MEDICINE

Clinical Manual Notes

(2010 Batch MIMS)

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Contents

History taking and analysis of symptoms...........................1

General physical examination........................................... 5
The cardiovascular system.................................................12
The respiratory system.......................................................28
The abdomen.....................................................................40
The central nervous system................................................50
Anemia...............................................................................68

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HISTORY TAKING AND ANALYSIS OF SYMPTOMS

History is a record of the medical events that have already taken place in the patient's life. History taking
involves the elicitation of an accurate account of the patient, enquiry recording the past problems, family
background, description of the socio-economic background and past habits and practices.
The importance of a good history lies in the fact that it provides an insight into the exact nature of the
patients problems and the attitude of the patient towards the illness. it often provides valuable clues that
ultimately help in diagnosing the condition, rule out certain possibilities and help the examiner to focus
attention on the particular system/systems involved.
Art of good history-taking can only be learnt by practice and the following pages provide general
guidelines regarding the approach to history taking.
The examiner should first allow the patient to state the nature of his complaints and narrate his problems
in his own language. Listening to the patient's account helps not only in establishing a rapport but also helps
the examiner for further enquiries into the history. After the initial description of his/her complaints, the
examiner should clarify certain terms or phrases not clearly understood and may himself put some questions
to the patient to bring out more information which might have been inadvertently omitted by the patient.
Leading questions in such circumstances must be avoided as far as possible. However, in certain situations,
leading questions may become necessary. All the facts presented by the patient must be verified carefully
by cross-questioning before actually recording them. The recording or documentation of the history should
not be disjointed but should be in a lucid and logical sequence. It must be emphasized at this juncture that it
is as important to elicit and record the negative history (that a symptom was not present) as to record that it
is as that it was present. This should be done towards the end of the history after exclusion of irrelevant
aspects in the patient's account of his symptoms.
In case the patient is unable to speak, is unconscious, is in shock, or is a child, the history should be
taken from the nearest relative/friend who is known as the informant.
The examiners approach should be gentle, sympathetic and caring, which makes his/her task easier,
Findings in the history should be recorded under the following headings:A. PARTICULARS OF THE PATIENT or PRELIMINARY DATA:
Name: Importance of name is for 1) Identification 2) Communication purpose 3) Maintenance of records 4)
Medico legal importance.
Age: Its importance lies in the fact that it provides a means to classify the patient to a particular group keeping
in mind the common illnesses of that particular group and also for medico-legal purposes.
Sex: It is important because certain diseases are more commonly seen in people of a particular sex.
Address: Provides information on the geographical location. This is important because certain diseases are
present endemically in certain areas. Also address may be necessary for maintenance of records and followup.
Occupation: It provides a clue as to whether the present ailment is related to his occupation. It also helps in
rehabilitation of the patient after treatment.
Socio-economic status: Social background and religion provide vital clues regarding the prevalent customs
and practices and their relevance to the patent's problems.
Particulars of the date of admission and date of examination: It helps in assessment of the progress of
the patient's condition, suggesting an improvement or worsening.

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B. PRESENTING COMPLAINTS:

Presenting complaint is the complaint for which the patient has come to the doctor.
Define and record the main complaints and the duration of the presence of the complaints.
Complaints should be recorded in a chronological order, i.e., the earliest complaint being recorded first.
At this stage it must be emphasized that the examiner should not elaborate on the nature of the complaint or
record any associated symptoms as these come under the domain of the next section of the history.
It is also important to record only the main complaints. The examiner has to use his/her discretion and ignore
vague complaints or less important complaints which can be included in the detailed history of the symptoms
Furthermore, complaints should always be recorded in such a way as to include expressions used by the patient
himself rather than medical terms.
Duration of the complaints may be recorded in days, week, months or years. As far as possible the same mode
of description (e.g. days) should be used for all the complaints.

C. HISTORY OF PRESENT ILLNESS:

This involves the recording of the details of each complaint separately. The chief complaints, which are the
presenting symptoms, are analyzed threadbare, studying them carefully and recording:

The mode of onset (whether sudden or gradual )

The duration (in days,weeks,months or years)

Location or site (example: pain in angina is typically retrosternal)

Severity (enquire whether the symptoms interferes with his activities or disturbs his sleep)

Character (e.g. character of pain whether aching,stabing,throbbing etc) allow the patient to describe the
character of his symptoms particularly if it is pain, in his own word

Diurnal variation (enquire at what time of the day the symptom is present or more severe. Eg cough in chronic
bronchitis is more severe in early mornings)

Aggravating and relieving factors (certain may contribute to or bring on a symptom or make it worse-these are
called aggravating factor. e.g. pain in angina is aggravated by exertion. Also some measures/factors bring about
relief from the symptoms-these are known as relieving factors.eg pain in gastric ulcer is relieved by vomiting.)
Progression (symptoms may remain of same severity or may progress over days, months, years.progression is only
made out in chronic debilitating illnesses)

Exacerbation or remission (there may be periods of time where symptoms are absent or there is a temporary
relief (remissions) or there may be exaggeration of the nature of the symptoms(exacerbations).such
exacerbations and remissions may be diurnal,seasonal,annual etc)
Associated or related symptoms either recorded in the presenting complaints or not volunteered by the patient
should then be analyzed as described above and recorded.
It is important to remember during the analysis of symptoms that the symptoms thus far studied provide
valuable clues regarding the probable system effected. Attention should then be focused on that particular symptom
and careful review of all the symptoms related to that symptom should be done in a meticulous manner. At the end of
such a careful analysis may be possible to relate such symptoms to the chief complaints.
Negative history as to the absence of symptoms considered relevant should be recorded
As stated earlier the history of present illness should be recorded in patients own description avoiding medical
terminologies, after proper verification and exercising his/her discretion regarding the importance of the narrated
symptoms.
Leading questions (questions that themselves suggest the answers) should be avoided as far as possible.
Treatment history, which involves the description of the nature of the treatment taken by the patient for his
complaints previously, should be elicited and recorded. it may also indicate if any of the symptoms are actually
adverse reactions of the drugs taken for the treatment

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D.HISTORY OF PREVIOUS LLLNESS or PAST HISTORY:

This involves review of all the illnesses from infancy. It includes:

All past illnesses with particular references to the presence/absence of important diseases like diabetes
mellitus, hypertension, bronchial rheumatic fever etc.
Enquiry into illnesses relevant to the present illness/condition of the patient as found by the history of
present illness.
e.g. i) Enquiry into the history of ischemic heart disease in a patient with history of chest pain.
ii) History of transient ischemic attacks in a patient with a history of hemiparesis.
Injuries or trauma suffered during his/her lifetime.
Previous surgeries, if any.
History of ingestion of drugs which are potentially toxic.
History of childhood diseases.
History of exposure to sexually transmitted diseases, if relevant.
Last but not the least, history of similar complaints in the past, the duration and the nature of treatment
taken. This may suggest the nature of illness or may imply whether the present condition is a sequelae
or complication of the previous complaint.
Importance of history of previous illness lies in the fact that it directly or indirectly suggests
whether the present illness is related to or is a consequence of some past illness.
the nature of the present condition, ie, whether it has a tendency to recur or is chronic, is made out to a
reasonable extent.
E.FAMILY HISTORY:
This includes :
Presence of similar complaints in the family.
History of disease like epilepsy, diabetes mellitus, hypertension etc in the family.
History of any other illness dealing with the onset, the duration and the outcome of such illness in
relatives of the patient.
Family history may become relevant and important ascertaining the nature of the patients illness in early
diagnosis of certain disease and pointing out the genetic factor if any in causation of the patients present
illness.
F.PERSONNEL HISTORY:
This includes details of personnel habits such as diet,appetite,sleep,bowel and bladder habits and other
habits like smoking.
Appetite: indicates the impact/relation to illness.
Dietic history : involves enquiry into the nature of the diet (veg/non veg),quality of the diet in terms of
essential nutrients, approximate calculation of caloriesconsumed and other details. this may provide a
clue regarding the possibility of the dietary factor involved in causation of patients illness and may
further help in assessment of the nutritional status during subsequent examination.
Sleep: enquiry into the number of hours of sleep,any disturbance of sleep or any alteration or reversal
of sleep rhythm.
Bowel and bladder habits: enquiry into frequency, presence of any complaint during defecation or
micturation.
Habits:these include alcohol consumption,consumtion of tobacco in any form like
smoking,chewing,consumption of tes,coffee,consumption of addicting substances like heroin etc
should be enquired and recorded.
e.g. smoking-whether cigarette/cigar/beedi;number of such substances smoked per day/week; total
duration of consumption; the history of consumption of the above mentioned substances again provide
clues regarding their possible role.
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G.MENSTRUAL HISTORY:
In female patients, this should be recorded with details of age of attainment of menarche,duration of
cycles,flow,presence of pain and any abnormalities of menstrual cycle.

H.OCCUPATIONAL HISTORY AND SOCIO-ECONOMIC HISTORY:

Relation of the patients occupation to his illness can be established.

Socio-economic status and social history provide an insight into the domestic surroundings and
psychological state of the patient.

At the end of the history, it would be important to emphasize upon the following three points:

While presenting a case, the history should not be presented in disjointed, erratic sentences but should
be presented in a logical and lucid narrative style.
At the end of the history, the examiner should be able to present the summary of the history. the
summary should include the preliminary data, presenting complaint, history in brief including only
relevant points both positive and negative.
After summarizing the examiner should be able to arrive at differential diagnoses as concluded from the
points in the history.

SYMPTOMATOLOGY
Symptom is a subjective manifestation which brings the patient to the doctor.
Important symptoms that are required to be studied are as follows:1. Symptoms related to cardiovascular system: breathlessness, chest pain,edema,palpitation.
2. Symptoms of respiratory system :cough,expectoration,hemoptysis,wheeze,chest pain, breathlessness
3. Symptoms of gastrointestinal system: nausea,vomiting,pain
abdomen,diarrhea,constipation,dysphagia,hematemesis,malaena etc
4. Nuerological symptoms: motor weakness,sensory symptoms,disturbance of speech,involuntary
movements,tinnitus,vertigo,visual disturbances,headache,convulsions etc
5. Miscellaneous symptoms: anorexia,halitosis,hiccups,hoarseness of voice,polyurea etc

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GENERAL PHYSICAL EXAMINATION

A detailed, thorough physical examination must always be done. The proforma is as follows.
Your estimation of the age of the patient (Approximately).
Build- It is the skeletal structure in relation to the age and sex of the individual as compared to a normal
Stature of an individual is the sum total of the height from the vertex to soles.It includes the upper
segment(From the vertex to the upper border of the pubic symphysis) and the lower segment (from the
sympysis pubis upto the soles).Span is distance between the tips of the fingers with arms held horizontally
outwards from the body.normally upper segment=lower segment and stature=span.in infants and children
below 2 years upper segment:lower segment ratio is 1.7:1 and stature >span.this infantile type of body
proportion is seen in adults due to premature closure of epiphyses as in adrenocortical tumour, precocious
puberty etc. In curtain other conditions,delayed epiphyseal closure results in the lower segment being
greater than the upper segment and the arm span greater than the stature. E.g. marfans
syndrome,hypogonadism etc
Variants from the normal type of build:
a. Tall stature: When the height is more than 2 standard deviations above the mean. If height is >6 ft, it
is known as gigantism. Causes: Familial,Hyperpituitarism,Klinefelter's syndrome, etc.
b. Dwarfism: If the adult is <4 ft. Causes: Familial, Tuner's syndrome, Down's syndrome,
Nutritional,Hypopituitarism and Achondroplasia.
Dwarfism can be classified as proportionate and disproportionate dwarfism.
Proportionate Dwarfism: Here, upper segment lower = lower segment. Its causes are:
i. Metabolic-Glycogen storage diseases, secondary to infantile diabetes
ii.nutritional
iii.endocrinal-cretinism,hypopituitarism
iv.chromosomal-turners syndrome.
Disproportionate Dwarfism: There are many types:i. Short limb dwarfism- eg, Achondroplasia, Osteogenesis imperfecta, Hypochondroplasia, etc,
ii.Short trunk- eg Spondyloepitholial dysplasia, osteitis fibrosa cystica, Hurler's symdrome, Morquoi
syndrome,renal rickets etc
Nutrition- Ideally, it must be determined using the Body Mass Index (BMI).
BMI=wt in kgs/(ht in mts)2
Normal range- 10-25 over weight- 25-30
Under weight- <18
obese- >30
whether the patient is alert,conscious and cooperative.
Decubitus: it is the attitude or position or posture of the patient when lying in the bed. For eg
a.in hemiplegia, the patient lies with the affected side immobile, the affected arm flexed and the affected
leg externally rotated and extended.
b. In emphysema, the patient is more comfortable in sitting position and bends slightly forwards
and breathes with pursed lips.
c, in pneumonia and pleurisy, the patient is more comfortable lying on the affected side because the
movement of the affected side is restricted.
observe whether the patient is toxic or dysphoeic or dehydrated or edematous.
Pallor: Look for the pallor at the junction of bulbar conjunctiva and palpebral conjunctiva of the lower
lid, tongue, palate, nail beds, palm and palmar creases.
If palmar creases are pale the Hb% is probably <7gm%
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 Icterus: Yollowish discolouration of the skin and the mucus membranes. Look for icterus in the bulbar
conjunctiva, palate, sublingual mucus membrane, nail bed and the skin (especially in the neonates).
icterus can be made out clinically only if the bilirubin level is <2-3 mg%.
There are three types of jaundice- a. Hemolytic b.Hepatocellular c.Obstructive
Features
Causes

Hemolytic

Bilirubinemia

Hemoglobinopathies
like sickle cell anemia
Red cell membrane
defects like
hereditary
spherocytosis
Infections like malaria
Drugs like
methyldopa,quinine &
phenacetin
Immunological
Unconjugated

Hepatocellular

Cirrhosis of liver
Infections like
hepatitis,spherocytosis
Anti-tubercular drugs like
rifampicin &isoniazid
Heavy metals like
mercury & arsenic
Anticoagulant therapy
Alcoholic hepatitis

Obstructive

Extra-hepatic causesstones,strictures, tumour

&biliary atresia
Intra-hepatic causescholestatis due to heptitis

Conjugated & Unconjugated

Conjugated

Color of urine

Normal

Yellowish

Yellowish

Color of stools

Yellowish

Yellowish

Clay colored

Associated
symptoms
Tests
LFT-SGOT,SGPT
Alk phosphatase
Urine
Bilirubin
Urobilinogen
Stool
stercobilinogen

Abdominal pain only in

hemolytic crisis

anorexia, nausea, vomiting, pruritus, pain abdomen

pallor, transient pain abdomen

All are normal

All are raised

All are raised (alkaline

phosphatase markedly so)

-+

+
+

+
--

--

Clubbing: Bulbous enlargement of the soft tissues of the terminal phalanges with increase in curvature
of the nail because of interstitial edema and dilatation of the capillaries.
Mechanisms of clubbing:
a) Hypoxic theory: Hypoxia leads to the opening of the deep atrio-venous fistulae which increase the blood
supply to the fingers and toes to hypertrophy.
b) Ferritin theory:increased reduced ferritin escapes oxidation in the lungs and enters the systemic
circulation. This causes dilatation of the AV anastomoses.
c) Neurogenic theory: Vagus nerve
d) Harmonal

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Grading of clubbing
I.
II.

III.
IV.

Fluctuation of the nail be present

Obliteration of the angle between the nail and the nail fol. This angle ia called the
LOVEBONDS ANGLE and is normally 1600.
Parrot-beak appearance or drum-stick appearance it is due to increase in the
longitudinal curvature of the nail.
Pain and swelling in the wrist due to hypertropic pulmonary osteoarthropathy

Distal phalanx diameter (DPD)/Intermediate phalanx diameter (IPD): this is normally <1(0.895).it is >1 in
clubbing.
Psuedo-clubbing:it is seen in hyperparathyroidism where there is excess of bone resorption leading to the
swollen appearance of the soft tissue.but there is no increase in the curvature of the nail and the angle
between the nail and nail fold is normal.

How to elicit fluctuation of the nail bed?

The finger to be tested is supported by placing it on the pulp of the examiners thumbs. Stabilizing
the distal interphalangel joint with the middle fingers,the dorsum of the patients finger should be
palpated immediately proximal to the base of the nail with the index fingers.a sensation of
fluctuation or rocking movement can be elicited.

How to look for obliteration of the angle of the nail bed?

Normal angle of the nail bed i.e. the angle between the nail and the nail-fold,called lovebonds
angle is 1600 .it is increased in clubbing. It can be demonstrated by viewing the side of the distal
phalanx of the flexed index finger.it is called profile sign.it can also be demonstrated by holding
the fingers of the two hands together with the nails facing eaxh other wherein the normal space
seen at the proximal nail fold is lost.this is called schamroths sign.

Causes of clubbing
Pulmonary
Bronchogenic ca
Suppurative lung diseases
Diffuse fibrosing alveolotis
Long standing TB
mesothelioma

Cardiac
Cyanotic congenital heart
diseases
Infective endocarditis
Atrial myxoma
Eisenmenges syndrome

Alimentary canal
Cirrhosis
Crohns disease
Ulcerative colitis

Others :Herediatary,Idiopathic, Acromegaly

Unilateranl clubbing- in pancoast tumor,dialysis fistula,AV malformation
Unidigital clubbing-traumatic,tophi deposition etc
Differential clubbing-clubbing of the toes in the presence of normal fingers.seen in PDA with reversal of the
shunt.
Koilonychias:spooning of the nails,nails appear as concave hollows with raised thin edges and
depressed centers (platynychia-flattening of nails) causes:iron deficiency anemia,trauma & fungal
infection.
Note:Koilonychia manifests first in the thumb and then in other fingers,whereas clubbing manifests
first in the fingers.

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Cyanosis:bluish discoloration of the skin and mucus membranes due to the increased amount of
reduce hemoglobin (>5mg%) in the capillary blood.look for the cyanosis in the nails and the nail
beds,lips,tongue,oral cavity,mucus membrane and skin.
Mechanism:
a) Anoxemia:due to inadequate oxygenation of the blood in the lungs. It is mostly seen in central cyanosis
b) Stagnation:due to sluggish circulation there is increased oxygendissociation.
c) Admixture: due to mixing of the arterial and the venous blood as in cyanotic heart disease.
d) Replacement : due to the replacement of the oxygen ion of oxyhemoglobin by pigments.
Types of cyanosis:there are 3 types:1.central cyanosis 2.peripheral cyanosis 3.mixed cyanosis
Difference between central and peripheral cyanosis
Central cyanosis

Peripheral cyanosis

Its due to diminished arterial oxygen

saturation
Observed on skin,mucus membranes
&tongue
Temperature of the body is warm

Its due to diminished blood flow to the

peripheral part
Sen in the skin and ear lobule

Temperature of the body is cool

Its abolished by oxygen therapy

Local heat abolishes cyanosis

Chronic cases are associated with

clubbing and polycythemia
Causes:
Cyanotic heart disease
Eisenmengers complex
Congestive cardiac failure
Chronic obstructive pulmonary disease
Advanced cirrhosis

Not associated with clubbing

Causes:
Peripheral circulatory failure-shock
Increased viscosity of blood
Exposure to cold

Mixed cyanosis is seen in acute LVF,MS.

