is
carried out by supraspinatus. T h e remaining 60 is produced by deltoid.
CENTRAL NERVOUS
SYSTEM
241
INFRASPINATUS:Ask the patient to tuck his elbows into his sides

with the forearms flexed to a right angle. Then ask him to rotate the
limbs outwards. T h e muscle can be seen and felt to contract.
PECTORALES:Ask the patient to stretch his arms forwards and then
to clasp his handspectorales contract.
SERRATUS A N T E R I O R : A s k the patient
right angle. A "winged" scapula is noticed on
inferior angle projecting. Or ask the patient
and watch for digitations of the muscle and the
to lift the limbs above a

the paralysed side with its
to push against resistance
position of the scapulae.
LATISSIMUS DORSI:Ask the patient to clasp his hands behind his

body, or ask the patient to cough. In health, the latissimus contracts.
II.
The Head Muscles:
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:
ABDOMINAL MUSCLES:Ask the patient to raise himself in bed with

the hand of the examiner on the patient's forehead so as to resist the effort.
In paralysis of a portion of the anterior abdominal wall, the umbilicus is
displaced towards the sound side.
ERECTOR SPINAE:Ask the patient to lie in prone position and try
to raise his head from the bed by extending the neck and back. T h e
healthy muscles stand out prominently during the effort.
TRAPEZIUS:The upper part is tested, while examining the 11th
cranial nerve by asking the patient to shrug the shoulders while the observer
tries to press them down from behind. T h e lower part is tested by asking
the patient to approximate the shoulder blades and watch for the prominence of the muscles.
IV.
The Lower Limb:
INTEROSSEI:If weakened a "claw-foot" analogous to the "claw-hand"

results.
DORSIFLEXION A N D PLANTAR FLEXION are tested by asking the
patient to flex or extend the foot against resistance.
EVERSION AND INVERSION are also tested by asking the patient to
turn the feet outwards or inwards against resistance.
EXTENSORS OF T H E KNEE:Ask the patient to extend the knee that
is bent with the observer's hand on the sole of his foot.
FLEXORS OF T H E KNEE:Raise the limb from the bed supporting
the thigh with the left hand and the ankle with the right; then ask him
to bend his knee.
16
242
HOW
TO EXAMINE A
PATIENT
EXTENSORS OF T H E T H I G H : T h e knee being extended, lift the

patient's foot off the bed, and ask him to bring it back on bed against
resistance.
FLEXORS OF T H E T H I G H : T h e knee being extended, ask the patient
to raise his leg off the bed.
ABDUCTORS AND ADDUCTORS OF T H E T H I G H : T o
test
adductors, abduct the limb and then ask the patient to bring it back to
the middle line against resistance. In a similar way the abductors are
tested by bringing the limb in the middle line and then asking him to
move it outwards.
ROTATORS OF T H E T H I G H : W i t h the limb extended on the bed,
ask the patient to roll it outwards or inwards, while passive resistance is
offered by grasping the foot.
2.
Nutrition.
Compare the size and shape of the identical muscles on both

the sides. Note their bulk and measure their circumference,
if necessary. Carefully note any changes in the size of the
muscles, especially in the limbs, face, shoulder and pelvic
girdles, and small muscles of the extremities. See if there are
any fasciculations, trophic changes and contractures.
3.
Muscular Tone.
Note the tone of the muscles by moving the limbs passively

at their various joints. If hypertonic, see if it is clasp-knife
type, i.e. maximum resistance offered in the initial stages of the
movements as occurs in pyramidal diseases; or cog-wheel type,
where resistance to passive movements is steady but fluctuant
as occurs in extra-pyramidal diseases; or plastic type, where
resistance is continuous, smooth and uniform as occurs in midbrain lesions and in catatonia; or hysterical type where resistance is increased in proportion to the effort made by the
examiner to move the limb.
If hypotonic, note the range of movement of the muscles and
their flabbiness. Although toneless muscles feel soft and flabby
when palpated, this method of testing for tone is to be discouraged as being unreliable for clinical purpose. Hypotonicity occurs in lesions of the spinal reflex arc, tabes and infantile
paralysis; from depression of reflex activity by shock; from state
CENTRAL NERVOUS
SYSTEM
243
of unconsciousness; from disorders of the cerebellum and in

feme myopathies.
4.
Co-ordination.
(a) Upper limbs:Test the upper limbs by asking the patient

to touch the point of his nose with his forefinger (fingernose test) with the eyes open and note if there are gross
tremors as occur in disseminated sclerosis; or ask him
to bring the points of the two forefingers together. In
females a good test is to ask them to thread a needle.
(b) Lower limbs:For testing the lower limbs ask the patient
to walk on a straight line or to place one heel on the
opposite knee (knee-heel test)-, or ask him to follow with
his toe the examiner's forefinger as it describes circles in
the air.
(c) Romberg's sign:Test for this sign by asking the patient
to stand with his feet close together and if he can do so,
then with his eyes closed. An average person may not
stand quite as steadily with his eyes closed as when they
are open, but the unsteadiness associated with tabes
dorsalis, subacute combined degeneration and severe
polyneuritis, is perceptibly aggravated by closing the eyes,
as in these conditions there is a loss of proprioceptive
sensations in the muscles of the lower extremities.
T h e unsteadiness on standing with the legs together may
occur in cerebellar and even in vestibular disorders, but
such unsteadiness is not aggravated by closing the eyes.
(d) Adiadokokinesia:Test by asking the patient to execute
repeatedly rapid movements like opening and closing the
fists alternately or patting the knees with the palms
or pronating and supinating the hands alternately. In
cerebellar diseases such movements are slow and clumsy.
5.
Abnormal Movements.
Note if they are widespread or localized, tonic or clonic,

rhythmic or choreiform, coarse or fine. Factors aggravating or
diminishing the movements should also be noted, especially the
H O W TO EXAMINE A
244
PATIENT
effect of voluntary movement, sleep and emotion. See if there

are cramps, tics, spasms, tremors, fasciculations, intention tremors and associated movements. (See page 282.)
Rebound phenomena:Test as follows: Let the patient relax
the arm at the shoulders and flex at the forearms. T h e examiner
pulls on the wrists against resistance and suddenly releases
them. In cerebellar diseases, the hand flies up towards the
shoulder.
6.
Gait.
Note the attitude the patient adopts when standing and

while walking in addition to describing the gait. Also observe
the automatic movements such as swinging the arms while
walking. (See page 284.)
V.
SENSATIONS
Ask the patient if he feels any abnormal sensations, like pins

and needles, numbness, hot flushes, formication, hyperesthesia,
etc.
Test for the following forms of sensibility:
1. Tactile sensibility. Use cotton wool and the head of a
pin (for light pressure). Avoid testing hairy parts without
shaving as the sensibility of the hair is very acute. Compare
corresponding points on the opposite side of the body. Ask the
patient to localize the stimulus as sometimes a patient may be
able to feel the stimulus and yet not be able to localize it.
Note if the area affected is anaesthetic, hyperaesthetic or
hypoaesthetic or if there is delayed conduction as occurs in
tabes dorsalis.
2.
Pain:
(a) Superficial pain. Use a pin and prick gently different

parts of the body and make sure that the patient feels
the pain and not the touch of the pin.
Note if the area is analgesic, hypoalgesic or hyperalgesic.
CENTRAL NERVOUS
SYSTEM
245
(b) Deep sensibility. Press the calf muscles, tendoachilles

and testes. Loss of deep sensibility is typical of tabes
and tenderness over the calf muscles is characteristic of
peripheral neuritis.
3. Thermal sensibility. Use two test tubes, one containing
hot water and the other crushed ice, and touch the various
parts of the skin and note the reactions. In syringomyelia
there is "dissociation of sensations", i.e. thermal sensibility is
lost but the patient feels the touch.
4. Sense of position. With the patient's eyes closed, take
hold of one of his limbs and place it in some definite position
and then ask him to put the corresponding limb in a similar
position. In paralysis of a limb this test has no value. In case
of the upper limbs ask the patient to touch the point of his
nose with his forefinger with his eyes closed (finger-nose test).
For testing the lower limbs, move the patient's great toe twice
or thrice, and then ask him to say in what position it is with
the eyes closed. In posterior cord or column lesions the sense
of pkasition is lost.
5. Vibrations. Use a tuning fork of 128 vibrations per
second. Train the patient as to what is expected of him and
then place the vibrating fork on the bony parts to be tested.
It is absent in posterior cord or column lesions.
6. Tactile discrimination. Use a compass and ask the
patient whether he is being touched with one or two points.
Normally 1 c.m. of separation of the points is appreciated over
the D|ody.
7. Recognition of size, shape and form. Use familiar objects
of different sizes and shape, such as coins, pencils, etc. and the
patient is asked to identify these when placed in the hands
with the eyes closed.
8. Recognition of weights (for kinetic sense). Use small
objects of different weights and ask the patient if he can appreciate the difference.
246
HOW
TO EXAMINE A
VI.
PATIENT
REFLEXES
Reflexes are of four varietiessuperficial, deep, visceral

(organic) and tonic.
1. Superficial Reflexes.
(a) Corneal and conjunctival.
(b) Pupillary.
(See page 227.)
(See page 226.)
(c) Cilio-spinal. Pupil is often dilated on pinching the skin

on the side of the neck. It is due to reflex excitation of
the pupil-dilating fibres in the cervical sympathetics and is
abolished in the lesions of that nerve.
(d) Abdominal. Let the patient lie recumbent with the
abdominal wall thoroughly relaxed. Gently stroke the
abdomen with a pin obliquely downward and outward
for the upper quadrants, and upward and outward for
the lower quadrants. T h e normal response is a retraction of the area stimulated. The test is more effective,
if performed at the end of expiration. Its absence ordinarily is an indication of a lesion of the pyramidal system.
It is absent in infants because pyramidal fibres are not
myelinated. The normal response is difficult to evaluate
in ticklish individuals and may not be easily elicited in
those with lax abdominal wall, in old age, obesity, in
multiparae, in violent emotion such as fear, in abdominal distension, in acute abdominal disease and acute
meningitis. The abdominal reflexes are absent in pyramidal diseases below the level of the lesion; they may
also be absent in deep sleep, surgical anaethesia and in
coma.
(e) Cremasteric. Stroke the upper and inner aspect of the
thigh from above downwards and look for the retraction
of the testes, which occurs due to contraction of the cremasteric muscle. It is absent in pyramidal diseases and
may be absent normally in elderly males, in people with
hydrocoele or varicocoele, orchitis or epididymitis.
(f) Plantar. Stroking with a blunt pin from the heel towards
the toes on the soles of the feet causes flexion of the toes
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
REFLEXES, THEIR CENTRES AND ARCS.

247
248
H O W TO EXAMINE A
PATIENT
normally provided the toes, especially the great toe, are

not defective or ankylosed. T h e stimulus should not be
too fine or painful as this may give rise to reversal to
flexion in pyramidal lesions in which condition the reflex
is extensor, i.e. there is dorsiflexion of the great toe
and fanning of the small toes. Normal response is best
elicited on stroking the medial side of the foot and
abnormal response, i.e. extensor response or Babinski's
sign, on the outer margin; it is best elicited with the limb
fully extended with the patient lying in recumbent
posture. T h e abnormal response may not be easily elicited if the feet are cold, when the soles of the feet are
thick, in severe anaesthesia of the feet and when there is
interruption in the reflex arc which passes through the
first sacral segment. An extensor response is present in
pyramidal diseases; it is often elicited in profound sleep,
coma, post-epilepsy and in children before the pyramidal
tracts are myelinated. (See Fig. XXII.)
Other methods of eliciting "extensor response".
(i) Oppenheim's sign
Press with the thumb on the inner
aspect of the tibia from above down.

(ii) Gordon's sign
Squeeze the calf muscles.
(iii) Schaefer's sign:Press the Achilles tendon.

(iv) Chaddock's sign:Stimulate the lateral aspect of the
foot under and around the external malleolus in a
circular direction.
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
KNEE JERK IS EXAGGERATED in the following conditions due to loss

of control of the brain over the spinal centres.
1. Excitement.
2. Anxiety; hysteria.
3.
4.
Intoxicationbenzidrine, strychnine.
Infectionstetanus, meningitis.
5.
Pyramidal diseasesmost important.
251
KNEE JERK IS DIMINISHED due to interference with the conduction

of the impulse through the reflex arc, in the following conditions:
A.
B.
TEMPORARY:
1.
2
Shock.
3.
Spinal shock.
4.
Deep anaesthesia; narcosis.
5.
Deep coma; deep sleep.
Cerebral haemorrhage.
6.
Severe infections.
7.
Diabetic ketosis.
8.
Uraemia.
9.
Marked increase in the intracranial

cephalus, posterior fossa tumours.
OF LONGER D U R A T I O N .
ence in the reflex arc.
tensionmeningitis,
hydro-
In this group there is definite interfer-
1.
Diseases of musclesmyopathies, myotonia dystrophica, amyotonia

congenita.
2.
Diseases of peripheral nervesneuritis.
3.
Diseases of posterior rootstabes.
4.
Lesions in the spinal cord :

(a) Posterior columnssubacute combined degeneration.
(b) Anterior columnspoliomyelitis, progressive muscular atrophy.
(c) Spinal cordsyringomyelia, disseminated sclerosis, paraplegia in
flexion, myelitis and other lesions at the level of the 3rd and
4th lumbar vertebrae.
(f) Ankle-jerk. This is best elicited by asking the patient

to kneel on a chair with the feet projecting out. If lying
in bed, the thigh of the patient should be abducted and
rotated externally, the knee flexed and the foot dorsiflexed at the ankle. The examiner should place one hand
under the foot to give it a moderate tension and then
tap the tendo-Achilles. (See Fig. XXVII.)
(g) Clonus.
(i) Ankle-clonus. Raise the patient's thigh and the leg
slightly at the knee and support the leg with one
hand. With the other, grasp the fore-part of the foot
and suddenly dorsiflex it at the ankle. Maintain the
pressure of the hand upon the sole of the foot. This
causes a series of involuntary contractions, which
252
continue as long as the pressure is maintained.

Fig. XXVIII.)
(See
FIG. XXVII
Ankle-Jerk.
A real clonus is sustained and rhythmical, whereas

a spurious clonus as occurs in functional paralysis is
ill-sustained and irregular in rhythm.
Whereas the presence of sustained ankle clonus is
a conclusive proof of an upper neurone affection the
absence of a clonus does not exclude such lesions.
Ankle clonus is not met with until there is relatively
large amount of damage to the pyramidal tracts. As
a rule it appears later than the extensor plantar
response.
Ankle jerk is absent in tabes dorsalis, sciatica and
in pyramidal lesions at the level of Si and S2.
(ii) Patellar clonus. Extend the patient's leg and then
suddenly push down the patella towards the foot.
Maintain the pressure and a series of clonic contractions of the quadriceps will be noticed in some cases
where the knee jerk is exaggerated due to pyramidal
disease.
CENTRAL NERVOUS
SYSTEM
253
FIG. XXVIIl
Ankle-Clonus.
3.
I.
ORGANIC (VISCERAL) REFLEXES
Micturition:
Note whether there is only retention or incontinence of urine.

If there is incontinence, ascertain by the use of a catheter
whether it is due to overflow from a distended bladder or
whether it is a reflex incontinence, i.e. whether the bladder
merely fills up and then empties itself by reflex action.
Also note if the patient complains of precipitate micturition,
i.e. feels the desire to micturate and is unable to restrain the
act as commonly occurs in disseminated sclerosis.
Ordinarily this reflex act can be voluntarily controlled to a
great extent by the higher centres in the brain. It is normally
initiated by a voluntary effort, but once started, becomes a reflex
act which is difficult to interrupt. The stimulus for this reflex
is distension of the bladder with urine. T h e afferent fibres are
nervi erigentes. T h e controlling centres are in the spinal cord
at various levels, so that although the reflex arc is intact, spinal
cord and cerebral lesions still cause its disturbance.
254
2.
Defaecation:
Inquire if there is any difficulty in the act and also if he

feels when the rectum is full. Note also if there is incontinence
of faeces.
Incontinence does not necessarily follow that the patient has
a nervous disease. On the contrary, more often it is due to
depression of the nervous system as occurs in high fevers,
toxaemia, etc. The reflex depends upon the 4th and 5th sacral
segments.
3.
Deglutition:
This reflex is not easily affected unless the pharyngeal nerves

are involved; the patient may complain of dysphagia for fluids
or nasal regurgitation.
4.
Mass reflex:
In severe spinal cord lesions there occurs paraplegia in flexion

in course of time. On the application of a stimulus like pin
prick or pinching the skin of the thigh, the legs are vigorously
drawn up, marked extensor plantar response occurs, the skin
sweats below the lesion and the bladder is evacuated. It is
easily elicited in relatively complete transverse spinal lesions.
IV.
T O N I C REFLEXES
1. Neck rigidity:The examiner places his hand behind the

occiput and then flexes the head. In meningeal irritation this
effort causes pain in the neck and the movement is resisted by
spasm of the extensor muscles of the neck. Neck rigidity is
also caused by diseases of cervical spine. Head retraction as
occurs in severe meningitis and tetanus is an extreme degree
of neck rigidity.
2. Kernig's sign:With the patient recumbent, flex the
thigh to a right angle and then attempt to extend the leg on
the thigh. There is pain due to spasm of the hamstring muscles
and limitation of extension. This sign is typically present in
meningitis, meningism and subarachnoid haemorrhage. (See
Fig. XXIX.)
CENTRAL NERVOUS
SYSTEM
255
Fig. XXIX
Kernig's-Sign.
3.
Brudzinski's signs:
(a) Neck sign:Raise the head of the patient while placing

the other hand on his chest to prevent elevation of the
body. There is flexion of both the thighs and legs in
meningitis.
(b) Leg sign:Flex one hip with the knee extended.
opposite thigh and knee flex in cases of meningitis.
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
ANATOMY OF THE CENTRAL NERVOUS SYSTEM

A fairly good knowledge of the anatomy of the nervous system is essential
for a student to determine the site of a lesion in cases of Nervous Diseases.
Hence, this chapter giving a brief detail of the anatomy and physiology of
the nervous system, is included here.
A.
T H E BRAIN.
T h e brain is a greatly modified and enlarged portion of the central

nervous system. It is surrounded by three protective membranesthe pia,
the arachnoid and the dura from within outwards, and is enclosed within
the cranial cavity of the skull. T h e weight of the brain is about 1,400 gms.
and is 2% of the total body-weight.
For clinical purpose the brain may be divided into five partscerebrum,
basal ganglia, mid-brain, brain-stem and the hind-brain.
1.
Cerebrum.
This consists of two hemispheres which make up the largest portion of

the brain. T h e dominant hemisphere i.e. the one that plays a major part
in the control of a person's activities, especially that of speech, is situated
on the left side in right-handed people and on the right side in left-handed
people. T h e two hemispheres are joined together by corpus callosum.
Below the corpus callosum are the optic thalamus and corpus striatum.
Sensory cortex
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
In the centre of each hemisphere is the lateral ventricle. T h e outer surface

of the hemisphere contains several gyri and sulci. Each hemisphere may
be divided into four lobesfrontal (motor and intellectual area), parietal
(sensory area), temporal (auditory area) and occipital (visual area). Most
of the descending tracts pass through the cerebral peduncles from the cortex
and most of the ascending fibres relay in the optic thalamus and then
go up to the sensory area of the cerebrum.
2.
Extra-pyramidal SystemBasal Ganglia.
3.
Mid-brain.
(See page 307.)
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.
This consists of pons and medulla oblongata. The pons is situated at

the base of the brain between the medulla oblongata and the cerebral
peduncles in front of the cerebellum. The medulla, which can be considered as an upward continuation of the spinal cord, goes up to end
at the lower end of the pons in front of the cerebellum. The cranial nerve
nuclei in the pons include the 5th, 6th, 7th and 8th nerves. The cranial
nerve nuclei in the medulla are the 9th, 10th, 11th and 12th.
5.
Hind-brainCerebellum mainly.
B.
MOTOR SYSTEM.
C.
SENSORY SYSTEM.
D.
SPINAL CORD.
E.
PERIPHERAL NERVES.
(See page 308.)
(See page 289.)

(See page 304.)
(See page 308.)

(See page 312.)
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
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.
Temporary vasomotor instabilityshock, cardiac irregularities, internal

secretory disturbances, anaemia, hyperaemia, etc.
2.
Spasm of the arterieshypertensive encephalopathy.
3.
Sclerotic changesarteriosclerosis.
4.
Haemorrhagescerebral and subarachnoidal.
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
100 cc. to 120 cc.

Water-clear.
1006.
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
T h e chloride content of the C.S.F. (700 mgm.) is more than

in the blood (600 mgm.). Glucose is 70 mgm. in the C.S.F.
and 100 mgm. in the blood. Calcium is 5 mgm. in the C.S.F.
and 10 mgm. in the blood.
Proteins are absent as the C.S.F. leaves choroid plexus, is least
in the ventricular fluid and highest in the lumbar region. It
follows therefore that protein is added to C.S.F. by transudation from the walls of the ventricles and perivascular spaces
below.
Sugar is highest in the ventricles and lowest in the lumbar
fluid. The chloride content is same throughout and is more
than in the blood plasma.
There are hardly any white blood cells in the cisternal fluid,
but a few lymphocytes may be present in the lumbar fluid
not more than five per field.
Iodides, salicylates, nitrates, lipoids, bile pigments, organic
arsenic and immune bodies hardly enter from the plasma into
the C.S.F. In severe jaundice the fluid may be tinged yellow.
EXAMINATION OF T H E CEREBRO SPINAL FLUID
HOW
TO PERFORM
LUMBAR
PUNCTURE:
Take aseptic precautions and introduce a lumbar puncture

needle into the middle line of the spine about 1 cm. above a
line drawn horizontally at the level of highest points of the
iliac crests. This line intersects between Ls and L4. The patient
should be made to sit on bed and bend forward or lie in bed in
curved position.
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
400 lymphos. 50 mgm.

50-500 lymphos.
50 mgm.
200 lymphos. 50 mgm.
50-200 lymphos.
normal
300 c.c.
200 c.c.
increased
increased
meningitic
600 mgm. 20 mgm.
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.
700 mgm. 70 mgm.
Total Proteins Lange's Test Chlorides
20 mgm.
Cells
5 lymplios.
Appearance Quantity
Normal 130 mm. HaO

Clear 100 c.c.
Meningitis
Pyogenic
greatly
turbid
increased
Tubercular increased
'cob-web'
Syphilitic
slightly+
normal
Mumps
increased
normal
Benign
normal or
normal
increased
Meningism
slightly+
normal
G.P.I.
increased
normal
Encephalitis
normal
normal
Disease
CEREBRO SPINAL FLUID IN SOME IMPORTANT NERVOUS DISORDERS.

261
HOW
262
T O EXAMINE A
PATIENT
Lumbar puncture is performed for the following reasons:

1. Diagnostic purpose.
2.
T o relieve pressure.
3.
For therapeutic purpose.
4.
For spinal anaesthesia.
Contraindications for lumbar puncture are marked increase

in the intracranial pressure, especially due to infratentorial
tumours as in such cases removal of fluid may cause medullary
compression from herniation of the cerebellar tonsils into the
foramen magnum. If there are "chocked discs" in suspected
space-occupying lesions, avoid lumbar puncture.
T h e commonest reaction, excluding extraneous infections,
that is likely to occur in lumbar puncture is headache due to
leakage of the fluid through the puncture made by the needle.
I.
1. Pressure. Note whether it is high or low or stops

abruptly. In recumbent posture the C.S.F. pressure
varies from 80-180 mm. of FLO. Low pressure, which
has no clinical significance, may be found in surgical
shock, severe dehydration, diabetic coma, after lumbar
puncture for some days due to leakage of fluid through
the opening, and in complete subarachnoid block.
High pressure, which is of greater significance, results
from the following:
(a) Increase in the content of the skulltumours, abscess,
cerebral haemorrhage, subarachnoid haemorrhage,
cerebral oedema, uraemia, narcotic poisoning, etc.
(b) Excess in the rate of formation of
the rate of absorptionhydrocephalus,
meningism.
fluid over
meningitis,
(c) Increase in the cerebral venous pressurecongestive

heart failure, sinus thrombosis, obstruction to the
venous drainage in the neck.
CENTRAL NERVOUS
SYSTEM
263
2. Colour. Ordinarily it is like water.

Xanthochromia
(yellow colour) indicates an old haemorrhage in the brain
or very high protein content in the fluid. Cloudiness
suggests high cell content and occurs in infections of the
brain and meningitis. Cob-web formation occurs in
tubercular meningitis when the fluid is kept standing for
a few hours. Red colour suggests cerebral haemorrhage,
subarachnoid haemorrhage, leaking cerebral aneurysms,
fracture of the base of the skull and extraneous blood.
If the fluid is bloody, centrifugalise the same. If the
blood is extraneous the red cells will settle at the bottom
of the tube and the supernatent fluid will be clear. If
the blood comes from the brain the fluid on centrifugalising will remain yellow, if not red.
3. Its relation to pressure on jugular veins. T h e initial
pressure of C.S.F. is about 100-150. This is promptly
raised by jugular vein compression (Queckenstedt's sign),
or on coughing or abdominal compression. On releasing
the pressure on the jugulars the fluid falls to normal
within a few seconds. If there is obstruction to the flow
of fluid, compression of jugulars, although raising the
cisternal fluid pressure, fails to produce a rise in the
lumbar fluid. If the subarachnoid block is incomplete,
a slow, delayed rise may occur with a delayed and sometimes incomplete fall on relaxing the jugular compression.
II.
MICROSCOPIC
EXAMINATION.
1. White blood cells:Ordinarily, a few lymphocytes, not

exceeding five per field may be seen under the microscope. Excess of polymorphonuclears may be present in
pyogenic infections of the brain or its meninges. Lymphocytes are increased in tubercular meningitis, syphilis and
acute poliomyelitis.
2. Red blood cells:These are present in all conditions
that give rise to haemorrhages in the brain.
3. Examine a smear with suitable stain for cocci, M. tuberculosis, spirochaetes and tumour cells.
264
H O W T O EXAMINE A
III.
CHEMICAL
PATIENT
EXAMINATION.
Examine for globulins, sugar, chlorides and urea.

Globulin is increased in pyogenic meningitis, syphilis, tuberculosis and brain tumours.
Total proteins are increased in diseases of the Central
Nervous System in which venous stasis occurstumours of brain
or spinal cord, and below the level of obstruction in the spinal
cord (Froin's Syndrome).
Albumino-cytologic dissociation, i.e. increase in albumin with
little increase in cells, occurs in:
(a) Cord compression.
(b) Some brain tumours.
(c) Cerebral thrombosis near the basal cisterns.
(d) Cerebral haemorrhage.
(e) Landry's paralysis.
(f) Cauda equina tumours.
Cyto-albuminal dissociation, i.e. increase in cells with little
increase in proteins, occurs in:
(a) Poliomyelitis.
(b) Neurosyphilis.
(c) Disseminated sclerosis.
(d) Encephalitis.
Sugar is diminished in all infections of the
increased in hyperglycaemia; it is normal in
Chlorides are lowered in meningitis and more so
meningitis; they are increased in renal failure;
affected in cerebral abscess. Urea is increased in
IV.
brain; it is
encephalitis.
in tubercular
they are not
uraemia.
COLLOIDAL TEST (LAXGE'S).
This is based on the presence of excess of globulin in the

C.S.F. T h e high globulin content has the power of precipitating colloidal suspension of gold in certain dilutions. T o 10
dilutions of the C.S.F. (from 1 in 10 to 1 in 10,000) a constant
amount of colloidal solution is added and the result noted after
CENTRAL NERVOUS
SYSTEM
265
24 hours. In G.P.I, the first six dilutions show precipitation

(paretic curve); in tabes dorsalis, the 3rd and 4th dilutions show
the maximal precipitation (luetic curve); in myelitis, the 6th
to 8th dilutions are precipitated ( meningitic
curve).
V.
BIOLOGICAL TEST.
W. R., Kahn, etc.

VI.
BACTERIOLOGICAL TEST.
Culture, guinea pig inoculation, etc.

COMMON NEUROLOGICAL SYMPTOMS AND SIGNS
CONVULSIONS
Convulsions or fits mean involuntary tonic or clonic movements of the limbs, trunk and face with or without loss of
consciousness. They may occur in normal brain but are more
easily induced in persons subject to epilepsy. T h e factors that
induce convulsions are:
(a) Alkalosis which may be produced by deep breathing.
(b) Excessive retention of fluids in the tissues.
(c) Anoxia as occurs in heart block.
(d) Poisons like alcohol and cocaine.
(e) Products of abnormal metabolism as in renal diseases and
hypoglycaemia.
(f) Sudden sensory stimulus like a loud report, especially in
epileptics.
Common causes of convulsions:
A.
DISEASES OF T H E BRAIN.
1. Idiopathic epilepsy.
(See page 268.)
2. Traumas, including birth injuries.

3. Infectionsmeningitis,
culosis, cysticercosis.
encephalitis,
syphilis,
tuber-
4. Circulatory disordersembolism, haemorrhages, thrombosis, subarachnoid haemorrhage, hypertensive encephalopathy.
266
5. Growthstumours, abscesses.
6. Defective development of the grey matterhydrocephalus, microcephalus, agenesis of the grey matter.
7. Functional.
B.
CIRCULATORY DISEASES IN GENERAL.
2. Arteriosclerosis.
3. Hyperpiesia.
C.
ALIMENTARY DISORDERS
Autointoxication (common in children).

D.
ENDOCRINE DISORDERS.
1. Hyperadrenalism.
2. Hyperinsulinism.
3. Hypoparathyroidism.
E.
METABOLIC DISORDERS.
1. Rickets.
2. Tetany.
3. Alkalaemia.
4. Cyanosis.
F.
EXTRANEOUS POISONS
Lead, strychnine, absinth.

G.
GENERALISED INFECTIONS A N D TOXAEMIAS.
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
Fevers, otitis, phimosis, etc. (especially in children).
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.
FITS O C C U R R I N G SOON AFTER B I R T H :
1. Difficult or precipitate labour leading to cerebral

oedema or haemorrhage; may recur for few days and if
the injury is severe may go on for months and even end
in spastic paralysis and mental defect.
2. Asphyxia.
3. Reflexconstipation, enteritis, otitis.
4. Feverspneumonia, etc.
5. Congenitalsyphilis.
II.
CONVULSIONS A T YOUNG AGE:
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,
4. Alteration of alkali and calcium metabolism.

(a) Tetany.
(b) Rickets.
(c) Persistent thymus.
(d) Diarrhoeas and vomiting.
(e) Cyanosis of congenital heart.
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
Epilepsy is the most important condition that gives rise to

convulsions. It is due to paroxysmal and transient disturbance
in the function of the brain, which develops suddenly, ceases
spontaneously and exhibits conspicuous tendency to recurrences.
It is a symptom due to anoxia of the cortical neurones.
Originally epilepsy was classified under two vast groups
idiopathic and symptomatic. As the knowledge of this difficult
subject is fast increasing, the so called idiopathic group is
shrinking in size and today probably, not even 20 per cent of
epilepsies come under this etiology.
Differentiating features of idiopathic and symptomatic
epilepsies:
IDIOPATHIC.
SYMPTOMATIC.
1.
Appears early in life.
Comes later in life.
2.
Nocturnal generally.
Occurs
at any time.
3.
Pattern stereotyped.
Mixed pattern.
4.
Mental changes later.
N o mental changes.
5.
Fits generalised.
Generally Jacksonian.
Epilepsies, nowadays are classified in the following groups:

I.
II.
III.
IV.
V.
Grand mal.
Petit mal.
Jacksonian epilepsy.
Psychomotor epilepsy.
Myoclonic epilepsy.
CENTRAL NERVOUS
I.
SYSTEM
269
EPILEPSY MAJOR.
A typical fit consists of three stages:.

(a) Aurapresent
in almost all cases and which may be in any of the
following forms:motor (twitchings, paresis), sensory (flashes, noises,
vertigo, headache, numbness,
tingling, cramps), vasomotor ( f l u s h i n g ,
sweating,
palpitation,
flatulence),
psychical (anxiety,
depression,
euphoria, irritability,
fear, "dream
state").
(b) Fitstonic followed by clonic convulsions lasting for about 10-30 sec.
The patient falls, if standing. T h e 'epileptic cry', if present, is due
to sucking in of air through a narrowed glottis. During the clonic
phase there is often froth in the mouth, tongue-biting and loss of
visceral reflexes.
(c) Post-epilepsythe
most cases.
patient lies in deep sleep followed by headache in
II.
P E T I T MAL.
This is a momentary loss of consciousness in a patient who

is generally a child or young adult. The patient during the
attack has a vacant look or fixed expression, pallor of the face
and fails to talk or answer any questions. T h e focus of origin
in all these cases is said to be in the thalamus. Petit mal exhibits itself in any of these three forms:
1. Akinetic typesudden dropping on the floor if the
patient is erect; he is hardly aware of the loss of consciousness.
2. Myoclonic typejerky movements and a break in stream
of consciousness.
3. Short starefixed vacant stare; cessation of movements;
loss of consciousness. This is the commonest variety.
It can be easily provoked by hyperventilation.
III.
JACK.SONIAN EPILEPSY.
In this condition the convulsions are confined generally to

one side of the body which are mostly clonic, orderly and with
no loss of consciousness. The cause is probably old injury or
space occupying lesion in the brain.
IV.
PSYCHOMOTOR EPILEPSY.
This type is more common in adults. T h e attack may last

longer than 2 minutes. The patient is more confused than
comatose and often performs automatic movements after the
270
attack rather than go to sleep. The attack may even lead to

a period of amnesia. The patient is even capable of committing
a crime soon after the attack, that is, during the period of automatic action. The seat of stimulus is said to be in the temporal
lobe.
V.
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.
Exclude tetany, tetanus and fainting.
3.
Carefully examine the head for evidence of injury, past or present;

size and shape of the head, cutaneous naevi on the face, and for
evidence of middle ear disease.
4.
Examine the Central Nervous System, especially for rigidity of the

neck, pupillary reactions, paralysis of the limbs, deep and superficial
reflexes and do fundoscopy.
5.
Note if there is loss of visceral reflexesespecially micturition.
6.
Examine the Cardio-Vascular System for Stoke-Adam's syndrome and

hyperpiesia.
7.
Examine the blood for malarial parasites.
8.
Examine the urine to exclude uraemia.
9.
X-ray the skull, do ventriculography, electroencephalography, etc.
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:
1. Hysteriathe headache is described by the patient,

generally a female, by a lavish use of superlatives.
CENTRAL NERVOUS
SYSTEM
271
2. Anxiety statethe patient is anxious, gloomy and

demands sympathy while vaguely describing the headache.
3. Menopausethe age of the patient and associated menopausal symptoms will help in arriving at the diagnosis.
4. Excessive mental strainmay cause headache which is
relieved after a good rest.
DISEASES OF T H E B R A I N :
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
Neuritis, neuralgias, tic douloureux.

DISORDERS OF SPECIAL SENSES.
1. Eyeserrors of refraction, glaucoma, iritis.

2. Earsmiddle ear disease, mastoiditis, sea or air sickness.
3. Nosesinusitis.
DISEASES OF T H E SKULL.
1. Injuries.
2. Infectionsperiostitis.
3. Dental diseases.
HOW
272
F.
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.
CARDIO VASCULAR DISORDERS:
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:
Carefully go into details of the following:

1.
History of trauma, hypertension, renal disease, epilepsy,

etc.
migraine,
2.
Character of headache: If throbbing in character, suspect raised

blood pressure; such headaches are often relieved by rest and
increased on movement. Severe paroxysmal attacks may be due to
neuralgia and migraine.
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,
(d) If unilateralmigraine, tumour, abscess, middle-ear disease.

4.
Time of occurrence. Most headaches are relieved at night including

those of toxic origin; those due to organic diseases of the brain or its
meninges often persist or even become worse at night, especially the
headache of svphilitic origin. A headache which disturbs the patient's
sleep is definitely of organic origin. Headache experienced on rising
is generally due to lack of sleep, stuffy room, abnormal heat, etc.
Persistent morning headache is often associated with chronic nephritis
and chronic sinusitis; the latter tends to disappear during the course
of the day. Headache due to errors of refraction commonly occur
during the latter half of the day or after prolonged reading. Headache due to mental overwork is relieved after rest.
CENTRAL NERVOUS
SYSTEM
273
Some characteristic headaches.

Headache is one of the most important presenting symptom
in tumours of the brain. It is present in almost all posterior
fossa tumours and in 30 per cent cases of supratentorial tumours.
Such headaches are often nocturnal in character and often Come
on in paroxysms, especially on shifting of the position. It may
be localised and may give a clue as to the localisation of the
organic lesion. It may be associated with vomiting, disturbance
of vision and fits. T h e fundi may reveal neuritis of the optic
nerve. In cerebellar tumours, there is no optic neuritis, but
there may be nystagmus, ataxia and intention tremors. In
space-occupying lesions in children, headache may be inconspicuous when expansion of the cranium is possible.
In uraemic headache there may be vomiting, drowsiness,
dyspnoea, disturbance of vision and retinal changes. Albumin,
blood and casts are found in the urine.
In high blood pressure the headache is of throbbing character
and there may be a sense of fullness in the head; the blood
pressure is elevated.
In low blood pressure also there may be headache and giddiness on standing; the headache is relieved on lying down.
Headache of lumbar puncture comes on an hour after the
puncture and lasts for a few days, worsens on standing and
subsides on lying down.
In venous congestion the headache is dull and constant; there
is evidence of venous congestion elsewhere.
In migraine the headache is paroxysmal in character, often
unilateral and accompanied by nausea, vomiting and disturbance of vision.
In epilepsy the headache is often noticed immediately after
the patient recovers from the attack.
Adrenaline injection often produces severe throbbing headache immediately after the injection and lasts for half an hour
or so.
18
H O W T O EXAMINE A
274
PATIENT
Histamine headache need not necessarily be due to the use

of the drug; it is characterised by frequent and severe attacks
of unilateral headache lasting an hour or so; it commences and
terminates suddenly; the pain is boring in character in the
region of the orbit and often associated with watering of the
eyes; the headache often tends to awaken the patient in the
middle of the night.
In subarachnoid haemorrhage there is sudden, intense headache, rigidity of the neck and unconsciousness.
In meningitis the headache is constant, severe and throbbing
in character, associated with fever, rigidity of the neck and
positive Kernig's sign.
In lesions of the cranial nerves the headache is unilateral,
severe, sharp, paroxysmal and follows the distribution of the
nerve involved. T h e commonest cranial nerve sensitive to pain
is the 5th nerve and gives rise to trigeminal neuralgia.
Temporal arteritis is a condition that gives rise to headache
associated with low fever, anorexia, weakness and profuse
sweating. The pain is localised over the temporal vessels,
which are tortuous and tender to pressure.
COMA
Coma is defined as a state of unconsciousness from which the
patient cannot be roused. The depth of unconsciousness may,
however, vary considerably, and in a semi-comatose state it may
even be possible to wake the patient up by strong external
stimuli. In every patient who is deeply comatose from primary
cerebral causes, the breathing is stertorous and the deep reflexes
are abolished. Incontinence of urine and faeces usually occur,
though urine may be retained in the bladder in some cases.
Coma is to be distinguished from delirium which is a symptom
of disordered functions of all the higher cerebral centres. The
stimuli may reach the mind, but there is failure of recognition.
CAUSES
I.
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-
4. Vascularembolism, apoplexy, thrombosis, subarachnoid

haemorrhage, hypertensive encephalopathy.
5. Growthsprimary or secondary, abscesses.
6. Post-epilepsy.
7. Functionalhysteria.
II.
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.
Inquire into the history, especially of trauma, diabetes, renal

disease, epilepsy, hypertensionfrom relatives, friends, bystanders,
police, etc.
2.
Previous attacks, habits, occupation.
3.
Localitypresence
place.
PHYSICAL
of
fumes,
extremes of
temperature,
drinking
EXAMINATION.
This includes complete general examination of the patient including

temperature, pulse, respiration, blood pressure, evidence of injury, neurological examination.
276
HOW
TO EXAMINE A
PATIENT
1.
GENERAL APPEARANCElook for the following (flushed face

alcohol poisoning and hypertension,
sallow in uraemia, cherry-red
CO-poisoning,
yellow in jaundice,
blue in cyanosis, malar flush
mitral stenosis').
2.
AGEcerebral haemorrhage in elderly, epilepsy in young.
3.
ODOUR OF BREATHacetone smell in diabetes, ammoniacal smell

in uraemia, alcohol smell in alcohol poisoning.
4.
EYES AND PUPILSsoft tension in diabetes, unequal pupils in head

injuries, dilated pupils in barbiturate and datura poisoning, narrow
pupils in opium poisoning and pontine haemorrhage, papilloedema
in tumours and abscesses, retinitis in uraemia.
5.
EARSotitis, mastoiditis.
6.
FACE AND MOUTHfor unilateral signs of paralysis (pufflness of

one cheek, obliteration
of naso-labial fold), frothiness and tongue
bitting,
(epilepsy).
7.
NECK FOR STIFFNESSmeningitis, subarachnoid haemorrhage.
8.
RESPIRATIONair-hunger, (diabetes),
stertorous (apoplexy),
slow
rate (opium poisoning), Cheyne-Stoke's (high intracranial
tension).
9.
PULSEabsent or very slow (Stoke-Adam's syndrome), feeble

slow and bounding (hypertension),
slow and small (morphia
ing).
heat stroke,
(shock),
poison-
10.
TEMPERATLTREhigh (cerebral
the brain).
11.
PALPATION OF T H E SKINdry (diabetic coma), hot and dry (heat

stroke),
moist and clammy (hyperinsulinism),
cold and clammy
(collapse).
12.
BLOOD PRESSUREmay be high in uraemia and cerebral haemorrhage; low in shock.
13.
CENTRAL NERVOUS SYSTEMposture, involuntary movements,

tone of muscles, carphology (picking of imaginary objects), reaction to
stimuli, response to commands, position of eye-balls, pupils and their
reactions, corneal reflexes, evidence of paralysis, (the paralysed
limb
falls limply), condition of deep reflexes, plantar response.
14.
HEART EXAMINATIONfor enlargement,

Adam's syndrome.
15.
LUNGSfor bronchiectasis, cancer.
16.
malaria,
in
in
in
infections
mitral stenosis, Stoke-
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
pupils, very slow breathing,
Alcohol poisoningodour of alcohol, flushed face, suffused

eyes, dilated pupils, coma not profound.
Barbiturate poisoningflushed face, shallow or deep respirations, fever generally, dilated or pin-point pupils.
Uraemiasallow face, ammoniacal smell to the breath, hypertension, twitchings, retinitis, urine contains albumin and casts.
Diabetic comahistory of diabetes, gradual onset of coma,
air-hunger, acetone smell to breath, soft eye-balls, sugar and
acetone in the urine, elevated blood-sugar.
Hypoglycaemiahistory of having taken insulin, sweating,
twitchings, bloocl-sugar below 50 mgm. per cent. The coma is
not profound.
Cholaemiawasting of tissues especially of the face, jaundice
sometimes, "spider" angiomata on the face, liver small or
enlarged, ascites if liver is small.
CO-poisoninghistory
cheeks, fever.
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.
DEFECT IN F O R M U L A T I O N OF WORDS AFFECTING

HIGHER CENTRES IN T H E BRAIN (APHASIA).
A.
(DYSARTHRIA).
THE
DYSARTHRIA
When severe it is termed "anarthria" as occurs in advanced

cases of bulbar paralysis.
COMMON CAUSES:
I.
FUNCTIONAL.
1. Stammering. Difficulty in articulation characterised by

repetition of syllables. More common in males, because
of their self-consciousness.
2. Stuttering. T h e difficulty generally arises at the commencement of the word, usually a consonant. There is
no essential difference between this and stammering.
3. Lalling. T h e pronunciation is imperfect. Common in
normal children when learning to speak. The child
drops difficult consonants. May persist in mentally feeble
individuals.
4. Idioglossia. A child may invent his own word due to
defect in the approximation of sounds.
II.
BRAIN LESIONS.
1. G.P.I. T h e speech is slurring. The patient misplaces

syllables. "British Constitution" becomes "Brish Conssusshen". T h e defect is cortical.
CENTRAL NERVOUS
SYSTEM
279
2. Diplegia. T h e speech is thick and indistinct, associated

with dribbling of saliva. T h e patient is very emotional.
3. Pseudo-bulbar paralysis. T h e voice is dull and monotonous. T h e patient speaks suddenly and in order to
pronounce a few words uses an immense amount of
effort, which seems to exhaust him.
4. Striatal lesions.
(a) Paralysis agitansmonotonous speech or palilalia
(repetition of sentences or fraction of sentences).
(b) Choreahesitant and jerky speech.
(c) Post-encephalitismonotonous
speech or palilalia.
and
often
indistinct
5. Cerebellar disordersthe defect in the speech is due to

ataxia of the muscles of articulation.
(a) Lesion in the cerebellumslow, laboured, monotonous and jerky speech. T h e voice is often explosive.
(b) Disseminated
T h e patient
speaks slowly
"Artillery" is
sclerosisscanning or staccatto speech.

hesitates at the beginning and then
and deliberately as if scanning a poetry.
pronounced as "ar-til-le-ry".
(c) Friedreich's ataxia. T h e speech is slow, thick and

clumsy as if the patient has a foreign body in his
mouth "hot potato speech".
(d) Alcoholic intoxication. Patient cannot pronounce
certain words and being aware of this defect endeavours to compensate by uttering some words with
emphasis (Alcohol acts on the cerebellum).
In
delirium tremens the speech is very tremulous; the
patient stumbles over words and often mispronounces
them.
INFRA-NUCLEAR LESIONS.
1. 12th nerve palsyspeech is clumsy, indistinct and lisping.

2. 7th nerve palsy, especially bilaterallips do not work
properly; hence, speech is indistinct.
280
H O W T O EXAMINE A
PATIENT
3. Bilateral paralysis of the palateoccurs in diphtheria,

botulism and other diseases that cause paralysis of the
palate; the voice is nasal; there is difficulty in swallowing liquids. In diphtheritic paralysis the voice improves
on lying down, because the paralysed palate falls back
and shuts off the naso-pharynx.
4. Bulbar paralysis, as occurs in
(a) Syringomyelia.
(b) Landry's paralysis.
(c) Amyotrophic lateral sclerosis.
(d) Myasthenia gravis.
(e) Myopathies.
In all the above conditions the speech is indistinct. In bulbar
paralysis the lips tremble while talking; there is dribbling of
saliva. T h e dysarthria may be complete so as to render the
speech inaudible (anarthria).
5. Mechanical defects of the palate:
(a) Congenital cleft-palate.
(b) Syphilitic perforation of the palate.
B.
APHASIA
Speech has an emotional as well as intellectual character.

T h e former being more primitive is less disturbed in lesions
of the speech centres. There are four speech centres and are
situated in the left side of the brain in right-handed subjects.
I n aphasia the patient has a loss or defect in the power of expression. He has not lost his ability to speak, but has lost his
ability to say what he wishes. He cannot utter the word he
wishes to express but often does, when the word he wants to
express is supplied to him. T h e speech centres are developed
in a child in the following order:
1. Auditory speech centrein the first left temporal convolution.
CENTRAL NERVOUS
SYSTEM
281
2. Motor speech centrein Broca's area in the third left

frontal convolution. Also known as motor area of
speech.
3. Visual speech centrein the angular gyrus.
4. Writing centrein the second left frontal convolution.
"2" and "4" are motor speech centresconcerned with performance of speechspoken or written, and "1" and "3" are
sensory speech centresconcerned with reception and comprehension of speech. According to their involvement one gets
motor or sensory aphasia.
I.
M O T O R APHASIA.
Motor aphasia, i.e. inability to speak or write occurs in left

sided lesions of the brain involving the Broca's area in front
of the Rolandic fissure. Internal speech may remain intact,
but there is inability to reproduce the requisite pattern of movement for verbal expression, although he can move his lips and
tongue. Agraphia (inability to write words) is often associated
with motor aphasia due to proximity of the "writing centre" to
the "speech area". Agraphia as such, is rare. If at all it occurs,
it may be due to involvement of the receiving mechanism
sensory aphasia (wonMeafness with inability to write from
dictation, or word-blindness with inability to copy from a book).
II.
SENSORY APHASIA.
In sensory aphasia the lesion is behind the Rolandic fissure

in the posterior part of the left superior temporal gyrus.
1. Word deafness:Sounds convey no meaning. T h e patient
may hear the spoken words but cannot comprehend their
meaning. If asked to close the eyes, th patient may
respond by closing the mouth. In mild cases, simple
sentences may be comprehended but not bigger sentences.
There is difficulty in recalling names of familiar objects
and often a knife is described as "something to cut with".
There may be jargon speech. T h e intellect is disturbed.
T h e voluntary speech is affected because, in order to use
correct words the patient must be able to hear himself.
HOW
282
2. Word blindness:Inability to understand written words,

though vision is not impaired; patient understands
spoken words; voluntary speech is not affected because
he can hear what he says. There is inability to write as
the patient cannot see the written words. The lesion is
in the angular gyrus.
Aphasia seldom occurs in a child under five years even after
destruction of Broca's area, because, by the time the patient
has recovered from the cerebral insult his other side of the brain
has taken up the function of the language. At the age of 20
years, it takes months for similar physiological changes to take
place. In later age, it is difficult to regain this power.
TREMORS AND TICS
Tremors consist of more or less rhythmical oscillations of a
part or parts of a limb and is due to the alternate contraction
of a group of muscles and its antagonists. While examining a
patient for tremors it is important to note their distribution,
rate, rhythm and the effect of movement and rest upon them.
Tremors may be classified under the following five headings:
I.
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.
These are usually due to organic diseases. They are generally

rhythmical in character in spite o their coarseness.
CAUSES:
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:
These are extremely variable, purposeless, coarse and jerky

and show no rhythmicity. Typically occur in disorders of basal
gangliachoreas of all types.
IV.
INTENTIONAL
TREMORS.
Tremors occur during movement and become more marked

towards the termination of the movement.
1. Functional.
3. Congenital cerebral diplegia.
4. Cerebellar disorderslesions of dentate nucleus.
V.
TICS.
These are brief, recurrent, irresistible, compulsive movements

involving a relatively small segment of the body. Frequently
psychogenic.
1. Simple ticslocalised to a small part of the body, like
neck.
2. Generalised ticscommon at the age of puberty characterised by complicated and widespread tics, often associated with explosive utterances and obvious mental
aberration.
H O W T O EXAMINE A
284
PATIENT
3. Co-ordinated ticsthe patient under emotional stress

carries out some complicated though co-ordinated act
which gives him relief.
4. Hystericalthe tics are bizzare in appearance.
WHILE
INVESTIGATING
FOLLOWING:
CASE
OF
TREMORS
NOTE
THE
1. Part of the body involved.

2. Pattern, rhythmicity and uniformity of movements.
3. Course, rate, amplitude and if constantly changing.
4. Relationship to posture, rest, exertion and voluntary
movement.
5. Relationship to emotion and excitement.
6. If controlled by attention.
7. If present or absent during sleep.
G A I T ABNORMALITIES
In every case of disturbance of gait, exclude the following,
before suspecting neurological disorders:
A.
Mechanical defects in the lower limbs and pelvis, dislocation of hips, ankylosis of the joints, deformities of feet,
etc.
B.
Pains in the legs, pelvis or lower spine as by arthritis,

injuries and intermittent claudication.
CHARACTERISTIC
A.
GAITS
OF NEUROLOGICAL
IMPORTANCE
U N I L A T E R A L DEFECTS
1. Hemiplegiacircumduction gait. T h e limb is stiff on

the affected side and plantar-flexed; hence, apparently
longer than the normal one; therefore the patient has
to circumduct the affected limb while walking. T h e
inner side of the toe of the shoe and the sole beneath
it is worn away more on the affected foot than on the
normal one. T h e arm on the affected side is adducted
at the shoulder, flexed at the elbow, and forearm is held
in-between pronation and supination.
SYSTEM
285
2. Paralysis of one external popliteal

steppage gait because of foot drop.
nerveunilateral
CENTRAL NERVOUS
3. Sciaticapatient generally leans on the same side as the

lesion, in order to relax the affected nerve.
4. Hysteriathe foot is dragged along while walking.
B.
I.
BILATERAL DEFECTS
CEREBRAL LESIONS.
1. Diplegiaspastic or "scissor" type of gait. T h e trunk

and upper limbs are jerked violently from one side to
the other while walking in order to facilitate the movements of the legs. There are generally adductor spasms
resulting in "scissor" type of gait, especially in advanced
cases.
2. Lacunar haemorrhageshort, slow, spastic steps.
is often loss of associated movements.
There
3. Little's diseasescissor type of gait.