Other causes for cyanosis:methhemoglobinemia & sulphhemoglobinemia.
Differential cyanosis:cyanosis occurring in one of the limbs only
e.g. 1. only in lower limbs in PDA with reversal of shunt.
2. Only in upper limb-PDA with reversal of shunt in transposition of great vessels.
3. In left upper limb and both lower limb-PDA with reversal of shunt and preductal coarctation of aorta.
Conditions where cyanosis does not occur:
a) If Hb % is <5gm%
b) In CO poisoning (bcz the blood will be cherry redin colour due to carboxyHb)
Edema: collection of fluid in the interstitial spaces or serous cavities.
Where do you look for edema in routine examination?
1. Above the medial malleolous
2. Over the shin of tibia
3. Over the sacrum(if the patient is recumbent)
How do you elicit?
Press the areas mentioned above with the thumb firmly for 30-40 seconds and then release. If the thumb
impression mark is palpable and lasts for more than 30-40seconds,it means there is edema.
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Causes of edema:
CCF
RVF
nephritic syndrome
anemia with hypoproteinemia
IVC obstruction
myxoedema(non pitting) angioneurotic edema
Local cause:- filariasis,lymphatic obstruction
idiopathic in perimenopausal women.
Types of edema :
1. Pitting :-in CCF,RVF,nephritic syndrome etc
Slow (the impression mark lasts for more than 30sec)
Fast (the impression mark disappears within 30 sec)-seen in anemia with hypoproteinemia.
2. Non-pitting:seen in lymphatic obstruction,myxoedema(here it is intracellular edema)

Lymphadenopathy:it refers to the enlargement of the lymph nodes. Lymphadenopathy at a particular

site indicates the pathology in the drainage area of the lymph nodes
Group of lymph nodes routinely examined are lymph nodes of neck,axillary lymph node,superficial
inguinal lymph nodes. examine the size,shape,consistency,number,mobility,presence and adherence to
skin.
Examination of lymph node of neck:
Lymph nodes of the neck are classified into:
a) Superficial includes submental,submandibular,preauricular,postauricular,suboccipetal and superficial
cervical(lie along the external jugular vein in the posterior triangle) lymph node.
b) Deep-includes superior deep cervical nodes which lie along the internal jugular vein beneath the
sternomastoid and inferior deep cervical(supraclavicular nodes).
Examination:
Examiner should stand behind the patient and place twohand on either side of the neck. Neck should be
slightly flexed and by gentle,slow,rotatary movements of the palpating fingers,various group of lymph
nodes should be palpated, systematically on both the sidesstarting from the submental group noticing the
size,shape,consistency,mobility,number and presence of matting.
Left supraventricular nodes(Virchows nodes)are enlarged in GI manifestation-Troissiers sign
Examination of axillary lymp nodes:
Lymph nodes in the axilla consists of five groups namely apical,central,anterior,posterior and lateral. To
examine the axillary lymphnodes,initially stand in front of the patient.for lymph nodes on the right side
support the slightly abducted limb of the patient on your right forearm. Palpate with the left hand,first the
anterior axillary fold for the anterior group,then place the fingers in the hollow of the axilla palpating for the
central group.further push the hand upwards and medially towards the apexof axilla looking for the apical
group.next move behind the patient and supporting the slightly abducted limb of the patient over the left
forearm,palpate with the right hand the posterior axillary fold(posterior group) and slide the hand laterally
over the medial surface of the arm palpating for the lateral group.
Same procedure is repeated on the opposite side as described above.
Examination of inguinal lymph node:
With the patient in the supine position and lower limbs extended at the hip, palpate just below the inguinal
ligament medial to the mid-inguinal point looking for the horizontal and the vertical groups of the superficial
inguinal nodes. The vertical groups is commonly enlarged in barefoot walkers.
Causes of lymphadenopathy:
Inflammatory-acute lymphadenitis, chronic lymphadenitis, TB, syphilis etc
Neoplastic-lymphosarcoma and secondaries
Hematological and immunological-lymphomas,CLL,AIDS,drug reactions,SLE & rheumatoid arthritis.
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Temperature:Body temperature measured during routine general physical examination gives an indication
of the temperature of the viscera and the tissues of the body.
Physiology of temperature regulation: temperature regulation is maintained by the hypothalamus (preoptic
and posterior regions) which acts as a thermostat maintaining a balance the heat gain and the heat loss.
Neurons in the preoptic and posterior hypothalamus receive signals from peripheral nerves and blood
which are integrated.
Normal body temperature is 36.6-37.20C. There is a circadian variation of 10C, the lowest being in the
early mornings and highest in the afternoon (4-6pm)

Normal
Fever
Hyperpyrexia
Hypothermia

Temperature
36.60-37.20C
- >37.20C
- >410C
- <350C

Fever or pyrexia: It is aa elevation of the body temperature above the normal circadian range as a result of
a change in the thermoregulatory center or any increase above the maximum normal temperature.
Mechanism of fever production:
Infectious
Agents &
toxins

monocytes

heat loss

Pyrogens
macrophages

(TNF,IL-1,6&IFNs)

Anterior
hypothalamus

Thermoregulatory
heat production
centre

Fever

Accompaniments of fever:
Chills: A sense of cold accurring during fever, patients even shiver,It is due to vasoconstriction and is a
mode of heat conservation.
Rigors: Profound chill accompanied by muscular contractions and chattering of teeth. It's a mode of heat
production.
sweating: occurs on elimination of febrile stimuli or on reaching thermostat point or an antipyretic therapy.
There is rapid dissipation of heat by evaporation.
others: Include headache, myalgia, arthralgia, nndrexia, nausea etc.
Convulsions: Triggered in children (<5 years), very old, patients with dementia, hepatic failure or CRF.
Measurement of temperature:Temperature is usually measured by a mercury thermometer, There are
twotypes ordinary and rectal.
Sites:
a) Oral cavity: It should be kept for a minute or two.The patient should be instructed to breathe through the
nose and keep the lips firmly closed while the mercury thermometer is under the tongue.
b) Groin or axilla: in young children the thermometer is kept in the groin with the thighs flexed on the
abdomen. It can also be kept in the axilla with the forearm closed to the side of the chest.
c) Rectum: rectal temperature is usually 0.060C more than normal body temperature.it is measured in
young children and In unconscious patients.
Types of fever: with the widespread use antibiotics and steroids the classical pattens of fever are rarely
seen. There are three classical patterns of fever described,
1. Continuous or sustained:when fever does not fluctuate more than 10C during the 24hours but at no
time touches the nommal. It is called continuous fever. e.g. pneumonia, enteric fever, infective
endocarditis, and urinary tract infection.
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2.Remittent fever: when the temperature remains above the normal through out the day but the fluctuation
exceeds 20C in 24 hours.E.g. Typhoid, infective endocarditis, viral fever and non infectious conditions like
collagen vascular disease etc
3.Intermittent fever: Fever present only for few hours in a day and remits back to normal for the remaining
hours. When the paroxysm of intermittent fever occurs daily it is called quotidian fever e.g. mixed infection
with malaria parasites. When the paroxysm of intermittent fever occurs on alternate days it is know as
tertian fever e.g. vivax/falciparum malaria. When the paroxysm of intermittent fever occurs on every fourth
day, it is known as quartan fever e.g. malaria by P.malariae.
Other causes of intermittent fever are brucellosis, rat bite fever, borrelia infection etc.
Other types of intermittent fevers:
Hectic/septic fever: Temperature variation between the maximum and the minimum is large
50C e.g. septicemia, malignancies, drug fever,deep seated systemic infections etc
Pel ebstein fever (9 day fever): fever in which there is regular alteration of recurrent bouts fever afebrile
periods. Temperature increases for 3 days, remains high for next three days and subsides in the next three
days, followed by the afebrile period of nine days. E g, Hodgkin's disease,brucellosis.
Low-grade fever: temperature is daily with fever being more in the cvening but not exceeding 37.8 0 C at
any time. It is exaggeration of normal circadian rhythm.
Fever with chills and rigor is seen in malaria, UTI, cholangitis, septicemia etc
Fever with rashes is seen with chicken pox, measles, rubella,drug fever,infectious
mononucleosis etc
Hyperpyrexia: Body temperature of more than 410C is called hyperpyrexia.It is seen in
malaria,encephalitis, pontine hemorrhage.In this hypothalamic thermostat is set at a higher level.
Hyperthermia: Elevation of the body /core temperature without elevation of the hypothalamic set point. It
is mostly due to inadequate heat dissipation or due to execessive heat production e.g. heat stroke,
malignant hyperthermia, etc.
Head to toe examination: Hair (whether malnourished, absent or decreased), any facial dysmorphism,
Eyes(phthisis bulbi, gross squint, signs of vitamin deficiencies like bitot's spots).Ear (low set ears, any
discharge etc), Nose (DNS, nasal polyps), Lips and oral cavity (aphthous stomatitis, angular stomatitis,
black pigmentation, fissures, ulcers in the mouth and oral hygiene), Tongue (macroglossia/microglossia,
any ulcers etc), Teeth (whether complete, any caries, etc) Gums-any hypertrophy, gingivitis, any bleeding
gums etc
Examination the vital signs: Pulse, Temperature, Respiratory rate, Bloud pressure and JVP
Examination of the vital signs is discussed in other chapters.

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THE CARDIOVASCULAR SYSTEM

Two important characteristics of cardiac diseases are,
1. They manifest late when the disease process has reached an advanced state.
2. Common symptomatolgy.
Cardiac diseases can be classified as follows
1. primary: Congenital, rheumatic, ischaemic, hypertensive and cardiomyopathies.
2.secondary: Anemia, collagen vascular disease, endocrine causes, etc
After history taking and clinical examination the diagnosis in a cardiac case should include,
1. Etiology : whether the discase is conginital or acquired. If acquired, whether it is ischemic,
hypertensive,infectious or secondary to other causes
2. Anatamical abnormality: The part of cardia involved, i.e, whether endocardium, myocardium or
pericardium. it should also include information regarding the involvement of valves or chambers and
involved whether right or left side.
3. Physiological disturbances: Any electrical like arrhythmias,mechanical disturbances like CCF or
presence of any ischemia or infarction.
4. Extent of disability: As made out of strenuous activity required to elicit symptoms.
SYMPTOMATOLOGY:The cardinal symptoms of cardiovascular disease are Breathlessness, Chest pain,
Palpitations, syncope,edema.
Breathlessness: It is defined as an abnormal, uncomfortable subjective awareness of ones breathing.
Breathlessness is a common symptom of cardiac disease. However it is also present in respiratory
diseases and diseases of other systems. Eg.severe anaemia,acidosis etc. It is important to remember that
the severity of breathlessness is not related to the severity of the disease.
Mechanism Breathlessness: Breathlessness can be due to,
a) Increased ventilator drive:as seen in lapse as seen in conditions causing increase in physiological dead
space. E.g. consolidation,collapse,congestive cardiac failure etc or stimulation of respiratory centers
e.g. acidosis.
b) Increased work of breathing: as seen in airway obstruction eg Asthma, COPD, etc
decreased compliance e.g. pulmonary edema,pulmonary fibrosis etc, and restriction of expansion
e.g.ankylosing spondylitis etc
c) Impaired respiratory muscle function: e.g. polio,myasthenia gravis,muscular distrophies etc
d) Multiple factors: eg pneumonia where decreased compliance, increased dead space, pain,
fever,hypoxemia and other factors contribute.
Causes of breathlessness: (4 'P's)
I.
Physiological:exercises, high altinude, etc
II. Pathological:
a) CardiacAcute: pulmonary edema, pulmonary embolism, CHDin neonates, etc
Chronic: CCF, acyanotic CHD, chronic thromoembolism.
b) RespiratoryAcute: pneumothorax, acute severe asthma, inhaled foreign body, acute exacerbation of
COPD,pneumonic consolidation, laryngeal edema etc.
Chronic:chronic pulmonary obstructive disease, asthma, pleural effusion(subacute), bronchogenic Ca,
pulmonary tuberculosis, interstitial lung diseases eg fibrosing alveolitis, etc
III.Pharmacological: Drugs beta-blockers, busulfan etc.
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IV. Psychological:Hyperventilation
V. Miscellaneous: Acute:Metabolic acidosis & respiratory muscle paralysis
Chronic: Anemia & ankylosing spondylitis
Analysis of breathlessness:Enquiring into onset, duration, progression, aggravating and relieving factors
and associated symptoms helps in arriving at the probable cause.
Onset & duration: It may be sudden, terms minutes to hours in foreign body
inhalation,pnuemothorax,pulmonary embolism and pulmonary edema or subacute in terms of days in
pleural effusion,pneumonia etc
Progression: may be over hours in acute causes,day or months or years in chronic causes.
Severity: Severity of breathlessness should assessed by asking the patient, whether breathlessness is
present at rest or is brought on by any activity,whether it interferes with his daily activities.
Accordingly breathlessness can be graded as per the NYHA classification as follows:
Grade 1: No breathlessness at rest or on moderate exertion
(breathlessness is present on unaccustomed work)
Grade 2: Breathlessness on moderateexertion (accustomed work)
(no symptoms at rest or at mild exertion)
Grade 3: Breathlessness on routine activities.
Grade 4: Breathlessaess at rest.
Further enquire if the patient has orthopnoea or paroxysmal noctumal dysproea.
Orthopnoea: It is defined as breathlessness on lying flat. The breathlessness being brought within 30
seconds of lying down. It is seen in CCF, where increase venous return further compromises the cardiac
output and severe emphysema where diaphragmatic movement causes orthopnoea.
Paroxysmal nocturnal dyspnoea (PND): It is a sudden severe breathlessness which wakes the patient
from sleep. Typically, the patient sleeps for 3-4 hours and wakes up suddenly, sits up gasping for breath
and coughs,expectorating frothy sputum.He goes to the window for fresh air and is relieved of these
symptoms aftyer 20-30 minutes.enquire the actual number of episodes,frequency and recent attack.it is
due to acute pulmonary edema as a result of left heart failure. This cardiac asthma has to be differentiated
from bronchial asthma which can also cause episodes of chronic dyspnoea.

Cardiac asthma

Bronchial asthma

1. Patient is middle aged (usually: 40)

2. History of heart disease present
3. Patient usually has cough with frothy sputum
which may be pink or blood tinged.
4. Patient is relieved by sitting up for sometime
5. Cyanosis and sweating are seen early
6. Breathing is shallow and rapid
7. The duration of inspiration is same as expiration
8. crepitations are heard on auscultation

-Usually young
-History of asthma/allergic disorders
-Cough with mucoid sputum which is not
blood tinged
-Patient is not relieved by sitting up.
-Cyanosis and sweating are late changes
-Breathing is deep and rapid
-Expiration is prolonged
-Rhonchi are heard on auscultation

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Possible mechanisms of PND:

Redistribution of fluid into the lung. Redistribution of fluid from tissue spaces to the blood column.
Elevation of diaphragm in sleeping position.
Decreased adrenergic stimulation during sleep
Decreased ventilatory drive due to fall in PaO during sleep. Fall in left atrial pressure during sleep
Platypnoea: Breathlessness is present on sitting or standing up and is relieved by lying flat. Seen in left
atrial myxoma, ball valve thrombus.
Trepopnoea: Breathlessness is present on lying to a particular side. Seen in unilateral pleural effusion on
lying to the opposite side.
Associated symptoms:
1. Chest pain: in pneumonia, pulmonary infection, pneumothorax (in all those pain is lateralised) and in MI
(central pain).
2. Cough and wheeze: In asthma,pulmonary edema etc.
Chest pain: Analyze chest pain enquiring into the site, character, radiation, severity,duration, aggravating
and relieving factors und associated phenomena.
Differential diagnosis of chest pain:
Angina: A characteristic chest pain present retrosternally, constricting or severe aching in character
radiating to either arm, hand, wrist, jaw, to neck, back or epigastrium which is brought on exertion, lasting
for 10-15 mins and relieved by rest or nitrates.
Myocardial infarction:Chest pain similar to angina in character, site and radiation but is much more
severe.not necessarily precipitated by exertion, not relieved by rest or nitrates. Lasting for more than 30
mins and associated with increased sympathetic activity like sweating, anxiety etc and fear of impending
death.
Pericarditis:Retrosternal pain which is stabbing in character radiating to shoulder, present or increased in
inspiration and varies with posture and is associated with pericardial rub.
Dissecting aneurysm:Pain of sudden in onset,which is severe tearing in nature, radiating to back
between shoulder blades and associated with disproportionate bradycardia.
Oesophageal spasm: often mimics angina but is not rapidly relieved by rest. But is relieved by
nitrates.History of chest pain related to food intake may be present
Pleuritic pain:it is described as lateralised, localized chest pain. Pain is typically present over the later
aspect of the chest wall,increases with deep inspiration and cough and is associated with pleural rub.
Pneunothorax:Pain is onen sudden in onset similar to pleuritic pain but with no history of ill health. Might
occur following trauma. Usually associated with rib fracture if due to trauma.
Pulmonary infarction: Pain is similar to onset and nature to the pain seen in pneumothorax, in addition
features of increased sympathetic activity like sweating, anxiety etc are present.
Musculo-skeletal: Pain is variable in site and intensity,may vary with movement and posture and
commonly accompanied by local tendemess over a rib or costal cartilage.
Other causes: retrosternal pain- MVP, AS, aortitis, tracheitis, anxiety neurosis etc.
lateralised- pneumonia, rib fracture, costochondritis (Teitz's syndrome) etc,
Palpitations: It is an abnormal, uncomfortable,subjective,awareness of one's own heart beat.
Causes:
Increased awareness by the patient himself as seen in anxiety, emotional excitement, neurocirculatory
asthenia, etc
Any alteration in rate and rhythm.This is seen in cardiac aarythmias like sinus tachycardia, paroxysmal
tachycardia, atrial fibrillation and flutter, intakeof drugs like ephedrine, atropine,caffeine etc.,
exercise,fever, thyrotoxicosis
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 Increased force of contraction as seen in MR, AR, anac nia, exercise, CIID, etc
Enquire into:
Onset: sudden in paroxysmal tachycardias, and insidious in regurgitant lesions.
Whether regular or irregular? Regularity is seen in anxiety.
Whether present throughout the day or brought on by any activity? or presence of any precipitating
factors
Duration of each attack
Presence of associated symptoms like chest pain, fever, breathlessness, etc
Description of palpitation:eg missed beat in extrasystole, racing beat supraventricular tachycardia
Syncope: transient loss of consciousness due to reduction in cerebral blood flow either due to decrease it
cardiac output or increase! peripheral vasodilatation or both.
Presyncope or faintness: Sense of impending loss of consciousness.
Causes:
Vasovagal syncope
Postural syncope: Occurs after prolonged standing. Its occurrence suggests impaired vasomotor
reflexes (autonomic neurupathy), vasodilator therapy, dehydration etc
Cough syncope: occurs after prolonged paroxysm of cough.
Micturition syncope: Seen in elderly with prostration, occurring on straining in upright position after
raising from bed.
Carotid sinus syndrome: in hypertensive individuals
Cardiogenic: due to inadequate cardiac output
Miscellaneous: dehydration,hypoglycemia etc.
Enquire into:
a) precipitating factors like prolonged standing, coughing, exertion etc.
b) premonitory symptoms like nausea, sweating, pallor etc
c) history of drugs like nitrates etc.
d) history of associated symptoms like chest pain, palpitations etc
e) history of TIAs (vertebro-basilar insufficiency)
Edema:
Usually bilateral swelling of limb is present in association with other symptoms of
right heart failure, pitting edema is demonstrable on accumulation of 5-6 liters of fluid.
Edema in cardiac failure is due to
impairment of renal blood flow (activation of RAAS system promoting excessive salt and water
retention)
increased venous pressure
Decreased oncotic pressure: due to decreased albumin production in liver because of its chronic
passive congetion.
Other symptoms
1) History of fever (to rule out infective endocardities)
2) History of weight and night sweats
3) History of jaundice, pain abdomen, (in liver congetion due to RHF), distention of abdomen
4) History of cough with expectoration.