4. Birth injuriesscissor type of gait, but with a tendency
to improve as the child grows.
5. Hysteriadifficulty in walking and standing (astasiaabasia). T h e gait is nondescript and bizarre. Often
irregular and changeable.
II.
E X T R A PYRAMIDAL DISEASES.
1. Paralysis agitansfestinating gait. T h e patient walks

with the head and body bent forward, usually takes
sharp, quick steps and gives the appearance as if "running after his centre of gravity"a phenomenon known
as festination. In some cases, if he is suddenly pushed
forward or backward or even sideways, he is unable to
stop himself (propulsion, retropulsion or
lateropulsion).
T h e arms, while walking do not swing freely.
2. Choreajaunty or dancing gait; no one step is equal to
another.
III.
CEREBELLAR DISORDERS.
In all cerebellar disorders the patient develops "reeling gait"

which is clumsy and uncertain. T h e patient walks on a broad
286
H O W T O EXAMINE A
PATIENT
base to steady himself. T h e ataxia is equally severe whether

the eyes are open or not, in contrast to posterior column lesions
where the ataxia becomes much more severe on closing the eyes.
1. Alcohol poisoningreeling gait; walks on a broad base
to steady himself. Alcohol mainly affects the cerebellum.
2. Vestibular disorderspatient leans on one side while
walking. T h e associated vertigo makes the patient feel
disorientated; the gait is unsteady with a tendency to
deviate to the affected side.
3. Cerebellar diseasesstaggering gait. In bilateral lesions
the patient's legs run away before the trunk muscles are
able to co-ordinate themselves; hence, he can be pushed
over easily. In unilateral lesions the gait is of reeling
type, the arm hangs motionless on the affected side, the
foot deviates one or two steps and then the patient corrects himself. T h e occiput is turned towards the lesion
and the face on the opposite side. T h e patient shows
tendency to fall usually towards the side of the lesion
owing to loss of muscle tone on that side. T h e arm on
the affected side does not swing freely as the patient
walks.
4. Friedreich's ataxiathe ataxic gait is chiefly due to
involvement of the cerebellar tracts and to a lesser extent
due to the involvement of the posterior columns.
IV.
SPINAL CORD LESIONS.
1. Lateral cord lesions(myelitis, Pott's disease, latliyriasis,

etc.). T h e gait is spastic in character because the limbs
are rigid at the joints. In later stages "scissor gait" is
seen due to spasticity of the adductor muscles of the
thigh. "Scissor gait" is typically present in lathyriasis.
2. Subacute combined degenerationspastiq-ataxic gait.
V.
POSTERIOR ROOT LESIONS.
Tabes and Friedreich's diseasestamping gait. T h e patient

walks on a broad base, the limbs are flail-like, the patient lifts
the limbs too high due to loss of sense of position and brings
them down with a peculiar thud, the heel usually striking the
CENTRAL NERVOUS
SYSTEM
287
ground first or the entire sole at the same time. T h e patient

watches his feet and keeps his eyes on the floor while walking.
VI.
PERIPHERAL NERVES.
Peripheral Neuritissteppage gait. T h e patient has a foot

drop and, hence, lifts the limbs too high in order to avoid
damage to the toes. T h e toes come in contact with the ground
first, while walkingthe reverse of normal walking.
VII.
MUSCULAR DISORDERS.
1. Pseudo-muscular hypertrophywaddling gait, i.e. the

body sways from side to side as each step is taken with
an exaggerated movement of the pelvis due to weakness
of the pelvic muscles. There is pronounced lordosis
which maintains the pelvis in a steady position while
walking.
2. Myotonia congenitapatient starts to walk badly and
drags the legs; later, walks normally. There may be
family history of the illness.
3. Dystrophia myotonicathe gait is unsteady due to weakness and atrophy of the quadriceps and dorsiflexors of the
feet. Premature baldness, early cataract and testicular
atrophy indicate the correct diagnosis.
4. Myasthenia gravisthe gait is normal at first, but
becomes unsteady, weak and shuffling soon after.
5. Amyotonia congenitathe weakness and extreme hypotonia in the child prevents him from learning to walk
early in life, and when able to do so, the gait is very
unsteady.
VIII.
CONGENITAL DISLOCATION OF T H E HIPS.
T h e gait is
IX.
waddling.
FUNCTIONAL.
Difficulty to stand and walk (astasia-abasia). There is no set

pattern and the gait is bizarre and inconsistent. This is a typical gait in most cases of hysteria.
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
This occurs in the limbs as a result of sensory loss, especially

deep sensibility.
T H E COMMON
ARE:
DISEASES T H A T
CAUSE THIS TYPE OF
ATAXIA
1. Lesions of the peripheral nervespolyneuritis in severe

form.
2. Lesions of the posterior rootstabes dorsalis, Friedreich's
ataxia.
3. Lesions of the posterior columnssubacute combined
degeneration.
4. Lesions of the fillet, thalamus and sensory cortex.
In sensory ataxia, the execution of movements are difficult
and clumsy and are much aggravated on removal of visual guidance by closing the eyes, especially in lesions of the posterior
roots and posterior columns (Romberg's sign).
B.
CEREBELLAR ATAXIA
This is distinguished from sensory ataxia by the presence of

normal postural sensibility.
Each cerebellar hemisphere exerts controlling influence on
the co-ordination of movements on its own side of the body.
When diseased, the cerebellum loses the modifying and regulating influence on the muscular movements with the result that
the movements become jerky due to imbalance between the
agonists and antagonists and failure to walk in a straight line.
SYSTEM
289
These disabilities are not increased by closing the eyes as occurs

in sensory ataxia.
This type of ataxia may occur in lesions in the pre-frontal
area of the cerebral hemisphere on the opposite side, or of the
vestibular system, the cerebellum and the spino-cerebellar tracts
(Friedreich's ataxia) on the same side. Of these, the cerebellar
ataxias are the most common.
I.
COMMON CAUSES OF CEREBELLAR ATAXIAS:
I. Disseminated sclerosis.
2.
Thrombosis of the posterior inferior cerebellar artery.
3. Cerebellar abscess.
4. Tuberculoma.
5. New growths.
RARE CAUSES:
1. Encephalitis.
2.
Schilder's disease.
3. Congenital cerebellar disorders.

4. Platybasia (causing compression of the cerebellar tonsils
due to upward displacement of the basi-occiput).
5. Head injuries.
II.
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
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
1. Loss of voluntary movements.

2. Spasticity of clasp-knife type.
3. Increase in deep reflexes; ankle clonus may be present.
4. Loss of superficial reflexesextensor plantar response.
5. Associated movementsyawning or stretching may produce movements in the paralysed limbs.
6. Negative findingsno wasting, no sensory changes, no
reaction of degeneration.
PARALYSIS
I.
PARALYSIS OF ONE EXTREMITY (UPPER)
ETIOLOGY:
A.
WITHOUT
ATROPHY.
1. Pyramidal lesions:
(a) Vascular causesthrombosis, embolism, haemorrhage,
hypertensive encephalopathy.
(b) Infectionsabscess, encephalitis, meningitis.
(d) Tumours.
(e) Trauma.
2. Extra-pyramidal lesionschorea, paralysis agitans.
3. Functional disorders.
B.
W I T H ATROPHY.
1. Lesions in the spinal segments between C5 and D.

Syringomyelia, haematomyelia, poliomyelitis, progressive
muscular atrophy, amyotrophic lateral sclerosis, Pott's
disease, syphilis, tumours.
2. Lesions in the brachial plexusinjury, cervical ribs,
enlarged glands, etc., leading to Erb's palsy (5th and 6th
SYSTEM
291
cervical roots affected) or Klumpke's palsy (roots of C 8

and Di involved).
3. Lesions of the peripheral nerves. (See page 312.)
(a) Long thoracic nerveSerratus Magnus is paralysed
giving rise to winging of the scapula.
(b) Suprascapular nerveinfraspinatus is affected giving
rise to fatigue while writing, flattening of infraspinatus fossa and weakness in rotating the humerus
outwards against resistance.
(c) Circumflex nervedeltoid is involved giving rise to
difficulty in abducting the arm.
(d) Radial nervewrist drop.
(e) Median nerve"ape-hand".
(f) Ulnar nerve"claw-hand".
4. Lesions of the musclesmyopathies, ischaemic paralysis.
II. PARALYSIS OF ONE E X T R E M I T Y (LOWER)
AETIOLOGY:
A.
W I T H O U T ATROPHY.
1. Conditions giving rise to Brown-Sequard's syndrome, such

as myelitis, gumma, tumours and disseminated sclerosis.
2. Functional.
B.
W I T H ATROPHY.
1. Lesions in the spinal cordpoliomyelitis, progressive

muscular atrophy, tumours of the spinal cord.
2. Lesions of the rootsmalignancy, syphilitic meningitis of
the lumbo-sacral cord.
3. Lesion of the nerves.
(a) Anterior crural nervegives rise to difficulty in
flexing the thigh on the trunk.
(b) Obturator nervedifficulty in abducting the thigh;
and on sitting, inability to cross the leg on the
normal leg.
(c) Sciatic nervepatient leans on the side of the lesion;
presence of Lasegue's sign; tenderness along the nerve.
H O W T O EXAMINE A
292
PATIENT
(d) External popliteal nervefoot-drop.

(e) Internal popliteal nerveinability to extend the foot
and stand on tip-toe.
4. Lesions of the musclesperoneal muscular atrophy.
III.
PARALYSIS OF ONE HALF OF T H E BODY

HEMIPLEGIA
Hemiplegia means paralysis of one half of the body due to

diseases of the upper motor neurones. It is not to be used for
unilateral Parkinson's disease or paralysis of one arm and leg
by poliomyelitis or for the apparent paralysis of hemichorea.
ETIOLOGY:
A.
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-
(c) Air bubblesoperations on the lungs, pneumothorax,

insufflation of air in the vagina.
(d) Septic matterbronchiectasis, puerperal sepsis, criminal abortion.
(e) Malignant cellsfrom the lungs chiefly (a rare cause).
(f) Fat globulesfractures (fat globules can pass through
the air filter).
(g) Parasitescerebral malaria.
The commonest cause of embolism is a blood clot
detached from the left ventricle in cases of mitral stenosis.
2. Cerebral haemorrhage.
(a) Hyperpiesia, atheroma.
(b) Subarachnoid haemorrhage.
(c) Bleeding in a new growth.
SYSTEM
293
(d) Blood dyscrasiaspurpuras, leukaemias.

(e) Trauma, especially in a new-born during birth.
(f) Erythroblastosis foetalis.
Of these, hyperpiesia is the most important and the
commonest
cause.
The lenticulo-striate
artery is
involved.
3. Thrombosis.
(a) Syphilitic endarteritiscommon between 35-50 years.
(b) Atheroma,
of 60.
arteriosclerosiscommon
after the
age
(c) Chronic kidney diseasedue to secondary damage to

the arteries.
(d) Tlirombo-angitis obliteranscarotid artery is generally involved.
(e) Abnormal condition of the circulatory systemlow
blood pressure as during typhoid, convalescence, weak
heart, septicaemia, puerperal sepsiscerebral veins
are thrombosed.
(f) Abnormal condition of the bloodleukaemia, polycythaemia, anoxia as in cardiac arrest.
In all these, conditions the middle cerebral artery is
involved in 75 per cent cases. Posterior cerebral artery
may be. affected in 10 per cent cases; basillar artery in
10 per cent cases and anterior cerebral in 5 per cent
cases.
4. Vascular spasmhypertensive encephalopathy.
B.
SLOW
ONSET.
1. Inflammations.
(a) Meningitis, encephalitis.
(b) G.P.I.
(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:
1. In the cortex:As the neurones are widely dispersed at

this level, involvement in this area gives rise to a
localised paresis or paralysis on the opposite sidemonoplegia, incomplete hemiplegia, often accompanied by
Jacksonian fits. Commonest causes are depressed fractures, tumours, old cicatrix.
2. Subcortical:In corona radiata the pyramidal fibres
begin to converge and hence, a lesion at this level predominantly involves one limb and to a mild extent the
other limb on the opposite side of the lesion (incomplete
hemiplegia).
T h e commonest cause is tumours.
3. Internal capsule:The fibres converge at this level and
hence, a lesion in this area causes complete hemiplegia
on the opposite side with involvement of the lower half
of the face. Common causes are embolism, thrombosis
and cerebral haemorrhage. There may be hemianaesothesia if the posterior end of the internal capsule is
involved.
4. Thalamus:This body may be involved in extensive
capsular lesions resulting in hemiplegia and ataxia on
the opposite side and hypersensitiveness to crude sensations.
5. Mid-brain:
(a) Upper level of crushemiplegia on the opposite
side and involvement of the 3rd cranial nerve on
the same side (Weber's syndrome).
Chief causes
are tumours in the interpeduncular space and
syphilis.
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.
(b) Lower level of crussame as Weber's syndrome with

involvement of the red nucleus on the same side
as the lesion leading to athetoid movements on the
opposite side, i.e. on the hemiplegic side (Benedikt's
syndrome).
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.
(See chart on page 298.)
Cerebral thrombosis constitutes two-thirds of all cerebral

strokes. Syphilis is the commonest cause between 35-45 years,
and arteriosclerosis, after 55. In 30 per cent cases patients have
had a previous cerebrovascular accident of a minor degree.
Consciousness is retained in 66 per cent cases and convulsions
occur in 10 per cent cases. Headache, if present, is rarely severe
and blood pressure is more often lowered than raised.
Cerebral Haemorrhage.
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
SYSTEM
297
conjugate deviation of the eyes"the patient looks at his

stroke". T h e C.S.F. is under tension and tinged with blood.
Cerebral Embolism. (See chart on page 298.)
The incidence is 5 per cent of the cerebrovascular accidents.
The commonest cause is a detached piece of clot from a
thrombus in the left auricle in mitral stenosis. The onset
is instantaneous with coma in 40 per cent cases lasting for about
half-an-hour and convulsions in 10 per cent cases.
Subarachnoid Haemorrhage.
Commonest cause is rupture of a congenital arterial aneurysm
of the circle of "Willis. Rarer cause is arteriosclerosis. Congenital disorders can cause subarachnoid haemorrhage at any
age. The stroke starts with lightning rapidity with rigidity of
the neck and quadriplegia, rather than hemiplegia. The patient
generally recovers from the first attack.
Hypertensive Encephalopathy.
This occurs in hyperpietic patients. Previous to the attack,
there is generally headache which may be intense. During the
attack the patient is unconscious with evidence of transient
paresis and extensor response. If the patient is not unconscious
he will complain of severe headache, apathy, weakness, paraesthesias, anxiety, restlessness and even convulsions.
METHOD
OF INVESTIGATION:
1. Determine if the hemiplegia is functional or organic:

(a) Superficial reflexes are never abolished in functional disorders, i.e. extensor response is not elicited
in functional diseases, but is present in pyramidal
lesions.
(b) Facial nerve is not involved in functional conditions.
(c) The rigidity is characteristicclasp-knife type in
pyramidal diseases and hysterical type in functional
disorders.
298
HOW
TO EXAMINE A
PATIENT
SYSTEM
299
(d) Side-gait. The hemiplegic patient moves sideways

towards the paralysed side fairly well, but badly
towards the healthy side. In hysteria the side-gait
is impaired on both sides.
2. Determine if the lesion is upper or lower neurone type
3. Determine the cause of the lesion.
(See page 292 )
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
6. Toxins and poisonslathyrism, arsenical and lead poisoning.

7. Fracture-dislocations.
B.
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
Upper neurone lesions.
Lower neurone lesions.
1.
Paralysis.
Movements rather than

muscles affected.
Individual muscles or
groups of muscles
affected.
2.
Tone.
Spastic.
Flaccid.
3.
Wasting.
From disuse only.
Rapid
4.
Sensory changes.
Absent.
Present generally
5.
Superficial
reflexes.
Lost; plantar reflex is

extensor.
Not affected.
6.
Deep reflexes.
Exaggerated.
Absent.
7.
Trophic changes.
None.
Skin often coloured

blue and shiny.
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
301
SYSTEM
limbs are spastic, the gait is "scissor" type and has

all other features of pyramidal disease. The legs
are more affected than the arms.
(b) Porencephalusthere is spasticity and mental defect.
The kidneys are often enlarged and cystic.
(c) Schilder's diseasea hereditary degenerative disorder. There is paralysis, cortical blindness, deafness, fits and dementia.
(d) Cerebro-macular degenerationthere is paralysis,
gradual loss of vision, dementia, "cherry-red" spot
at the macula.
2. Acquired:
(a) Injuries at birtharms are more involved
legsopposite of Little's disease.
(b) Meningitis
helpful.
and encephalitisprevious
than
history
is
(c) Hydrocephalusmay produce paresis in course of

time.
(d) Thrombosis of the superior longitudinal sinus
common in marasmic children; often leads to paresis
of the legs.
B.
LESIONS OF T H E SPINAL CORD.
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
(d) Friedreich's diseaseunsteady gait, nystagmus, loss

of deep sensibility, loss of deep reflexes, extensor
plantars, pes cavus, explosive speech.
2. Acquired:
(a) Pott's diseaseprogressive spasticity, deformity of
the spine.
(b) Poliomyelitisonset with fever, wasting of muscles,
loss of tendon reflexes.
C.
LESIONS OF T H E NERVES.
1. Hypertrophic interstitial neuritiswasting and weakness

of the anterior tibial muscles, foot-drop, pain in the
hands and legs, thickening of the popliteal nerves.
2. Acute infective polyneuritismay occur in children with
sudden weakness of the legs, pains and hyperaesthesias.
D.
LESIONS OF T H E MUSCLES.
1. Pseudo-hypertrophic paralysisdelay in walking, wasting

of muscles, apparent prominence of glutei and calves,
paresis rather than paralysis of the limbs.
2. Peroneal type of atrophywasting confined to lower
limbs upto the junction of middle and lower third of
the thigh; foot-drop and pes cavus.
METHOD
A.
OF INVESTIGATION
OF A CASE OF
PARAPLEGIA.
EXCLUDE FUNCTIONAL DISORDERS:

No extensor response, no loss of visceral reflexes, presence of hysterical
type of rigidity. Sensory changes may be present and deep reflexes
may be exaggerated.
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
note the following:
UPPER
OR
LOWER
(a) Suddenacute myelitis, haematomyelia, fracture dislocations.

(b) Gradualtumours,
myelia.
Pott's
disease,
degeneration,
(c) Transientdisseminated sclerosis, G.P.I.
G.P.I.,
syringo-

2.
AGE OF T H E
303
PATIENT.
(a) ChildrenPott's disease, spina bifida.

(b) AdultsPott's disease.
(c) At 30-40 yearssyphilis, disseminated sclerosis,
syringomyelia,
motor neurone diseases, subacute combined degeneration.
(d) At 50-60 yearstumours
bined degeneration.
(may occur at any age), subacute
com-
3.
H I S T O R Y OF SYPHILISa common cause of myelitis.
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.
L O C A T E T H E SITE OF LESION AS FOLLOWS:

(a) Motor symptoms:
(i) Power diminished at the level of and below the lesion,
(ii) T o n e of the limbs increased below the lesion.
(b) Sensory changes:
(i) Anaesthesia at the level of the lesion.
(ii) Hyperaesthesia just above the lesion due to irritation of
posterior roots.
the
(iii) Hypoaesthesia below the level of the lesion.

(c) Reflexes:
(i) T e n d o n reflexes are exaggerated below the lesion and lost at
the level of the lesion due to involvement of the reflex centres,
(ii) Superficial reflexes are abolished below the level of the lesion.
Normal flexor plantar response is converted into extensor.
(d) Localization by myelography:By injecting radio-opaque substances,
the exact location of the compression can be detected.
If the paralysis
is of flaccid type,
the possibilities
are:
(a) POLIOMYELITISacute onset with fever, muscular weakness, flaccid

paralysis; several muscles are affected first and later a group of
.muscles are damaged permanently. If bilateral, the wasting is not
symmetrical.
(b) N E U R I T I S t i n g l i n g and numbness, tenderness over the calf muscles,
loss of tendon reflexes, global and bilaterally symmetrical wasting.
(c) S U B A C U T E C O M B I N E D D E G E N E R A T I O N " g l o v e and stocking"
type of anaesthesia, deep reflexes exaggerated or lost, deep sensibility
lost, extensor plantar response, associated anaemia and achlorhydria.
(d) TABES DORSALISlightning pains, Argyll-Robertson pupils, positive
Romberg's sign, tendon jerks lost, deep sensibility lost.
(e) C A U D A E Q U I N A T U M O U R S p a i n in the back, saddle-shaped
anaesthesia around the glutei, loss of ankle jerks, trophic disturbances.
304
SENSORY TRACTS AND T H E I R DISORDERS

Sensation is an essential part of the protective mechanism of the body.
In general, sensations may be divided into two groupssuperficial and
deep.
A.
Superficial group comprises of the following sensations:light

pain, temperature, and two-point discrimination.
touch,
B.
Deep sensibility include:pressure, posture, vibrations, joint

and ability to recognise size and weight of objects.
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
T O U C H S E N S A T I O N S : T w o paths carry these sensations:

(a) Posterior columns o n the same side via column o Goll and Burdach
to end in the nucleus gracilis and cuneatus respectively. From here
the fibres decussate and ascend to the thalamus.
(b) Crossed sensory pathfibres enter the posterior horns and end
around the cells in this area. T h e 2nd relay starts here and the
fibres cross to form the spino tectal tract and go up to the thalamus.
2.
PAIN A N D T H E R M A L IMPULSES. T h e s e enter into the posterior

horns and end in their cells. T h e 2nd relay starts here, ascends a few
segments of the spinal cord and t h e n crosses to the lateral spinothalamic tract and then goes up to t h e thalamus.
3.
DEEP SENSIBILITY A N D P O S T U R A L SENSATIONS. T h e neurones

ascend in the posterior columns and g o up through the column of
Goll (lower limb) and Burdach (upper
limb) and terminate in the
nucleus gracilis and cuneatus. In these nuclei a 2nd group of fibres
arise and cross to the opposite side ( m e d i a n fillet) and reach the optic
thalamus.
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
Amyotrophic lateral sclerosis involves
5. Lesions in the spinal canalthere is loss of pain and

temperature sensations, but sensations of touch and
pressure in the affected parts are preserved (dissociation
of sensations) . Syringomyelia is the chief cause.
6. Brain-stem lesions. As all the sensory fibres on the
opposite side of the body are closely packed together in
this area, including the fibres of the trigeminal nerve,
lesions in this area usually affect all forms of sensations
on the opposite side. A little lower down in the medullary
region, the anaesthesia may be widespread. Common
causes are thrombosis, disseminated sclerosis and syringomyelia.
Fig. XXXIV
BASAL GANGLIA.
CNCaudate Nucleus. PPutamen. GPGlobus Pallidus.
OTOptic Thalamus. ICInternal Capsule.
SYSTEM
307
7. Thalamic lesionscause spontaneous pains in the

opposite side of the body; threshold for pain is raised
on the opposite side; athetoid movements are present
sometimes.
8. Lesion in the sensory cortexthere is impairment of
sense of position and of two-point discrimination, and
inability to recognise objects placed in the hand on the
opposite side. Tumours and vascular lesions are the
common causes.
EXTRA-PYRAMIDAL SYSTEM
T h e extra-pyramidal system is a primitive pyramidal system and consists
mainly of basal ganglia, its tracts and subthalamic nuclei.
T h e basal ganglia consists of optic thalamus and the corpus striatum.
T h e latter consists of two nucleicaudate and lenticular. T h e lenticular
nucleus is divided into outer putamen and inner globus pallidus. T h e
internal capsule separates the lenticular nucleus from the medially located
caudate nucleus and the thalamus.
T h e corpus striatum has hardly any connections with ihe cortex or
pyramidal fibres or the corpus striatum of the opposite side. It receives
afferent fibres through the thalamus. Its efferent fibres lead to the red
nucleus and other substriatal centresthe corpus Luysii, substantia nigra,
etc. They innervate the non-striated sarcoplasm of the slender musclefibres in the body and control the involuntary, automatic and associated
movements, in contrast to the motor fibres arising from the cortex which
innervate the coarse striated muscle-fibres and control the voluntary movements.
T h e optic thalamus is a sensory relay station for all the impulses of the
body, but olfactory. It is also a relaying station for fibres that come from
the opposite side of the cerebellum to the cortex. It is by this means that
the cerebellum guides and controls the cerebral cortex when it is carrying
out voluntary movements. An injury to the thalamus, therefore, produces
signs of cerebellar disturbance on the opposite side of the body.
Sensations of pain, hunger, thirst, and sexual feeling end in thalamus
mainly.
T h e cortex exercises an inhibitory effect on the thalamus on certain occasions and thus, very often, sensations of the special senses may fail to reach
the cortex. For example a busily engaged man may fail to hear the tick
of a clock in the room.
COMMON DISORDERS OF T H E BASAL GANGLIA

1. Parkinson's syndromegives rise to muscular hyper tonicity, disturbance of automatic movements (lack of blink-
HOW
308
TO EXAMINE A
PATIENT
ing of the eye-lids), loss of associated movements (lack of

swinging of the arms while xvalking), loss of emotion,
rhythmic tremors, festinating gait.
2.
Chorearesults in inco-ordination, spontaneous movements, muscular weakness and "dancing gait".
3. Thalamic syndromegives rise to outburst of severe,

poorly localised pain, ataxia, involuntary movements,
paraesthesias and inability to discriminate or localise
simple crude sensations. Slight stimuli may evoke severe
and disagreeable sensations.
CEREBELLUM
T h e cerebellum is located in the posterior fossa of the skull behind the
pons and medulla and is separated from the overlying cerebrum by an
extension of the dura mater, tentorium cerebelli. It consists of two lobes
and a median portion, the vermis and is connected to the brain by superior
and inferior peduncles and to the spinal cord by cerebellar tracts.
Each half of the cerebellum is connected with:
(a) T h e same side of the spinal cord.
(b) Both sides of the medulla.
(c) Opposite side of the cerebrum, thalamus and pons.
Its main functions are:
Keep the individual oriented in space, control the tone of the muscles
and volitional movements.
Its involvement causes:

1. Disturbance of motor functionhypotonia, asthenia, reeling gait.
2. Lack of co-ordinationRombergism (present even when
the eyes are open), dysmetria (finger-nose test) adiadokokinesia, rebound phenomena.
3. Involvement of
speech, vertigo.
cranial
nervesnystagmus,
slurring
4. Reflexespendulous deep reflexes.

SPINAL CORD AND I T S LESIONS
T h e spinal cord is 42-45 cms. long and occupies the upper two-thirds of
the vertebral canal. It extends from the upper border of the 1st cervical
vertebra to the upper border of the 2nd lumbar vertebra. It is continuous
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
(b) Rubro-spinal tractmuscle tone and synergy.

(c) Olivo-spinal tractfunction not known.
2.
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).
DISEASES OF T H E SPINAL CORD

In lesions of the spinal cord, the general examination of the
nervous system is sufficient to enable one to detect the site of
the lesion and the amount of damage done to the nervous
structures; but, in order to determine the nature of the lesion,
the history of the case, examination of the other systems of the
body and special tests may be necessary.
Since the cord ends at the upper level of the 2nd lumbar vertebra, spinal
segments evidently do not correspond numerically with the vertebrae overlying them. T o determine which spinal segment is related to a given
vertebra follow this procedure:
For the cervical vertebra, add I.
For dorsal 1 to 6, add 2.
For dorsal 7 to 9, add 3.
T h e 10th dorsal arch overlies
T h e 1st lumbar arch overlies
Li & L2 segments.
L 3 & I.4 segments.
L5.
the sacral & coccygeal segments.
Several diseases involve the spinal cord invariably giving rise

to paraplegia. (For classification see page 311.) However
one has to bear in mind the more common diseases of the spinal
cord such as Pott's disease in children and young adults, transverse myelitis especially of syphilitic nature at the age of 35 to
50, tumours, disseminated sclerosis, syringomyelia, subacte combined degeneration and virus diseases.
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.
5th & 6th.
Cervical.
3rd & 4th.
III.
II.
I.
Segment.
Muscles involved. Reflexes involved.
Cremasterics lost.
Knees lost.
Muscles below the knees.
All reflexes normal.
Ant tibials and small muscles

Ankles lost.
of the feet.
External sphincter paralysed.
Anal and micturition affected.
Oblique abdominal muscles.

Adductors and quardriceps.
Paresis and anaesthesia around

the anus.
No paresis.
Paresis.
Paraplegia.
Paraplegia.
Paraplegia, and trunk

Flexors of the wrist. Lower reflexes brisk,
affected.
Paraplegia, and abdomen
Intercostals and abdominals.
Epigastric lost,
affected.
Paraplegia.
Upper abdominals.
Abdominals lost
Paraplegia.
Lower abdominals.
Lower abdominals lost.
Pain behind the neck, paresis

Lower trapezius, supra and
None,
of the arms, anaesthesia of
infraspinati muscles of the
the face on the same side.
arms.
Quadriplegia.
Deltoids, biceps, brachialis,
Biceps and supinators lost;
supraspinati.
inversion of the radial reflex.
Paraplegia
Triceps & extensors of the
Triceps lost.
wrist.
Features.
SEGMENTAL INVOLVEMENT OF THE SPINAL CORD.