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PAST HISTORY:
* History of ischaemic heart disease * History of DM/HT/epilepsy.
* History suggestive of rheumatic heart disease in childhood (fever with fleeting joint pains and swelling
involving of particularly knee, ankle, elbow, etc or long term history of penicillin prophylaxis )
* History of similar complaint in the past. * History of recurrent respiratory tract infections
* History of cyanotic spells or squatting episodes
FAMILY HISTORY: History of HTN/DM, history of IHD or CHD.
PERSONAL HISTORY :Lay emphasis on dietic history and personal habits like smoking & alcoholism.
GENERAL PHYSICAL EXAMINATION:
General appearance of patient, presence of any dyspnoea, anxiety, etc
Decubitus: examine whether comfortable lying down or requires to rest in propped up position.
Extremities: whether warm and flushed (high output states) or cold (cardiac failure)
Nails: For clubbing (infective endocarditis, cyanotic CHD), splinter hemorrhages(infective
endocarditis)& koilonychia (iron deficiency anemia)
Pallor: in anemia, shock, peripheral vascular diseases
Cyanosis: whether central (right to left shunt) or peripheral MS) or mixed(CCF).
Signs of atherosclerosis: arcus juveniles,xanthomas,xanthelesmas, dancing brachialis,
Edema: (discussed undor the chapter on GPE)
Icterus; (discussed under the chapter on GPE) seen in CCF, infective endocarditis,pulmonary
infarction,cardiac cirrhosis due to chronic congetion of liver.
Cogenital defects of extremities like syndactyly,polydactyly,etc.
Facies:for presence of congenital anomalies
Congenital disorders

Features

Associated cardiac anomalies

Turner syndrome
Marfans syndrome.
Klepel feil syndrome
Elfin facies
Down's syndrome

webbed neck, short stature

Long limbs, ectopia lentis
Low hair line, short neck
Pointed nose,low set ears
Mongoloid face

Congenital rubella syndrome

Blind, deaf

Coarctation of aorta
AR,MVP
VSD
AS
Endocardial cushion defect
ASD, VSD
PDA

Lymphadenopathy: Lymphomas, secondaries from breast and bronchogenic Cas, may cause
pericardial effusions.

Signs of infective endocarditis: Janeway lesions( erthyma over palms and soles), petichial
hemorrhages, Osler nodes (painful 3-4 mm tender vegetations in nail bed)
Rheumatic arthritis
Asymmetrical involvement
Involve larger joints
No residual deformity

Rheumatoid arthritis
Symmetrical involvement
Involves smaller joints
Residual deformity present
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Vital signs: pulse, blood pressure, respiratory rate, temperature and JVP
Pulse: it is defined a wave form produced by ventricular systole which is propagated peripherally along the
arterial tree .Examination of pulses is an important prerequisites for the examination of the cardiovascular
system as it reflects the hemodynamic changes in the heart. Examine all the peripheral pulses including
the radial,carotid, brachial, femoral, popitial posterior tibial and dosallis pedis.
Comment on the following:
Rate, rhythm, volume, character or quality ,condition of vessel wall and radio femoral delay.
RATE:Radial pulse is used to access the rate.Normally the pulse rute is 70-90 beat per minute. Rate
>100/min is tachycardia,Rate <60/min is bradycardia.
Bradycardia (<60/min) : seen in vasovagal syncope, hypothyroidism, athletes, heart block &
drugs: atenol. Etc
Tachycardia (>100min): seen in anxiety, fever, pregnancy, hyperthyroidism, tachyarrhythmia's and drugs:
salbutamol and terbutaline.
Rhythm: completely irregular (irregularly irregular is seen in AF, frequent extrasystoles; Regularly irregular
in sinus arrhythmia, pulsus bigeminus and occasional irregularity in extrasystoles.
Volume and Character:They are assessed by palpating the carotid artery. Low volume pulse is
seen in decreased left ventricular stroke volume and increased peripheral vascular resistance and
bounding (high volume) pulse is seen in hyperkinetic states, wide pulse pressure and decreased peripheral
resistance.
Based on character, the variations of pulse are as follows:
Pulsus parvus et tardus:this is a small volume(parvus) pulse that rises slowly (tardus) to a late
systolic peak. This is the result of mechanical obstruction of left ventricular ejection and is seen in
aortic stenosis)
Anacrotic pulse: It is a variant of pulsus parvus et tardus, in which a notch is palpable on the
upstroke of the pulse wave. It is seen in severe aortic stenosis
Dicrotic pulse: It has two palpable wave. One in systole and other in diastole (it is due to low stroke
volume) It is seen in dilated cardiomyopathy, late stages of cardiac failure.
Bisferiens pulse: It is a pulse with two waves both in systole. It is seen in combined presence of
aortic stenosis and aortic regurgitation, severe aortic regurgitation and HOCM.
Collapsing pulse (water hammer pulse): It is a high volume pulse characterized by a rapid upstroke.
Mechanism- Rapid upstroke is due to increase in stroke volume and the collapsing character is due to
diastolic leak back to the left ventricle and rapid run-off to the periphery because of low systemic vascular
resistance.it is typically seen in aortic regurgitation,hyperkinetic circulatory states(anemia,fever,
thyrotoxicosis), large AV fistulae, PDA and severe MR.

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Pulsus alternans: It is alteration of large and smaIl volume beats, with a normal rhythm and associated
with a difference of 10-40 mm Hg in systolic pressure between beats (it is due to ventricle alternatively
contracting strongly and then weakly). It is seen in acute left ventricular failure.
Pulsus paradoxus: It is characterized by a decrease in systolic pressure more than 10 mm during
inspiration and the radial pulse smaller in volume during inspiration and larger in volume during expiration.
It is merely an exaggeration of the normal decreased systolic pressure(by 3-10 mmHg) during inspiration
and not a reversal of this. The paradox is that heart sound are still audible at time whenno radial pulse is
felt.
Mechanism: normally, during inspiration there is reduction of intrathoracic pressure
resulting pooling of blood in the pulmonary circulation and in the right ventricle(increased venous return
with a net effect of reduction of cardiac output and drop in systolic pressure by 5-10 mmHg. pulsus
paradoxus the increased volume of blood causes bulging of the inter-ventricular septum.This is responsible
for further reduction in cardiac output and exaggeration of the fall in systolic blood pressure.
Conditions associated with pulsus paradoxus are:
Constrictive pericarditis,cardiac tamponade, pericardial effusion, restrictive cardiomyopathy, chronic
obstructive airway disease, severe bronchial asthma.
Radiofemoral delay: It occurs in simultaneous palpation of right radial artery and one femoral artery.
Blood pressure: Measurement of blood pressure is an essential part of the examination of cardiovascular
system, It is measured using sphygmomanometer which consists of a mercury manometer, an inflatable
rubber bulb, cuff, tubing and inflation-deflation device.
Preliminaries:
1. The patient should be comfortably seated or recumbent and completely relaxed.
2. Arm should be freed from the clothing and supported at the level of the heart.
3. Cuff should be tied snugly around the arm above 2.5cm above the cubital fossa covering 2/3 of the arm
with tubings over the brachial artery.The cuff should be neither too tight nor loose (to avoid erroneously
high and low values respectively)
4. Cuff size should be appropriate: Normally the cuff size is 12-15 cms for adults, 5 cm for infant ,5-7 cms
for children and 18 cm for thigh. Length of the cuff is double the width.
5. Manometer should be well supported and upright.
6. Avoid parallax error.
Method:
After tying the cuff measure the systolic blood pressure by palpatory method. first and
then follow it up by auscultatory method.
1. Palpatory method : palpate for radial artery at wrist and inflate the cuff till the pulse is obliterated.The
reading in the manometer gives the approximate value of systolic pressure.
2. Auscultatory method:Inflate the cuff 30mmHg above the systolic pressure obtained by Palpatory
method and apply the stethoscope over the brachial artery. slowly deflate the cuff listening for
appearance of Korotkoffs sounds. The sounds have five phases as shown below
3. Oscillatory method:
Phase I: Appearance of some sounds, tapping

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Phase II :Softening of sounds to murmur like quality

Phase III:Reappearance of sharp tapping sounds.

Phase IV :Muffling of sounds.
Phase V: Disappearance of sound.
Point of appearance of two consecutive clear cut sounds is taken as the systolic pressure and the point or
disappearance of sounds is taken as diastolic pressure. The blood pressure is expressed as
systolic/diastolic in mmHg.
Normal blood pressure is 120/80mmHg. Normally the blood pressure is 5mmHg higher in the right limb
than the left lower limb.Also the blood pressure is 10mmHg higher in lower limb than in the upper
limb.(because lower limb vessels are direct continuation of aorta) This is exaggerated in aortic
regurgitation-Hills sign
**Palpatory method is done to avoid missing the silent gap (Auscultatory gap) which is seen
certain cases of hypertension where in after initial appearance of sounds they disappear completely only to
reappear at a lower pressure. The silent gap is attributed to venous hypertension because of which
transmission of sound from brachial artery is poor.
Pulse pressure: lt is the difference between systolic and diastolic pressures.
Mean arterial pressure:diastolic pressure+ 1/3 pulse pressure.
Hypertension: A systolic blood pressure 140mmHg and diastolic blood pressure is more important
because it less affected by extraneous influences and rise in diastolic pressure is more significant.
Hypotension:Systolic blood pressure 80mmHg and 60 mmHg diastolic.
NOTE: In conditions characterized by wide pulse pressure like aortic regurgitation, anaemia
pregnancy, muffling of sounds rather than the disappearance of sounds indicate the diastolic pressure
(particularly when the disappearance of sounds is >10mm Hg below the muffling point).
Measurement of BP in special situations:In cases of atrial fibrillation and aortic regurgitation ,average of
two readings should be taken and muffling point taken as diastolic pressure.
other uses of sphygmomanometer
a) Hills sign in AR
b)pulsus alternans

c)pulsus paradoxus d)Hess test e)Trosseau's sign

Jugular venous pulsation and Jugular venous pressure(JVP)

observation of the jugular venous pulsation provides information regarding
a) Tone of the venous system
b) Right heart hemodynamics
c) Atrial activity-reflecting volume and pressure changes
Usually the vein used for such observations and measurement of venous pressure is the internal
vein and not the external jugular vein. This is because
a) It is in direct continuity with the right atrium
b) There are no valves
c) There are no intervening fascial plane
d) it is less affected by sympathetic tone.
Surface marking for IJV: A curved line from medial end of clavicle to the ear lobe.
Normal jugular venous pressure: Normally pulsations of the internal jugular vein are seen only when the
patient is recumbent.
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How to look for jugular venous pulsation?

Patient should be instructed to lie flat with the head propped up by the pillows, observe the neck of the
patient with the head in the midline position simultaneously palpating opposite carotid. Also observe the
neck after making the patient reclining at 45 degree and sitting upright as in case of high pressure the
pulsations may be missed.
Normal jugular venous pulsations consists of positive waves or crests namely A, C and V and 2 negative
waves or troughs X and Y.however clinically only 2 positive waves A and v are made out A wave -due to
right atrial contraction-absent in atrial fibrillation, decreased in RHF,exaggerated in tricuspid stenosis
atresia,pulmonary stenosis,pulmonary hypertension, pericardial effusion,constrictive pericarditis and
HOCM.
C wave-due to bulging of tricuspid valve into right atrium and impact of adjacent carotid artery.
Vwave- due to passive filling of right atrium during ventricular systole-large V waves are seen in TR
X wave (descent) due to downward displacement of tricuspid valve and continued relaxation of the right
atrium-absent in TR and RHF prominent in constrictive pericarditis.
Y wave (descent)-due to opening of tricuspid valve and rapid flow of blood into the ventricle rapid in
TR,RHF and constrictive pericarditis and slow in TS.
Jugular venous pulsation
Position is more lateral
It is better seen than felt
Two wave forms seen
Inward movement is maximum
venous pulse decreases with inspiration and
increases with expiration and in supine position
Pressure over the site obliterates with pulsation
Pressure over the abdomen causes transient
increase in pressure

Carotid pulse

Medial
Better felt than seen
Single brief wave palpable
outward movement is maximum
Unaffected by posture and respiration

Pressure does not obliterate the pulsation

No change

Measurement of JVP
Sternal angle is the point of landmark for JVP measurements as it roughly corresponds to the middle
of the right atrium and represents the normal pressure approximately with the body in horizontal or erect or
in intermediate position.
The pressure is expressed as centimeters for vertical distance between top blood column and sterna
during normal quiet respiration.
Patient is instructed to lie down reclining at an angle of 45degree with the neck relaxed. The neck
slightly away from the side under observation to make the vein more prominent. Observe for the upper
level of pulsation and place a ruler horizontally.place another ruler at the sternal angle, at right angle to the
fist one and measure the height of level of pulsation. To this pressure at 45 degree 5 cm is added which
gives the JVP Eg: if the height of column is 3 cm.JVP 3+5=8cm. Normal JVP is 5 to 8 cm.
Causes of raised JVP
*Right heart failure is the commonest cause *Pericardial effusion, constrictive pericarditis and tricuspid
stenosis where the capacity of right heart is reduced * Hyperkinetic circulatory states like fever, anemia,
thyrotoxicosis,AV aneursym etc. * Raised intrathoracic or intraabodominal pressure as in pregnancy ,large
pleural effusion abdominal tumors etc * superior venacaval obstruction *Increased blood volume *
Pulmonary diseases like emphysema and bronchial asthma.

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Kussumaul's sign:
Normally there is a fall in the height of jugular venous pulsations and decrease in JVP during inspiration
because of the fall in thoracic pressure. However in certain conditions there is a paradoxical increase in the
height of pulsations and a rise in JVP during inspiration This is known as Kussumaul's sign. It is seen in
constrictive pericarditis, severe RHF ,acute severe asthma and restrictive cardiomyopathy.
Hepatojugular reflux:
Normally when pressure is applied over abdomen for 10-30 seconds there is a transient rise (due to
increase venous return) and fall of height of jugular venous pulsations (due to capacity of normal heart to
accommodate the venous return)
Positive hepatojugular reflux is defined as a sustained increase in JVP more than 1cm for more than 1
minute on firm compression of upper abdomen for 10-30 seconds.This is seen in right heart the failing
failure as the failing heart cannot accommodate increased venous return.
EXAMINATION OF CARDIOVASCULAR SYSTEM
Inspection :patient is examined both in upright and supine position and looking for the following.
Shape of the chest: Examine for the presence of skeletal deformities like pectus excavatum,
kyphoscoliosis etc as these deformities can give rise to abnormalities live shifting of apex beat, systolic
murmurs etc without any organic disease of the heart.
Precordium :Look for any bulging or retraction.
Bulging of the precordium is present in a)long standing heart disease (congenital or rhemautic) having its
onset when the bones are soft and incompletely ossified b)massive pericardial effusion c)large pleural
effusion d)skeletal deformities like kyphoscoliosis ,rachitic rosary e) mediastinal growths f)localized bulging
seen in ventricular aneurysm.
Retraction or Flattening of the precordium present in fibrosis of lung skeletal deformities and long standing
cases of pleural effusion.

Apical impulse: It is defined as the lowermost and outermost forward thrust of the heart. Nomal
position of the apical impulse is in the 5th intercostal spice 10cm from the midsternal line. (0.5-1cm from
the midclavicular line) and is limited to one intercostal space and 2.5cm in diameter.Inspection for the
apical impulse is best done with the patient sitting up and slightly bent forwards. If not visible in this
position turn the patient to the left lateral position and examine, wherein the apical impulse is visible in
the mid-axillary line (shifted by 2-3cms).

Apical impulse may not be visible in the following situations: thick chest wall,emphysematous chest,
obesity,massive pericardial effusion etc
Double or bifid apical impulse: two consecutive thrusts of the apical impulse during each heartbeat. is see
in HOCM, ventricular aneurysm, gallop rhythm, bundle branch block.

Visible pulsations: Look for visible pulsations over the precordium, particularly over the juxta-apical
area, left Parasternal areas. Also examine for the apical impulse in the epigastrium, 2nd left intercostal
space and suprasternal regions in the neck.

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Causes for the pulsation

*Epigastric pulsations:RVH, aneurysm of the aorta, aortic pulsations in normal individuals, liver pulsations
and transmitted pulsations.
*Left Parasternal pulsations: RVH, left atrial enlargement & aneurysm of aorta.
*2nd left space: dilated pulmonary artery & aneurysm of aorta.
*Suprasternal area: AR, hyperkinetic states & pulsating thyroid gland.
*Neck: AR, aneurysms of the carotid and subclavian arteries.
Suzzman's sign: pulsations over the scapular region due to development of anastomotic channels seen in
Coarctation of aorta.

Dilated veins: examine for dilated veins over the chest wall. They are seen in obstruction of the superior
and inferior venacava.
Scars and sinuses

Palpation: palpate the pericardium to determine the following:

Apex beat: It s the lowermost and outermost point from the manubrium sterni where the cardiac impulse
transmitted across the precordium can be felt. It is the result of the heart rotating, moving forward and
striking against the left lateral part of the chest wall. It is usually produced by the left ventricle during
systole. In severe RVH, the right ventricle may produce it.
How to palpate for the apex beat?
Place the whole of the palm on the chest in such a way that the middle three fingers are pressed
gently against that part of the chest just below and lateral to left nipple. The fingers should be
placed in the intercostal spaces only. Feel for the cardiac impulse, if not go downwards and
laterally till you localize it.
Now for the assessment of the character of the apical impulse ask the patient to turn to the left
lateral position and palpate. Put the patient back to the supine position and look for any
displacement, extent- localized or diffuse and other features.