311
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
6. Chronic vascular diseasesarteriosclerosis, thromboangitis obliterans, periarteritis nodosa.

7. Cachexiascancer, tuberculosis, etc.
F E A T U R E S OF N E U R I T I S I N
GENERAL.
1.
Radiating pains.
2.
Tenderness along the nerves and tender spots.
3.
Subjective sensationstingling,
4.
Weakness of the affected muscles.
5.
Wasting of muscles, foot-drop, wrist-drop etc.
6.
Hypotonia.
7.
Ataxia.
numbness,
etc.
8.
Objective sensationshypoaesthesia,
9.
D e e p sensibilitytenderness over the calf muscles.
anaesthesia.
10.
Depression of the deep reflexes.
11.
Relaxation of the involved limbto avoid stretching of the

or nerves.
12.
T r o p h i c and vasomotor changesloss of hair, brittle nails, ulceration,

etc.
13.
Presence of reaction of degeneration.
NEUROMUSCULAR DISEASES
(See under Locomotor System, Chapter VIII)
nerve
CHAPTER VI
GENITOURINARY
SYSTEM
A.
INTERROGATION.
B.
C.
GENERAL EXAMINATION.
D.
EXAMINATION OF T H E GENITO URINARY

SYSTEM.
E.
EXAMINATION OF T H E URINE.
F.
RENAL EFFICIENCY TESTS.
316
A.
INTERROGATION
Particularly inquire into the family history of kidney diseases,

hypertension, gout, haematuria, etc.
In personal history inquire into the past history of scarlet
fever, tonsillitis, disorders of micturition, bleeding tendencies,
renal colic, toxaemias of pregnancy, etc.
B.
HAEMATURIA.
SYMPTOMS
(See page 344.)

1. Amount passed per day.
2. Colour of the urine.
3. Relation to micturitionbefore, during or after.
4. If associated with pain.
5. Other urinary symptoms.
POLYURIA.
(See page 348.)

1. Frequency.
2. Approximate amount passed.
3. Ratio of day to night urine.
4. If voided periodically or constantly.
5. Accompanying thirst, if any.
OLIGURIA.
(See page 349.)

1. Amount passed.
2. Frequency.
3. Duration of symptoms.
4. Appearance of the urine.
5. History of renal or heart diseas.e.
GENITO URINARY
DYSURIA.
SYSTEM
317
(See page 339.)

1. T h e exact time of difficulty in micturitionwhile starting
or during the flow.
2. If flow stops abruptly.
FREQUENCY.
(See page 339.)

1. Number of times urine passed.
2. Whether at night, day or both.
3. Amount passed each time, and the total in 24 hours.
INCONTINENCE.
(See page 332.)

1. If it occurs at night only.
2. If there is dribbling.
3. If there is bed-wetting (enuresis).
PAIN.
1. Whether continuous or intermittent.
2. If colicky.
3. If present only while passing urine.
4. Exact locationback, abdomen, bladder, testicles, epididymes.
5. If it deviates in any particular direction.
C.
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
318
oculi for papilloedema, haemorrhages, thickening of the arteries

and "cotton wool" patches.
D.
1.
E X A M I N A T I O N OF T H E GENITO-URINARY
SYSTEM
KIDNEYS.
(See page 146.)
Palpate the kidneys with the patient in recumbent position

and with the head slightly raised on a pillow. Sit beside the
patient on the side to be examined. Put one hand over the
loin behind with the tips of the fingers resting against the
erector spinae, i.e., just below the twelfth rib. Place the right
hand (for, the right kidney and vice versa) flat on the abdomen
with the fingers pointing upwards towards the costal margin.
Instruct the patient to take a deep breath and apply firm pressure with both hands, so that if the kidney is palpable it moves
down into the space between the examining hands. When the
kidneys can be felt in this way it is recognised as a swelling
with a rounded lower pole, and if sufficient of it can be grasped
between the hands the characteristic reniform shape can be
recognised.
2.
T H E BLADDER
If distended with urine, the bladder can be seen and felt

as a rounded swelling arising from the pelvis and extending
upwards, sometimes as far as the umbilicus. Percussion gives
a dull note over the swollen area.
3.
T H E E X T E R N A L GENITALIA.
Carefully look for phimosis (which can give rise to urinary

obstruction, especially in infants), epididymitis, vaginal infection and congenital defects.
4.
R E C T A L AND VAGINAL EXAMINATION.
Rectal examination is necessary in all cases of suspected

urinary diseases. It is desirable especially in males to use the
knee-elbow position which gives better access to the organs
lying around the base of the bladder.
G E N I T O URINARY
SYSTEM
319
Examine the prostate, which is normally felt as an elastic

swelling with a median groove terminating in a notch at the
top. If enlarged, the upper surface of the notch is not easily
felt. Irregularity and hardness in the prostate suggest malignancy or prostatic calculi.
Vaginal examination is also necessary to exclude diseases of
other pelvic organs, e.g. uterus and its appendages which may
involve or irritate the bladder and cause urinary symptoms.
E.
COLLECTION
OF A
URINE ANALYSIS
SAMPLE-.
In males, a specimen of urine as passed into a clean glass

vessel is sufficient for ordinary tests. For females, a catheter
specimen is preferable to exclude contamination from vaginal
discharge. For diabetes a 3-hour post-prandial urine is desirable.
In cases of nephritis a morning specimen should be examined.
NORMAL FEATURES OF URINE
I.
PHYSICAL EXAMINATION
1. Quantity. Normal quantity passed in 24 hours is about

1,500 c.c. generally voided during the day, or at the most,
the normal ratio of day urine to night is 4 : 1. Approximation of the night quantity to that of the day is always
abnormal and especially apt to occur in renal failure.
2. Colour. Normally is pale yellow or amber. An acid
urine is darker than the one which is alkaline. Concentrated urine, as occurs in high fevers, is high coloured
as compared to that voided by normal individuals.
ALTERATION
PALEwhen
nephritis.
IN THE
COLOUR
OF
URINE.
excessive as in diabetes mellitus or insipidus and
chronic
H I G H COLOUREDfevers, dehydration and congestive heart failure due

to concentration of the urine.
YELLOWISHbile, administration of B-complex.
YELLOWISH-GREENacriflavine intake.
REDDISH, SMOKY
melanin, phenol.
OR
BROWNISHpresence
of
blood,
haemoglobin,
320
HOW
TO EXAMINE A
PATIENT
PINKISHingestion of dyes, dindevan, alkaptonuria.

ORANGEjaundice, santonin or rhubarb intake.
PORT WINEblack water fever, haematoporphyrinuria, haemochromatosis,
methaemoglobinuria, meianuria.
GREENISHbile
derivatives.
or
administration
of
carbolic
acid
or
other
coaltar
BLACKISHalkaptonuria, melanin from malignant melanomas.

CLOUDYpus, phosphates or urates.
MILKYfat, chyle or pus.
OPALESCENTmicro-organisms.
BLUEtyphus or administration of methylene blue.
3. Consistencygenerally transparent with no deposits. If

cloudy, it may be due to presence of mucus, pus, oxalates,
urates or alkaline phosphates. If the turbidity has a
pinkish colour, it is due to salts of uric acid.
4. Odourmildly aromatic due to presence of volatile fatty
acids. On standing the urine is decomposed and has an
ammoniacal smell. A cloudy urine with an ammoniacal
smell suggests pyelitis or cystitis. In ketosis the urine
may have the smell of rotten apples due to the presence
of acetone.
5. Densitygenerally the specific gravity varies from 10
25. Low specific gravity suggests diabetes insipidus or
chronic renal disease. High specific gravity is characteristic of diabetes mellitus and may also occur in haematuria and albuminuria; it is also increased in fevers,
congestive heart failure, dehydration, acute nephritis and
nephrosis. In all cases where there is albumin in the
urine, for every 1 per cent increase the specific gravity
rises by three points, and in cases of glycosuria for every
1 per cent increase in the glucose the specific gravity rises
by two points.
If the urine to be tested is insufficient, dilute it so as to enable
the urinometer to float into the fluid and then multiply the
last two figures of the specific gravity by the dilution.
321
GENITO URINARY SYSTEM
II.
CHEMICAL E X A M I N A T I O N
A. Reaction. Normally the urine is slightly acidic to litmus

due to presence of acid sodium-phosphate; it becomes alkaline
on standing due to decomposition (conversion of acid phosphate
into alkaline phosphate).
I n cystitis, the urine is alkaline in
reaction; it is also alkaline in constant vomiting, severe anaemias
and crises of pneumonia. Strong acid reaction is found in
acidosis, diabetes mellitus, chronic nephritis, leukaemias and
scurvy.
NORMAL C O N S T I T U E N T S
Total solids excreted in normal urine per day is 50 Gms. of
which 20 Gms. are voided as inorganic and about 30 Gms. as
organic constituents.
N O R M A L C O N S T I T U E N T S OF T H E U R I N E
Output per day
A.
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
C H L O R I D E S . T h i s is the chief inorganic constituent of normal urine

and is mainly found as sodium chloride and in small quantities as potassium
salt. Daily excretion is about 10-12 gms. It is diminished i n fevers a n d
21
322
may be completely absent in pneumonia; also diminished in chronic

nephritis, during formation of large exudates, severe diarrhoea and excessive sweating.
P H O S P H A T E S . Salts of phosphoric acid with calcium and magnesium
(earthy phosphates)
are often found in an alkaline urine as a cloudy
precipitate. A clear urine on boiling may also show a precipitate of
phosphates d u e to liberation of C 0 2 by the action of heat, which converts
acid sodium phosphate into alkaline phosphate. T h i s precipitate quickly
disappears on adding a few drops of acetic acid. Daily excretion is about
2 gms. of phosphates. T h e y are found in excess in vegetarians and increased in nervous diseases. T h e y are considerably diminished in renal
disorders. If fresh urine contains a deposit of phosphates it means there
is an infection of the urinary tract.
S U L P H A T E S . Sulphuric acid occurs in the urine as inorganic salts mainly,
and to a small extent as organic sulphates in combination with indol,
skatol, etc. Average daily excretion is 2 gms. in 24 hours. It is increased
in fevers in general, and in other conditions where there is increased protein
metabolism.
OXALATES. T h e average excretion is about 0.015 gm. per day. It is
increased o n taking certain vegetables such as cabbage, spinach and rhubarb. T h e y are best seen under the microscope as "envelope-like crystals"
and also as "dumb-bells".
2.
ORGANIC CONSTITUENTS
OF T H E
URINE
T h e s e are mostly nitrogenous substances whose total output is about

30 gms. per day of which 85% is voided in the form of urea (25 gms.
per day).
UREA. T h e excretion of urea which is normally about 20-30 gms. per
day is increased in excessive protein intake, fevers, diabetes, convalescence
and in phosphorus and arsenical poisoning. It is diminished in starvation,
chronic kidney diseases and liver destruction.
A M M O N I A . On an ordinary diet the average daily excretion is about
one gramme per day. It is increased in ketosis, such as in advanced
diabetes, delayed chloroform poisoning, in severe vomiting of pregnancy
and in those conditions where there is failure to synthesise urea in the body
as in liver cirrhosis.
U R I C ACID. T h i s occurs in urine in combination with alkalis as urates.
These may be seen in the urine as "brick dust" deposit. Excess in the
urinary passages may lead to "gravel" or stone formation. T h e average
amount of uric acid excreted per day is 0.4 to 0.7 gm. It is increased by
the intake of food containing nucleo-proteins; it is also increased whenever
a large destruction of nucleins is going o n in the body, as in myeloid
leukaemia, acute fevers, resolving pneumonia, acute yellow atrophy and
other acute destructive diseases of the liver; it is also increased during
X-ray treatment and after an attack of gout. It is diminished during an
attack of gout and during quinine administration.
C R E A T I N I N E . Creatinine is creatine minus water. Daily output is
remarkably constant and is 1.5 gms. Its significance is not yet very clear.
GENITO-URINARY
SYSTEM
323
It is increased in pneumonia, typhoid and tetanus. It is decreased in

anaemia, leukaemia, thyrotoxicosis, advanced degeneration of the kidneys
and liver, and in muscular atrophy.
P U R I N E BODIES. A m o n g the chief products of disintegration of nucleins
are uric acid and some basic bodieshypoxanthine, xanthine, adenine and
guanine. T h e y total about two grammes. T h e y are increased, just as
uric acid, in conditions associated with increased destruction of nucleins as
in leukaemia, etc.
TESTS FOR ABNORMAL CONSTITUENTS

Albumin.
1. Heat Test. Boil upper portion of a test tube filled three
quarter full of urine If turbidity appears, add five drops of
10 per cent acetic acid which causes carbonates and phosphates
to dissolve. Cloudiness persists if the urine contains albumin.
This test is not very reliable if urine has very low specific gravity.
Heating at about 50C precipitates Bence-Jones' proteins,
which disappear on boiling and reappear on cooling. BenceJones' proteins are found in myeloma, leukaemia, osteomalacia
and sometimes in nephritis with high B.P. and oedema.
2. Sulphosalicylic Acid Test. Urine must be clear and acid
in reaction. Add three cfrops of 20 per cent solution of sulphosalicylic acid to 1 c.c. of urine; the urine becomes cloudy if
albumin is present. If cloudiness disappears on boiling and
reappears on cooling, it is Bence-Jones' protein.
3. Nitric Acid Test. Pour urine in a test tube containing
a little nitric acid. A white ring appears at the junction, if
albumin is present.
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
(a) Sugarsglucose, laevulose, lactose,
pentose.
(b) Normal constituents in the urine w h e n present in high concentration

glycuronic acid, uric acid and creatinine.
(c) Homogentisic acid as occurs in alkaptonuria. ( T h e urine darkens on
heating with Fehling's and Benedict's reagents.)
(d) Mucins.
f(e) Drugs like chloral, chloroform, copaiba, benzoic acid, salicylic acid,
morphia and aspirin.
2. Benedict's Test. Add 8 drops of urine to 5 c.c. of

Benedict's solution and boil for three minutes. Allow it to
cool. Green, yellow or red colour appears if sugar is present.
This test reveals even 0.08 per cent sugar. A rough idea of
estimating the percentage of sugar in the urine may be based on
the final colouration of the urine. Green colour suggests 0.5
per cent, yellow 1 per cent, and red above 1 per cent. Benedict's
test is more reliable than Fehling's as it is more stable and less
reactive to non-sugar reducing substances. This test is also
positive to lactose, pentose and laevulose (fructose); so also to
homogentisic acid. Fermentation test may be necessary to detect
the correct reducing agent.
Acetone.
Rothera's Test. Saturate a few c.c. of urine with ammionium
sulphate and add to it a few drops of freshly prepared sodium
nitro-prusside solution. Then pour gently down the side of the
test tube strong ammonia solution. A violet ring appears at
the junction. A brown colour is negative. T h e test being very
delicate, a weak positive reaction has little significance. I n
diabetic patients, a progressive increase in acetone is a grave
prognostic sign. Acetone is also present in starvation, toxaemic
vomiting of pregnancy, high ketogenic diet and chloroform
poisoning.
Aceto-Acetic Acid.
Gerhardt's Test. To be tested only if acetone is present.
Add 10 per cent ferric chloride solution to the urine to precipitate the phosphates; filter and to the filtrate add a few more
drops of ferric chloride solution. Brownish-red colour appears
if aceto-acetic acid is present. This disappears on boiling.
Typically present in diabetes along with acetone.
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.
Use fresh urine.
1. Iodine Ring Test. Pour gently a 1 /10th alcoholic iodine

solution in a test tube containing urine. A green ring
at the junction of the two fluids indicates presence of
bile.
2. Gmelin's Test. Filter 100 c.c. of acid urine, remove the
filter paper and allow it to dry partially and then add
a drop of concentrated nitric acid to the precipitate. A
play of coloursgreen, blue, red and yellowindicates
the presence of bile pigments. Their presence in the
urine signifies obstructive or infective jaundice.
Bile Acids.
Place urine in a beaker (not test tube). Sprinkle a few
flowers of sulphur on the surface. If bile acids are present, due
to lowering of the surface tension of the urine, the sulphur sinks
to the bottom.
Indican.
T o 1 / 3rd test tube of urine add 1 / 3rd strong hydrochloric
acid and 5 c.c. of chloroform plus a few drops of H 2 O 2 . Invert
the tube several times without shaking violently. Bluish colour
due to indigo formed from indican appears in the chloroform.
It is increased in intestinal obstruction, cholera, typhoid, lack
326
of bile in the intestine and other conditions of intestinal putrefaction.

Chyle.
Shake urine with etherfat is dissolved and urine becomes
clear.
Pus.
Add liquor potash to the deposita ropy gelatinous mass is
formed.
Urobilin.
T o 10 c.c. of urine slightly acidified, add a few drops of iodine
plus 10 c.c. of saturated alcoholic solution of zinc acetate. Shake
and allow the test tube to stand for a few minutes and then
filter. The appearance of the fluid becomes greenish against
daylight. Urobilin is present in toxic necrosis of the liver,
haemolytic and pernicious anaemias. It is nearly always absent
in obstructive jaundice.
III.
Use sediment after centrifuging the urine.

Look for:
1. R.B.C.signifies haematuria.
2. W.B.C suggests pyelitis, cystitis, etc.may be present in
a non-catheter specimen in a female.
3. Epithelial cellstheir presence is of not much significance and may be normally present and coming from the
bladder.
4. Casts. These are linings of the kidney tubules and
hence, are cylindrical in shape; they may have rounded
ends or one end may be ragged as if fractured. Although
their presence in the urine is significant of renal disease,
an occasional hyaline cast may be found in normal urine.
GENITO-URINARY
TYPES OF CASTS.
SYSTEM
327
(See Fig. X X X V I . )
(a) E P I T H E L I A L CASTSthe casts are completely filled with epithelial

cells with or without a nucleus. T h e y are generally found in chronic
inflammation of the prostate and hence, of not much significance so
far as diseases of the kidney are concerned. T h e y may be present
in toxaemias, poisoning by heavy metals, and in amyloid disease.
(b) B L O O D CASTSthe casts are thickly covered with red
T h e y are typically present in acute nephritis.
corpuscles.
(c) G R A N U L A R CASTSfine granules are seen in the casts. Such casts

are commonly present in sub-acute and chronic parenchymatous
nephritis.
(d) H Y A L I N E CASTSthese are pale, transparent and homogeneous in
appearance. T h e y may be present in normal urine. T h e y are frequently seen in chronic nephritis, nephrosis, congestive heart failure,
eclampsia, dehydration and diabetic coma.
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
(e) F A T T Y CASTSlipoid matter is present in the casts and indicates

that the tubules are undergoing lipoid degeneration. T h e y are present in sclerotic diseases of the kidney and nephrosis.
(f) W A X Y CASTSwaxy matter is deposited in the casts which have
remained long in the urinary tubules. T h e y occur in amyloid disease
of the kidney, advanced stages of glomerulonephritis and myelomas.
5.
BACTERIA.
6.
OVA A N D PARASITES.
Stain the slide with appropriate reagents.
7.
CRYSTALS.
Use deposit after centrifuging the urine.
T h e following crystals are often seen in the urine:(See Fig. X X X V I I . )

(a) U R I C ACIDthese are reddish brown in appearance due to absorption of urinary pigments. Under the microscopic the crystals look
either like rhombic prisms or some modifications of these forms.
Sometimes numerous crystals are clustered together producing rosettes
ifM
ACID
A
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XXXVII
Microscopic appearance of crystalline urinary deposits.

A. A m o r p h o u s urates. B. Uric acid crystals. C. Calcium-oxalate crystals.
D . Leucine crystals. E. Tyrosine crystals. F. Cystine crystals. G. Sulphonamide crystals. H . Calcium phosphate crystals. I. T r i p l e phosphate
crystals. J. Urate crystals.
GENITO-URINARY
SYSTEM
329
and other composite forms. T h e i r presence suggests a stone in the

urinary tract or abnormal uric acid metabolism as in gout.
(b) U R A T E S t h e s e have considerable affinity for the urinary pigments
and hence are generally brick coloured. Under the microscope they
look like small granular particles arranged in clumps. Some may
form spheres with numerous spines radiating from their surface. T h e y
are f o u n d in the urine during fever.
(c) PHOSPHATESthese are salts of phosphoric acid and calcium, or of
phosphoric acid with a m m o n i u m and magnesium. T h e y are present
in an alkaline urine only. T h e y are f o u n d in excess in neurasthenia,
osteitis fibrosa and in disorders that give rise to alkalosis.
(i) CALCIUM-PHOSPHATESoccur i n colourless prismatic crystals
which occur either singly or in radiating clusters.
(ii) A M M O N I U M - M A G N E S I U M
OR
TRIPLE
PHOSPHATES
occur as triangular prisms and often described as "coffin-lid"
crystals.
(d) OXALATESgenerally occur as calcium oxalates and under the
microscope are seen as "envelopes" or minute " d u m b bells". T h e y
are present in those w h o have excess of tomatoes, spinach, rhubarb
and other vegetables rich in oxalic acid. T h e i r presence in fresh
urine is suspicious of calculi.
(e) CARBONATESgenerally occur in the urine as calcium carbonates.
T h e y look like "dumb bells" or spheres with a radiating structure.
KIDNEY EFFICIENCY TESTS

These tests fall under two headings:
A.
ALTERED
URINE.
PHYSIOLOGICAL B A L A N C E B E T W E E N
BLOOD
AND
T h i s is best detected by the analysis of blood, urine or both.
B.
1.
B L O O D U R E A . Blood analysis is done mainly for urea content

which is normally 20 to 40 mgm. per 100 c.c. of blood. Over
50 mgm. is evidence of disturbed renal function. If this goes
above 80 mg., it is strongly suggestive of uraemia t h o u g h not
necessarily kidney disease.
2.
B L O O D C R E A T I N I N E . Creatinine content of the blood, which is

normally 1 to 1.5 mgm. per 100 c.c. of blood, is increased in
kidney damage and if it goes to even 2 mgm. it is a sure sign of
kidney disease.
E L I M I N A T I N G P O W E R OF T H E
KIDNEYS.
Several tests are employed to test the efficiency of the kidneys,

the following two are fairly good for routine purposes.
1.
UREA CONCENTRATION
TEST.
2.
WATER CONCENTRATION
TEST.
but
330

UREA CONCENTRATION
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.
T h e bladder is emptied at 9, 10 and 11 a.m. and each specimen is tested

separately for urea concentration. Normally a concentration of 2 % is
reached in at least one of the specimens. Mild impairment is indicated
by a concentration of 1.8% and severe impairment by less than 1.6%.
WATER CONCENTRATION
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
(j) T U M O U R S OF T H E O M E N T U M , MESENTERY OR PANCREAS

these are more median in position, do not project into the loin and
rarely resemble a renal tumour.
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.
The common causes of abnormalities in micturition can be

grouped under two headings:non-neurological and neurological causes.
A.
1.
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
(d) Inflammation of the surrounding organssalpingitis,

pyosalpinx, appendicitis, ovarian cysts, fibroids, gravid
uterus.
(e) Other irritative conditions, especially in children
phimosis, balanitis, worms, oxaluria, bacilluria.
2. Changes in the Stream of Urine.
(a) Congenital disorders like hypospadias.
(b) Stricture of the urethra (stream thin, but
forcible).
GENITO URINARY SYSTEM
(c) Enlarged prostate (stream slow and
333
forceless).
(d) Vesical calculus or papilloma (sudden stoppage of the

flow).
3.
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
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
lesions, because the contractions of the bladder walls

become so vigorous that they cannot be resisted by the
external sphincter and urine escapes suddenly.
COMMON SYMPTOMS A N D SIGNS IN KIDNEY
DISEASES
ALBUMINURIA
Presence of albumin in the urine does not necessarily signify
a disease of the kidney. Several conditions outside this organ
may also cause albuminuria. Very small amounts may arise
from the urinary passage, especially vagina. Nearly all the diseases of the pelvis of the kidney, bladder and the urethra are
accompanied by albuminuria. Any urine containing blood
(haematuria), haemoglobin (haemoglobinuria)
or pus (pyuria)
also contains albumin. T o diagnose kidney diseases, an appreciable amount of albumin should be present in the urine,at
least one gramme per litre.
Albumin per se is probably never present in
urine. It is found as a mixture of albumin and
the proportion of about 10: 1. T h e molecule of
much smaller than that of globulin, and, hence is
voided in the urine.
CAUSES
I.
OF
pathological
globulin in
albumin is
more easily
ALBUMINURIA.
I N T H E KIDNEY:
A.
Primary.
1. Bright's disease:Inflammations, degenerations

and
sclerotic conditions. T h e history of the illness and the
presence of casts in the urine will reveal the true nature
of the disease.
2. Calculi:History of colic may help to arrive at the
diagnosis.
3.
Tumours of the kidney:Examine the lumbar region

for swelling, the urine for red cells and general examination for wasting and anaemia.
336
4. Renal tuberculosis:Pus is found in the urine which is

acid in reaction and often red cells are present.
5. Hydronephrosis:The swollen kidney may be felt; there
is generally a history of Dietl's crisis. Albumin is found
intermittently in the urine.
6. Pyelitis: Pyelonephritis:There
urine than albumin.
is more pus in
the
7. Polycystic kidneys:The disorder is present from an early

age. There may be high blood pressure.
8. Injury to the kidneys:There will be history of trauma.
In most of these cases X-ray of the genito-urinary
is indicated.
B.
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.
Most of the conditions listed under ureter, bladder and

urethra, cause haematuria or pyuria rather than albuminuria.
ANURIA
Anuria means suppression of urine and must be distinguished
from retention of urine in which case urine is secreted by the
kidneys but retained in the bladder. Anuria may result from
blocking of the tubules of the kidney, gross obstruction to the
urinary tract or rapid fall of blood pressure.
CAUSES:
I.
Pre-renal:
T h e anuria is non-obstructive in character. Whatever causes

rapid fall in blood pressure results in lack of urinary secretion
in the glomeruli.
II.
Renal causes:
Anuria is partly due to obstruction in the kidney tubules.

1. Nephritis. In acute nephritis anuria may occur but is
very rarely complete. It may also occur in amyloid
kidneys, tuberculosis of both the kidneys, polycystic disease and suppurative pyelonephritis. In all these condi22
338
tions there is blockage of the renal tubules with cellular

debris.
2. Tubular blocking or degeneration.
(a) Products of haemolysis, e.g. blackwater fever, incompatible blood transfusion, intravascular haemolysis.
(b) Sulphonamide therapy causing deposition of crystals
in the tubules.
(c) Compression anuria or "crush syndrome", due to
blocking of the tubules by myohaemoglobin.
(d) Poisoning by turpentine, cantharides, etc.due to
direct damage to the tubules.
III.
Post-renal:
Anuria is due to obstruction of the urinary passages.