Normal apex beat is felt in the left 5th ICS 10cm from the midsternal line, is forcible, is confined to one ICS
and is 2.5cm in diameter. A normal apex beat is displaced laterally in pneumothorax and displaced
medially in fibrosis and collapse.
Other types of apex beats:
Hyperdynamic apex beat: The apex beat is displaced laterally and slightly downwards with the palpating
fingers lifted up by the impulse, but the lift is ill sustained (<2/3 of systole) and the impulse is diffuse &
>2.5cm in diameter. It is seen in cases of left ventricular dilation due to volume overload as in
Hyperdymamic output states like anemia, thyrotoxicosis, mitral regurgitation and aortic regurgitation.
Heaving apex: The impulse is displaced laterally and downwards, the finger is lifted up by the impulse, the
lift being sustained(>2/3 of systole) and the impulse is confined to one intercostal space and is <2.5 cm in
diameter. It is seen in conditions of pressure overload of the left ventricle such as aortic stenosis,
coarctation of aorta, hypertrophic cardiomyopathy and hypertensive heart disease.
Tapping apex: The apex beat is felt as a short sharp systolic tap.It is seen in mitral stenosis

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 other pulsations:
Epigastric pulsations are palpated by placing the thumb just below the xiphisternum in the direction of the
apex of the heart with the breath held in inspiration. If the impulse is felt at the tip, it is due to RVH; at the
pulp is due to liver pulsations and more distally is due to aortic pulsation.
Parasternal pulsations/heave: with the chest held in expiration place the ulnar border of your hand over
the 3rd 4th and 5th IC spaces adjacent to the sternum. Pulsations are seen in conditions of volume
overload and heave is present in conditions of pressure overload.
Palpable P2 or Diastolic shock: Present in second left intercostal space in cases of pulmonary
hypertension.
Thrill:It is defined as a palpable murmur. It is felt as a sensation of purring of a cat.
It is produced by transmission of vibrations that are generated during passage of blood through a narrowed
valve the chest wall. Presence of a thrill is a definitive evidence of organic disease of the heart and the
diagnosis of thrill is justified in the presence of definite vibration of moderate duration and an
accompanying murmer.Thrills are commoner with the systolic lesions and rare in regurgitant lesions.
To palpate for a thrill place the palm of your hand lightly over the chest wall and determine the site of
maximum palpability, its extent and timing i.e. whether systolic or diastolic.systolic thrill is that which occurs
synchronously with apical thrust and one that precedes is the diastolic thrill. Usually systolic thrills are
common and better heard at the base and diastolic thrills are better heard at the apex.
Timing
Disease
Site
Systolic
AS
Aortic area
PS
Pulmonary area
VSD
3rd &4th left ICS
Diastolic
MS
Apex
AR
Aortic area
Continous
PDA
Pulmonary area
Percussion:
The purpose of percussion in a cardiac case is for the following:
l. To determine the cardiac borders.
2. To determine the abnormal areas of the cardiac dullness such as due to presence of pericardial effusion.
Normally the left, right and the upper borders are percussed.
Left border is percussed in the 4th and the 5th spaces in the midaxillary line and then medially towards the
left border of the heart. The resonant note of the lungs become dull. Normally the left border is along the
apex beat.If it is outside the apex beat it suggests presence of pericardial effusion.
The upper border is percussed in the 2 and the 3 intercostal spaces in the parasternal line. Normally it is
resonant in the 2nd space and dull in the 3rd space. A dull note in the 2nd space may suggest pericardial
effusion ,aneurysm of aorta ,pulmonary hypertension and left atrial enlargement.
Right border: The patient is percussed in MCL on the right side unt il the liver dullness is obtained.Then
percuss one space higher from MCL to the sternal border:normally the border is parasternal. Any dullness
in the right parasternal indicates the pericardial effusion,aortic aneurysm or right atrial enlargement,
Dextrocardia,Mediastinal mass.
Auscultation.
Principles of auscultation
l. The patient should be in a semi recurmbent position or in a position in which he is comfortable.
2. The examination room should be quiet.

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3. A good stethoscope of about 25 cm sound proof rubber tubing should be used.

4. High pitched sounds such as first and second heart sounds,all systolic murmurs and aortic diastolic
murmur s are best heard with the diaphragm.
5. Low pitch sounds such as third and fourth heart sounds and mitral diastolic murmurs are best heard with
the bell of the stethoscope.
Area of auscultation over the precordium:
I. Mitral area: area where the apex beat is felt.
2. Tricuspid area: just to the left of lower sternum.
3. Aortic area:just to the right of the sternum in the 2nd intercostal space.
4. Pulmonary area: just to the left of the sternum in the 2nd intercostal space
5 Erb's area: just to the left of the sternum in the 3rd intercostal space
Note: These areas do not correspond to their respective valves but represent areas to which the sounds
from the valves are conducted best.
Look for the following aspects in auscultation.
Heart sounds
Assess the rate rhythm, intensity ,splitting and presence of 3rd and 4th heart sounds.
All these aspects should be observed for in all auscultatory areas over the precordium.
S1( first heart sound): It is produced by the closure of mitral and tricuspid valves. It is
identified by its coincidence with carotid pulse.Normally splitting of S1 is not appreciated.
Variations in the intensity of S1:
Loud S1: Mitral stenosis, Hyperdynamic states like exercise, anemia, thyrotoxicosis, pregnancy, fever and
Pagets disease, Short P- R interval.
Soft S1: Mitral regurgitation, Myocarditis, Myocardial infarction, Severe aortic regurgitation, obesity,
Emphysema, Pericardial effusion, LBBB, Long P-R interval.
Varying intensity of S1 is seen in atrial fibrillation and complete AV block.
S2(second heart sound): It is produced by the closure of aortic and pulmonary valves
Variations in the intensity of S2
Loud A2: Hyperdynamic state,syphlitic AR, essential hypertension.
SoftA2: AS
Loud P2: PHT
Soft P2: PS, TOF, Pulmonary atresia
Splitting of S1:
1.Wide splitting (M1T1) complete right bundle block ebstein anamoly.
2.Reversed splitting (T1M1) complete left bundle branch block severe MS, Large left atrial myxoma.

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Splitting of S2:
1. No splitting: In elderly patients, severe AS/ PS, Fallot's tetralogy
2. Reversed splitting: (P2A2) LBBB, IHD, PDA, Severe AS, WPW syndrome
3.Wide splitting (mobile): RBBB, PS /Pulmonary embolism, VSD ,MR
4. Wide splitting and fixed: ASD, severe AS Severe RVF.
S3 (The third heart sound):It is because of the rapid filling phase of the ventricular diastole when the
blood flows from the atria to the ventricles.
Presence of S3:Physiological in children, athletes and pregnancy.
Pathological in Left sided S3-LVF, AR/MR ,Right sided S3 RVF
S4 (The fourth heart sound): It is produced by atrial contraction and is always pathological.
Presence of S4:
Left sided S4 -Systemic hypertension, acute MI, acute MR ,anaemia, thyrotoxicosis.
Right sided S4- Right ventricular hypertrophy due to pulmonary HTN and pulmonary stenosis.
Murmurs
Comment on 1. their presence 2. the timing and character 3. the area in which the murmur is best heard
4.whether it is best heard with the bell or the diaphagm 5. relation of the murmur with the position of the
patient and some manoeuvre 6 its relation to respiration 7. whether its radiating or conducting 8.grading
of the murmur.
Types of the murmur based on the time and character:
Systolic: These are the murmurs heard of S1.The murmur may be present throughout the
systole when it is called pansystolic. Pansystolic murmurs may mask S1 and are usually of blowing in
character .Systolic murmurs can also be ejection type when they are harsh and have a rise and fall in the
intensity much before S2.Late systolic murmurs start much after S1 and continue upto A2. They are
blowing in nature.
Diastolic :These murmurs start after S2 and end before S1. Early diastolic murmurs are heard in the early
phass of diastole and end much before S1. Mid diastolic murmurs are heard in the later phase of the
diastole and may mask S1.
Continous murmurs: They are present throughout the systole and diastole and are blowing in nature.
Causes of murmurs:
Pansystolic murmurs: MR,TR, VSD.
Ejection systolic murmurs:
1. Organic valvular disease : AS, PS, HOCM, TOF etc
2. Flow murmur from intracardiac causes like ASD, AR MR etc
3. Flow murmur from extracardiac causes like hyperdynamic output states like fever exercise,
pregnancy,thyrotoxicosis, severe anaemia etc.

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Late systolic murmurs : MVP,mild ischemic, MR etc

Early diastolic murmurs: AR, PR etc
Mid diastolic murmurs:
At the apex:Organic:MS,Carey coombs murmur of rheumatic carditis, left atrial myxoma.
Functional :Austin Flint murmur of AR, MR, VSD, PDA etc
At the tricuspid area:Organic: TS
Functional: asd, TR etc
Continous murmurs: PDA coarctation of aorta, AV fistula, jugular venous hum, mammary souffle.
Murmurs whichI. Increase with valsalva manouvre : in TR, PS, TOF, HCM, etc.
2. Decrease with sustained handgrip: in AS, HCM,etc
3. Increase with sustained handgrip :in MR, etc
4. Increase with transient exercise :in VSD, MR, etc
5. Decrease during squatting
:in HCM, etc
6. Increase with inspiration and decrease with expiration (De Carvallo's sign): in right sided murmurs
except pulmonary ejection click.
7.Increase with expiration and decrease with inspiration: all left sided murmer.
8. MDM of MS is better heard in left lateral position.
9. ESM of AS is better heard when the patient bends forward
Radiation of murmurs: Murmurs radiate in direction of blood flow causing murmurs
Murmurs due to pulmonary and tricuspid valve lesions are well localized.
Systolic murmurs arising from the aorta radiate towards the neck, sternum and also towards the apex.
Murmurs due to MR where anterior valve leaflet involved radiate towards the aortic and pulmonary area
and also to the axilla; whereas those due to posterior valve leaflet lesions radiate to the back.
MDM of MS is usually localised.
Grading of intensity ofthe mumurs
1. Heard by an expert in optimum conditions
2. Heard by a non-expert in optimum conditions
3. Easily heard; no thrill
4. Aloud murmur with thrill.
5. Very loud, often heard over wide area; with thrill
6, Extremely loud; heard without stethoscope
Note: 1. It is always important to differentiate an innocent murmur from a pathological murmur. An
innocent murmur is usually soft systolic, especially ejection systolic not associated with thrill and not
associated with any other abnormal sounds or murmurs.
2. Functional murmur is one which is usually rumbling or soft diastolic, not associated with thrill but
may be associated with other abnormal sounds.
Characteristic features of some murmurs
1. Murmur of aortic stenosis: Loud, harsh, ejection systolic murmur best heard in the second intercostals
space (aortic area),radiating to carotid arteries. It diminishes with sustained handgrip.
2. Murmur of tetralogy of fallot: Loud, harsh, ejection systolic murmur best heard at the
2nd and 3rd left intercostal spaces, due to pulmonary stenosis.

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3. Murmur of coarctation aorta: ejection systolic murmur over the spine posteriorly, from the coarctation
itself.
4. Murmur of mitrial regurgitation: High pitched, blowing,pansystolic murmur best heard at the apex. It
commonly radiates to axilla and back when anterior mitral leaflet is predominantly involved. With
predominant posterior mitral leaflet involvement, the murmur radiates to left sternal border and base of
heart.it increases during expiration, sustained handgrip and transient exercise. The murmur is unchanged
or decreases during inspiration.
5. Murmur of VSD: Harsh pansystolic murmur best heard at the 3rd or 4th left inter costal space, but
radiating all over the precordium. The murmur increases during transient exercise, but is unchanged by
respiration.
6. Murmur of mitral stenosis: Mid diastolic murmur often with a presystolic accentuation, well localised to
the apex. It is low pitched, rough and rumbling character, best heard at the apex with the bell of the
stethoscope, with patient in left lateral position and during expiration. Murmur is accentuated during
exercise carried out just before auscultation
7. Carey coombs murmur of rheumatic carditis: Soft, mid diastolic murmur, well localised to the apex.
8. Austin Flint murmur ofaortic regurgitation:Rumbling, midiastolic murmur, without a presystolic
accentuation even in the presence of sinus rhythm. It is best heard at the apex.
Other sounds:
Opening snap: It is a high pitched, loud snapping or clicking sharp sound due to sudden tensing of cusps
of the valves. It is heard midway between the 2nd and 3rd heart sounds in MS & TS just inside the apex. It
is best heard with diaphragm and is not related to respiration or posture. It has to be distinguished from
split S2 which is softer, heard in normal individuals in 2nd and 3rd ICS and the interval between two
sounds is shorter.
Pulmonary Ejection click: It is high pitched click like sound coming immediately after S1. It present in PS,
PHT and best heard during inspiration.
Pericardial rub: A superficial leathery or cracking sound synchronous with heart beat both during systole
and diastole. Variation with posture is seen, but affected by respiration. It is heard in pericardial effusion
EXAMINATION OF OTHER SYSTEMS:
Respiratory system: To rule out pleural effusion, presence of COPD that might have led to right
ventricular enlargement and to rule out other respiratory diseases.
Per abdomen: Examined for ascites and hepatomegaly as a consequence of CCF.
Central nervous system: To rule out embolic cascades secondary to heart disease.
NOTE: 1) whenever you suspect atrial fibrillation while examining the pulse( irregularly irregular pulse)look
for pulse deficit. Pulse deficit is the difference between heart rate( on auscultation) and the pulse rate. It is
assessed by simultaneously auscultating the heart and palpating the radial pulse .This is done with the
help of an assistant. Note the difference between the heart rate and the pulse rate.This is known as pulse
deficit and is significant if the difference is more than 10 beats. Pulse deficit is seen in atrial fibrillation.
Mechanism: In atrial fibrillation, the rate is irregular. So the length of the diastoles is variable.This leads to
varying stroke volumes. Only the stroke volume which is sufficient enough to produce the pulse wave can
be palpated. Thus there is pulse deficit.
2) In a case of suspected aortic regurgitation, always record the BP in both the upper and lower limbs. In
either case, take an average of at least two readings.
To record BP in lower limb, tie the cuff to the thigh (a larger cuff is used) and palpate/ auscultate the
popliteal artery (the procedure is similar to that in the upper limb). If a larger cuff is not available, use the
upper limb cuff and tie the cuff to the calf and palpate/ auscultate the tibialis posterior artery.

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THE RESPIRATORY SYSTEM

CLINICAL ANATOMY
The respiratory tract for the sake of convenience is divided into upper respiratory tract consisting of
nasopharynx, pharynx larynx and lower respiratory tract consisting of trachea, bronchi, small airways and
lung parenchyma. The level of division is at the cricoid cartilage C4.
Surface marking
1. Apex of lung: it extends superiorly 1 inch above medial 1/3rd of clavicle. The margin of pleura
corresponds to lung borders.
2. Inferiorly: the lung extend upto 6th,8th &10th ribs in mid clavicular, mid axillary and mid scapular line
respectively. Similarly the pleura extend upto 8th,10th, 12th rib in the MCL, MAL, and MSL respectively.
3. Each lung is divided by oblique fissure called the major interlobar fissure into upper and lower lobes. A
line drawn front 2nd thoracic spine which runs forwards, downwards and medially meeting the 5th in mid
axillary line and further ending at 6th costal cartilage fissure in the anterior aspect represent this fissure.
4.The right lung is further divided by horizontal fissures.a line drawn from the sternum to oblique fissure at
the level of 4th costal cartilage represent this fissure.Thus the right lung is divided into three lobes upper,
middle & lower lobes.
As a result of obliquity of horizon fissure, major part of the lower lobe is posterior and the upper lobe&
middle lobes are anteriorly placed.
For convenience of examination, the area of chest is divided as follows:
Anteriorly: (upper and middle lobe on right side and upper lobe on left side)
* Infraclavicular: extend from clavicle to 3rd rib.
*Mammary :extended from 3rd rib downwards.
Laterally:
Axillary: extends from the 6th rib (parts of all the 3 lobes are present)
Infraaxillary: extends arbitrarily downwards from 6th rib onwards (parts of lower lobe)
Posteriorly:
Suprascapular and interscapular (parts of upper lobe)
Infrascapular and lower interscapular (parts of lower lobe)
Louis angle: It is the bony prominence at the junction of manubrium sterni and body of sternum. It is at the
level of 2nd costal cartilage. It represents the level which*Lungs meet anteriorly
*Trachea bifurcates
*Upper level of atria
*JVP is measured
* Convenience for counting the intercostal space

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SYMTOMATOLOGY
THE 6 PRINCIPAL SYMPTOMS OF RS are: cough, sputum, hemoptysis, chest pain, breathlessness, and
wheeze.
The symptoms should be recorded in chronological order and analyzed. Proper documentation of the
symptoms provides a vital clue regarding the probable diagnosis for e.g. In COPD if breathlessness
preceded cough is most likely emphysema & if cough with sputum has precede breathlessness is most
likely to be chronic bronchitis.
SYMPTOM ANALYSIS
COUGH: forced expiration against closed glottis which clears the trachea bronchial tree of any foreign
material or secretion. it is a protective reflex and can be voluntary or involuntary being provoked by
physical,chemical, or mechanical stimuli irritating the mucosa of any part of the respiratory tract and even
from irritation of the pleura.
Cough reflex: afferent 5th, 9th, & 10th CN. Centre- medulla & efferent- 10th and spinal nerve supplying the
abdominal and intercostals muscle.
Analyze the following aspects in cough.
Nature:
Dry- In pharyngitis, allergic bronchitis
Productive- In lower respiratory tract infection like pneumonia, bronchitis, bronchiectasis,
pulmonary Tuberculosis etc
Onset:
Sudden- In acute asthma,massive pulmonary embolism & pneumothorax.
Gradual-In chronic bronchitis.
Duration:
Short duration- In Acute bronchitis, pharyngitis etc,
Long duration- in COPD, TB, allergic bronchitis, fibrosing alveolitis etc,
Diurnal variation:
Early morning and night-chronic bronchitis, bronchiectasis
Cough disturbing patients sleep in nights-pulmonary edema,asthma.
Postural variation:
In bronchiectasis & lung abscess when the patient lies in the opposite side of the lesion. This is
because the postural drainage of the mucus into the healthy bronchi stimulates cough reflex.
Sputum production:
Comment on quantity, colour ,consistency, odour & presence of blood.
Note the quantity in term of spoons, cups, or any other container
Normal
Scanty
Moderate
Copious

75 to 100 ml in 24 hour
100 to 200 ml in 24hour
200 to 500 ml in 24 hour
>500ml in 24hour

Note the character (colour and consistency) of the sputum as follows:

* Serous (if watery)-In acute pulmonary edema.
* Mucoid (if sticks to the container)-chronic bronchitis, chronic asthma(tenacious sputum).when allowed

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to settle in a container, mucoid sputum is uniformly thin and is whitish in colour.