1. Stone in the kidney or ureters.
2. Vesical carcinoma involving both the ureteral orifices.
3. Cancer uterus infiltrating both the ureters.
4. Large pelvic or abdominal tumours obstructing
ureters.
the
In obstructive anuria the symptoms may not be present for

several days. The patient passes a very small quantity of urine
of low sp. gr. containing very little urea or solids; albumin is
absent unless there is haematuria or cystitis; the patient may
complain of aching in one or both the loins. After a week or
so the patient becomes drowsy, the tongue dry, temperature subnormal, appetite poor and pupils small; twitchings, convulsions
and coma set in and the episode may last for even three weeks.
T h e commonest cause of obstructive anuria is calculous disease
and occurs at about the age of 40 years.
The sequence is very different in anuria of non-obstructive
types. The nervous system is markedly disturbed with headache, giddiness, convulsions, delirium, dyspnoea and vomiting;
the pupils are small and the episode lasts not more than a
week.
GENITO-URINARY SYSTEM
339
DYSURIA
Dysuria means difficulty in micturition.

THE COMMON
I.
CAUSES
ARE-.
LOCAL CONDITIONS OF T H E LOWER URINARY T R A C T :
1. Cystitisthere may be pain while passing urine.

2. Stone in the bladderthere may be sudden stoppage
while passing urine due to impaction of the urethral
orifice.
3. Enlarged prostatethere is hesitancy in starting the flow
which is also lacking in force.
4. Stricture of the urethrathere is difficulty in starting the
flow; the stream is thin, but forceful.
5. Phimosis, balanitis, vaginitisexamination
ternal genitalia will reveal the real cause.
II.
III.
of the ex-
MUSCULAR WEAKNESS IN OLD AGE.

DEFECTIVE INNERVATION OF T H E BLADDER.
FREQUENCY
OF
MICTURITION
Frequency of micturition must not be confused with polyuria

as the amount of urine voided may be within normal limits
in spite of frequency.
CAUSES OF FREQUENCY:
1. Irritation of the bladdercalculus, cystitis.

2. Irritation of the bladder by extrinsic pressurepregnancy, fibroids, etc.
3. Irritation caused by abnormal constituents in the urine
highly acid urine, blood or pus. Frequency is a
common symptom of pyelitis.
4. Polyuria, whatever the cause, also leads to frequency.
DECREASE IN THE FREQUENCY.
This generally occurs in conditions that cause partial or

complete retention of urine in the bladder as in:
1. Lesions of the spinal cord.
340
2. Obstructive lesions in the bladder or urethra.

3. In all conditions that causes diminution in the secretion
of urine.
GLYCOSURIA
Glycosuria ordinarily signifies presence of sugar in the urine.
T h e sugar need not necessarily be glucose. Other sugars like
laevulose, pentose, lactose and galactose are often found in the
urine and they are all grouped under Glycosuria. T h e correct
term should be Melituria.
CAUSES
A.
OF GLYCOSURIA
ENDOCRINE
DISTURBANCES.
1. Pancreatic diseasesdiabetes mellitus and pancreatic

calculi; may occur in haemochromatosis and chronic
pancreatitis; not so common in cancer of the pancreas.
2. Pituitary disordersacromegaly often terminates in
diabetic coma. Cushing's syndrome may cause glycosuria.
Both these conditions probably stimulate the nerve centres at the base of the brain and the nerve-pathways
(splanchnic nerve) cause increase in the adrenalin secretion.
3. Hyperthyroidismglycosuria is not unknown in Grave's
disease and is due to increased adrenalin formation
resulting in glycogenolysis in the liver.
4. Adrenal conditionsemotional glycosuria may occur due
to oversecretion of adrenalin; it may also occur in phaeochromocytoma.
5. Pregnancy glycosuriasugar may be present due
lowering of the renal threshold.
B.
to
R E N A L GLYCOSURIA:
T h i s condition is asymptomatic and independent of diet.

T h e threshold value for sugar is low, and the sugar tolerance
test shows a low curve. (See Fig. XXXIII.)
GENITO-URINARY
C.
SYSTEM
341
CEREBRAL CONDITIONS:
In fracture skull, cerebral haemorrhage, tumours and other

conditions that cause increased intracranial pressure, stimulation of hepatic glycogenolysis takes place via the splanchnic
nerves resulting in glycosuria.
D.
DISEASES OF T H E L I V E R :
In advanced cirrhosis or cancer of the liver, due to failure of

the storage mechanism, there may be mild glycosuria.
E.
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:
Staphylococcal infections, especially boils and carbuncles,

often cause temporary impairment of glucose tolerance and
result in glycosuria. This may be due to temporary pancreatic
insufficiency or lowering of the renal threshold.
G.
CHEMICAL A G E N T S :
1. Phlorhidzinlowers renal threshold.

2. Curare, carbon monoxideprobably damages the liver
cells.
3. Caffeine, diuretin, morphia, strychninestimulate the
nerve centres at the base of the brain and hence, the
splanchnic nerves.
4. Anaesthesia, asphyxiadue to acidosis, the Co combining power of the blood falls and sugar rises in the blood.
342
H.
CHRONIC
DEGENERATIONS:
1. Chronic nephritis and nephrosisprobably due to lowering of the renal threshold.

2. Hypertensiondue to overactivity of the sympathetic
nervous system and also renal damage.
3. Malignancymay be due to impaired carbohydrate metabolism.
HOW
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.
Consider the question of other non-glucose reducing substances.

history and clinical features are very important.
4.
Detect the exact sugar in the urine.
5.
D o glucose tolerance test.
GLUCOSE
If present, most probably the patient has diabetes.
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.
N O R M A L CURVE. Fasting-sugar is 80-100 milligrammes; reaches

peak of 180 mgm. in half an hour and comes back to the original
after two hours.
2.
D I A B E T E S MELLITUS. Fasting-sugar is 120 mgm. Reaches peak

of even 300 mgm. in half an hour and touches the original level
after more than two hours.
3.
R E N A L GLYCOSURIA. Fasting-sugar is below 80 mgm.

Reaches
peak of 160 mgm. within half an hour and drops to original in less
than two hours.
4.
A L I M E N T A R Y GLYCOSURIA. Fasting-sugar is normal. Reaches

above 180 mgm. within an hour and returns to normal a little after
two hours.
S U G A R F O U N D IN T H E
1.
PENTOSE.
URINE.
Found in the urine in the following conditions:
(a) After eating excess of grapes, prunes and cherries.

(b) As an inborn error of metabolisma condition which is hereditary, mainly occurring in Jews.
(c) In some cases of diabetes mcllitus, along with glucose.
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.
Occurs during pregnancy and lactation; hence,
physio-
3.
GALACTOSE. Often excreted in the urine after the substance is

given to test the efficiency of the liver; when present, it signifies
hepatic derangement. It is sometimes present in nursing infants
during disorders of the gastro-intestinal tract. In hyperthyroidism
this sugar may be present, probably due to acceleration of its
absorption from the intestine.
4.
LAEVULOSE (FRUCTOSE). Some persons for no apparent reason

lack tolerance for laevulose. It may be due to an inborn error of
metabolism. It is, on rare occasions, found in severe diabetes along
with glucose. T h e tolerance for laevulose is less in persons with liver
disease and, hence, may be present in hepatic impairment.
344
5.
GLUCOSE.
T h i s is found in the urine chiefly in diabetes mellitus.
The most reliable

by ozazone test and
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.
Papilloma especially, often causes haema-
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
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.
1. Blood-dyscrasiaspurpura, leukaemia, haemophilia.

2. Scurvy.
3. Malignant hypertension.
4. Congestive heart failure sometimes.
5. Acute infectionmalaria, small-pox, yellow fever.
6. Incompatible blood transfusion.
7. Essential haematuriableeding comes on suddenly without any apparent cause, or may be after exercise.
8. Vicarious menstruation.
WHILE INVESTIGATING
FOLLOWING POINTS:
A.
B.
CASE
OF
HAEMATURIA
NOTE
THE
SYMPTOMS.
1.
Age. In elderly persons suspect calculus or neoplasm; in young

adults, tuberculosis of the kidneys and acute leukaemia; in infants,
vitamin K deficiency.
2.
Distribution of pain. If at the end of the penis, the cause is in

the bladder; if there is unilateral lumbar pain with occasional
attacks of colics, suspect stone; sacral pain with haematuria suggests
malignancy of the prostate.
3.
Haematuria with frequency of micturition suggests vesical disease.
E X A M I N A T I O N OF T H E U R I N E .
1.
Colour of the urine. If smoky, it may be coming from the kidney;

if bright redfrom the bladder and below.
2.
Quantity of urine and blood. Small quantity of urine and smoky,

suggests nephritis. Large quantity of blood suggests growth. If
there are definite colics, suspect stone.
3.
Distribution of the blood in the urine during micturition. If the

terminal urine is stained red, probably it comes from the bladder;
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.
Presence of other elements in the urine. Presence of urinary

crystals suggest stone; plugs of mucustuberculosis; pus cells
pyelitis; epithelial cellscystitis; castsnephritis. Excessive albuminuria generally suggests renal disorders.
PHYSICAL E X A M I N A T I O N OF T H E
PATIENT.
1.
Carefully examine
swelling, etc.
the urinary organs,
especially
for
2.
D o P.R. examination for prostatic enlargement and P.V. for vaginal

disorders.
3.
Examine the heart, lungs, blood and liver especially.
4.
D o cystoscopy wherever indicated.
5.
D o radiological examination and pyelography.
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
3. Septicaemia and severe infections like yellow fever.

4. Toxaemias of pregnancy.
C.
Blood dyscrasiasacute haemolytic anaemia, especially of

Lederer; crisis in sickle-cell anaemia.
D.
Extensive bums, probable cause being direct damage to the

red cells by the heating of the blood.
E.
"Crush syndrome"due to presence of myohaemoglobin in

the urine.
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 :
1. Excessive drinking of water and other liquids, especially

tea, coffee and alcohol.
2. Neurosis and anxiety.
3. Hydronephrosis with periodic emptying of the renal sac.
4. During convalescence, especially after fevers.
5. During recovery from oedema.
6. Induced by diureticsdiuretin,
pituitrin, digitalis.
caffeine,
mercurials,
CAUSES OF C O N T I N U O U S P O L Y U R I A :
1. Diabetes mellitushistory of intense thirst, glycosuria

and loss of weight.
2. Chronic nephritisthe urine is of low specific gravity
and contains traces of albumin, granular and hyaline
casts; there is hypertension and left ventricular enlargement.
3. Arteriosclerosisadvanced age, moderate
and thickening of the arteries.
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:
1. Acute and sub-acute nephritis.

2. Loss of fluid as in diajrrhoea and/or vomiting.
3. Fevers.
4. Low blood pressure.
5. Congestive cardiac failure.
6. During the formation of exudates and transudates in the
body.
7. Obstruction to the urinary passages.
8. Shock.
MELANURIA
Melanuria means passing of black coloured urine. In some
cases the urine is clear on voiding and becomes dark on
standing.
CAUSES:
1. Jaundiceif very severe.

2. Haemoglobinuriathe urine may be dark; on dilution
with water the colour becomes red.
3. Haematuriathe colour is smoky rather than dark.
350
4. Porphyrinuriathe colour may be extremely dark; on

dilution with water, the colour becomes pinkish.
5. Drugsresorcin, carbolic acid.
G. Berrieseating of black cherries may give a blackish
colour to the urine.
7. Malignancyin melanotic sarcoma the colour of the
urine is dark and becomes black on standing or on addition of ferric chloride. Sometimes, the patient passes
black urine (true melanuria).
8. Alkaptonuriathe urine becomes black on standing or
on addition of alkalis.
9. Indicanuriathe patient may pass dark urine on very
rare occasions.
PYURIA
Presence of a few pus cells in the urine has little significance,
especially in a non-catheter specimen of a women.
Presence of pus in adequate quantity indicates an inflammatory lesion of the urinary tract especially cystitis, pyelitis and
pyelonephritis; while smaller amount may occur in prostatitis
and urethritis. In rare cases pus may be found in the urine
in diseases of the surrounding organs.
I.
Diseases of the urinary organs.

1. Renalpyelitis, pyelonephritis,
culosis, calculus.
renal
abscess,
tuber-
2. Uretericcalculus.
3. Vesicalcystitis, tuberculosis, calculus, tumours, bilharzia
infection.
4. Ureteralurethritis, prostatitis.
II.
Diseases outside the urinary organs.

1. Vaginitis, balanitis, phimosis.
2. Iliac, pelvic or psoas abscesses.
3. Pyosalpinx.
GENITO URINARY
SYSTEM
351
4. Cancer of the uterus, rectum, caecum, sigmoid or pelvic

colon.
5. Ulceration of the intestine, appendicular abscess, diverticulitis.
HOW
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.
The cause of uraemia in such cases is lack of adequate flow

of fluids in the kidney circulation. The renal blood flow and
glomerular filtration rate are reduced and oliguria results. The
urine thus formed is of high sp. gr. and the concentration of
352
urea in the blood gradually rises. T h e additional factors are

hypotension, which further reduces the effective glomerular
filtration pressure and to a certain extent, an increased destruction of the body proteins. T h e blood urea may rise to 50-100
mg. per 100 ml. blood, but rarely reaches a higher figure.
CAUSES:
A.
LOSS OF BODY FLUIDS.
1. Loss of blood, as in trauma, post-partum haemorrhage,

gastro-intestinal bleeding, etc. Unless the bleeding is
profuse, uraemia as a result of haemorrhage is not so
common provided there is no marked fall in the blood
pressure; however, if the haemorrhage occurs into the
stomach or intestine the absorption of amino-acids from
the blood proteins results in increased load on the
kidneys, thereby causing retention of N-products in the
blood. T h e associated dehydration and low blood pressure may lead to uraemia.
2. Loss o plasma, as occurs in extensive burns and crush
injuries. In the latter, also known as "crush syndrome",
fatal anuria and uraemia may occur when there is heavy
pressure on a mass of muscle thereby depriving it of its
blood supply fpr some time. A few hours after the pressure has been released there occurs a massive effusion of
plasma in the underlying muscle and the blood in the
circulation becomes concentrated. T h e urine becomes
high coloured with a slight albuminuria and presence of
a few hyaline casts. Within ten to twenty minutes an
ominous change may ensue. T h e urine becomes red and
smoky due to presence of myohaemoglobin. Oliguria and
anuria set in and the patient's condition rapidly deteriorates with symptoms of uraemia.
3. Loss of fluids:
(a) From the alimentary tract:
(i) Severe vomiting. In such cases there is not only
loss of fluids but also loss of chlorides and the
resultant alkalosis further contributes to the
development of uraemic symptoms.
GENITOURINARY
SYSTEM
353
(ii) Acute diarrhoea. Causes loss of salts, and the

acidosis that follows may result in uraemia.
(iii) Acute intestinal obstruction. There is lack of
absqrption of fluids from the distended part of
the intestine.
(b) From the kidneys:
(i) Diabetic comadue to acidosis.
(ii) Addison's diseasedue to loss of salts and fluids.
(c) From the skin. Excessive sweating
leading to loss of salts.
B.
(heat
stroke)
L O W BLOOD PRESSURE.
1. Shock and peripheral circulatory failureresults in lack

of adequate circulation in the kidneys.
2. Coronary thrombosisthere is also lack of adequate
circulation in the kidneys due to collapse and improper
action of the heart.
3. Repeated vaso-vagal attacksmay cause inadequate bloodflow in the kidneys.
4. Severe haemorrhage anywhere in the bodycauses fall
in the blood pressure and hence, uraemia.
5. Addison's diseasethere is disturbance of salt and water
balance in the body tissues due to excessive excretion of
sodium by the kidneys thereby upsetting the distribution
of fluids between the intra-cellular and extra-cellular
spaces in the body.
C.
ABNORMAL
METABOLISM.
1. Fevers and toxaemias. In severe febrile and toxic states

there is acceleration of protein catabolism with consequent increase in the blood urea. If such conditions are
associated with dehydration, the urea elimination is considerably reduced.
2. Acidosis. This occurs in severe diarrhoea due to loss of
salts. In those whose kidneys are damaged there are
more chances for N-products being retained in the blood.
In such cases there is invariably a rise in the H-ion con23
354
centration of the blood. Diabetes mellitus often gives

rise to acidosis and leads to pre-renal uraemia.
3. Alkalosis. This occurs when alkalis are given in large
amounts especially to anaemic persons and to those suffering from kidney disease. Severe and persistent vomiting
can also give rise to alkalosis due to loss of chlorides.
T h e p H value of the blood is almost always reduced in
such cases.
4. Acute necrosis of the liver. This condition brings about
necrosis of the renal tubules and consequently uraemia.
(Hepato-renal
syndrome.)
5. Renal necrosis. Incompatible bloocl transfusion and
"crush syndrome" cause sympathetic stimulation resulting in local vasoconstriction of the blood-vessels in the
renal cortex. This action is primarily protective to the
cortex of the kidneys and is reversible without damage,
if not prolonged. As a result of lack of proper circulation in the kidneys the urea in the blood rises.
Whatever the cause of extra-renal uraemia, the symptoms are
the same as of renal uraemia but milder in form. There is
oliguria with high sp. gr., slight albuminuria and occasional
hyaline casts. The blood urea is about 50-100 mgm. per 100 ml.
of blood, but in rare cases may reach to even 200 mgm. T h e
blood pressure is low in most cases.
II.
RENAL
URAEMIA.
T h e damage to the kidneys must be extensive to cause

uraemia, as even two-thirds of one kidney is adequate to cause
sufficient elimination of urea.
CAUSES:
1. Acute nephritis, both type I and II. T h e blood urea

in these conditions rarely exceeds 100 mgm. per 100 ml.
of blood and uraemia does not usually occur unless the
blood-urea goes up to 150 mgm.
2. Chronic nephritis. In this condition the tempo with
which renal failure progresses is dependent upon the
hypertension present. A blood urea of 100 mgm. per
GENITO URINARY
SYSTEM
355
100 ml. of blood is compatible with survival for months

or even years provided the blood pressure is not very
high; but increased retention or a concentration of over
200 mgm. usually indicates terminal stages of the disease.
3. Essential hypertension. Malignant hypertension quite
commonly gives rise to uraemia. T h e high blood pressure quickens the onset of uraemic symptoms.
4. Other renal diseases. Urea retention may occur in neoplastic or polycystic renal diseases and in pyelonephritis.
In renal uraemia, whatever the cause, the blood urea generally
rises to 150 mgm. per 100 ml. of blood, blood cholesterol to
120-300 mgm., and blood calcium falls to as low as 6 mgm. per
100 ml. of blood. T h e onset of symptoms are insidious, with
drowsiness, dyspnoea, headache, vomiting, diarrhoea, twitching
of the muscles, cramps, transient palsies, visual disturbances
and finally coma. T h e blood pressure is high and the temperature subnormal.
III.
P O S T - R E N A L URAEMIA.
This is also known as latent uraemia or "Ascoli's
syndrome".
CAUSES:
1. Obstruction to the ureters by calculi.

2. Vesical neoplasm obstructing the openings of the ureters.
3. Obstruction by an enlarged prostrate.
In this group there is anuria first followed by uraemia.
Symptoms appear several days after anuria sets in. There is
no hypertension and hence, no headache or convulsions. There
is gradual and progressive drowsiness, asthenia and wastings
with slight twitchings of the face. Vomiting and hiccups
precede death, which comes after two weeks or more.
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
COMMON FORMS OF BRIGHT'S DISEASES AND THEIR FEATURES
Urea
356
CHAPTER YII
HAEMOPOIETIC SYSTEM
INTERROGATION.
EXAMINATION OF BLOOD.
1. Blood Cells.
2.
Haemoglobin Estimation.
3.
Examination of a Smear.
4.
Reticulocyte Estimation,
5.
Haematocritic Determination.
6.
Red Cell Indices.
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.
Volume:About 9 per cent of the body weight.

Specific Gravityof the whole blood, 1055; serum, 1030; red
cells; 1080.
Viscosity:3.5 to 4.5 times in relation to water.
Reaction:Alkaline, p H value being 7.4.
HAEMOPOIETIC SYSTEM
359
Total solids:20 Gm. per 100 ml. of blood, divided as

follows:Haemoglobin, 90 per cent; proteins, 7 per cent;
salts and lipoids, about 3 per cent. Total solids in the
serum:7.5 Gm. per 100 ml. of blood.
B.
RED BLOOD CELLS.
Total5 million in males and 4.5 million in females per

c.mm. of blood. Of these about 1% are reticulocytes.
Average diameter of a red cell7.5 u.
Total haemoglobin15-16 Gm. in males and 14-15 Gm. in
females per 100 ml. of blood. This is considered as 100%
haemoglobin.
Packed cell volume (P.C.V.)45 per cent in males and 40
per cent in females.
Mean corpuscular volume (M.C.V.)90 cubic u.
Colour, Saturation and Volume index1 in males and 0.9
in females.
C.
W H I T E B L O O D CELLS.
Normal total5-9 thousand.

blood.
Average 7,500 per c.mm. of
Average diameter8.15 u.
Differential Count
Polymorphonuclear cells
Lymphocytes
Monocytes
Eosinophils
Basophils
D.
60-70%
20-30%
2-5%
1-3%
o-i%
PLATELETS.
Normal total200,000 to 400,000 per c.mm. of blood.

Average diameter2-4 u.
E.
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.
ESTIMATION OF BLOOD CORPUSCLES.
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.
Draw blood in a haemocytometer upto "0.5" mark and dilute

it with Hayem's solution upto "101" mark, thereby diluting the
blood in 1:200 dilution. After mixing well, fill the counting
chamber under a cover glass. The depth of the chamber is
1/10 mm. and the area of each small square is 1 /20 x 1/20 mm.;
therefore the volume of each small square is 1/4000 c.mm. Count
the corpuscles in 64 squares. If the count is " N " there will be
N / 6 4 cells in each square and since dimensions of each of these
tiny squares is 1/4000, in one c.mm. there will be N / 6 4 x 4 0 0 0
red cells, and as the blood was diluted 200 times, the final figure
will be N / 6 4 x 4000 x 200. A simpler method of calculating the
total red blood cells in c.mm. is to count 80 small squares and
multiply by 10,000.
B.
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
Haemoglobin was formerly recorded for clinical purposes as

percentage of "normal". It is better to report it in grammes
per 100 ml. of blood. T h e Tallquist scale may be used for
rough estimation. It should be compared to the standard chart
as soon as the initial glistening appearance of the drop of blood
HAEMOPOIETIC SYSTEM
361
4rawn on a special absorbent paper has passed. 100 per cent

Hb. represents 15 Gm. of Hb. in 100 ml. of blood.
III.
EXAMINATION OF A SMEAR
Examine the slide after staining it with Wright's stain or with

methylene blue and eosin.
A.
FOR RED CELLSfor their size, shape and

reaction.
staining
Look especially for the following:

1. Anisocytosis, i.e. change in size. T h e size of a normal
red cell is 7.5u. T h e size of a microcyte is 6M or less;
of a macrocyte, 9-12M; and of a megalocyte, 12-25M.
2. Poikilocytosis, i.e change in shape May be oval, clubshaped, sickle-shaped, spherical, etc.
3. Polychromatophilia, i.e. irregularity in staining. Punctate
basophilia is a special type of polychromatophilia commonly present in plumbism.
B.
FOR D I F F E R E N T I A L
COUNT.
Count at least 100 white cells for the purpose of differentiation.

C.
FOR PARASITES, ESPECIALLY MALARIAL.
IV.
ESTIMATION OF RETICULOCYTES.
Draw a large drop of blood in a Wright's pipette and then

draw in an equal quantity of a saturated solution of cresyl blue
in 0.85% Nacl. After incubation at body temperature for 20
minutes, make blood films and stain with Leishman's stain. A
reticulocyte under the microscope appears slightly larger than a
normal red cell and contains a delicate basophil cytoplasmic
network. The normal count is 0.5 to 1%. It is increased in
states of active regeneration of the blood as in after haemorrhage
and during the administration of specific haemopoietic remedies.
V.
A.
HAEMATOCRITIC DETERMINATION.
PACKED CELL V O L U M E .
(P.C.V.).
This means the volume in c.mm. of the red cells contained in

100 c.mm. of blood. This is obtained by centrifuging oxalated
362
blood for 30 minutes in a Wintrobe tube filled upto "100" mark

and measuring the bottom layer of packed red cells. Normally
it is 45%. In macrocytic anaemia it is 18%; in normocytic,
25%; and in microcytic, 20%.
B.
M E A N CORPUSCULAR V O L U M E .
(M.C.V.).
It means the average volume of a red cell, expressed in cubic

microns. It is calculated as follows:
Volume of packed cells per 1000 ml. of blood.
Red cell count in millions.
The normal M.C.V. is 90 CM. It is increased in macrocytosis
and decreased in microcytic anaemias.
VI.
A.
RED BLOOD CELL INDICES.
V O L U M E INDEX.
(V.I.).
This is calculated as follows:

P.C.V. found
Normal P.C.V. (45)
R.B.C. found
Normal R.B.C. (5)
Normally, the V.I. is 1. In pernicious anaemia it is more than
1 and in secondary anaemia it is below 1.
B.
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.
This is calculated as follows:

Colour index
= 1 normally.
Volume index
VII.
E S T I M A T I O N OF PLATELETS.
Place a drop of 2% solution of Na-citrate on the tip of the

finger and then prick it with a sharp needle. Pick one loop-full
of the mixture, place it on a slide and cover it with a cover
glass. Using microscope with oil immersion lens, count the red
cells and platelets in several fields and work out the proportion.
Count 1,000 red cells and the platelets in the same fields and
calculate as follows:1,000 red cells: 5,000,000 red cells: :no.
of platelets found: X. Count the number of red cells with a
haemocytometer and if there is anaemia, correct accordingly.
VIII.
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:
Wintrobe's Method: Draw 5 c.c. of citrated blood and fill

Wintrobe's tube to 10 cm. mark with a capillary pipette. Set it
vertically and read the result after one hour. Normal E.S.R. is
10 mm. or less. It is increased in all conditions where there
is tissue breakdown, or when foreign proteins enter the blood.
THE COMMON
IS INCREASED
CONDITIONS
ARE:
WHERE
THE
SEDIMENTATION
RATE
1. Infections and toxaemias.

(a) Tuberculosis. T h e E.S.R. decreases when toxaemia decreases and,
hence, is a valuable aid from the prognostic point of view.
(b) Extensive inflammation and toxaemias.
(c) Active syphilis.
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.)
(c) Infective arthritis.

(d) Gout.
7. After operations and fractures.

8. After irradiation.
9. After vaccine and protein injections.
10. Cancer.
365
11. Pregnancy and puerperium.

12. Shock.
SLOW
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 .
Method. Make a deep skin puncture on the tip of the

finger. Gently remove drops of blood that ooze out with a filter
paper every 30 seconds. Normally the bleeding stops after half
to three minutes due to formation of a thrombus by the platelets
in the blood and not due to clot formation as occurs in stationary
blood. Hence, if platelets are diminished, the bleeding time is
prolonged as occurs in purpura haemorrhagica and symptomatic
purpuras. It is normal in haemophilia, scurvy, hereditary
telangiectasis and senile purpura.
B.
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:
1. Haemophilia. It is normal in purpura, scurvy, hereditary telangiectasis and senile purpura.

2. During administration of anticoagulants.
3. Obstructive Jaundice, due to lack of vitamin K.
4. Liver destruction by chloroform, benzol or phosphorus,
due to disturbance of fibrinogen function of the liver.
366
5. Excess of CO2 in the blood.

6. X-ray and radium exposures, due to less fibrinogen and
less platelet formation.
7. Leukaemia sometimes.
It is unaltered in thrombocytopaenia.
C.
CLOT RETRACTION TIME.
This should not be confused with coagulation time as clot

retraction depends upon the platelets in the blood.
Technique: Draw* 5 c.c. of blood, transfer it in a test tube
and incubate at 37C in a vertical position. Record degree of
retraction after 1, 18, 24 and 48 hours. Normally the retraction
is complete in 24 hours. It is impaired in thrombocytopaenia
and normal in haemophilia.
XI.
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%
Juveniles (have sausage shaped nuclei)
15%
17.5%
0%
0%
Bands (have band-shaped nuclei)
12.5%
1-2%
27%
50%
Myeloblasts
Promyelocytes
Neutrophile series:
Myelocytes (have round or oval nuclei)
Segmented (have 1-5 nuclei)

Eosinophils
4%
1-3%
Basophils
1%
0-1%
Lymphocytes
Monocytes
13%
20-30%
1.5%
4-8%
0.2%
0%
Nucleated Red Cells:

Megaloblasts
Erythroblasts
2.0%
0%
Pronormoblasts
4-5%
0%
15%
0%
Normoblasts
The marrow usually shows a characteristic picture in the following conditions:

1. In pernicious anaemia there is an enormous increase in
the nucleated red cellsmegaloblastsand they may even
outnumber white cells.
2. In acute leukaemia the marrow is full of myeloblasts or
cells of lymphocytic or monocytic series even in cases
where the peripheral blood is nearly normal.
3. In chronic lymphatic leukaemia the marrow contains a
large number of lymphocytes as compared with the normal
upper limit of 15%. This is of great diagnostic value
when the white count in the blood is not much raised.
4. In aplastic anaemia the marrow contains extremely few
nucleated white cells which gives a differential count
practically identical with the blood.
5. In myelomatosis the marrow contains 10-60 per cent of
typical myeloma cells.
368
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.
80-120 mg. in 100 ml. of blood.
GLUCOSE:
NORMAL
BLOOD
369
VALVES.
Hyperglycaemia occurs in the following:

(a) Diabetes mellitus.
(b) Vomiting of pregnancy.
(c) Anaesthesia.
(d) Asphyxia.
(e) Dehydration.
(f) Increased intracranial pressure.
(g) Endocrine disturbanceshyperpituitarism,
adrenalism.
hyperthyroidism,
hyper-
Hypoglycaemia occurs in the following:

(a) Pregnancy and lactation.
(b) Starvation.
(c) Hyperinsulinism.
(d) Severe anaemias.
2.
TOTAL
CHLORIDES-.570-620
mg. in 100 ml. of blood.
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.
T h e y are the following:
(i) Non-protein nitrogen:20-40 mg. in 100 ml. of blood.

(ii) Urea:15-30 mg.
per 100 ml. of blood.
(iii) Creatinine:1-2 mg. per 100 ml. of blood.

(iv) Uric acid:2-4 mg. per 100 ml. of blood.
All these products are increased in the following:
(a) Renal diseases, especially nephritis and nephrosclerosis.
(b) Extra-renal diseasesvomiting, diarrhoea, excessive burns, Addison's
disease, etc.
24
370
All non-protein N-compounds

are increased
conditions long before urea rises.
in the
above
Decreased urea occurs in the following:

(a) Liver diseases.
(b) Low protein diet.
(c) Coeliac disease.
(d) Acromegaly.
Uric acid is increased in the following conditions:
(a) Metabolic diseasesgout, rheumatoid
arthritis.
(b) Liver diseasesacute hepatitis, liver necrosis.

(c) Renal diseasesnephrosis,
hydronephrosis.
(d) Cardiac diseasessevere congestive heart failure.

(e) Blood
dyscrasiasmyeloma,
leukaemia,
remission
of
pernicious
anaemia.
4.
PLASMA
PROTEINS:
divided as follows:
6-7.5 gm.
per
100 ml. of blood.
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.
(b) Liver diseasescirrhosis, acute yellow atrophy.

(c) Intestinal diseasesprolonged diarrhoea or vomiting.
(d) Malnutrition in general.
5.
CHOLESTEROL:
130-200 mgm.
Cholesterolaemia occurs in the following conditions:

(a) Pregnancy.
(b) Metabolic disordershypothyroidism, severe diabetes, coeliac disease,
obesity, xanthomatosis. Gaucher's disease.
(c) Cardio vascular diseaseshyperpiesia,
arteriosclerosis.
(d) Liver diseaseobstructive and hepatogenous jaundice,

to the common bile-duct.
(e) Renal conditionsnephrosis and chronic nephritis.
(f) Ether anaesthesia.
obstruction
llAEMOPOIETICSYSTEM
371
Cholesterol is decreased in the following conditions:

(a) Metabolic disordershyperthyroidism, cachexia, coronary diseases.
(b) Liver conditionsportal
cirrhosis.
(c) Blood diseasespernicious
anaemia, haemolytic
anaemias.
(d) Infectionstuberculosis of the lungs, acute pancreatitis.

(e) High intestinal
6. INORGANIC
A.
obstruction.
SALTS.
Sodium:300-350 mg. in 100 ml. of blood.

It may be increased i n : a c u t e nephritis.
It is diminished in the following conditions:
(a) Metabolic disordersAddison's disease, diabetes mellitus.
(b) Alimentary diseasesprolonged diarrhoea,
(c) Kidney conditionschronic
vomiting.
nephritis.
(d) Excessive perspiration.
B.
Potassium:15-20 mg. in 100 ml. of blood.

It is increased in the following conditions:
(a) Addison's disease.
(b) Uraemia.
(c) Hyperparathyroidism.
(d) Intestinal obstruction.
It is diminished in the following conditions:
(a) Alimentary causesconstant vomiting
steatorrhoeas, ulcerative colitis.
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.
Calcium:9-11 mg. in 100 ml. of blood.

It is increased in the following:
(a) Hyperparathyroidism.
(b) Overdosage of vitamin D.
(c) Bone tumours.
It is decreased in the following:
(a) Hypoparathyroidism.
(b) Vitamin D deficiency and osteomalacia.
372

(c) Renal diseaseschronic nephritis and renal rickets.
(d) Alimentary disorderssteatorrhoeas, obstructive jaundice.
(e) Cachexia.
D.
Phosphorus:3-4 mg. in 100 ml. of blood.

It is increased in the following conditions:
(a) Hypoparathyroidism.
(b) Overdosage of vitamin D.
(c) Bone diseasesmultiple myeloma.
(d) Kidney disordersrenal rickets, polycystic kidneys.
(e) Blood dyscrasiasmyeloid leukaemia.
(f) Liver disordersacute yellow atrophy.
It is decreased in the following:
(a) Hyperparathyroidism.
(b) Osteomalacia.
(c) Sprue, coeliac disease.
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
AB, i.e. agglutinin o
A, i.e. agglutinin b
B, i.e. agglutinin a
-)-
O, i.e. agglutinin a &
ft
-f
' + ' represents agglutination and ' _ ' no agglutination.
It will be seen from the above chart that persons belonging

to the same group can safely donate their blood to one another.
Group AB can receive blood from groups AB, A, B and O
Group A can receive blood from groups A and O
llAEMOPOIETICSYSTEM
373
Group B can receive blood from groups B and O

Group O can receive blood from group O only.
It will be noticed from this chart that persons belonging to
Group AB can receive blood from all the other groupsuniversal recipients; and those belonging to Group O can donate to
those belonging to any other groupuniversal donors.
Although the chart given above serves in a great majority of
cases, transfusion in apparently compatible blood, occasionally
gives rise to severe and even fatal reactions; hence, factors like
Rh and others will have to be considered when blood transfusion is indicated.
INDICATIONS FOR BLOOD TRANSFUSION
In general, the object of transfusion is to restore the volume
of circulating blood and of any deficient elements.
CHIEF I N D I C A T I O N S :
1. Acute haemorrhage producing shock. Loss of two pints

and over of blood can cause shock. In such cases transfusion of whole blood is indicated.
2. Traumatic shock without haemorrhage, e.g. burns and
wounds. There is peripheral circulatory failure and this
is best overcome by giving transfusion of serum, as blood
in the patient is already concentrated and transfusion of
whole blood may increase cardiac embarrassment.
3. Chronic anaemias. Give transfusion slowly because the
heart is weak. Give whole blood or even concentrated
blood.
4. Haemophilia. Give whole blood.
5. Platelet deficiencythrombocytopenia.
Give whole
blood.
6. Coal-gas poisoning. Give transfusion after venesection.
7. Preparatory to major operations.
8. Agranulocytosis.
Give whole blood.
Give whole blood.
9. Sepsis and septicaemia. In such cases reaction may be

severe after blood transfusion.
374
10. Exsanguination transfusion, i.e. withdrawal of patient's

blood and simultaneous replacement by suitable blood as
in erthyroblastosis foetalis.
R E A C T I O N S OF T R A N S F U S I O N .
(a) Simple pyrexial reactions.

(b) Allergic reactioncommon in repeated transfusions,
especially when the same donor is used. There may be
dyspnoea, cyanosis and urticarial rashes.
(c) Haemolytic reactionsoccur due to incompatibility.
There is rapid respiratory distress, cyanosis, pain in the
lumbar region and collapse.
(d) Pulmonary oedema due to overloading of the circulation
may occur when the heart is weak or in cases of severe
anaemia. Give transfusion very slowly.
(c) Delayed reactionjaundice due to haemolysis; oliguria
or anuria probably due to deposition of haematin in the
kidney tubules.
(f) Sepsisfever, rigors, vomiting, diarrhoea. These are
generally due to infection of the blood to be transfused.
(g) Air and fat embolismthe latter may occur when transfusion is given in bone injuries.
(h) Transmission of diseasesespecially syphilis.
N O T E T H E FOLLOWING WHILE PERFORMING
TRANSFUSION:
BLOOD
1. Select a donor of the age between 15 and 60 years.

2. Reject blood from syphilitics and of those who suffered
from malaria or infective hepatitis during the previous
one year.
3. The safe limit for blood removal is 50 ml. for one stone
of body-weight.
4. Always warm the slides before testing for grouping as
agglutination may occur at low temperatures.
5. One pint of whole blood will raise the haemoglobin by
about 8% and one pint of concentrated red cells by 15%.
375
6. Ten ml. of 3.8% Na-citrate solution is required for 100

ml. of blood to prevent coagulation.
7. The ratio of infusion should not be more than 40 drops
per minute and less in severe anaemias.
8. Infants have hardly any agglutinins and hence, may be
injected with blood of any group in cases of emergency.
RED BLOOD CELLS.
T h e primitive cell, proerythroblast, is a large cell with basophilic cytoplasm and with n o haemoglobin; it has a finely reticulated nucleus containing many nucleoli. From this cell, by mitosis, is derived early normoblast
which is a smaller cell with denser nucleus and basophilic cytoplasm.
Complete maturation of the normoblast is reached w h e n the cell is fully
haemoglobinised, and contains a dense and pyknotic nucleus. T h e disappearance of the nucleus results in formation of the reticulocyte which
stains with cresyl-blue and shows fine reticulum in its body. Finally the
mature erythrocyte is formed and enters into the circulation as a biconcave
disc with a remarkable uniformity in size, which is 7.4 u.
SUBSTANCE NECESSARY FOR RED BLOOD CELLS.
A.
PROTEINS.
B.
MINERALSIron; copper, manganese and cobalt in traces.
C.
VITAMINS:
1.
Vitamin B 12 and folic acid.
2.
Vitamin C.
3.
Some B-complex substances.
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.
Proteins of h i g h biological value are very important for haemoglobin

formation. If the body stores are depleted as in nutritional disorders and
pregnancy, anaemia results. Kwashiorkor is an ideal example fundamentally
due to gross protein deficiency.
B.
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
and sufficient for a woman or a growing child if it reaches to 15 mgm. T h e

average diet does contain 15 m g m . of iron. Hydrochloric acid in the
stomach, bile, and traces of copper h e l p the absorption of iron from the
intestine; so also ascorbic acid.
Copper also assists in
haemoglobin.
the
utilization
of
iron by
converting
it
into
Manganese probably acts as a catalyst.

Cobalt is necessary for the formation
is n o evidence that h u m a n anaemias
deficiency. T h e fact that Vitamin B 12
that this metal is necessary for normal
C.
of haemoglobin in animals. There

are in any way caused by cobalt
contains about 5% of cobalt, shows
nutrition of m a n as well.
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.
T h y r o x i n e is a general metabolic stimulant which increases the needs of

the tissues for oxygen and to this demand the marrow responds.
Other internal secretions like A C T H and cortisone appear to have some
relationship to the red cell formation which as yet is not clearly understood.
E.
INTRINSIC FACTOR IN T H E
STOMACH.
T h i s is very necessary for a proper mitosis of the proerythroblasts.

absence produces pernicious anaemia.
F.
Its
PIGMENTS.
Bile appears to h e l p the absorption of iron and chlorophyll,

substance accelerates the utilization of iron by the body tissues.
which
ALTERATION IN T H E APPEARANCE OF RED CELLS.

I.
ANISOCYTOSIS.
(Change in size):
1. Macrocytosis (size 9-12u)occurs in anaemia due to

deficiency of haemopoietic factor as in pernicious
anaemia; sometimes in leukaemia, myeloma, malignancy,
Hodgkin's disease,
myxoedema,
plumbism,
acute
anaemias, severe haemorrhages and erythroblastosis.
llAEMOPOIETICSYSTEM
377
2. Microcytosis (size 6u)occurs in Fe deficiency anaemia,

chlorosis, chronic bleeding, polycythaemia and anaemias
secondary to infections.
II.
POIKILOCYTOSIS.
(Change in shape):
1. Pernicious anaemia is the commonest cause; the red cells

are irregular in shape.
2. Ovalocytosis. T h e only mammalian corpuscles that are
oval in shape are those of the camel. It occurs in some
human families and inherited as a simple Mendeliandominant so that males and females are equally affected
and have equal power of transmission. Such a condition
does not cause ill-health but a small minority may manifest haemolytic phenomena.
3. Spherocytosis. Spherocytes may be seen in congenital
haemolytic icterus and in certain acute haemolytic
anaemias. T h e red blood cells are fragile.
4. Sickle-cells. In arterial blood the red cells are normal
in shape, but in venous blood some cells assume the shape
of sickles. This phenomenon arises by reason of the
abnormal type of haemoglobin (S-type) present in the cell
which readily crystallises when converted into the
reduced form. Sickle-cell anaemia is commonly present
in Negroes.
III.
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.
Extravasated blood loss.

1. External or internal bleeding.
2.
II.
B.
Haemorrhagic diseases.
Intravasated blood loss (blood destruction)haemolytic

anaemias.
D U E T O DEFECT IN T H E FORMATION
I.
OF B L O O D .
Damage to blood forming organs.

1. Disorders of the bone-marrow, liver, spleen and lymph
glands.
2. Chronic infections and sepsis.
II.
Deficient intake or defective absorption of blood forming

substancesiron, B-vitamins, folic acid, ascorbic acid,
copper and protein deficiency.
HAEMOPOIETIC SYSTEM
PATHOLOGICAL
CLASSIFICATION
OF
379
ANAEMIAS.
This classification is mainly based on the size of the red cells

present in the circulation. Accordingly, anaemias are divided
into three groups:
I.
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:
1. Deficiency of the extrinsic factornutritional anaemias,

pellagra, pregnancy anaemia, tropical anaemia.
2. Absence of intrinsic factorAddison's anaemia, cancer
stomach, total gastrectomy.
3. Failure of absorption of the anti-anaemic substance from
the intestinesteatorrhoeas, infection by D. Latus.
4. Failure of the liver to store the anti-anaemic substance
cirrhosis, cancer liver.
5. Failure of the bone-marrow to utilize the anti-anaemic
substanceuntreated megaloblastic anaemia, aplastic
anaemia.
II.
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
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,
2. Inadequate absorption of ironidiopathic hypochromic

anaemia.
3. Inadequate intake of ironstarvation, dietary deficiency,
anaemia of milk-fed children, chlorosis, etc.
4. Excessive need of ironduring growth, pregnancy, lactation.
5. Inadequate utilization of haematinicsmyxoedema,
chronic sepsis, cancer, chronic renal diseases.
I N V E S T I G A T I O N OF A CASE OF ANAEMIA.
1.
Personal history.
(a) Diet to exclude nutritional
anaemias.
(b) Intake of drugs like sulpha, etc.

(c) Occupation to exclude plumbism, etc.
2.
Family historyof Addison's anaemia, purpuras,
3.
Previous diseaseskala-azar, black-water fever, etc.
4.
History of bleedingpiles, menorrhagia, blood dyscrasias.
5.
Examine carefully for evidence of jaundice, subacute combined degeneration, Plummer-Vinson syndrome, etc.
6.
Examine in detail blood and also d o gastric analysis for achlorhydria,

stool for ankvlostome ova and sputum for T . B .
7.
Perform bone-marrow examination.
8.
X-ray the bones whenever indicated.
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 :
1. Severe vomiting, especially in toxaemic vomiting of

pregnancy.
381
2. Severe diarrhoea as in cholera, ptomaine and arsenical

poisoning.
3. Insufficient fluid intake or excessive fluid loss as in prolonged high fevers, hyperthyroidism, excessive sweating,
diabetes mellitus or insipidus.
4. Traumatic shock, when there is loss of plasma into the
tissue fluids as in extensive burns.
II.
SECONDARY
POLYCYTHAEMIA.
1. Congenital heart diseasesmorbus coeruleus.

2.
Acquired heart diseasesmitral stenosis especially.
3. Chronic pulmonary diseasesemphysema, fibroid lungs,

chronic bronchitis, bronchiectasis, silicosis and Ayerza's
disease.
4. Residence at high altitudemountain sickness.
5. Chemical substancesaniline
sulpha, phosphorus, etc.
III.
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.
T h e primitive cell which arises from the bone-marrow is the myeloblast

with basophilic non-granular cytoplasm and a nucleus with fine reticular
structure and several nucleoli. About 2% of the white cells in the bonemarrow are myeloblasts. T h e i r mitotic division leads to the formation
of myelocytes, which are the progenitors of polymorphonuclear leucocytes.
About 30% of the white cells in the bone marrow are myelocytes. T h e s e
are smaller than myeloblasts with a coarser nuclear reticulum and no
nucleoli. As they mature, myelocytes acquire granules in the cytoplasm
which, according to their staining reactions become neutophils,
eosinophils
or basophils.
As the maturation proceeds the nuclei become condensed,
later kidney-shaped (metamyelocytes)
and finally lobulated (granulocytes).
T h e older the cell the more lobes there are in its nucleus. T h e multinucleated white cells are found in a normal individual in the circulation
in the following proportion :
396 HOW TO EXAMINE A PATIENT

One-lobed, about 10%.
Two-lobed, 25-35%.
Three-lobed, 35-45%.
Four-lobed,
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 Arncth index is based on the number of nuclei present in the white

cells. In acute infections there is shift to the left i.e. there are more
immature white cells (of less nuclei in the circulation). If the sum total
of group one and two exceeds 45%, the count is said to shift to the left
and occurs in most infections. A shift to the right is f o u n d in pernicious
anaemia, sprue and vitamin deficiency anaemias due to presence of mature
white cells in the circulation, which are multi-lobed due to lack of effective
stimulation of the bone marrow resulting in leucopenia.
Metamyelocytes in small numbers and granulocytes are the only cells
found normally in the peripheral blood. T h e presence of myeloblasts or
myelocytes in the peripheral blood usually suggests myelofibrosis and may
also occur when the bone marrow is stimulated by severe pyogenic infections
or irritated by metastatic deposits.
2.
T H E L Y M P H O C Y T E SERIES.
T h e primitive cell is the lymphoblast which arises from lymph nodes.

It closely resembles the myeloblast in appearance. From the lymphoblasts
are derived large and small lymphocytes.
Lymphoblast (HasNudeott
iBrffi lymphocyte
Lymphoblastic
plasma cell
Granular
small lymphocyte
Granular
large lymphocyte
Fig.
XLI
Development of Lymphocytes.
3.
T H E MONOCYTES SERIES.
T h e primitive cell, the monoblast, is derived from the reticulum cells,

chiefly from the spleen. T h e cell resembles a myeloblast. T h e monoblasts
give rise to monocytes.
384
The primary function of the white blood cells is defence of body against
infection by phagocytosis and probably by the production of antibodies.
VARIATIONS IN WHITE BLOOD CELLS.

An absolute increase in the polymorphonuclear cells is known
as leucocytosis and of lymphocytes as lymphocytosis.
LEUKOCYTOSIS.
Normal average is 7,500 per c.mm. of blood. A count above
10,000 is considered as leucocytosis. Below 5,000 is considered
as leucopenia. In infants the normal white count is over 10,000.
CAUSES:
1. Physiological.
(a) After exercise, exposure
digestion.
to sunlight
and
during
(b) May occur during pregnancy, parturition and at the

time of menstruation.
(c) Adrenaline excess, whatever the cause.
2. Chemicals and infections:
(a) Chemicalsether, chloroform, lead, carbon monoxide.
(b) Infectionsbacterial, B. Coli and B. pyocyaneus
chiefly.
(c) Intoxicationsacute gout, uraemia, acute yellow
atrophy, diabetic coma, intestinal obstruction, cirrhosis of the liver.
3. Sudden blood losshaemorrhage or haemolysis.
4. Severe injuries, burns or after surgical operations.
5. After convulsive seizures.
6. Malignancy, especially of the alimentary tract.
7. Severe cachexia and terminal states.
8. Injection of tissues extractspentnucleotides.
9. Infarction and gangrene in any part of the body.
10. Myeloid leukaemia.
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-.
1. Starvation and malnutrition.

2. Infections like typhoid, undulant fever, influenza, dengue
fever, malaria, kala-azar and virus infections.
3. Exhaustion of the bone marrow:
(a) Aplastic anaemias, cachexia, debility and malnutrition.
(b) Poisoning of the bone marrowby sulpha, benzol,
amidopyrine, arsenic, gold, thiouracil, after exposure
to X-rays and radium.
(c) Crowding out of the haemopoietic tissue by abnormal
erythropoiesispernicious anaemia, acholuric jaundice, acute leukaemia, Banti's and Gaucher's diseases.
4. Anaphylactic shock.
5. Acute traumatic shock.
6. Haemoclasic crisis. When liver is damaged, protein food
fails to produce the normal slight increase in the leucocytes. Instead, there is leucopenia and is due to the
damaged liver allowing to pass the toxic products into
the circulation instead of being detoxicated. For this
reason a slight protein shock occurs and this causes
leucopenia. This condition is known as Widal's haemoclasic crisis.
AGRANULOCYTOSIS.
Severe drop in the white cells is of a grave omen and the
condition is known as agranulocytosis. T h e polymorphonuclear
cells are considerably diminished or even absent in the circulation. There is failure on the part of the marrow to produce
mature granulocytes. This condition occurs more often in
women than in men and is more common at and after middle
25
386
age leading to sore throat, fever, great prostration and necrotic

ulceration in the mouth. The disease is serious, and may rapidly turn fatal.
CAUSES:
1. Idiosyncrasy or sensitivity to, or poisoning by a variety of

drugs, the most important being amidopyrine, gold salts,
sulpha, organic arsenicals, thiouracil, butazolidine, chloramphenicol and certain benzol derivatives.
2. Excessive irradiation.
3. Aplastic anaemia and acute leukaemia.
4. Severe infections sometimes.
5. Idiopathic, where no discoverable cause is detected.
6. Marasmus in children.
LYMPHOCYTOSIS.
CAUSES:
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.
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:
1. Allergic diseasesbronchial asthma, eosinophilic lungs,

hay-fever, urticaria, angioneurotic oedema. The average
in such conditions is 5-20%. In eosinophilic lungs it
may even reach 80%.
2. Skin diseasesin pemphigus and dermatitis herpetiformis
it may reach 50%. In smaller quantity, eosinophilia is
found in eczema, exfoliative dermatitis, mycosis fungoides,
psoriasis and prurigo.
3. Parasitic diseasestinea, bilharzia and in ankylostome
infections eosinophilia is almost always present and may
go upto even 50%. Generally it is about 20%. It is less
constant in filariasis and ascaris.
4. Infectionsmay occur in scarlet fever and chorea and may
go upto even 10%.
5. Blood dyscrasiasleukaemia, polycythaemia, Hodgkin's
disease, pernicious anaemia and following splenectomy.
6. Diseases of unknown aetiologyperiarteritis nodosa.
388
7. After X-ray irradiation especially in ovarian growths.

8. Drugscamphor, phosphorus, copper sulphate, mercury,
arsenic.
9. Bone diseasesosteomalacia, chronic osteomyelitis, rickets,
Paget's disease, malignancy.
10. Congenital or familialseveral members of a family show
very high eosinophilia without any symptoms.
BASOPHILIA.
CAUSES:
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.
1. Poisoning of the marrow as by benzol, infection, X-ray and

radium exposures.
2. Obliteration of megakaryocytes by overgrowth of other
cells as in leukaemia, metastasis, pernicious anaemia, etc.
3. Atrophy of the bone marrowaplastic anaemia.
389
4. Failure of inhibition of platelet formation from megakaryocytesessential thrombocytopaenia.

II.
D E S T R U C T I O N BY T H E SPLEEN
Essential thrombocytopaenia, Banti's disease, Gaucher's

disease.
III.
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 :
1. Repairing damage to the endothelium.

2. Agglutination by organisms as in septicaemias.
PLATELETS
ARE
INCREASED
IN:
1. Recovery after haemorrhage.

2. Recovery after severe acute illness like pneumonia.
3. Recovery after parturition.
4. Recovery after splenectomy.
5. After severe trauma.
6. Chronic tuberculosis.
7. Hodgkin's disease.
8. Blood transfusion.
9. Myeloid leukaemia sometimes.
LYMPH GLANDS.
These may be enlarged locally or all over the body.
Causes of generalised enlargement:
A.
BLOOD DYSCRASIAS.
1. Lymphatic leukaemiaanaemia, progressive

enlarged spleen, high lymphocytosis.
weakness,
2. Hodgkin's diseaseneck glands generally involved first,

remain discrete and do not suppurate; spleen is enlarged
and anaemia is well marked.
3. Lymphosarcomainvolved glands enlarge rapidly with
fatal consequences.
4. Lymphomaa single mass of glands is invaded, commonly
in the axilla or neck and which are shotty and painless.
390
B.
INFECTIONS.
1. Glandular fevercervical glands are particularly involved

associated with fever and lymphocytosis.
2. Secondary syphilisin secondary syphilis all the glands
may be involved with coppery-red eruption over the body.
3. Bubonic plaguestarts as an acute infection involving
the glands in the groins, as the infected flea commonly
bites the legs.
4. Sarcoidosisall the glands in the body may be infiltrated
and may also affect the other tissues in the body.
LOCALIZED ENLARGEMENT OF LYMPH GLANDS.
The four important conditions that cause enlargement of the
glands locally are:
1. Syphilisthe affected glands are hard and shotty; skin
and the subcutaneous tissue around the glands are not
involved. Commonly involve the glands in the groin and
epitrochlears.
2. Tuberculosisthe enlarged glands are often matted
together and may adhere to the skin and subcutaneous
tissue.
3. Sepsisthe affected glands are tender to pressure and in
pyogenic infections may show fluctuation and may
adhere to the surrounding tissues. In chronic infections
the involved glands are firm to the feel and may not be
tender.
4. Malignancythe involved glands are stony hard to the
feel.
C H A R A C T E R I S T I C F E A T U R E S OF SOME COMMON
O F GLANDS A N D T H E I R CAUSES:
ENLARGEMENTS
(a) Occipital glandssepsis by pediculosis, scalp wounds, dermatitis, etc.