* Mucopurulent(If sticky and yellowish)-In infections (due to myeloperoxidase).When allowed to settle in a
container, it separates into three layers:an upper thin layer, middle thick layer and a lower thick layer.
* Purulent (If yellowish green /foul smelling)-In infections (in asthma,sputum can be yellow without
infection due to the presence of eosinophils. If the sputum is very foul smelling,think of anaerobic
infections).When allowed to settle in a container, it is uniformly thick.
* Frothy- In acute pulmonary edema.
* Rusty- In pneumonia.
* Black-in aspergillosis, soot depositions.
* Anchovy sauce-In rupture of amoebic liver abscess into the lung,
* Red current jelly-In bronchogenic carcinoma.
Hemoptysis: Expectoration of blood.
Causes:
1.Respiratory: TB, bronchogenic ca, pulmonary embolism, lung abscess, bronchiectasis, bronchial
adenoma, trauma.
2 Cardiac:
Mitral stenosis, aortic aneurysm, primary pulmonary hypertension.
3 Immunological: Good pasteur's syndrome,wegener's granulomatosis and PAN.
4 latrogenic: Lung biopsy, bronchoscopy.
5.Bleeding disorders: Thrombocytopenic purpura, hemophilia,leukemia.
6 Spurious:Trauma,ulcers and lesions in the mouth,pharynx and larynx.
7 Functional
Commonest cause for hemoptysis in India-Tuberculosis
* Note the frequency and quantity of blood expectorated.
* Note the type.
Types of hemoptysis
*Frank blood-TB,Ca bronchus,bronchiectasis.
*Blood stained-(inseparable from sputum)-Pulmonary edema.
*Blood streaked (Blood streaks can be separated from the sputum)- chronic bronchitis
Always diferentiate bw hemoposis and hematemesis so that the appropriate investigation can be
started as early as possible.
Hemoptysis
Sensation of tingling in throat& cough
precedes the outpour of blood
Blood is usually bright red
May be associated with sputum
Frothy due to mixture with air
Massive hemoptysis >500ml

Hematemesis
Nausea,abdominal discomfort precede the
outpour of the blood
Coffee ground
Associated with gastric contents
not frothy

Chest pain:
Enquire into the following aspects:
*Onset: Sudden onset-In spontaneous pneumothorax.
Gradual-pleurisy.
*Site of pain: To differentiate from cardiac, gastrointestinal. Respiratory chest pain is
lateralized.
*Type: Sharp/stabbing, related to deep breathing and coughing-In pleuritis (this
usually subsides after pleural effusion develops)
Lateral/low down, aching pain-ln spontaneous pneumothorax.
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usually

32

*Aggravating /relieving factors:

Costochondral pain is aggravated by movements.
To differentiate from cardiac causes-angina is aggravated by stress & relieved by
rest while pleural pain is aggravated on deep breathing and coughing.
*Any preference to sleep on a particular side?
In almost all respiratory diseases,the patient prefers to sleep on the side of affectation of the
disease so that he can comfortably breathe with the help of the unaffected side.
Breathlessness: It is the abnormal uncomfortable subjective awareness of ones own breathing.
Enquire into:
*Onset: Gradual in emphysema.
Sudden-in acute pulmonary embolism, spontaneous pneumothorax.
*Progress-It worsens day by day, despite treatment in emphysema.
*Aggravating factors-exercise/weather/smoke/anxiety(especialy in asthma)
*Relieving factors-humidified air in bronchiolitis.
*To what extent is it exertional?
*orthopnea/Paroxysmal nocturnal dyspnea (to differentiate from cardiac cause)
Wheeze:
*onset

* Aggravating factors

Associated symptoms:
*Fever continous-in pneumonia
Evening raise in TB
Why is there evening of temperature in TB?
Actually there is no definite evening rise of temperature of the body,but the patient feels so tired at the end of the day
that the relative cool climate in the evening makes him feel that he has fever.

*Anorexia -TB/brochogenic Ca
*Weight loss-TB/bronchogenic Ca
*Abdominal symptoms
*Headache- CO2 narcosis
*Edema- Corpulmonale
PAST HISTORY:
h/o bronchial asthma/allergy/TB.
GENERALPHYSICALEXAMINATION:
Observe the build, the nourishment of the patient (emaciation occurs in chronic diseases like TB,Ca)
See if he is toxic or dyspnoeic
Criterla to say a patent is dyspnoeic
1.Respiratory rate >40/min
2.Accessory muscles of respiration in use
3. Patient is unable to speak in sentences or even worse in words
Make a note of the following aspects:
Temperatures
Pulse rate(pulsus paradoxus is seen in severe bronchial asthma)
Respiratory rate
BP
JVP: It is pulsatile and raised in RVF.
It is nonpulsatile, but raised in SVC obstruction.
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Pallor: An anemic patient can become polycythemia due to chronic hypoxaemia as in chronic Bronchitis.
Cyanosis: In COPD,central cyanosis is seen.
In SVC obstruction due to Ca bronchus, peripheral cyanosis is seen.
Lymphadenopathy (scalene nodes- in ca bronchus, TB)
Pedal edema-In corpulmonale in RVF.
Clubbing- seen in lung abscess, empyema, bronchiectasis, bronchogenic Ca.
Head to toe examination:
o Eyes- Horner's syndrome (in Ca bronchus), phlyctenular conjunctivitis (TB)
o Face- swelling in SVC obstruction, pursed lip breathing in emphysema.
o Neck- Scalene lymph nodes (in TB, Ca bronchus)
Upper Respiratory Tract Examination.
RESPIRATORY SYSTEM EXAMINATION:
Examine the patient in standing position.
Inspection:
Shape of the Chest:
Transverse diameter and antero posterior diameter.
The normal T-diameter : AP diameter=7:5 The ratio reverses in emphysema.

How to measure subcostal angle?

Place the 2 thumbs in the subcostal region in such a way that they meet in the midline.
Measure the Angles between them.
How to measure the diameter?
For Transverse diameter-Place 2 books parallel to each other one in each armpits and
measure the distance between them.
For AP diameter-Place 2 books one over the back and the other over the anterior chest
wall,both parallel to each other. (Take the help of the patient or an assistant) Measure
the distance between these two.
Hemithoracic diameters on both sides should be measured at the level of T10 vertebra

Observe for any bulging/ depression

Bulging - in pleural effusion, pneumothorax.
Depression- in fibrosis, collapse, muscle wasting,
Subcostal angle: Normally it is 700. It is increased in emphysema.
Shoulders: Drooping-in apical fibrosis, scoliosis.
Spine :See for any kyphosis/scoliosis. Because these can give rise to signs mimicking fibrosis.
Spinoscapular distances:
Increased in pleural effusion, pneumothorax.
Decreased in fibrosis, collapse.

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Various shapes of the chest:

1. Normal shape:Bilaterally symmetrical. On cross section it appears ellipsoidal. The transverse diameter
is greater than the antero posterior diameter (7:5). the subcostal angle is about 700 and intercostal
spaces are broader anteriorly than posteriorly.
2. Funnel chest (pectus excavatum): Depressions in the lower part of the sternum. It could be
congenital or due to rickets or occupational as in cobblers. There may be displacement of apical
impulse & trachea & may cause murmurs due to Compression of the heart.
3. Barrel shaped chest : AP diameter is more than Transverse diameter. Angle of Louis is prominent
and ribs are less oblique. It is seen in emphysema.
4. kyphosis : leads to barrel chest.
5. Scoliosis: due to congenital deformity, rickets, poliomyelitis. It shifts the trachea and apex beat.
6. Bulging of one side of the chest:In pleural effusion, pneumothorax.
7. Depression of one side of the chest: in fibrosis and collapse.
8. Pigeon chest (Prominent sternum or Pectus carinatum): here AP diameter is increased. It can be
congenital, in rickets, nasopharyngeal obstruction.
9. Typical shape in rickets:
Rickety rosary (prominent costochondral junction)
Harrison's sulcus (a groove passing from the xiphisternum to the midaxillary line)
Pigeon chest.

Respiratory rate:
Normal -16 to 20 per minute.
Decreased [<10/min]-in opium poisoning, brain tumors,
Increased [>40/min]-in fever,excitement,anoxemia,acidosis.
Rhythm:
Types in rhythm
1. normal- regular, duration of inspiration more than expiration.
2.cheyne Stokes respiration or periodic breathing-rhythmical alteration of apnoea & hyperpnoea.Occurs in
LVF,opium/barbiturate poisoning, damage to medulla.
3. Kussmaul's respiration- deep and rapid breathing. occurs in diabetic ketoacidosis and in uremia.
4. Biot's respiration -irregularly irregular breathing. Occurs in meningitis
Character of breathing:
Abdominothoracic- In males
Thoracoabdominal-In females,
Only thoracic-In diaphragmatic paralysis, peritonitis, severe ascites
Only abdominal- In pleurisy, collapse
Movements of the chest:
Normally both sides of the chest wall move uniformly & there is no bulging or in-drawing of the
ICS.Accessory muscles of respiration are seldom used.
Movements of chest can be observed by Making the patient lie in the supine position & observing the
movements from foot end of the patient.
The movements are decreased in: Consolidation, fibrosis, collapse, pnemothorax & emphysema.
Any accessory muscles used, intercostals retraction etc.
Any sinuses, dilated veins, scars, etc.
Mediastinum: to know the shift
1. Trachea: on inspection look for Trail's sign. Presence of it indicates upper mediastinal shift.
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What is Trail's sign?

The clavicular head of sternocleidomastoid appears prominent on the side of towards
which the trachea is shifted.This is because the shift of trachea makes the pretracheal
layer of the deep cervical fascia lax & thus making the muscle more prominent.
2. Apex beat: shift of apical impulse indicates lower mediastinal shift.

Same side

Mediastinal shift in various disease

Collapse, fibrosis, pleural thickening

Opposite side

Pleural effusion, pnemothorax, hydropneumothorax

Palpation:
l. Local rise of temperature-seen in empyema
2. Intercostal tenderness-empyema, ameobic,liver abscess
3. Confirm all inspectory findings including the position of trachea
4. Respiratory movements & chest expansion
How to palpate for the trachea?
Slightly flex the neck of the patient & stabilize it & place your index & ring fingers on the
medial ends of the clavicle on either side & gently push the middle finger inwards.
Normally the resistance of trachea is encountered. When the trachea is shifted to one
side the palpating finger slides to the opposite side.
How to assess the respiratory movements during palpation?
Anteriorly:
a) Infraclavicular areas: Place your palms over the chest wall over the infraclavicular areas. Instruct
thepatient to breathe deeply. Observe the anteroposterior movements of your palm & compare the
move on the two sides.
b) Supraclavicular areas:stand behind the patient & place your hand in such a way that the fingers lie
anteriorly over the supraclavicular areas & the thumbs meet posteriorly firmly in the midline. Instruct the
patient to breathe deeply. Observe the upward & downward movement of fingers and compare the two
sides.
c) Posterior parts of the chest: Place the hands in such a way that the thumbs meet in the midline with a
fold of skin in between them & the fingers are spread laterally. observe for the separation of thumbs.
d) Next keep the thumbs firm & observe for the outward movements of the rest of the fingers on both the
side to know the chest movements on the lateral side. Compare movements on both sides.
Measure the maximum expansion using a measuring tape placed at the level of the nipple. Also
measure the hemi-thoracic expansion on both sides.
5. Tactile vocal fremitus: Place the ulnar border of your hand on the chest wall & ask the patient to utter
consonants like "one", ninety nine", repeatedly & feel for the vibrations. Compare respective areas
alternately on both sides.
variation of TVF are discussed under VR.
Percussion:
Percussion was discovered by Arnold vonbrugger'

36
PESCADOC

Cardinal rules of percussion:

1. Pleximeter (usually the middle finger of the examiner's left hand) is firmly applied to the chest wall so
that no air pockets are interposed between chest wall.
2. Plexor (usually the middle finger of the examiner's right hand ) is kept flexed at a angle & must hit the
middle phalanx of the pleximeter perpendicularly with the pad & not the tip of finger.
3. Percussion note must be sudden, the plexor being withdrawn immediately after the stroke & the
movement of percussion should originate at the wrist.
4. Percussion should proceed from resonant to dull or from more resonant to less resonant areas.
5. Force of percussion stroke must be varied according to purpose of percussion, tissue/organ being
percussed, area of the chest wall percussed etc. however the force of stroke must be kept absolutely
constant while comparing symmetrical areas the chest.
6. During percussion of the chest pleximeter should be kept along the interspace rather than obliquely
across the ribs.
7. When delineating the borders of an organ such as liver, heart, the long axis of pleximeter should be
kept parallel to the expected position of that border.
8. Area percussed must be more or less equidistant from the two ears of the examiner in order to prevent
wrong interpretation.
The areas to be percussed on the chest wall are as follows:
Posteriorly
Laterally
Suprascapular
Axillary
Interscapular
Infraaxillary
nd
rd
Infrascapular
Infraclavicular (2 & 3 ICS)
Anteriorly
Kronig's isthmus
Clavicle

Mammary (4 & 5th ICS)

Inframammary (6th ICS&

downwards)
Kronig's isthmus is a band of resonance 5-7 pm in width connecting lung resonance over the anterior and
posterior aspects of each side of the chest. It is bounded medially by the dullness of the neck muscles &
laterally by the dullness of the shoulder muscles.
Variants of percussion notes over the chest wall:
Tympanic -pneumothorax, empty cavity
Subtympany- above the level of pleural effusion
Hyperresonant- pneumothorax, emphysema, severe asthma
Resonant- normal lungs, bronchial asthma, bronchitis, interstitial lung diseases
Impaired- localised fibrosis, cavitation, bronchopneumonia
Dull-collapse, consolidation, pleural thickening
Stony dull- pleural effusion
Liver dullness-The span of normal liver dullness is 5th right ICS in MCL, in the 7th ICS in anterior MAL
and in the 9th ICS in MSL.
Alterations in liver dullness:
Shifted up- liver abscess, diagphragmatic paralysis, collapse of lower lobe of lung.
Shifted down-emphysema, rt. sided pneumothorax.
NOTE: while doing the liver dullness simultaneously do the tidal percussion.
Tidal percussion- first percuss the upper border of liver dullness.Ask the patient take deep
breath and now again. Normally the upper border of liver dullness shifts by 1-2 spaces down
during inspiration due to expansion of the lungs. This doesnt happen in emphysema, massive
pleural effusion, hepatic amoebiasis etc
37
PESCADOC

Cardiac dullness- normally the dullness extends upto 3rd & 4th ICS in the left parasternal region & 5th
ICS in the MCI,
It is decreases in- emphysema, left pneumothorax
Increased in- pericardial effusion, cardiomegaly
Percussion of Traube's area- It is a quadrangular area having
Boundaries: above-lung resonance. below-costal margin. On right- left border of liver.On left-spleen.
Normally it is tympanic due to air in the underlying fundus of stomach.
It becomes dull in left sided pleural effusion (this is the earliest sign in pleural effusion.) other causespericardial effusion, massive cardiomegaly, ca stomach
In case of suspected hydropneumothorax always do the following tests:
Shifting dullness
Coin test
succussion splash
Ideally in all cases of pleural effusion these tests have to be performed to rule out hydropnemothorax.
Shifting dullness- Make the patient to sit down and percuss from the clavicle
downwards up to the level of dullness and then one space downwards. Now, ask the
patient to lie down supine with your pleximeter over that space ( do not remove the
finger until the procedure is over). Now percuss. If u get resonant note now it implics
hydropneumothorax due to displacement of air.
Coin test-place a one rupee coin at the junction of resonance and dullness (i.e. at the
junction of air and water) and ask somebody else to percuss the coin with another coin.
And you keep the stethoscope diaphragm over the posterior part of the hemithorax at
the same level. Hear the sound produced. It'll have a metallic quality. Compare with
normal side to appreciate it.
Succussion splash- ask the patient to sit down, keep the stethoscope at the junction of
dullness and resonance with the help of one hand. Now with the other hand shake the
shoulder of corresponding hemithorax in a jerky manner once or twice. A splashing
sound will be beard through the stethoscope.
NOTE:
1)In pleural effusion the percussion note is stony dull which is highest laterally and lower anteriorly and posteriorly,
(ELLIS 'S' shaped CURVE)
2) In moderate to large sized pleural effusion a triangular area of dullness or impaired note can be percussed over
the back of the chest on the opposite side of pleural effusion. It is probably due to shifting of posterior mediastinum to
the opposite side of the pleural effusion. This area is known as GROCCO'S TRIANGLE, and
the sign is called as GROCCO'S SIGN.

AUSCULTATIONPrinciples1. Ask the patient to breathe well.

2. Put the diaphragm gently but firmly over the chest wall and listen whether the air entry is good
throughout the chest.
3. Now concentrate on the type of the breath sounds and adventitious sounds heard.
4. First auscultate on normal side and then compare it with other side.
5. The areas to be auscultated are same as those of percussion
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PESCADOC

Breath soundsEvery breath sound has phases. A phase of active inspiration, followed by a phase of expiration. Active
inspiration is due to the passage of air into the bronchi and alveoli and passive expiration is due to the
elastic recoil of the alveoli.
Normally on auscultation inspiration is longer than expiration without a pause in between. The sound is
low pitched and rustling in quality due to the alveolar phase. This is known as vesicular breath sound.
In certain conditions like consolidation (pneumonia), the alveolar phase is absent. So the expiration is as
long as inspiration. And since there is no alveolar phase, there is no rustling quality and there is a pause
between inspiration and expiration. Instead it is blowing in quality. This is known as bronchial breath
sounds.
Bronchial breath sound is normally heard over trachea. It is also heard over a cavity, open pneumothorax
and above the fluid level in pleural effusion.
There are 3 types of bronchial breath sounds
1. Tubular- high pitched. Heard over consolidation, cavity, above the level of pleural effusion.
2. Cavernous- low pitched. Heard over an irregular cavity.
3..Amphoric- low pitched with high pitched overtones. Heard over smooth walled cavities and open
pneumothorax.
In obstructive lung diseases (bronchial asthma, COPD), the inspiratory phase is normal but the expiratory
phase is delayed due to obstruction. This type of vesicular breath sounds with prolonged expiration is
known as BRONCHOVESICULAR BREATHING.
Added Sounds:
Rhonchi: These are musical sounds heard due to the passage through the narrowed airways there are
two types
a) Monophonic: Partial obstruction of a single airway causes a single type of sound
Example- foreign body/tumor compressing over an airway
b) Polyphonic: Partial obstruction of more than two airways causes more than one type of sound
Example- Bronchial asthma. Chronic bronchitis
Note: Rhonchi or wheezes should be differentiated from stridor which is almost always inspiratory while
Rhonchi may be both inspiratory or expiratory. In addition stridor results from partial obstruction of the
upper respiratory tract and Rhonchi originate from lower airways.
Crepitations: These are cracking type of sounds. There are two theories for their cause:
a. Sudden opening of the airways due to the passage of the air through the almost collapsed airways.
b. Passage of air through the secretion in the airways.
The first theory holds good in pneumonia. The second theory holds good in pulmonary edema.
There are three types 3
(1) Fine crepitations-in pulmonary edema
(2) Coarse crepitations- in pneumonia
(3) Leathery crepitations- in bronchiectasis
Post tussive rales-These are crepitations heard after the patient takes a deep inspiration and coughs out
Presence of these rales is pathognomonic of TB cavity.
Vocal Resonance:
1. vocal resonance is decreased/absent in pleural effusion, pneumothorax, thickened pleura, emphysema.
2. It is increased in consolidation

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3. Alterations in vocal resonance are:

a) Bronchophony-sounds are loud and clear, but words can't be distinguished. Seen in consolidation.
b) Aegophony- when spoken are auscultated they sound like the bleating of the goat.Seen above the level
of pleural effusion.
c) Whispering pectoriloqy- when words are whispered, They are clearly picked up by
the steth. Seen in
cavity communicating with bronchus,consolidation.
EXAMINATION OF OTHER SYSTEMSCVS: As a routine, to rule out any cardiac abnormalities that might have lead to respiratory complications
and to rule out corpulmonale secondary to respiratory disease.
Per abdomen: As a routine, to rule out ascites in case of pleural effusion [e.g. in Meig's syndrome]
CNS: As a routine, to rule out CO2 narcosis. etc...

Note: Blue bloaters are called so because they suffer from recurrent attacks of cyanosis (blue) and CCF
(blotted due to edema)
Pink puffers are called polycythaemic (pink) secondary to hypoxemia and breathe through punctured lips
(puffers)

40
PESCADOC

HOW TO ARRIVE AT DIAGNOSIS

Disease

History

G.P.E

consolidation

Fever,chest
pain,breathle
ssness

Chronic
bronchitis

chronic
cough with
mucoid
sputum for 3
months in 2
years
dyspnea of
gradual onset
& progressive

May or
maynot be
toxic/
dyspnoeic
Blue
bloaters in
advancedsta
ge

Emphysema

Bronchial
asthma

collapse

fibrosis

Pleural
effusion

pursed lip
breathing &
pink puffers
in advanced
Stage

Insp/palp
----------

Percussion
Impaired dull

normal

Barrel chest,
Tracheal tug,
retraction of
lower
ICS

Hyper
resonant,
obliteration of
liver &cardiac
dullness.

cyanosis
may be
present

sudden onset
of
breathlessne
ss
history of
Koch's

dyspnoeic

dyspnoeic

chest
retraction
movements,m
ediastinal
shift to
the same side

impaired

H/O of
breathlessne
ss & or fever
with cough
h/o evening
rise of
temperature

may be toxic

fullness on
affected
side,moveme
nts,effusion
mediastinal
shift to
the opposite
side

Stony dullness

flattering of
the affected
side

Dull note

gradual onset
of
breathlessne
ss

pneumothorax

sudden onset
of
breathlessne
ss,may be
spontaneous
or traumatic

VR

normal

normal

Whispering
pectoriloquy

Added
sounds
Crepitations
in resolving
phase
Rhonchi,
crepitations

-----------

episodic
cough
wheeze chest
tightness

Pleural
Thickening

Breath
sounds
Tubular
bronchial

normal

Bilaterally
--------------

diminished

normal

Rhonchi

---------------

-------------

impaired
--------------

dyspnoeic

crepitations

Or absent

------------

-------------hyperresonant

----------------

---------------

41
PESCADOC

THE ABDOMEN

Examination of the abdomen involves study of the GIT, the hepatobiliary system and the genitourinary
tract.
In the following chapters we concentrate mainly on GI diseases.
Symptoms of GI diseases are complex and often vague which require careful analysis to be followed by
thorough clinical examination.

Symptomatology
disorders of the GIT may present will following symptoms: Nausea, vomiting, dysphagia, dyspepsia, pain
abdomen, distension of abdomen, diarrhoea, constipation, hematemesis,melena, jaundice, anorexia
haematochezia, heart burn, water brash and flatulence.
Symptom analysis
Nausea: It is an impending sense of vomiting.
Vomiting: Forceful expulsion of the contents of the stomach outside.
Retching:Rhythmic contractions of the abdominal muscles preceding or associated with vomiting
Belching : Chronic repetitive eructations.
Regurgitation: appearance of previously swallowed food in the mouth without vomiting, e.g.achalasia
cardia.
Anorexia: Loss of appetite or lack of desire to eat.
Causes of Vomiting
Non alimentary

Gastritis
Peptic ulcer
Gastroenteritis
Biliary colic
Acute abdomen
Viral hepatitis

Alimentary
Neurological- anxiety, meningitis, raised
ICT,middle ear disorders, migraine.
Psychological- bulimia, anorexia nervosa
Metabolic -CRF, diabetic ketoacidosis,
pregnancy, uremia.
Drugs- alcohol, morphine, opioid.
Severe pain eg: MI, renal colic.

Vomiting is often preceded by nausea in acute gastritis, gastric outlet obstruction, acute GE, acute
abdomen and in other alimentary causes.
Vomiting occurring without being preceded by nausea is called 'Projectile Vomiting'. It is seen in
conditions causing raised ICT like cerebral tumour, hemorrhage and other space occupying lesions.
Vomiting Reflex
Afferents from GIT (carried by the vagus)

CTZ (floor of fourth ventricle)

Efferents through spinal nerves, phrenic nerve, vagus.

NOTE: the frequency of vomiting, the taste colour, smell and diurnal variation.

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PESCADOC

Yellowish and bitter vomiting is seen in biliary causes.

Foul smelling in pyloric stenosis, carcinoma stomach (due to gastric outlet obstruction)etc.
Faeculent in ''gastrocolic fistula, intestinal obstruction (below the level of caecum) etc.

Enquire into the presence of blood in the vomitus and the colour of the blood.
Hematemesis is bright red in pharyngeal and esophageal lesions.
It is coffee ground (true hematemesis) in erosive gastritis, peptic ulcer, and oesophageal varices.
It is important to differentiate hemoptysis from hematemesis and this has been discussed in the chapter
Respiratory System'.
Vomiting has to be differentiated from regurgitation' which is passive expulsion of stomach contents
without accompanying contraction of the abdominal muscles.eg:Achalasia cardia.
Dysphagia:
1. It is difficulty in swallowing.
2. It is mostly seen in oesophageal diseases like achalasia cardia, malignancy, scleroderma,
strictures,pharyngeal pouches and webs.
3. Dysphagia is intermittent in pharyngeal pouch etc.
4. It is progressive to solids in CA, progressive to liquids in achalasia cardia.
5. It is painless in neurological disturbances.

Aphagia: Complete inability to swallow.

Odynophagia: Retrosternal pain during swallowing.
Phagophobia: Fear of swallowing.
Sitophobia: Fear of eating because of subsequent abdominal discomfort seen in regional enteritis and in
chronic mesenteric vascular insufficiency (abdominal angina).
Aerophagia: Air swallowing
Globus pharyngeus: Sensation of lump lodged in the throat.
Water brash: sudden filling of the mouth with as a reflex response to a variety of symptoms from upper
GIT.
Hematemesis: vomiting of blood
Haematochezia: Passage of frank blood per rectum.
Dyspepsia
It is a vague upper abdominal discomfort accompanied by nausea and a sensation of bloated abdomen.
Causes are peptic ulcer, upper GI dysmotility, reflux oesophagitis etc.
Pain abdomen
Note the following aspects:
1) Onset: Acute in acute abdominal conditions like acute appendicitis.
Chronic in peptie ulcer etc.
2)duration of pain

43
PESCADOC

3) Nature of pain : Colicky in intestinal colic, biliary colic,ureteric colic.

Aching in peptic ulcer and pancreatitis etc.
4) Intensity of pain
5) Radiation pain:
Pain of acute appendicitis is initially periumbilical and later radiates to right iliac fossa.
Pain of acute pancreatitis is epigastric in origin and radiates towards the interscapular region.
Pain of ureteric colic is lumbar in origin and radiates towards the groin.
6)aggravating and relieving factors:
Pain of gastritis is aggravated on ingestion of spicy/oily food, alcohol etc. and relieved on ingesting
milk,banana, egg etc.
Pain of gastric ulcer is aggravated immediately after taking food.
Pain of duodenal ulcer is relieved on taking food. Actually in duodenal ulcer, pain is aggravated after
about 1-2 hours after ingestion of food because it takes that much time for the stomach to empty its
contents into the duodenum. This delay in aggravation of the pain makes the patient think that intake of
food relieves the pain when actually it does not.
7) Associated symptoms:
vomiting/diarrhoea in gastroenteritis.
vomiting/constipation in intestinal obstruction.
Urinary disturbances (Increased frequency of micturition on cystitis, retrocolic appendicitis, etc).
Rashes over the skin in Henoch Schonlien purpura.
Bloating of abdomen and vomiting at the end of the day in pyloric stenosis,
Associated symptoms like sweating, breathlessness, menstrual disturbances, scrotal pain and
unconsciousness should be asked to the patient to rule out non GIT causes of abdominal pain.
Causes of abdominal pain
Non GI causes
Peptic Ulcer
Gastritis
Pancreatitis
Biliaryl Intestinal colic

GI causes
Interior wall MI
Pleurisy
Lower lobe consolidation
Diabetic Ketoacidosis
Ureteric colic, torsion of ovarian cyst/testis

Distension of the abdomen.

Acute in acute intestinal obstruction, peritonitis, paralytic ileus, hepatic/portal vein obstruction.
Chronic in ascites due to cirrhosis, tuberculous peritonitis, CCF etc
.
Generalized in ascites.
Localised in tumors, organomegaly etc
Painful distension in acute intestinal obstruction
Painless distension in chronic constipation, obesity.
The principal causes of abdominal distension have been known as 5 F's: Fat, flatus, faeces, fluid and fetus.
Diarrhoea
There are three criteria to define diarrhea
a. More than 200g of stools per day
44
PESCADOC

b. Frequency of >3 times a day

c. Loose consistency
Enquire into the frequency, duration, consistency, associated symptoms, presence of blood or mucus etc.
Tenesnus is a feeling of incomplete evacuation with a persistent desire to defecate.
Constipation: It is defined as passing stools less than 3 times per week.Enquire if the stools are hard,
if there is excessive straining, any bleeding per rectum (as in case of hemorrhoids), etc.
Melena: Passing of dark tarry stools that stick to the container.
It is seen in upper GI bleeding. For melena to manifest, blood loss should be >60ml with a transit time in
GIT of 6-8hrs. (Upper GIT is the portion above the ligament of Treitz)
Haematochezia- Passing of frank blood in stools. It is seen in hemorrhoids, CA rectum, polyps, and anal
fissure.
Jaundice: This is discussed under the chapter "The general physical examination".
Other symptoms: Loss of appetite and significant weight loss.
PAST HISTORY:
H/o similar complaints in the past
H/o acid peptic disease
H/o jaundice in the past.
H/o any blood transfusion, drug intake
H/o DM/HTN/TB
History suggestive of cardiac disease.
H/o previous surgeries
PERSONAL HISTORY
Particular emphasis on diet, appetite, bladder and bowel movements, loss of weight, alcohol intake,
smoking and other habits is required.
GENERAL PHYSICAL EXAMINATION
Concentrate on the following things in addition to the general proforma given in the beginning of the book.
Condition of the patient: whether delirious/toxic/drowsy,
Build/nutrition
Signs of dehydration: loss of skin turgor, sunken eye balls, dryness of tongue. Conjunctiva etc,
Pallor/koilonychia: to rule out anemia
Clubbing (seen in cirrhosis of liver, ulcerative colitis, crohn's disease)
Pedal edema (look for sacral edema and comment on it in a bed ridden patient)
Lymphadenopathy (especially supraclavicular to rule out abdominal malignancy)
Signs of liver failure
Spider naevi: They are complexes of central arterioles with radiating capillaries found usually in the
areas of superior vena caval drainage like chest, arms, face, shoulders etc. They are identified by their
red color which blanches on pressure and when the pressure is released they fill from the centre to the
periphery.They are due to hyperestrogenism.
Palmar erythema: This is seen in thenar, hypothenar eminences and soles. It blanches on pressure
and it is also due to hyperestrogenism.
Parotid swelling (seen more in alcoholic hepatitis)
Loss of body hair especially in the axilla, chest and the chin.

45
PESCADOC

Testicular atrophy
Dupuytren's contracture (seen more in alcoholic hepatitis)
White nails (due to hypoalbuminemia)
Flapping tremors (in hepatic precoma)
Gynaecomastia in men and breast atrophy and virilisation in women.
Jaundice
Clubbing and central cyanosis (due to AV shunts)

Other causes of spider naevi and palmar erythema

2% of healthy individuals
Alcoholic hepatitis
rd
3 trimester of pregnancy
Rheumatoid arthritis
Other causes of flapping tremors
CO2 narcosis
Uremia

Thyrotoxicosis

any organ failure especially renal failure

How to look for flapping tremors?

Ask the patient to outstretch his arms and gently dorsiflex the hand at the wrist The sign consists
of irregular to and fro movements due to flexion and extension of the wrist and the fingers.

Signs of specific vitamin deficiency: bitot's spot (vitamin A deficiency), angular stomatitis(vitamin B
deficiency), bleeding gums and dry skin (vitamin C deficiency)ETC
Skin and hair
Oral cavity: oral hygiene, aphthous ulcers, pigmentation E.g. Addison's disease, Peutz Jegher's
syndrome, gum hypertrophy and bleeding,breathe odour etc.
Vital signs: Particular emphasis on JVP, pulse and temperature.

PER ABDOMEN EXAMINATION

Regions of the abdomen
RH -Right hypochondrium
LH Left hypochondrium
EEpigastrium
RL -Right lumbar
LL -Left lumbar.
UR -Umbilical region
RI -Right iliac
LI -Left iliac
H -Hypogastrium

Abdomen is divided into nine regions by two horizontal lines one across the tip of the ninth costal cartilage
at the level of L1 and the other across upper border of the iliac crest at the level of L3 and the vertical lines
being along the mid clavicular lines.
Examination is done with the patient in supine position. Instruct the patient to flex the lower limbs at the
knee so as to relax the abdominal muscles and breathe deeply.Abdomen and adjoining portions of the
chest and the lower limb are exposed for examination.
INSPECTION
shape of the abdomen
46
PESCADOC

a. Inspect for the shape of the abdomen. In normal individuals the abdomen is usually scaphoid in
shape.on inspection tangentially the abdomen wall appears sunk below the level of the plane connecting
the xiphisternum and the symphysis pubis. Scaphoid shape of the abdomen is exaggerated in
malnutrition,malignancies(cachexia,muscle wasting etc)
b. Inspect for any fullness/distension.Distension may be generalised or localised. Generalised distension of
the abdomen occurs due to ascites,obesity,etc & localized distension may be seen in organomegaly or
tumour like growths,
c. observe and comment on the fullness of the flanks: Seen in massive ascites and term pregnancy.
Umbilicus:
Shape: Inverted-normal umbilicus, obesity etc.
Everted- hernia, massive ascites etc.
Transversely stretched (smiling umbilicus) -in ascites
Colour: Bluish discoloration in and around the umbilicus acute hemorrhagic pancreatitis (Cullens sign)
Cherry red- in inflamed Meckel's diverticulum
Discharge : Ascitic fluid- in massive ascites etc
Faecal matter-in enteric fistula
Clear fluid-in patent urachus (crying umbilicus)
Distance between the xiphisternum and the umbilicus (XU) and the distance between the umbilicus & the
pubic symphysis (UP)
XU=UP in normal abdomen
XU>UP in ascites
XU<UP in ovarian tumour
Distance between the umbilicus and the anterior superior iliac spine on both the sides
The distances increased on the corresponding side of the localised distension in case of a
tumour.
Movements of the abdomen:
See whether all the regions of the abdomen move correspondingly" with respiration
Abdomen bulges during expiration in diaphragmatic paralysis.
Abdomen does not move or moves minimally with respiration in peritonitis.
Pulsations:
Aortic pulsations are felt in thin individuals
In aortic aneurysm, the pulsations are expansile
Pulsations from a tumour sitting over the aorta are of transmitted type and they disappear on putting
patient in knee-elbow position
Pulsations in the epigastrium are seen in tricuspid regurgitation

Dilated Veins:
How to know the direction of the flow?
Put two fingers over the dilated vein one next to the other and separate them, thereby
emptying the vein. Now lift one finger and note the direction of the flow.
Blood flow from below upwards is seen in IVC obstruction (Because the blood from
the lower limbs enters the thoracic veins via superficial abdominal veins)
Blood flows away from the umbilicus radially in portal vein obstruction (Caput medusae)(Because
they are one of the sites of anastamoses between the systemic and portal veins)

47
PESCADOC

Peristalsis:
How to examine for peristalsis?
Make the patient to drink about a litre or two of water. After a few minutes inspect the
abdomen. Tap the abdomen gently and observe tangentially from one side.

Peristalsis is seen
From left to right across the midline over the epigastrium and the right hypochondrium: in pyloric
stenosis.
From right to left over the same regions in transverse colon obstruction.
Step ladder pattern over the periunbilical region in small intestinal obstruction.
Hernial sites: Ask the patient to stand up and cough and inspect the following sites for any
swelling:Superficial inguinal ring, Hasselbach's triangle, femoral triangle, umbilicus and previous
operation scars.
Divarification of recti: Normally the recti muscles on both the sides are continuous with one
another without any gap in between, if there is a gap it is called divarification of recti. This occurs in
congenital defect, massive ascites, pregnancy (multiple) and in obesity.
Skin over the abdomen:Glossy skin-in ascites, abdominal wall edema etc.
o Striae- in previous pregnancy, obesity, massive ascites etc.
External genitalia: Look for meatal stenosis, ulcers, scrotal swelling etc. in males. In females Look
for vulval edema, ulcers, discharge PV, etc.
PALPATION:
Instruct the patient to lie on his back with legs flexed enough to relax the abdomen and to breathe through
mouth quietly and deeply. Use the flat of the hand to palpate, but feel any mass/viscera using the pulp of
fingers.
Look for the following features:
Local rise of temperature
Whether the abdomen is soft: it is usually soft, if it is not, it could be because of guarding/rigidity.
Doughy feeling of abdomen is seen in T.B. ,ascites.
Tenderness: It is present over inflammatory lesions of the viscera and the surrounding peritoneum.
Rebound tenderness can be elicited by exerting a firm pressure with the hand and
releasing it suddenly. A gentle way of performing this test is by gentle percussion. It is a test for deep
seated pain.
Gaurding: It is voluntary and is due to muscular contraction ever a tender region, but the muscles
gradually relax when the patient is put to ease and taken to confidence and asked to breathe slowly and
deeply.
Rigidity: It is involuntary and is due to reflex muscular contraction over a tender region. It cannot be
relaxed. It occurs in peritonitis, perforation, pancreatitis.
Confirm the inspectory findings.
Palpation for the liver ,the spleen and the kidney.

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How to palpate for the liver?

Patient lies in supine position with the lower limbs flexed at the knee. Instruct the patient
to breathe deeply.palpate the abdomen with the flat of the hand keeping the palm in
such a way that the fingers are parallel to the right costal margin, start from the right
iliac fossa and move/slide the palpating palm upwards and deeply with each deep
inspiration, trying to feel for the edge of the enlarged organ which is felt as increased
resistance.Once the edge of the enlarged liver is palpated,find out whether the edge is
rounded/sharp, then palpate over the organ looking for consistency, tenderness and the
surface (nodular or smooth), At the end of your palpation percuss over the organ.
Enlarged liver is dull to percuss.Further measure the liver span by percussion.

How to pulpate for the spleen?

There are three methods for palpation of the spleen
Method 1
With the patient in supine position and instructed to breathe deeply ,palpate from the
right iliac fossa towards the left hypochondrium sliding the hand upwards and deeply
with each deep inspiration.The edge of the spleen is felt during deep inspiration.A notch
may be felt along the edge of the organ.
Method 2.
With the patient in right lateral position ,support the lower ribcage with left hand and
palpate the abdomen with the right hand looking for the edge of the spleen as described
above.
Method 3.
with the patient in right lateral position,stand on the left side of the patient and hook your
fingers under he left costal margin.
Dipping method
This method is used when there is massive ascites,with the patient in supine
position,dip the fingers into the abdomen with each palpation ,so that the fluid is
displaced temporarily and palpation of the organ is facilitated.

Hacket's grading for splenomegaly:

0: not palpable
1: just palpable
2. palpable just above the midpoint between the costal margin and the umbilicus
3: palpable just below the midpoint between the costal margin and the umbilicus
4: palpable below the umbilicus
5: palpable below the midpoint of the spino-umbilical line
Splenomegaly can also be arbritrarily classifed as;
Mild: when it is palpable just below the left costal margin
Moderate: when midway between the costal margin and the umbilicus
Massive: when palpable at or below the level of the umbilicus
How to palpate for the kidney?
With the patient in supine position the left kidney is palpated keeping the left hand posteriorly in
the left loin and the right hand anteriorly in the left lumbar region,Asking the patient to breath
deeply. The left hand is pressed forwards and the right hand backwards,upwards and inwards.lf
palpable,the kidney is felt as a round ballotable mass.The right kidney is palpated likewise.
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How to differentiate between spleromegaly and enlargement of kidney?