(b) Pre-auricular glandssepsis from the cheeks, ear, eye-lids
and sarcoma.
391
(c) Sub-maxillaryseptic absorption from the mouth, tonsils,

fauces (diphtheria).
(d) Cervicaltuberculosis, lymphadenoma, lymphosarcoma,
secondaries from the tongue, pharynx, larynx or
oesophagus.
(e) Supraclavicularif on the left side, suspect cancer stomach;
if on the right side, suspect intrathoracic growths. Other
causes are sepsis from the skin, neck, upper extremities,
pharynx and larynx.
(f) Axillarysepsis from the upper extremity, secondaries
from cancer breast, lymphadenoma, Hodgkin's disease,
tuberculosis (without involvement of the neck glands is
not common).
(g) Epitrochlearsyphilis, infections of the arm.
(h) Mesenterictuberculosis, ulcerative colitis, malignancy.
(i) Inguinalmay be felt normally in males, but not in
females. Often involved in sepsis, gonorrhoea, syphilis,
lymphogranuloma inguinale, secondaries from the genitals
and legs.
(j) Poplitealsepsis from the legs and feet.
CHAPTER VIII
LOCOMOTOR SYSTEM
A.
INTERROGATION.
B.
GENERAL EXAMINATION.
I.
II.
Muscles.
Bones.
1.
SkullHead and Neck.
2. Vertebral Column.
3.
Long BonesExtremities.
4.
Small BonesFingers and Toes
III.
Joints.
IV.
Gaits
394
A.
INTERROGATION.
Ordinarily a student should be in a position to assess the

amount of involvement of the Locomotor System during the
General Examination of the patient or during the examination
of the Nervous System.
However, as a matter of convenience, all disorders of the
Locomotor System, which includes muscles, bones and joints are
included in this chapter.
I.
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.
These are classified under the following three groups:

A.
D U E T O LESIORS OF T H E NERVOUS
T h e most important of these are:
SYSTEMMYELOPATHIES.
1. Progressive Muscular Atrophyoccurs at 30-40 years,

starting with wasting of the muscles of the hands with
fasciculations and later, involving the legs.
2. Amyotrophic Lateral Sclerosisinvolves the antero lateral
columns resulting in spasticity and muscular atrophy.
3. Peroneal Atrophyoccurs at about the age of 4 leading
to a symmetrical atrophy of the legs rising up to the lower
third of the thighs.
B.
D U E T O LESIONS IN T H E MUSCLESMYOPATHIES.
important of these are:
T h e most
(a) Pseudohypertrophic Paralysisa familial disease starting

in early youth, characterised by bulky calf muscles, progressive weakness, difficulty in rising while sitting (climbs
upon himself) lordosis and waddling gait.
(b) Erb's & Degerine's type of atrophy involving the muscles
of the arms in the former and face, arms and even legs
in the latter.
LOCOMOTOR SYSTEM
395
(c) Due to lesion at the myo-neural junctionMyasthenia

Gravis. This gives rise to excessive fatiguability of the
voluntary muscles, especially those innervated by the cranial nerves resulting in ptosis, diplopia, dysphagia, and a
'myasthenic smile'.
II.
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:
1. AchondroplasiaThe head appears large in contrast to

the small stature of the body. The vault of the head is
large with prominent frontal and parietal eminences.
The face is small and the nose depressed so that the
nostrils tend to point directly forwards.
2. Hydrocephalushead globular in shape, forehead overhangs and the eyes pushed down so that a part of the
sclerotic is exposed. Sutures may be wide open and there
may be bulging of the fontanelles.
3. Leontiasis Ossealarge masses of bone appears on the
skull giving rise to terrible disfigurement. The cavities
of the mouth, nose and orbit may be greatly lessened.
The eye-balls often protrude beyond the lids.
4. Microcephalusabnormally small head associated with
mental defect. The skull is roundish.
5. Mongolismthe skull is small and round, eye-slits narrow and tilted obliquely inwards and downwards towards
a broad and flat nose; eye-lashes scanty, tongue fissured,
scanty and silky hair on the scalp. (See Fig. XLII.)
6. Osteogenesis Imperfectathe head is protuberant, temporals tilting the ears outwards; so also protuberance of
the occipital and frontal regions. Sclerotics are bluish.
Bones are fragile and break frequently.
396
Fig.
Cretin
XLII
Mongol
7. Oxycephalusthe skull is short from front to back, vertex

high and pointed, forehead much increased in height
giving the appearance as if the ears are placed at a lower
level than normal.
8. Paget's Disease (Osteitis Deformans)progressive increase
in the size of the head. Face is ovoid in shape with
broader end up. The forehead becomes prominent and
is held forward. Deafness often present due to pressure
on the 8th cranial nerve.
B.
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'.
is broad, with thick eye-lids, broad and

and coarse ears, lips fissured, large coarse
coarse skin, scanty or brittle hair, stunted
(See Fig. XLII.)
(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
3. Hypogonadismabsence of hair on the face which is pale

and sallow with furrows on the forehead (eunuchoid face).
C.
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
(c) M Y O P A T H Y : Ptosis, wasting of the facial muscles

"transverse smile", inability to blow or whistle.
of
with
the
a
(d) PARALYSIS A G I T A N S : Expressionless face, staring eyes, elevated

eye-brows, absence of normal blinking, rigidity of the body.
398
Fig. XLIV
Bell's Palsy
E.
Leprosy
DEFICIENCY DISEASES.
Ricketsthe skull is somewhat enlarged, elongated and

flattened on the vertex. The anterior fontanelles remain wide
open with "hot-cross bun" appearance due to thickening of the
parietal and frontal eminences.
RETRACTION
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.
Superior longitudinal sinus thrombosis.
4.
Abscess of cerebellum (especially of vermis).
DRUGS AND TOXINS.

1.
Tetanus.
2.
Strychnine poisoning.
3.
Hydrophobia.
NEOPLASTIC.
1.
Lesions in the cerebellum.
2.
Lesions below the tentorium cerebelli.
LOCOMOTOR SYSTEM
V.
GENERAL
399
INFECTIONS.
1.
Broncho-pneumonia with asphyxia (especially in children).
2.
Laryngeal
3.
Meningism (typhoid or otitis media).
obstruction
2.
(especially in
VERTEBRAL
diphtheria).
COLUMN.
The Vertebral Column in a normal upright position has two

curvatures.one with a concavity forwards in the upper dorsal
region and the other with slight convexity forwards in the dorsolumbar region. T h e anatomical landmarks are the 7th C.V.
(vertebra prominens) in the back of the neck and the last rib
which articulates with the 12 D.V.
T h e examination of the vertebral column, just as the skull,
demands special attention. Carefully look for any abnormalities, angular deformities, local swellings and areas of tenderness
(if necessary, thump the spine at various levels and note the
maximum point of tenderness).
Ask the patient to bend forward and backward and notice
the degree of mobility and pain, if any. Also ask him to move
sideways and note if there is any limitation of movements. These
movements cannot be measured, but should be compared with
the probable normal for the patient's age.
CURVATURE
I.
OF THE
SPINE.
SCOLIOSISlateral curvatures of the spine.

CAUSES:
1.
2.
CONGENITALwedge-shaped deformity of the vertebra; present

from birth.
ACQUIRED
(a) Habitual or posturalcarrying heavy weight in one arm.
(b) Compensatoryless length in one lower limb; wry neck.
(c) Paralyticpoliomyelitis,
hereditary
ataxias,
syringomyelia,
muscular dystrophies, peripheral neuritis, neurofibromatosis.
(d) Rickets.
(e) Cicatricalscars of burns, muscle injuries, shrivelling on one
side of the chest due to emphysema or lung fibrosis.
(f)
Reflexto relieve pain in sciatica, renal diseases, etc.
(g) Functionalhysteria.
400
II.
KYPHOSISabnormal curvature of the spine with dorsal prominence.

CAUSES:
1.
ANGULAR.
(a) Pott's diseasecommonest
cause.
(b) Growths of the spine(not common).

(c) Hydatid disease(rare).
(d) Fracture of the vertebral body.
(e) Congenital wedge-shaped vertebra.
2.
DIFFUSE
KYPHOSIS.
(a) Muscular weakness

paralysis).
(muscular dystrophies,
congenital
spastic
(b) Faulty posture in adolescents or carrying heavy weights o n

the back.
(c) Rickets.
(d) Osteitis deformans.
(e) Spondylitis deformans.
(f)
III.
Osteo-arthritis.
LORDOSIScurvature of the spine with forward convexity.

CAUSES:
1.
Myopathiespseudo-hypertrophic
2.
Secondary to h i p disease.
paralysis.
3.
Congenital dislocation of the hips.
4.
Large abdominal tumours.
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
of injury, difficulty in standing erect.
(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
bilateral and the muscles are tender to pres-
common in thin women or in unduly obese people.
3.
PELVIC DISORDERSthis is the commonest cause of back p a i n i n

females; retroverted uterus is perhaps the most important cause.
4.
VISCERAL DISEASES OF T H E ABDOMENrenal stones is one of

the chief causes; as a rule there is history of renal colic.
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.
Examine the bones for alteration in shape, outline, localised

swellings, tenderness, trophic changes, evidence of fracture, etc.
Common conditions that cause alteration in shape, size or
outline of the long bones are:
ACROMEGALYthe bones are large and hands, broad and spade-like.
MYXOEDEMAthe bones are broad and hands stubby.
RICKETSthe ephiphyses are enlarged at the wrists and ankles; knockknees arid bow legs are common accompaniments.
OSTEOMALACIA ( A D U L T RICKETS)the pelvic bones and the long
bones are distorted in shape.
OSTEITIS D E F O R M A N S (PAGET S DISEASE)lower limbs are o f t e n
affected along with the face. Tibiae are particularly enlarged and the
legs may be bowed.
RAYNAUD'S DISEASEthe extremities are shrivelled and bluish.
PULMONARY-OSTEO-ARTHROPATHYthe
and feet are enlarged.
lower ends of the hands
FRAGILITAS OSSEUM (OSTEOGENESIS IMPERFECTA)the bones are

abnormally fragile and break easily resulting in gross deformity.
OSTEITIS FIBROSA (VON RECKLINGHOUSEN'S DISEASE)the bones
are decalcified w i t h cyst formation and with tendency to break or fracture
easily.
Localised Swelling of the bones may occur in the following

conditions:
(a) OSTEOMYELITIS.
(b) EPHIPHYSITIS.
(c) P E R I O S T I T I S .
(d) T U M O U R S m y e l o m a , sarcoma, secondaries.
26
402
All the local swellings of the bones produce pain and tenderness of the affected area.
4.
SMALL BONESFINGERS A N D TOES.
Look at the fingers and toes for deformities, tenderness, ulcers,

tophi, trophic disturbances, etc.
Following are the common deformities:
U L N A R D E V I A T I O N OF T H E FINGERSrheumatoid arthritis.
RADIAL D E V I A T I O N OF T H E FINGERSosteo arthritis.
C L A W - H A N D (flexion of the interphalangeal joints and extension of the
metacarpophalangeal joints of the ring and little fingers)ulnar nerve
paralysis, progressive muscular atrophy, syringomyelia.
W R I S T - D R O P (flexion at the wrist)radial nerve palsy.
" A P E - H A N D " (the thumb is in the same plane as the other fingers)
median nerve paralysis.
" A C C O U C H E R H A N D " (the tips of the fingers meet together)tetany.
" T R I D E N T H A N D " (all fingers are more or less of the same size and
diverge from one another)achondroplasia.
Following are the common nodes found on hands and fingers:
NODES O N T H E
FINGERS.
HEBERDEN'Ssmall painless bony outgrowths at the terminal phalangeal

joints. Found in osteo-arthritis.
ASCHOFF'Sfound near wrist rather than the fingers; painless.
in rheumatism.
Present
OSLER'Ssmall painful nodes felt in the p u l p of the finger-tips in cases

of subacute bacterial endocarditis.
T O P H I c o m m o n l y present in the ears, they may also be present over
the knuckles of the hands in the form of hard, painless nodes of variable
size.
III.
EXAMINATION OF JOINTS.
If joints are involved inquire into the following:

1. How the trouble startedinjury, infection, etc.
2. Duration of the illness.
3. History of similar attacks in the past.
4. Past illnesses of rheumatism, tonsillitis, gout, venereal
diseases, etc.
LOCOMOTOR SYSTEM
403
5. If pain is shifting in character.

6. Size and shape of the joints involved.
7. Progress of the disease.
Examine the affected joints by inspection and palpation for
enlargement, evidence of inflammation, irregularity and bony
outgrowths.
Next, test the joints for the range of movement by gently
moving them passively with one hand and feeling the joint with
the other. Note the range of movement and the degree of limitation and compare them with the fellow on the opposite side.
If tenderness is present, localise it as accurately as possible and
determine if it arises in the joint itself or in the neighbouring
structures.
If there is suspicion of fluid in the joint, test for its presence
by "fluctuation test" as follows:Use the two index fingers and
gently press one of them; a fluctuation sensation will be felt by
the other finger if there is fluid.
While testing for the movements, feel for grating sensation
over the jointan evidence of degenerating joint disease.
In general, the following points must be noted while examining the joints:
(a) Shape. Some joints acquire characteristic shape in certain
diseases. They may be fusiform in rheumatoid arthritis,
distorted in tabes and syringomyelia, nodular in gout and
osteo-arthritis.
(b) Mobility and tenderness. Almost all joint conditions are
painful and movements restricted, except in arthropathies
due to syringomyelia, tabes and leprosy.
(c) Joints involved. Large joints like knees, elbows, ankles
and shoulders are involved in rheumatism. Small joints
of the hands are affected in rheumatoid diseases and
osteo arthritis. Ankylosing spondylitis generally involve
the spinal joints. Gout classically affects the great toe.
Peri-arthritis and oseteo-arthritis generally involve the
shoulders. Tuberculosis chiefly affects the hip-joint and
the vertebral column.
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.
or more joints are involved which may
(e) Reiter's syndromeankle generally

urethritis and conjunctivitis.
2.
associated
with
COLLAGEN DISEASES.
Rheumatismacute
never suppurate.
3.
affected
onset, big joints involved, shifting in character,
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.
cause chronic involvement of the knees due t o
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.
Particularly inquire into the family history of skin diseases,

previous diseases of the skin, occupation to exclude sensitivity
to drugs, etc., and history of taking medicines or using local
applications.
B.
HISTORY OF T H E PRESENT ILLNESS.
Inquire into the symptoms with special reference to:

1. The mode of onsetwhether sudden, gradual, constant
or intermittent; whether localised or spreading; its course
and progress.
2. Predisposing factorssensitivity to food, handling of
drugs, etc. Substances that aggravate the disease.
C.
EXAMINATION OF T H E SKIN.
I.
INSPECTION.
Note the following:

1. Colour of the skin.
2. Eruptions.
3. Haemorrhages.
4. Ulcers, excoriations, fissures, etc.
5. Boils, carbuncles, scars, trophic changes, etc.
Colour of the Skin.
T h e colour of the skin may take a different hue in certain diseases.
PALEanaemia, aortic regurgitation due to constriction of the peripheral
arteries, fainting attack and severe nausea.
FLUSHEDpneumonia, malaria and other high fevers.
CYANOSEDcardiac and respiratory embarrasment, congenital heart
diseases, poisoning by coal-tar derivatives.
YELLOWISHjaundice, haemolytic anaemias, carotinaemia,
drugs like atebrin and picric acid.
DUSKY REDpolycythaemia, scarlet fever, erythema.
SLATY-GREYpoisoning by silver (argyria).
BROWNISHchronic arsenical poisoning.
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.
Pigmentation (melanin) of the skin.

Common causes:
(a) RACIALcharacteristic of certain races in Africa.
(b) PHYSICALexposure to sunlight, ultra-violet rays and X-rays.
(c) DEFICIENCYpellagra (mainly present in the exposed parts of the
body); kwashiorkor (skin wasted and pigmented).
(d) ENDOCRINEAddison's disease (skin and mucous membranes involved); Cushing's syndrome (orbits, nipples and legs afEected); thyrotoxicosis (orbital area mainly affected); pregnancy (localised to nipples).
(e) METABOLICochronosis (blackening of the conjunctivae along with
cartilages and ligaments); haemochromatosis (bronzed diabetes)the
skin is slate-coloured rather than black; cachexia (pigment more
marked o n the wasted parts of the body).
(f) B L O O D DISEASESpernicious anaemia (pigmentation is well-marked
in the skin and mucous membranes); moderately present in tropical
sprue, haemolytic anaemias, Hodgkin's disease and methaemoglobinuria.
(g) INFECTIONSkala-azar;
chronic
malaria;
secondary
syphilitic
lesions; tuberculosis (especially abdominal); leprosy (skin lesions may
be pigmented);
rheumatoid arthritis (involved joints may
be
pigmented).
(h) SKIN DISEASESneurofibromatosis (pigment localised); lichen planus;
chronic dermatitis; achantosis nigrans.
(i) Cancerousmelanotic sarcoma (urine
stomach (face is often darkened).
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,
E R Y T H E M A T O U S (a large area o macular rash with fading edges)

may be present in typhus, early stages of measles, skin disorders, etc.
410
PAPULAR (raised as tiny nodules)present in chicken-pox,

measles, drugsespecially bromides and sulpha.
small-pox,
PUSTULARraised as 'papular' but contain pus.

L E N T I C U L A R (a papule with a flat top)found in skin diseases.
N O D U L A R (solid projections from the skin of the size of a pea i.e. a
large papule)occur in erythema nodosum, leprosy, secondary syphilis,
tuberculoma and secondary deposits.
VESICULAR (small blisters)occur in herpes, chicken-pox,
Vesicles with umbilication is characteristic of small-pox.
erysipelas.
BULLOUS (large blisters)occur in burns, scalds, pemphigus.

WEALS (slightly elevated patches on the skin, the centre of which is
paler than the periphery)occur in urticaria.
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.

(v) N A T U R E OF T H E FLOOR.
evidence of healing. Slough is
gummatous lesions. Bone may
Fungating appearance suggests
411
If covered with granulations, it is

present in unhealing ulcers and in
form the floor in a trophic ulcer.
carcinoma.
(vi) C H A R A C T E R OF T H E EDGE. In a spreading ulcer the edge is

inflamed and oedematous. In a healing ulcer, the edge is surrounded by a bluish line. In tuberculosis, the edge is undermined.
In syphilis, it has a punched-out appearance. It is raised, everted
and hard to the feel in cancer.
(vii) DISCHARGE. In healing ulcer, the discharge is scanty and serous.
In spreading ulcer, it is purulent. In B. Pyocyaneus infection it is
offensive.
In
cancerous
conditions
the
discharge
may
be
sanguineous.
(viii) T E N D E R N E S S . Acute ulcers are tender to the feel. Tubercular,
syphilitic and neoplastic ulcers are rarely tender. Varicose ulcers
are generally tender.
(ix) S U R R O U N D I N G SKIN. Inflamed ulcers are red and oedematous;
varicose ulcers are hard and pigmented; may be normal in appearance in tuberculosis, syphilis and malignancy.
(x) LYMPH NODES. T h e y may be palpable and tender in acute and
inflamed ulcers; enlarged and slightly tender in chronic ulcers; firm
and shotty in syphilis; very hard in malignancy.
II.
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.
2. Textureif smooth or rough, thick or thin. T o test the

elasticity pinch the skin which flattens to normal when
released; when the skin is wasted the crease persists for
some time.
Thick skin is found in myxoedema, acromegaly, scleroderma and
in chronic skin diseases. T h i n skin is found in wasting diseases
and in old people. Wrinkled skin suggests old swelling now
cleared. Pinched skin suggests severe dehydration.
3. Tendernessif present, suggests inflammation.
412
4. Oedema. Press with the finger over a bone and note if

there is pitting. The places to press are tibia, behind the
maleoli or over the sacrum in those confined to bed. T h e
swelling of lymphatic obstruction does not pit on pressure.
5.
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.
This is very necessary to investigate parasitic diseases, like

scabies and pediculosis; so also in fungus infections and scaly
diseases.
D.
EXAMINATION OF T H E HAIR.
The appearance of the hair in a patient may give a clue

in the diagnosis of certain diseases. The following changes in
the appearance of the hair may be met in some diseased conditions:
FALLING OF T H E H A I R a f t e r infective fevers, especially typhoid.
PATCHY LOSS OF HAIRalopecia areata, syphilis.
T H I C K , COARSE A N D
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.
ABSENCE OF AXILLARY, PUBIC A N D FACIAL

hypogonadism and hypopituitarism.
LOSS OF EYE-BROWS O N T H E O U T E R
HAIRinfantilism,
SIDEmyxoedema.
P R E M A T U R E GREYNESSSimmond's disease, Grave's disease, worries

and anxiety.
SILKYmongolism.
E.
EXAMINATION OF T H E NAILS.
Look carefully at the nails for the following:

CLUBBING'drumstick' appearance of the fingers, nails large, broad
and curved over the tips of the fingers. Commonly present in chronic
infections of the lungs, cyanotic congenital heart diseases, chronic enteritis, cirrhosis liver, subacute bacterial endocarditis, amyloidosis and myxoedema sometimes. Such conditions are often associated with pulmonary
osteo-arthropathy.
413
KOILONYCHIAspoon-shaped deformity of the nails.

in iron deficiency anaemia.
Typically present
ONYCHIAdeformity of the nails due to fungal, tubercular or syphilitic

infection.
D I S C O L O U R A T I O N m a y occur in silver or mercurial poisoning
in Addison's and Raynaud's disease.
H A E M O R R H A G E S m a y be present under
dyscrasias and subacute bacterial endocarditis.
OPAQUE AND
IRREGULARcongenital
RIDGED A N D BRITTLEsprue,
the
nailbeds
in
and
blood
syphilis.
hypoparathyroidism.
T R O P H I C CHANGESribbing or brittleness may occur in diseases like

syringomyelia
T h e nails may even fall off in tabes and leprosy. Nails
are often blackened and striated longitudinally in median nerve paralysis.
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.
Be tactful and show genuine sympathy while handling the

children so as to gain their confidence.
HISTORY OF T H E PATIENT.
Go into the details of the following:

A.
FAMILY
HISTORY.
1. Health of both parents and of all brothers and sisters

of the patient.
2. History of abortions and still-births.
3. Health of the mother during pregnancy.
4. Obstetrical details of the labour, noting especially whether
asphyxia, birth-injury or jaundice were present during
birth.
5. The birth-weight and a general outline of the subsequent
growth in weight and height.
6. Exact details of feeding especially in young children.
7. Physical
walking.
progresswhen
crawling,
sitting,
standing,
416
8. Mental and educational progress.

9. History of important previous diseases.
10. Possibility of recent contact with infections, especially
tuberculosis.
B.
HISTORY
OF PRESENT
ILLNESS.
(a) Mode of onset.

(b) Behaviour and temperament.
(c) Appetite.
(d) Appearance.
(e) Bowel-actionfrequency and character of stools.
(f) Vomiting and colics.
C.
CLINICAL
1.
GENERAL
EXAMINATION.
EXAMINATION.
(a) Weight and height.

The weight of an infant, at birth is 7 lbs.; in 3 months it is
12 lbs.; at 5 months15 lbs. (double the birth-weight); at
6 months16 lbs.; at one year 21 lbs. (treble the birthweight); at two years28 lbs. (quadruple of birth-weight);
at six years 48 lbs.; and at 14 yearsabout 100 lbs.
A child that is gaining weight at less than the average
normal rate is equivalent to the adult who is losing weight.
The height of a full-term baby is 19-20 inches; at one year
28 inches; and thereafter a gain of
inches a year upto the
5th year and later 2 inches per year upto the 15th year.
(b) Cardiac and respiratory rates.
At birth, the pulse rate is 120-140 and respiratory rate is
35 per minute; it is 100 and 20 respectively at the age of 5.
After that, there is gradual diminution to the adult rate,
which is reached at the age of 13 or so in both and by the
13th year they reach the normal adult rate.
(c) Temperature.
Use groin for taking the temperature.
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.
Certain diseases produce a characteristic appearance of the

face. The following are the most important:
Anxiouspneumonia and infective fevers.
Oedematousnephritis.
Eruptioneruptive fevers, skin diseases.
Sunken eyesdehydration.
Photophobiameningitis.
Sunken bridge of the nose,congenital syphilis.
Frontal bossesrickets, congenital syphilis.
Wizened expressioncongenital syphilis.
Mongolismbrachycephalus, sloping palpebral apertures,
delicate skin and soft silky hair, protruding tongue, muscular hypotonicity, incurving little fingers, wide separation
between the 1st and 2nd digits of the feet.
Cretinismcoarse dry skin, firm subcutaneous tissue, scant
and dry hair, large tongue, thick lips, stunted stature, low
temperature, slow pulse and tendency to constipation.
(i) Skull.
Note the size of the skull, especially for hydrocephalus,
microcephalus, localised bulging, etc. Note the fontanelles
and sutures.
27
418
The head circumference of an infant at birth is 13 inches;

at 6th month16 inches; at 1 year18 inches; at 3 years
19 inches; at 7 years20 inches; and at 12 years21 inches.
The head of a premature born child is larger in relation
to the rest of the body than that of a full term child.
In full-term babies, the circumference of the head is slightly
greater than that of the chest until the age of 6 months,
when they are equal. Thereafter, the circumference of the
chest is greater than that of the head.
Examination of the fontanelles and sutures is an essential
part of the examination in a child. The fontanelles ordinarily close by the 18th month. In hydrocephalus, they
may be found to be bulging and the sutures abnormally
separated. Ossification of the sutures may be delayed by
rickets. A microcephalic baby will show retardation in
development.
(j) Neck.
Look for haematoma, torticollis, thyroid enlargement, cervical glands, scars and sinuses.
(k) Ears.
Otitis in children may cause a little pain and local tenderness. Examine the tympanic membrane and look for enlargement of cervical, post-auricular and preauricular
glands. Otitis often gives rise to fever in infants and even
rigidity of the neck.
(1) Limbs.
Note if they are cold and blue; see if there is oedema, joint
swelling, periostitis, deformities, purpuric haemorrhages,
spasms, rheumatic nodules, paralysis.
2.
CHEST.
Healthy infants frequently breathe irregularly from time to

time. One often notes an inverted form of respiration in which
the long pause occurs between the inspiration and expiration
while the interval between the expiration and inspiration is
comparatively short. In infants, the rate of respiration is about
35 per minute, becoming less and less as he grows and comes
419
to 18 at the age of 12. Respiration is mainly abdominal in

type.
Constant sighing respiration may indicate a serious intracranial lesion such as tuberculous meningitis. The breath
sounds on ausculation are puerile normally and should not be
mistaken for harsh or bronchial breathing.
The chest must be carefully examined for deformities, especially for "rickety rosary", "pigeon-breast" chest and for subcostal indrawingan evidence of respiratory obstruction.
3.
T H E C A R D I O VASCULAR SYSTEM.
The radial pulse may be difficult to palpate in babies. T h e

tension of the anterior fontanelles gives information comparable
to pulse volume.
At birth the heart rate is 120 per minute; thereafter, there is
gradual falling till it reaches about 75 at the age of 12. As
nervousness is a frequent cause of temporary tachycardia, the
cardiac rate in a child should be recorded during sleep whenever possible.
Sinus arrhythmia frequently occurs in normal infants.
The blood pressure results are not likely to be of value in
young children. Average normal readings are:
1 year
6 years
12 years
80/60
90/65
110/70
The younger the patient, the higher is the position of the

apex-beat and before 6 years the cardiac thrust may be normally
outside the mid-clavicular line.
Displacement of the heart by pleural effusion, pneumothorax,
lung collapse, ascites, etc. occurs more easily in children than
in adults.
The younger the child, the more "tic-tac" are the cardiac
sounds. A persistent and loud systolic murmur at the base or
to the left of the sternum is suggestive of congenital heart lesion.
A persistent apical systolic murmur, harsh in character, is sug-
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.
Upper and lower lateral incisors (4)

Upper molars (4)
Canines
9-12 months.
12-18 months.
(4) first, the upper ones
2nd molars (4)

PERMANENT
6-8 months.
18-20 months.
24-28 months.
TEETH
1st molars (4)
(32 teeth)
6 years.
Central incisors (4)
7 years.
Lateral incisors (4)
8 years.
First premolars (4)

Second premolars (4)
Canines (4)
9-10 years.
10-11 years.
12 years.
2nd molars (4)
12-13 years.
3rd molars (4)
17-25 years.
Delayed dentition is frequently due to rickets or malnutrition.