Features
1. Direction of enlargement
Movement with respiration
2. Margins
3. Bimanual palpation
4. Ballotability
5. Finger insinuation between the
mass and the costal margin
6. To get above the mass
7. Fullness of the loin
8. Percussion note

Splenomegaly
Towards the right iliac fossa
Moves well
sharp with a notch in the
anterior border
Not palpable
Not ballot able
Not possible

Kidney
Towards the left iliac fossa
Moves less
Rounded margins
no notch
Palpable
Ballotable
Possible

Not possible
Not seen
Dull

Possible
Seen
Band of resonance due to the
overlying colon

Palpate for any other mass per abdomen looking for the shape, size, consistency, borders, mobility and
the plane of the mass.
Measure the abdominal girth at the level of the umbilicus and at the level of maximum distension.

Percussion:
Confirm the span of the enlarged organ by percussion
For distension of the abdomen do percussion to differentiate between gas and fluid.
In ascites, the following features can be observed
a. Horse shoe dullness: This is because the fluid accumulates in the flanks as a result of
producing dullness of horse shoe shape.
b. Shifting dullness

gravity

How to elicit shifting dullness?

With the patient in supine position, percuss the abdomen from the xiphisternum towards the umbilicus up
to the level of the dullness. The pleximeter should be perpendicular to the saggital plane. Go one finger
below and change the direction of the pleximeter i e, parallel to the saggital plane without lifting the
finger. Now percuss towards the flanks. Then without lifting the finger ask the patient to turn to the
opposite side. Now percuss after about 30 seconds. A change of note from dull to resonant confirms the
presence of fluid. Again percuss tack towards the umbilicus till the dull note is obtained. Repeat this on
the other side. This confirms shifting dullness. The minimum quantity of fluid required for shifting dullness
is around one liters.

c. Puddle's sign (in minimal ascites): When fluid present is minimal, it is not detectable either by fluid thrill
or by shifting dullness. In such a case, puddle's sign is helpful in detecting the presence of fluid. It can
detect fluid of around 120ml.

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How to elicit Puddle's sign?

Put the patient in knee elbow position and wait for few seconds. Place the diaphragm of the
stethoscope over the umbilicus and flick the abdominal wall around the umbilicus. A characteristic
puddle sound is heard through the stethoscope

d. Fluid thrill: For fluid thrill, the amount of fluid required is usually >2 litres.
How to elicit fluid thrill?
Fluid thrill is demonstrable in the presence of tense ascites. To demonstrate fluid thrill, the patient
lies in supine position. Instruct the patient to place his/her hands in the saggital plane to avoid
transmission of impulses via the abdominal wall. Flick the abdominal wall on one side and feel for
the impulse on the opposite side with the palm of the other hand.
Auscultation:
1. Bowel sounds: These are exaggerated in partial bowel obstruction and absent in bowel atony/paralytic
ileus.
2. Arterial bruit: In atherosclerosis of aorta and hepatoma.
3. Venous hum: In Porto-systemic shunting.
EXAMINATION OF OTHER SYSTEMS
CVS: To rule out any heart disease leading to ascites, hepatomegaly, etc.
RS :To rule out pleural effusion.
CNS: To rule out hepatic encephalopathy (look for flapping tremors, altered sensorium etc.)

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THE CENTRAL NERVOUS SYSTEM

Diseases of the CNS present in many ways. Whatever may be the mode of presentation, detailed history
must be taken and examination of all the aspects of the Central Nervous system and also the other
systems must be done to arrive at a correct
diagnosis.
PRESENTING COMPLAINTS:
1. Those concerned with the disturbances in the motor system like inability to move the limb or inability to
comb the hair,inability to walk ,stand etc
2. Those concerned with the disturbances in the coordination like inability to walk steadily, or to reach a
particular thing.
3. involuntary movements like tremors.
4. Sensory symptoms like tingling, hyperaesthesia, numbness, shooting pains, dificulty in feeling the
ground, etc.
5. Disturbances of bladder and bowel
6. Disturbances of cranial nerve functions like loss of smell, disturbances in visual acuity, etc.
7. Disturbances of higher function like speech disturbances, vomiting, convulsions, etc.
Record the presenting complaints in a chronological order.
HISTORY OF PRESENTING COMPLAINTS:
In all cases the following aspects should be elicited carefully.
Onset of the symptoms, their progress, duration, any period of relief from symptoms. Enquire whether
symptoms progressed or were stationary and how long the symptoms lasted.
Part of the body affected, as to where the symptoms exactly started, whether they affect both the sides
symmetrically, whether the involvement is that of proximal or distal portion of the limb.
Enquire about precipitating factor, if any, like exercise, sleep posture, reading, eating, coughing,
urination, sex or any other external stimuli.
Associated symptoms if any:
a) Numbness/paraesthesia/cold/warmth
b) Any weakness/clumpsiness/stiffness
c) Headache/nausea/vomiting/loss or alteration of consciousness
d) Any changes in Higher Mental Function like disturbance in consciousness/ behavior/ speech/
memory etc.,
e) Any disturbances suggestive of cranial nerve dysfunction like loss of smell/visual disturbances,
numbness over face, difficulty in chewing, dribbling of saliva from mouth,vertigo/tinnitus/deafness, any
hoarseness of voice,dysphagia,dysarthria, nasal regurgitation
f) Any bladder disturbances: whether the patient has control over his bladder, whether he is having the
sensation of fullness, whether there is any dribbling or retention or incontinence.

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g) Any bowel disturbances--whether the patient is able to have control over his bowel
motion.Whether he is able to perceive defecation reflex.
h) Any mental symptoms like impairment of memory, abnormal change in behavior, etc
i) Any convulsions
j) Any abnormal movements
Any history of trauma should be asked in detail
History of fever: onset, duration, altered sensorium and its relation to the complaints of the patient.
PAST HISTORY: (Ask only relevant questions)
History suggestive of diabetes mellitus, hypertension
History of transient ischemic attacks
History suggestive of cardiac disease
History of head injury
History of fever with altered sensorium
History of epilepsy
History of past drug in take
FAMILY HISTORY
History of similar complaints among family members
History of epilepsy/migraine/vascular disease
History of diabetes mellitus,hypertension
PERSONAL HISTORY:
Enquire in detail about appetite, any alteration in sleep rhythm, bowel and bladder disturbances, any
habits like smoking / alcoholism
GENERAL PHYSICAL EXAMINATION:
Age of the patient
Build nutrition
Whether the patient is alert, conscious, cooperative and comfortable?
Whether his facial appearance is normal?
Whether he is right handed or left handed? (to know the dominant cerebral hemisphere)
Are there any noticeable involuntary movements of the body or the neck and spine?
Decubitus (posture and attitude of extremities) For e g: in hemiplegia, the patient lies the bed with the
affected side immobile, the affected arm flexed and affected leg externally rotated and extended.
Pallor (anemia to vit B12 deficiency can lead to sensory symptoms-subacute combined degeneration)
Icterus (in hepatic encephalopathy, Wilson's disease, etc)
Clubbing (in syringomyelia)
Lymphadenopathy (in disseminated TB, lymphoma, secondaries)
Cyanosis and koilonychia
Edema-pedal/sacral
Skin-neurocutaneous markers like :caf au lait spots in neurofibromatosis and adenoma sebaceum in
tuberous sclerosis, hypopigmented patches in leprosy, hemangiomas, etc Thickened nerves in leprosy,
hereditary polyneuropathy, etc
Spine-to rule out spinabifida, disc prolapse, etc
Head and neck examination

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Thyroid (thyroid disease can cause muscle weakness, cerebellar ataxia, etc)
Signs of meningeal irritation-neck rigidity etc.
Any bruits (seen in AV malformations)

NEUROLOGICAL EKAMMINATION:
Higher functions: The following aspects describe the higher mental functions
Consciousness
General appearance, behaviour and mood
Intelligence
Memory of the past and the present
orientation of time, place and person
Any hallucinations/ delusions
speech and language
Released reflexes
Consciousness-A state of awareness of one's self and one's environment
Alterations in consciousness:
Sleep- patient can be aroused to normal consciousness
Drowsiness- patient can be aroused to normal consciousness but goes back to drowsy state.
Stupor- patient requires very strong stimulus to be aroused.
Coma-an abnormal deep stupor where in the patient cannot be aroused by external stimuli.
Catatonia- limbs are in rigid postures for long hours: seen in psychosis
Akinetic mutism- patient is immobile, makes no sounds but moves his eyes and allows to be nursed:
seen in bilateral frontal lobe lesions.
Delirium- it is an acute confusional state involving global impairment of mental function of acute onset .lts
characteristic features are
a) Impairment of consciousness especially during the evening
b) memory disturbances
c) Perceptual disturbances, especially visual and tactile.
d) Difficulty in thinking.
e) Psychomotor changes
f) Emotional changes.
General appearance, behaviour and mood:
These can be assessed by the following methods:
observe the patient's appearance and manner in which he/she is dressed.
Is he/she cooperative?
Is there any alteration in the behaviour like aggressiveness, childishness, etc?
It there is any change in the mood like mood elation, depression, etc?
Intelligence
Intelligence is assessed by asking simple arithmetic problems like l+2=?, etc.
Memory of the past and the present
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This is assessed by asking the patient what he had for breakfast in the morning, where did he have his
schooling, etc.
Dementia- It is defined as a clinical syndrome characterized by loss of previously acquired intellectual
function in the absence of impairment of consciousness. The commonest causes are Alzheimer's disease
and cerebrovascular disease.
The key features are:
a) Loss of general intelligence
b) Personality changes
c) Memory impairment
d) Emotional changes
Orientation of time, place and person:
This is assessed by asking the patient which place he belongs to? How many children he has? What could
be the time now? (Approximately without looking into the watch) what is his occupation?
Any hallucinations, delusions etc- these should be asked since the patient will not volunteer the
information.
Delusions
Delusion is a persistent false belief despite evidence to the contrary
Types and causes
Holistic (about once body)- seen in schizophrenia
Delusions of guilt-seen in depression
Delusion of grandeur (high estimation of oneself) seen in GPI mania ,schizophrenia etc
Hallucination
Perception of sensation in the absence of any sensory stimulus is called hallucinations
Causes
Visual hallucinations: in migraine
auditory hallucinations: in temporal lobe epilepsy
Delirium tremens: hallucinations of small animal or insect crawling through the room or under the
bed. This occurs during alcohol withdrawal

Speech and language:

The following aspects are tested to assess speech.
1. Comprehension
2. Reception
3. Word output
4. Reading and writing
5. Naming
Disorders of speech
Dysphasia /aphasia: It's a disorder of central speech mechanism where in comprehension and or
expression of meanings and thoughts are deranged partially or completely.
Dasarthria: it's a peripheral speech defect where the abnormality is in articulation or enunciation of
speech.
Types of aphasia
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1) Sensory aphasia: Dysfunction in the afferent area. i e, failure to comprehend visual or written
messages but word output is normal. It is seen in the lesions of the dominant posterior perisylvian
area(temporal lobe)
There are two types:
i)
Wernicke's aphasia (repetition is defective)
ii)
Transcortical sensory aphasia (repetition is preserved)
2) Motor aphasia: Dysfunction in the afferent area. i e, spoken speech is non fluent but comprehension is
normal. It is seen in lesion of the anterior perisylvian area(frontal lobe)
i)Brocas aphasia (repetition is defective)
ii)Transcortical motor aphasia (repetition is preserved).
3) Conduction aphasia: here repetition of words is lost. It is seen in the lesion of arcuate
fasciculus
4) Global aphasia: All faculties of speech are deranged.
Types of dysarthria :
Cerebellar dysarthria: the patient speaks slowly syllable by syllable stressing on each syllable. It is
called scanning speech.eg cerebellar is pronounced as ce-re-be-lla-r. It is seen in crebellar disease
Psuedobulbar or spastic dysarthria: Here constant pronunciation is lost. For eg: constitution is
pronounced as conshihushon .It is seen in pseudobulbar palsy.
Bulbar dvsarthria: There is nonspecific slurring of speech due to difficulty in pronouncing labial, lingual
and palatal syllables. Palatal air escape may be a audible during phonation. There may be associated
dysphagia it is seen in bulbar palsy.
Cortical dysarthria:There is irregular hesitancy in word production. There is always associated orofacial
apraxia.it is seen in left frontal and temporal lesions.
Release reflexes:
These are present during infancy but disappear during growth. They reappear in disease like
dementia,acute confutional states, Parkinsonism and frontal lobe diseases.
l. Grasping reflex: it elicited by stroking the palmer surface of the patients hand on the radial aspect. In
response, patient's hand grasps examiner's hand.
2. Glabellar tap reflex: series of taps over the glabella elicits another series of blinks with each tap
3. other reflexes are- (i) palmomental reflex
(ii)suckling reflex
(iii) snout reflex, etc
CRANIAL NERVE EXAMINATION
Pure motor nerves
CN IV (trochlear) - nucleus in the midbrain supplies superior oblique
CN VI (abducent) - nucleus in the pons supplies lateral rectus.
CN XI (accessory) - spinal part (nucleus ambiguous in lower 1/3rd of medulla) supplies
sternocliedomastoid and trapezius.
-cranial part (along with vagus) supplies muscles of larynx, pharynx and soft
palate
CNXII( hypoglossal) -hypoglossal nucleus in the medulla supplies muscles of tongue and
depressors of hyoid bone (sternohyoid, sternothyroid and omohyoid)
Mixed nerves
CN III (occulomotor)
-Somatic motor (from midbrain) supplies extraocular muscles except lateral rectus and superior oblique.
-Parasympathetic (from Edinger Westphal nucleus) supplies pupil and ciliary muscles
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CN V (Trigeminal)
-Motor (from nucleus in the pons) supplies muscles of mastication.
-Sensory from face, mouth and conjunctiva.
CN VII (Facial)
-Sensory-sensation of taste from anterior 2/3rd of the tongue to the brain (nucleus of tractus solitarius).
-Parasympathetic (from superior salivatory nucleus) supply submandibular and sublingual,glands
-Somatic motor fibres (from pons) supply muscles of facial expression and scalp
CN IX (Glossopharyngeal)
-Parasympathetic fibres (from inferior salivatory nucleus in medulla) supply the parotid gland.
-Sensory fibres carry taste sensations from the posterior 1/3rd of the tongue, they also carry sensations
from the baroreceptors.
-Somatic motor (nucleus ambiguous in medulla) fibres supply stylopharyngeus and middle pharyngeal
constrictor.
CN X (vagus)
-parasympathetic fibres (from the dorsal nucleus of the vagus in the noor of the fourth ventricle) are
viscerormotor and cardioinhibitory.
-Sensory fibres supply the respiratory passages the larynx and the heart.
-Somatic motor fibres (from the nucleus ambigous via the cranial accessory) supply the muscles of the soft
palate, larynx and the pharynx.

Pure sensory
CN I (olfactory) -Fibres carry olfactory sensations from the bipolar sensory cells in the olfactory epithelium
to the uncus and the parahippocampal gyrus,
CN II (optic)- Fibres carry visual sensations from the retina to the temporal lobe and the parietal lobe and
finally to the occipital cortex around the calcarine fissure.
CN VIII (vestibulocochlear)- The auditary fibres arise from the cochlear ganglion and are distributed to
the dorsal and ventral cochlear nuclei. The vestibular fibres arise from the vestibular ganglion (in the
labyrinth and semicircular canals) and terminate in a group of nuclei in the pons and the medulla.

EXAMINATION
NOTE: Always test the nerves on both the sides.
1: olfactory nerve
Test for the sense of smell in both the nostrils. Use asofoetida (ingu), coffee powder. etc
Ask the patient to close his eyes and also close one of his nostrils. Bring one of the above substances near
his unclosed nostril and ask him to identify the substance. Repeat this on the other nostril.
2: The optic nerve: Test for the following aspects on both the sides
l. Visual acuity at a distance of one meter
3 Pupillary reflexes
2. visual fields
4. color vision (using color ribbons.etc)
Always ask the patient to close one of his eyes while testing the other.

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How to test for pupillary reflexes?

Use a shady indirectly illuminated room and examine each eye separately. Ask the patient to look into
the distance to be sure accommodation is relaxed.shine a bright light into one eye
the pupil should contract almost immediately. Then dilate again a little and after undergoing a few slight
oscillations settle down to a smaller size. This is known as reaction to light.
Consensual pupillary reaction-if bright light is shown into one eye only, both pupil contract and if light
is shut off from one eye both the pupils dilate slightly. This is known as consensual papillary reaction and
is due to optic nerve decussation on the optic chiasma.
How to test for visual fields?
Finger confrontation test- Stand opposite to the patient. Test each eye separately. To test right
eye of patient, he is asked to close his left eye and keep gazing at your left eye. Close your right
eye and gaze in the patient's right eye with your left eye. The four quadrants of vision namely the
upper and the lower ,nasal and temporal are tested separately by moving your finger of one of
your hand along the plane midway between you and the patient inwards from various points at
periphery towards the centre. The patient is asked to say 'yes when he begins to see your finger.
This normally coincides with the point at which you yourself can see the finger, presuming that
your field of vision is normal.
Lesions and their effects at various levels of visual pathways.
Lesion at the level of optic nerve produces blindness of corresponding eye with loss of direct light reflex
of that eye.
Lesion at the level of intersection of optic fibres from both the sides produces bitemporal hemianopia.
Lesion at the level of optic chiasma produces blindness of the eye of which all the fibres are involved
and temporal hemianopia of the opposite side.
Lesion at the level of optic tract produces homonymous hemianopia of the opposite side with macular
(splitting) involvement.
Lesion at the level of optic radiation produces homonymous hemianopia of the opposite side without
macular involvement.
Lesion at the level of optic cortex produces homonymous central (macular) hemiscotoma of the
opposite side.
III, IV & VI nerves: The oculomotor, the trochlear and the abducent nerves.
To test the above nerves look for the following aspects.
l. Presence of any ptosis, or strabismus or nystagmus.
2. External ocular movements in all directions i e. abduction, adduction, elevation, depression, intortion and
extortion.
Observe whether the movements are conjugate or not this is important because infranuclear lesions
(LMNL) of III, IV &VI nerves lead to weakness of individual eye muscles or a group of muscles. whereas
supranuclear lesions (UMNL) lead to paralysis of conjugate movements of the eyes.
Infra nuclear lesions of III, IV and VI nerves
III N Lesions:
Ptosis
Defective movements of the eye
Squint
Diplopia
Pupillary dilatation and loss of accommodation
(Note: In Diabetic Ill N palsy, pupil is spared)
VI N Lesions:
Inability to move the eye laterally
Diplopia on looking in that direction
IV N Lesions:
Impaired downward movement: on attempting to look downwards in the mid-position of gaze, the
eyeball is rotated outwards by the unopposed action of the inferior rectus.
Diplopia below the horizontal plane
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3. Examination of the pupils: The following aspects must be noted: Size of both the pupils: Normal size of pupils- 3-4mm, both the pupils are almost of the same size. If
one is larger than the other, the one with weaker eye movements is probably the diseased eye,
shape of the pupils: Normal shape is circular; irregular outlines are usually due to adhesion of the iris to
the lens,
Reaction to light (Pupillary light reflex discussed under tests for optic nerve)
Reaction to accommodation
Hold up one finger close to the patient's nose. Ask the patient to look away at a distant object. Then
ask him to look quickly at your finger. As the eyes converge to accomplish this, the pupils become smaller.
This is known as accommodation.