Congenital syphilis may reveal itself in the 2nd dentition
(Hutchinson teeth and Moon's molars).
The abdomen in children is relatively larger and more prominent than in adult life. Inspection and palpation are most
valuable methods of examination. Liver and spleen may be
palpable in normal infants. The younger the child, the higher
421
is the position of the urinary bladder and in a new-born baby

it is located in the abdomen, rather than in the pelvis.
Examine the stool for colour, consistency, reaction, etc.
5.
GENITO URINARY
SYSTEM.
Especially look for phimosis, vulvitis, vaginitis and ulcers.

Examine the urine for abnormal constituents.
6.
N E R V O U S SYSTEM.
Examination of the Central Nervous System is more difficult

in childhood because the patient's co-operation is lacking. Note
especially the back for deformity of the spine like kyphosis,
lordosis, spina bifida, meningocoele, etc. Proceed in the
examination of the Nervous System as in adults.
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.
Illustrate with significant quotations from patient and/or

other informant.
Facts and evidence should be stated in detail (even though
negative) rather than use technical terms and conclusions, such
as "patient has auditory hallucinations" or "memory normal".
Subjective and objective data should not be mixed up. History
and present mental state should not be mixed either. It is also
undesirable to make the greater part of the record a mere
transcript of what the patient has said. The physician's observations, summaries and conclusions should be recorded as well.
B.
FAMILY HISTORY.
This should date back to three generations.

C.
PERSONAL HISTORY.
1. Development of the patient from birth.

2.
3.
4.
Habits.
Social activities.
Career of the patient.
5.
Tantrums, convulsions, etc. during childhood.
6.
Intellectual adoptionschool reports, if truant, untruthful, etc.
7.
Sexual developmentsbad habits, menstrual history,

pregnancy, abortion.
8. General diseasessyphilis, endocrine disturbances.
9.
Previous attacks of mental disorders.
424
D.
IIOVV TO EXAMINE A PATIENT

HISTORY OF P R E S E N T
ILLNESS.
Note the date and details of first deviation from normal.

E.
E X A M I N A T I O N OF T H E P A T I E N T .
1. General behaviour. Describe as completely and accurately

as possible of what the examiner and the nurses observe in the
patient's behaviour, especially if abnormal. (The
following
points may be considered, though not exclusively.)
Does the
patient look ill? Is he in touch with his surroundings, in general, in particular? Does he look untidy, tense, violent, hostile,
irritable? Relationship to other patients, to the nurses, the
doctor who examines and treats him. How does he respond to
various requirements and situations? Does he make gestures,
grimaces, or other motor expressions such as tics and mannerisms? If so, are they constant or abrupt, spontaneous or provoked? Is he attentive, apathetic or pre-occupied? Is he
violent or depressed? Does the patient, if inactive, resist passive
movements, or maintain an attitude, or obey commands, or
indicate awareness at all? Habits of eating, sleep, bowels, cleanliness in general. Way of spending the day. If the patient
does not speak the description of his mental state may be limited
to a careful report of his behaviour.
2. Talk. T h e form of the patient's utterances rather than
their content is here considered. Does he say much or little,
talk spontaneously or only in answer, slow or fast, hesitantly
or promptly, to the point or wide of it, coherently, loosely with
interruptions, sudden silences, changes the topic, comments on
happenings and things at hand; is he using strange words or
syntax, rhymes, puns? How does the form of his talk vary with
its subject?
3. Mood. T h e patient's appearance may be described, so
far as it is indicative of his mood. His answers to "how do
you feel?" "what is your mood", "how about your spirits?", or
some similar enquiry should be recorded. Many varieties of
moods may be present, not merely happiness or sadness, but
such states as irritability, suspicion, confusion, fear of death,
suicidal tendencies, unreality, day dreams, phobias, worry, restlessness, nightmares, bewilderment, and many more which are
EXAMINATION OF PSYCHIATRIC PATIENTS
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
there is selective impairment of memory for special incidents,

periods, recent or remote happenings. Tell the patient simple
stories and ask him to repeat them in his own words. Give
him digits to repeat and record how many he can repeat immediately after.
9. Insight and judgement. What is the patient's attitude
to his present state? Does he regard it as an illness and needing
treatment? Is he aware of mistakes made spontaneously, or in
response to tests? How does he regard them and other details
of his conditions? Does he recognise and acknowledge any
special incapacity he may have? Does he exaggerate or minimise its importance? What is his attitude to recovery? How
does he regard previous experiences, psychological symptoms, etc.
that are relevant? What is his attitude towards social, financial,
domestic and ethical problems? Is his judgement good? What
does he propose to do when he has left the hospital?
Examination of a psychiatric patient is extensive, if

not exhaustive and the above scheme is only a concise
one for the guidance of a student.
Appendices
Retards growth.
(c) B(;Pyridoxine.
(d) B4 and B5.
Yeast, kidney, wheat-bran.
Yeast, liver, cereals.
Not yet identified.
(c) B 3 Pantothenic acid.
2 mgm.
5 mgm.
Seborrhoeic dermatitis. Controls pregnancy vomiting.
"Burning feet" syndrome, premature greying of the hair.
1 to 2 mgm. Cheilosis, angular stomatitis,

glossitis (magenta tongue).
Beri beri.
Anorexia, constipation.
4 to 5,000 units.
(b) BoRiboflavin. Eggs, milk, liver, yeast.
2 to 3 mgm.
(a) BiThiamine. Yeast, rice polishings, pulses.
Meat, yeast, legumes.
Milk, liver, eggs.
(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
COMMON VITAMINS, THEIR SOURCES AND DEFICIENCY DISORDERS
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. PRutin. Tobacco leaves, citrus fruits. 2 mgm.
Green vegetables, alfalfa,

egg-yolk.
Vit. KNaphtoquinone.
! 3UU
..
f
j
J
unlts
1 to 3 meg.
5 mgm.
"]
Rickets, osteomalacia.
Teeth decay.
Scurvy.
Hypoprothrombinaemia.
Megaloblastic anaemia, subacuti

combined degeneration.
Sterility. Habitual abortion in

laboratory animals.
"
Megaloblastic anaemia, sprue.
Pellagra.
Dry and scaly skin. Retards

growth.
Capillary bleeding.
50 mgm.
Streptomyces Griseus, liver.
Vit. B12Cyanocobalamin.
Synthesized to D2 in the skin

when exposed to U-V rays.
(c) D3Ergosterol.
Germinating seeds, wheat
germ oil.
Fish-liver oil, milk, eggs.
(b) D2Calciferol.
V i l . ETocopherol.
Fish-liver oil, milk, eggs.
50 mgm.
1 to 2 mgm.
1 to 3 mgm.
10 mgm.
(a) DiDehydrocholesterol.
Vit. D.
Citrus fruits.
Eggs, yeast, meat, legumes.
Green vegetables, eggs.
Vit. CAscorbic acid.
(h) Biotin.
(g) Folic acid.
(f) B,Nicotinic acid. All flesh foods, yeast.
APPENDIX A
429
I.
A.
Stimulates thyroid.
Parathyroid influencing.
CHO influencingdiabetogenie.
Lipid influencingketogenic
6.
7.
8.
In females, helps to develop corpus luteuir
Controls fat metabolism.
Helps carbohydrate metabolism,
Stimulates parathormone.
In females, induces mammary secretion.
In males, no known action.
Lactogenicprolactin.
5.
(b) Luteinizing hormone. In males, helps to produce testosterone.
EXAMINE
In females, helps maturation of Graffian

follicles.
In males, helps spermatogenesis,
Gonad influencing:
(a) Follicle stimulating.
4.
Thyrotrophic hormone.
Stimulates adrenal cortex.
Stimulates tissue growth,
TO
(b) chromophil cells, which are

active. These consist of two
groups acidophils, producing
growth hormones and basophils, producing the rest.
Growth hormone.
ACTHcorticotrophic.
1.
Chief action.
HOW
(a) chromophobe cells, which are

inactive.
3.
2.
Important hormones.
Common Hormones, Their Source and Actions
Anterior Pituitary consists of two

types of cells:
Pituitary.
Glands.
I.
ENDOCRINE SYSTEM
APPENDIX B
4 3 0
PATIENT
Gonads.
VI.
Blood pressure influencing

(pitressin).
3.
Progesterone.
(b) Corpus lutcum.
Prepares uterus for implantation of

fertilized ovum.
Develops female secondary sex characteristics

and regulates menstrual cycle.
Develops male secondary sex characteristics.
1. 2.Corticosteroids.
Controls metabolismStimulates
of water and
salts.
Adrenalin; nor-adrenalin.
nerve-endings;
constricts
capillaries.
Controls blood sugar level.
Oestrogens.
Testosterone.
Helps metabolism.
Controls Ca and P metabolism.
Insulin.
Parathormone.
Thyroxine.
animals.
Regulates blood pressure,
Helps water reabsorption from the tubules

of the kidneys.
Stimulates contraction of gravid uterus and

secretes milk.
No known action in human beings.
Vasopressin (antidiuretin).
2.
Oxytocin (pitocin).
Pigment influencing in lower
1.
(a) Ovarian secretion.
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-
Cushing's syndrome"mooning" of the face,

plethora, hypertension, adiposity.
Simmond's diseaseanorexia, cachexia, loss
of axillary and pubic hair, genital atrophy.
Hypersecretion of the basophil cells.

Hyposecretion of the basophil cells.
(d) Progeriadwarfism, premature greyness

of the hair, wrinkled and wizened face.
(c) Lawrence-Moon-Biedl
hypogonadism, mental
tinitis pigmentosa.
(b) Frohlich'sobesity, sexual infantalism,

may be of stunted growth.
(a) Lorain typedwarfism, sexual infantalism, mentally normal, look young for
their age.
Hyposecretion of the acidophil cells. The common syndromes are:
(b) Acromegaly in 3rd decadeenlarged face

and spade-like hands.
Hypersecretion of the acidophil cells. (a) Gigantism in young adults before

epiphyses have united.
Headache due to increased intracranial

pressure; bi temporal hemianopia; papilledema, obesity, polyuria.
Common Endocrine Dysfunctions
Adenoma of the gland due to excessive

formation of the chromophobe cells.
II.
432
K>
CC
Thyroid
Parathyroids
III.
Posterior Pituitary
II.
B.
achlor-
Hyposecretion.
Hypersecretion.
Osteitis
(a) Cretinism in youngcoarse

skin, large tongue.
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.
(b) Myxoedema in oldpuffy face, coarse

skin, hoarse voice, anaemia, low B.M.R.
face, dry
(a) Grave's diseaselarge eyes, large throat,

large
heart,
tremors,
tachycardia,
anxiety, high B.M.R. Common in the
age group of 20 and 30 years.
(b) Toxic goitretachycardia and increase
in the B.M.R. are the prominent
features. Eyes and the gland may not
be prominent. Common after the age
of 50.
hydria.
macrocytic anaemia,
Diabetes insipiduspolyuria, loss of weight.
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
No known clinical syndrome.
high blood pressure, giddiness and sweating.
Phaeochromocytomaparoxysmal attacks of
diseaseasthenia, pigmentation,
hypotension.
Hypoglycaemiagiddiness, sweating, palpitation and syncope. Blood-sugar falls below

50 mgm. per cent during the attack.
Diabetes mellituspolyuria, increased appetite, thirst, loss of weight. Blood-sugar is
high.
Addison's
(ii) Acquiredtendency to change of

sex in females (virilism). Males may
show evidence of feminization.
(i) Congenitalpseudohermaphroditism
in females and pubertas praecox in
males.
(c) Adrenogenital syndrome.
(b) Cushing's syndromeobesity, asthenia,

osteoporosis, hypertension, loss of libido.
(a) Conn's syndromehypokalemia, polyuria, hypertension, asthenia, muscular

weakness.
434
Hydatid disease.
Tapeworm (D. Latus).
Undulant fever (Malta fever).
Plague.
Enteric. Dysentery. Cholera.
Typhus. Relapsing fever. Trench fever.
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
Relapsing fever. Typhus.
Kala-azar. Sand-fly fever.
Malaria. I'ilaiia. Yellow fever. Dengue.
plague.
Trichiniasis, T. Solium.
(abortus).
Encephalitis.
Glanders.
II. Insect Vectors
Sheep.
Rodents.
Pigs.
Mice.
Cat-scratch fever.
Cats.
Horses.
Ornithosis. Psittacosis.
Birds.
I. Animal Reservoirs in Important Diseases
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
Macular, papular, vesicular,

rarely pustular.
4th to 5th day.
2nd week.
3rd day.
Punctate & erythematous.
Small-pox.
2nd day.
Macular.
EXAMINE
2 to 4 days.
1st day.
Rubella (German measles). 14 to 19 days.
^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.
Features of the rash
Initial1st day.
Punctate.
Appearance of rash
2 to 6 days.
Terminal4th day.
Incubation period.
Denoue
"
Disease
III. Eruptive Fevers
436
PATIENT
f.
Ova.
Remarks.
of
the
anus
Ova, thin shelled and
contain
coiled embryos.
Wide spread.
l/8"-l/4" long. Head

pointed
with 4
suckers. Double row
of hooklets; has 4
segments.
16-25 ft. long. Head
club-shaped, no hooklets, no suckers, 3000
segments.
T. Kcchinococcus.
T. Lata (D. Latus).
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.
Ova brown, barrelshaped with terminal

knobs.
Hydatid cyst.
No symptoms.
Over 1" long.
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.
About 3/4 cm. long.

Itching
and genitals.
Anaemia, eosinophiTransparent with 2-8

Widely spread in soil,
lia.
stages of segmentanear fresh water.
tion.
Trichuris trichuria,
(whipworm).
Strongyloides
stercoralis.
Clinical features.
Common Pathogenic Infestations
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.
About 1 cm. long.
Round.
Oxyuris vermicularis
(thread worms).
Ankylostoma
duodenale.
Ascaris.
Feature of the worm.
Intestinal worms.
Name.
IV.
in
APPENDIX
C
4 3 7
Clinical features.
7-10
Trich. Spiralis.
Size 1-2 ml.
S. Haematobium. 10-20 mm. long.
Size 40-80 cm.
Ova with a terminal

spine.
mediate host.
Larvae ejaculated
from ulcer.
Snail is the inter-
Animal host is
cyclops.
Gastric and intestinal

Embryos may be Rats are the animal
symptoms,
myositis
found in the blood.
hosts,
due to migration of
embryos.
Haematuria, eosinophilia.
Urticaria, ulcer,
cellulitis.
swellEmbryos found in the

Animal host is anopings,
eosinophilia,
blood at night. heles mosquito,
lymphangitis.
ft. long. Head

Digestive and nervous
Ova nearly spherical
Pig the intermediate
has 4 suckers and
disorders, cysticercosis
containing segments.
host. Man can act as
hooklets;
segments
from embryos.
intermediate
host
about 800.
leading to cysticercosis.
Resemblefinecatgut;
Fever, painful
75-100 mm. long.
Guinea worm.
Remarks.
Ova oval, contain

Cattle, the intersegments. mediate host,
Ova.
14-24 ft. long. Head

Digestive and nervous
has 4 suckers,
no
disorders.
hooklets;
segments
over 1000.
Feature of the worm.
Blood infestation.
l'ilaria.
If.
T. Solium.
T. Saginata.
Name.
438
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
Auscultation of the chest, 33

of the heart, 73
Austin-Flint murmur, 118
Ayerza's disease, 53
Babinski's sign, 248
Bacillary dysentery, 190
Backache, 400
Basal ganglia, 307
Basophilia, 388
Bell-sound, 32
Bell's palsy, 232, 397
Benedict's test for urine, 324
Benzidine test for blood, 325
Beri-beri, 428
Biceps reflex, 249
Bickele's sign, 255
Bigeminus, pulse, 84
Bile acids, test, 325
Bile pigments, test, 325
Bilirubin in blood, 195
Bisferiens, pulse, 84
Bladder urinary, 318
Bleeding time, 365
Blood analysis, 358
Blood chemistry, 368
calcium, 371
chlorides, 369
cholesterol, 370
creatinine, 360
N-compounds, 369
phosphorus, 372
plasma proteins, 370
potassium, 371
sodium, 371
sugar, 369
urea, 369
uric acid, 369
Blood pressure, 86
high, 88
low, 92
Blood transfusion, 373
Blood in urine, 325
Body configuration, 6
Bone marrow examination, 366
Brain, anatomy, 256
Brain-stem, 257
Breath, smell, 135
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
Haematemesis, 180, 130

Haematoma, 410
Haematuria, 344, 316
Haemic murmurs, 124
Haemoglobin estimation,
Haemoglobinuria, 347
Incompetence, aortic, 120

mitral, 116
pulmonary, 122
Incontinence, urine, 317
Indican, test, 325
Indigestion, 129
Infectious diseases, 435
Insect vectors, 435
Intestinal obstruction, 191
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
Jacksonian Epilepsy, 269

Jaw jerk, 249
Joints, examination, 402
Jaundice, 195, 131
Kernig's sign, 254
Kidneys, 146, 318
efficiency tests, 329
enlargement, 330
Knee jerk, 250
Koilonychia, 413
Kussmaul's breathing, 23
Kyphosis, 400
Lange's test, 264
Laryngeal obstruction, 54
Larynx, 20
Lawrence-Moon-Biedl syndrome. 432
Leontiasis ossio, 395
Leprosy, 397
Leucocytes, 381
Leucocytosis, 384
Leucopenia, 385
Leukaemia, 384
Lips, 9, 133
Litten's diaphragmatic sign, 26
Liver, 192, 144
cirrhosis, 194
enlargement, 193
Lordosis, 400
Low blood pressure, 92
L u n g resonance, 32
Lungs, surface marking, 18
Luttenbacher's disease, 113
444
Lymph glands, 389

Lymphocytes, 383
Lymphocytosis, 386
Macrocytic anaemia, 379
Macrocytosis, 379
Malignant sclerotic kidneys, 356
Mass reflex, 254
Mean corpuscular volume, 362
Melaena, 191
Melanuria, 349
Meniere's syndrome, 234
Menigitic curve, 265
Microcephalus, 395
Microcytic anaemia, 380
Micturition, abnormal, 317, 332
frequency, 339, 317
reflex, 254
Mid-brain, 257
Millard's syndrome, 296
Mitral murmurs, 116
regurgitation, 116
stenosis, 118
Mongolism, 395
Monocytes, 383
Monocytosis, 387
Monoplegia, 290
Moon's molars, 133
Motor function tests, 239
Motor tracts, 289
Mouth, examination, 132
Movements, ocular, 219
Mucous membranes, examination, 10
Murmurs, cardiac, 115
aortic, 119
Austin-Flint, 119
congenital, 118
diastolic, 118, 120, 122
endocardial, 116
exocardial, 124
functional, 115
Graham-Steel, 122
haemic, 124
machinery, 123
mitral, 116
myocardial, 124
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
Packed cell volume, 361

Paget's disease, 396
Pain, abdominal, 168, 128
in children, 173
colicky, 172
in the chest, 45, 17
neuralgic, 313, 208
praecordial, 94, 62
peritoneal, 169
visceral, 169
Painful micturition, 317
Palate, examination, 135
Palpitation, 69, 63
Pancreas, 434
Pansystolic murmur, 116
Papilloedema, 218
Progeria, 432
Paralysis, 290, 208
agitans, 397
Degerine's, 394
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
Potassium in blood, 371

Pott's disease, 299, 310
Praecordial pain, 94, 62
Presystolic murmur, 118
Progressive muscular atrophy, 394
Proteins in blood, 370
Prothrombin deficiency, 366
time, 366
Pseudohypertrophic paralysis, 394
Psychiatric examination, 423
Psychogenic epilepsy, 269
Ptosis of eye-lids, 220
Puerile breathing, 34
Pulmonary murmurs, 121
Pulmonary stenosis, 113
Pulsation, epigastric, 66
neck, 66
praecordial, 65
thoracic, 66
Pulse, 80
abnormal, 82
alternans, 84
anacrotic, 84
bigeminus, 84
bisferiens, 83
bounding, 83
collapsing, 83
Corrigan's, 83
dicrotic, 84
irregular, 84
paradoxus, 84, 85
thready, 83
Punctate basophilia, 377
Pupillary reactions, 226
Pupils, 224
unequal, 226
Purine bodies, in urine, 323
Purpura, 389
Pus in urine, test, 326
Pyuria, 350
Queckenstedt's phenomena, 263
Rachitic chest, 24
Rales in the chest, 35
Reaction of urine, 321
Rectal examination, 147, 318
Red blood cells, 375, 359

cell estimation, 360
cell formation, 375
Reeling gait, 285
Reflexes, 246
abdominal, 246
ankle, 251
biceps, 249
cilio-spinal, 246
conjunctival, 227
corneal, 227
cremasteric, 246
defaecation, 254
deglutition, 254
grasp, 255
hepato-jugular, 67
jaw, 249
knee, 250
mass, 254
micturition, 253
organic, 253
plantar, 246
pupillary, 226
supinator, 249
tonic, 254
triceps, 249
Regurgitation, aortic, 120
mitral, 116
pulmonary, 122
Rales in the chest, 35
Renal asthma, 56, 58
efficiency tests, 329
Resonance, lung, 32
skodaic, 32
tympanitic, 32
Respiration, rate, 22
rhythm, 22
Retraction of the head, 398
Reticulocyte estimation, 361
Rhythm, gallop, 75
tic-tac, 77
triple, 77
Rhonchi, 35
sibilant, 35
sonorous, 36
Rickets, 398
Riedl's lobe, 194
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
Stenosis, aortic, 119

mitral, 118
pulmonary, 121
Stomach, 144
ulcers, 157
Subacute combined degeneration,
299
Subarachnoid haemorrhage, 297
Sugar in blood, 369
in urine, 340
Sugar, test for 323
Sulphates in urine, 322
Supinator jerk, 249
Suprarenals, 434
Surface marking of the heart, 64
of the lungs, 18
Swelling of the abdomen, 160
Sympathetic nerves, 238
Syncope, 100, 63
Syndrome, Adie's, 227
Benedickt's, 295
Brown-Sequard's, 296
Conn's, 434
Cushing's, 434
Foster-Kennedy's, 218.
Foville's, 296
Frohlich's, 432
Froin's, 264
Horner's, 225, 226
Lawrence-Moon-Biedl, 432
Millard-Gubler, 296
Pancost's, 225
Weber's, 294
Syphilis, congenital, 397
Syringomyelia, 306
Systolic murmurs, 116
T a b e s dorsalis, 397
Tachycardia, 99
paroxysmal, 99
T e e t h , 420, 133
fluorosis, 133
Hutchinson's, 133
Moon's molars, 133
Temperature, 11
Tetralogy of Fallot, 113
Thalamic syndrome, 308
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
Urea concentration test, 330

in urine, 322
Uric acid in urine, 322
Urinary bladder, 318
casts, 328
crystals, 328
Urine analysis, 319
Urobilin test, 326
Vagus nerve, 235
Valvular diseases, heart, 115
Vascular diseases, brain, 296, 297
murmurs, 124
Ventricular septal defects, 113
Venous congestion, 63, 102
Venous h u m , 125
Vertebral column, 399
Vertigo, 233, 208
Vesicular breathing, 34
Vestibular nerve, 233
Visual defects, 214, 215
Vitamins, 428
Volume index of blood, 362
Vomiting, 178, 129
in children, 180
Waddling gait, 287
Water-brash, 132
Water concentration test, 330
W a x y casts, 328
Weber's syndrome, 294
test, 233
W h i t e blood cells, 381, 358
W h i t e cells, estimation, 360
Xanthochromia,
263
Ziehl-Neelsen's stain, 40
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PREFACE TO THE SECOND EDITION

PREFACE TO THE SECOND EDITION

PREFACE TO THE SECOND EDITION

Examination of the Mouth and Throat

ness 209; Tremors 209; Unconsciousness 209; Diplopia

Albuminuria 335; Anuria 337; Dysuria 339; Frequency

Appendix A: Vitamins and their Deficiencies

Endocrine Glands and their Dysfunctions 430

VI. FAMILY HISTORY.

1. Briefly list presenting complaints and their duration.

Give chronological story of the illness, beginning with the

3. Factors modifying the symptomsfood, deep breathing,

If the diagnosis of the previous diseases is not clear, describe

HOW TO EXAMINE A PATIENT

2. Occupation: Nature of work and its surroundings. If

If disturbed, its cause.

(f) Bowels and micturition; their frequency during day

1. Of parents, brothers, sisters and childrentheir state of

CONSCIOUSNESS AND INTELLIGENCE

Note the degree of co-operation; promptness or delay in

Many nervous patients, particularly those suffering from Grave's disease,

The posture a patient adopts, especially when lying in bed,

In pleural effusion and pneumonia, patients prefer to lie o n the same

In severe respiratory or cardiac embarrassment the patient finds some

VOICE AND SPEECH

T h e character of the voice is often

helpful in arriving at the

HOW TO EXAMINE A PATIENT

voice is husky and in laryngeal paralysis, it is feeble. (For

GENERAL DEVELOPMENT AND N U T R I T I O N

Under this heading the following are to be considered:

Height and Weight.

Examination of the Head, Neck and Face.

Configuration of the Skull and Face.

Examination of the Skin, Hair and Nails.

Examination of the Lymph Glands.

Examination of the Genitalia and Breasts.

Examination of Joints and Extremities.

Note the posture and attitude of the patient, especially the

3. Height and Weight

If the patient is under-nourished, find out if it is

Rapid or gradual in onset.

If the stature of a patient is far above or below limits, he may be classified

4. Examination of Head, Neck and Face

HOW TO EXAMINE A PATIENT

PUFFYrenal disease, anaemia, myxoedema.

Examination of the eyes also includes examination of the

EYE-BROWSif fallen or scantythyroid disorders.

T h e complexion of a patient is mainly dependent upon the

FLUSHEDhectic fever, mitral stenosis.

The appearance of the lips may be of some importance to

(e) DRYtoxaemia, h i g h fever.

(j) FISSUREDangular cheilitis, riboflavin deficiency.

and myxoedema; large and

HOW TO EXAMINE A PATIENT

Carefully examine the ears including the meatus and the

Examine the following:

for perforation as occurs in

(e) GUMSfor bleeding,