Gunn's pupil: consensually mediated light reflex of the eye is more active than its
direct reaction.It is due to a lesion in the optic nerve.
Argyll Robertson pupil: The pupil is small and irregular, reacts briskly to
accommodation, but doesn't react to light directly or consensually, It is the classical
papillary abnormality of neurosyphilis.
Hippus: Rhythmic dilatation and constriction of the pupil, either in response to light or
occurring spontaneously. It is seen in retrobulbar neuritis
Adie pupil: Absent or delayed papillary constriction to light or accommodation. It is due
to partial parasympathetic denervation.
Horner's syndrome: It consists of ptosis, papillary constriction even on instillation of
cocaine and abolition of ciliospinal reflex. It is due to paralysis of the cervical
sympathetic nerve.

Note: Dilatation of the normal pupil when the skin of the neck is pinched is known as ciliospinal reflex and
is due to reflex excitation of the pupil dilating fibres in the cervical sympathetic chain.
V N: The Trigeminal Nerve
It is the sensory nerve of the face. It has 3 divisions the ophthalmic, the maxillary and the mandibular
divisions. The division in addition supplies the masseter, temporalis, lateral pterygoid and the medial
pterygoid muscles.
The following aspects have to be tested to determine the function of the nerve.
Motor functions: Ask the patient to clench his teeth the temporal and masseter muscles should stand
out with equal prominence on each side. It is better to palpate and confirm this. If there is any paralysis,
that muscle will not be prominent and on opening the mouth, the jaw will deviate towards the paralysed
side. Further, ask the patient to open the jaw, move it sidewards with and later without resistance given
by your palm.
Corneal, conjunctival and jaw reflexes
Corneal & conjunctival reflexes: Ask the patient to gaze into distance. Touch a wisp of cotton to the
lateral edge of the cornea. If the reflex is present, the patient blinks. Repeat this over the conjunctiva.
Jaw reflex: Place your finger over the chin of the patient and gently tap it using a knee hammer. If the
reflex is present, the jaw depresses opening the mouth.

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Reflexes

Afferent

light reflex

optic nerve

Accommodation
Conjunctival and
Corneal

optic nerve
Ophthalmic div. of
5th N

Gag reflex

9th N

Reflex Centre
Edinger Westphal
nucleus
Nucleus of Perlia
Sensory nucleus in
Pons

Efferent
3rd N
3rd N
7th N

10th N

Test the sensory functions as discussed under the examination of the sensory system.

VII N: The Facial Nerve:

It is the motor nerve of the face. It supplies the stapedius, posterior belly of the digastrics,
stylohyoid, muscles of facial expression and platysma. The chorda tympani branch transmits taste
sensations to the anterior 2/3rd of the tongue.
Testing the facial nerve:
Ask the patient to shut his eyes as tightly as possible and try to open the eyes while the patient
attempts to keep them closed. Normally, if the orbicularis oculi is functioning well, it is impossible to
open the eyes against patient's effort.
Ask the patient to smile, to whistle, to show the upper teeth, to inflate his mouth with air and blow out
the cheeks. Palpate each inflated cheek and feel the strength of the muscles.
Test the sense of taste on the anterior 2/3rd aspect of the tongue.
Examine the lacrimation of each eye.
Examine for any abnormal perception of not-so-loud sounds as loud sounds (Hyperacusis-in stapedius
paralysis)
Note: Bell's phenomenon, in which the eyeball rolls upwards during attempted forced eye closure, is a
normal phenomenon which is preserved in facial palsies of LMN type.
Supranuclear facial palsy:
The lower part of the face is chiefly affected because the upper part is bilaterally innervated.
Taste is not affected
Facial reflexes elicted by lightly tapping the facial muscles around the mouth are often
exaggerated.
Infranuclear facial palsy: Eg-Bell's lesions
Both the upper and lower parts of the face are equally involved.
Loss of taste sensation in the anterior 2/3rd of the tongue in most cases.
Hyperacusis on the affected side
VIII N: the vestibulocochlear nerve: it is the nerve of hearing and balancing. It carries sensations from
the cochlea, labyrinth and semicircular canals
The function of hearing is tested as follows,
Test the hearing in both the ears separately
If hearing is abnormal perform Rinne's test and Weber's test to differentiate between conduction deafness
and nerve deafness

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How to do Rinne's test?

Place a vibrating tuning fork (256 or 512 Hz) on the mastoid process and just lateral to the
external ear.Ask the patient which of the two sounds appears louder Normally air conduction is
better than bone conduction. If this is reversed it indicates the presence of conduction deafness.
How to Weber's test?
Place a vibrating tuning fork on the middle of the forehead. Ask the patient whether the sound is
heard loudest in the midline or preferentially to one side. In conduction deafness, the sound is
lateralised to the diseased, in nerve deafness he sound is lateralised to the normal ear.

IXand X cranial nerves: the glossopharyngeal and the vagus.

Testing t f the IX and X cranial nerve:
Examine the movements of the palate and the uvula with the help of a tongue depressor and asking the
patient to say 'ah'
Ask him to pronounce words like egg, rub etc, which need complete closure of the nasopharynx. In
case of paralysis they sound 'eng' 'rum'.
Assess the volume and quality of the patient's speech.
Elicit the gag reflex using a thin stick covered with sterile cotton. Touch the posterior wall of the pharynx
with this. Contraction of the pharyngeal muscles proves the reflex
The XI nerve: the accessory nerve.
Testing for the XI nerve:
Ask the patient to move his chin to a side against resistance( test for sternocleidomastoid)
Ask the patient to shrug his shoulders against resistance while the examiner presses downwards on the
them(test for trapezius)
The XII nerve: the hypoglossal nerve.
Testing for the XII nerve:
Examine the tongue for symmetry,deviation etc.
Examine for any fasciculation of the tongue. Ask the patient to open his mouth wide and keep his
tongue inside the mouth and then examine,
Examine the movement of the tongue like lateral movements, shortening of the tongue, lengthening of
the tongue etc.
Examine the strength of contraction of tongue by asking the patient to press his tongue against the
cheek.Now palpate the tongue through the cheek to know the strength of contraction.
Examination of motor system:
Assessment of the motor system is done in the following manner:
Inspection of the muscles and the limbs
palpation of the muscles
Assessment of tone
Testing of power
Elicitation of superficial reflexes
Elicitation of deep tendon reflexes
Testing of coordination
Gait
Inspection of the muscles and the limbs
Inspect all individual muscle groups(flexors, extensors etc) separately.
Any muscle asymmetry?
Any atrophy or hypertrophy and its distribution?

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any fasciculations?
any involuntary movements?

any postural abnormality?

any incoordination of voluntary movement

Types of involuntary movements:

Fasciculations: they appear as subcutaneous twitches overlying muscle bellies when the muscles are at
rest.They result from disease of lower motor neurons.
Myoclonus: it is a sudden shock like contraction which involves one or more muscles of a whole
limb.theymay occur in normal people, particularly when falling asleep.some patients with primary
generalized epilepsy experience myoclonic jerks especially after waking.
Choreioform movements: they are irregular jerky, semipurposive and ill sustained movements seen in
Huntington's chorea, rheumatic chorea,etc
Tics and habit spasms: they are stereotyped and localized movements which can be resisted by the will
of patient.
Tremors: they are rhythmic movements resulting from alternating contraction and relaxation of group of
muscles.
Types of tremors:
Action/postural tremor :hyperthyroidism, anxiety and fatigue.
Intension tremors: cerebellar lesions,
Resting tremor: parkinsonism
Dystonic movements: they are slow and writhing movements often leading to sustained
abnormal contractures and limb postures. They are seen in spasmodic torticolis following infantile
hemiplegia and in dystonia musculorum deformans.
Athetosis: slow writhing movements of distal parts usually fingers and toes.
Palpation of the muscles:
Tender in myositis
Doughy in Duchennes dystrophy(due to fatty infiltration of the pseudohypertrophied muscle)
Woody in acute muscle necrosis(eg alcoholic or rhabdomyolysis.)
Tapping muscle bellies is an useful way of enhancing the production of fasciculations
Movement disorder
Site of lesion
Parkinsonism
substantia nigra & corpus striae
Chorea
caudate nucleus
Athetosis
putamen
Hemiballismus
subthalamus muscle
Dystonia
not known

Assessment of tone:
Muscular tone is a state of tension or contraction in the healthy muscles. In other words, it is the resistance
offered by normal muscles to passive movements. An increase in tone is called hypertonia and a reduction
hypotonia. Muscle tone is mainly regulated by corticospinal and extrapyramidal pathways.
Hypertonia:
Hypertonia following lesions of the corticospinal system (UMN) is termed Spasticity. lt describes a state
of increased tone which is of "Clasp-Knife" type i.e. the resistance is increased only in the beginning or
at the end of passive movement.

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Spasticity due to cerebral or brainstem lesion has a characteristic distribution shown by typical posture
of the limbs in such patients. The upper limbs are held in flexion and the lower limbs in extension with
the feet in plantar flexion (Physiological extension).This is known as Decerebrate rigidity

Hypertonia due to disease of the basal ganglia is termed as extrapyramidal rigidity.The resistance is
present throughout the range of passive movements but it is rhythmically jerky. It is like rubbing teeth of
cog wheel. This is known as Cogwheel rigidity.

Some times a plastic type of rigidity is found in which the resistance developed to passive movements
is uniform during all phases of applied movement. This is known as Paratonic rigidity or "Gegenhalten
Phenomenon'. It is found in catatonic state and dementia.

In hysterical rigidity, the resistance to passive movement increases in proportion to the effort applied by
the examiner.

Hypotonia: It occurs in LMN lesions, in lesions of afferent sensory pathways as in tabes dorsalis and in
cerebellar disease. Tone may also be reduced in sleep.
UMN Lesions
Groups of muscles involved. Hence individual
movements are affected.
Spasticity
Disuse atrophy in the late stages
Deep tendon reflexes exaggerated.
Superficial reflexes diminished or absent.
Extensor plantar response
No fasciculations.
EMNG shows normal potentia

LMN Lesion
Individual muscles are affected.
Flaccidity.
Atrophy in early stages also.
They are diminished or absent.
They are diminished or absent.
Plantar reflex response is normal or mute
Fasciculations present
Fibrillation potential seen.

Extrapyramidal Lesions
Rigidity involves muscles through out the body
Involuntary movements may be seen
Deep tendon reflexes are normal or
exaggerated
Superficial reflexes are normal
Plantar reflex is normal
Muscle bulk is normal
Muscle weakness absent.

Pyramidal Lesions
Spasticity involves specific muscle groups
Involuntary movements not seen
They are exaggerated
They are diminished or absent
Plantar reflex extensor
There is disuse atrophy
Muscle weakness present

Testing of power:
Always examin individual muscle groups in both the limbs alternatively or in some instances
simultaneously so that the strength of the right and left sides can be directly compared.
How to test for power?
1. In the upper limb examine for:
Abduction and adduction of shoulder.
Flexion and extension of shoulder
Flexion and extension of elbow
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flexion and extension of wrist

supination and pronation of forearm
Finger and thumb flexion ,extension, adduction and abduction
Extension of finger at both metacarpophalangeal & interphalangeal joints.
2. In the lower limbs examine for
Hip flexion and extension, adduction and abduction
Knee flexion and extension
Foot dorsiflexion, plantar flexion inversion and eversion,Toe plantar flexion & dorsiflexion
3 Test the abdominal muscles by asking the supine patient to flex the neck or sit forward.
MRC Scale for muscle power
0-No muscle contraction
1-Muscle contraction visible, but no movement of joint
2 Joint movement along the gravity
3 Movement sufficient to over come the effect of gravity
4.Movement overcomes the gravity plus added resistance
5 Normal power
Trunk muscles and respiratory muscles are spared in hemiplegia because of bilateral representation in the
brain.
Patterns of weakness of muscles
Hemiplega- Paralysis of one side of the body, involving the arrn and leg, usually also face (facio-brachio
-crural hemiparesis)
Crossed paralysis -Paralysis of ipsilateral cranial musculature with contralateral hemiparesis.It is a sign
of brain stem lesion.
Paraplegia- Paralysis of both the legs
Monoplegia- Paralysis of one limb (Arm- brachial monoplegia,Leg- crural monoplegia)
Quadriplegia-Paralysis of all four limbs
Myasthenic weakness-commonly affects external ocular and bulbar muscles and is characteristically
exacerbated by repeated contraction of affected muscles.
Neurogenic weakness-In LMN lesions there is weakness and atrophy of affected limb
Myopathic weakness- In myopathies, dystrophies and polymyopathy muscle weakness is strikingly
proximal, usually symmetrical often affects pelvifemoral muscles more severely than the pectoral girdle
muscles. Affected muscles are atrophic and firmer than normal.
Myotonia-In inherited muscular diseases like myotonic dystrophy relaxation is impaired following
contraction of n muscle.
Pentaplegia- When diaphragm is paralysed along with all four limbs.
Superficial reflexes
The following reflexes are tested,
1)Planter reflexes(root value S1, L5)
Put the patient in supine position. Stroke the lateral border of the foot from the heel towards the tip of the
little toe with tip of a key. Stop as soon as the first movement of the big toe occurs.
Response types:
Normal: Flexion of the great toe at metatarsophalangeal joint with adduction of other toes.
Absent: In thick sole, LMN lesions.
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Extensor response: In infants and children upto the age of two years,in sleep and in lesion of the
corticospinal tract above S1 segment. This is known as Babinskis response
In the major corticospinal lesions,the area from which extensor plantar reflex can be elicited
enlarges,spreading first inwards and over the sole of the foot, and then upwards. So, the reflex can also be
elicited by squeezing the calf(Gordon's reflex) or pressing heavily along the inner bordel of the tibia
(Oppenheim's sign) or by pinching the calcaneous tendon(Schaeffer's sign).
2) Abdominal reflex(T7-T12):
Put the patient in supine position. Stroke all the four quadrants with the tip of a key and watch for
muscle contraction. Direction of stroking should be from outside to the centre in both sides. The reflex can
be read by observing the movement of umbilicus.
3) Cremastric Reflex( L1-L2):
Put the patient in supine position.Rotate the thigh externally and abduct it. Stroke the skin of
upper thigh with the tip of a key. Observe the response in the form of elevation of ipsilateral testicle.

Deep tendon reflexes

Grade all the reflexes as follows:0= Absent
1= Present (like normal ankle jerk)
2= Brisk (like normal knee jerk)
3= very brisk
4= Presence of clonus
Biceps jerk(C5- C6):
Put the patient in supine position. Flex the elbow to a right angle. Feel for the biceps tendon with
the thumb and place the thumb over it. Now strike the hammer over the thumb. Observe for biceps
contraction.
Triceps jerk(C7- C8):
Put the patient in supine position. Flex the elbow and allow the forearm to rest across the patient's chest.
Tap the triceps tendon just above the olecranon. Observe for triceps contraction
Supinator jerk(C5-C6):
Tap 5cm above the styloid process of radius and watch for the supination of the elbow.
Knee jerk(L2,L3,L4):
Put the patient in supine position.Pass your hand under the knee to be tested and place upon the opposite
The knee to be tested should rest upon the dorsum of your wrist, Strike the knee
hammer over the Patellar tendon midway between the patella and tibial tuberosity. Observe for
contraction of quadriceps
Ankle jerk (S1,S2):
Put the Patient in supine position.Place the lower limb so that it lies everted and slightly flexed. Then with
one hand,slightly dorsiflex the foot and with the other hand, strike the Achilles tendon. Observe for calf
muscle contraction.

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Finger jerk C7,8,T1):

Place the tips of your middle and index fingers across the palmar surface of the proximal
phalanges of the patient's relaxed fingers. Now tap your fingers lightly with a tendon hammer. The normal
response is slight flexion of the patient's fingers.
Hoffman's sign:
Place the examiner's right index finger under the distal interphalangeal joint of the patient's middle finger.
Now briskly flick down the patient's finger tip with the examining right thumb tip and allow it to spring back
to the normal position while observing the patient's thumb for any movement. Normally,the reflex is absent.
Its presence indicates a state of hyperreflexia.
Wartenberg's sign:
Supporting the patient's upper limb at the wrist with your left hand,hook the bent fingers of your
right hand into the bent fingers of the patient. Patient is asked to further bend his fingers and
exert pressure,at the same time pulling your fingers against the patient's fingers. Normally the thumb
remains immobile or moves very little. In extensive pyramidal tract lesions the thumb goes into
adduction,flexion and moves inwards.
Clonus:
It is a term applied to a rhythmic series of involuntary muscle contractions evoked by sudden stretch of the
muscles. It is seen in hyperreflexia.
a) Patellar clonus: Sharply push the patella towards the foot while the patient lies supine and relaxed with
the knee extended. Following the initial jerk exert sustained pressure with the thumb and index finger in a
downward direction on the patelia.If clonus is present patella will jerk up and down following a solitary jerk
stimulus.
b)Ankle clonus: support the flexed knee with one hand in the popliteal fossa so that the ankle rests gently
on the bed. Using the other hand,briskly dorsiflex the foot and sustain the pressure. If ankle clonus is
present,there will be a rhythmical beating (alternating plantar and dorsiflexion) of the foot as long as the
pressure is maintained.
Sustained clonus is a "hard" neurological sign.
Note: when a deep tendon reflex is difficult to elicit, the reflex can be reinforced by a voluntary
manoeuvre that increases the muscle tone all over the body. (This is mediated by the gamma motor
neurons). Such manoeuvers are jendrassik's' manoeuver. ( hooking the fingers of both hands into each
other and pulling apart, clenching the teeth etc).
Examination of the sensory system:
Various dermatomes of the body:
#Face: trigeminal nerve
#Back of neck:C2
#Lateral part of neck:C3
#Epauled area:C4
#over deltoid:C5
#Over thumb and index:C6
#Middle finger: C7

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#small&ring fingers: C8,T1

#Medial part of thigh: L2,L3
#Medial part of knee joint: L3
#Big toe: L5
#Lateral part of ankle :S1
#Posterior part of thigh:S2
#Perianal&genital:S3,S4,S5
The following aspects have to be examined:
Touch: with cotton
Pain: pin prick
Deep pain: test by squeezing muscle bellies
Temperature: hot & cold water
Joint and position sense
Vibration sense
Two point discrimination
Sensation of pain and temperature are carried by the lateral spinothalamic tract of opposite side.
Sensation of vibration, crude touch, joint sense, position sense & stereognosis are carried by the
posterior column of the ipsilateral side & those of fine touch by the anterior spinothalamic tract of
opposite side.
How to test joint position sense?
Show the patient intended movement of the joint and the movement and name them (eg: "that's
up and "that's down"). Ask the patient to look away and perform these movements randomly.
Ask the patients to identify the direction of the movements performed.Always go from the distal
joints to proximal joints.
How to test for the vibration sense?
Hold the vibration tuning fork (128Hz) over the area to be tested. Prefer regions over bony
prominences. Always go from proximal to distal.
How to check 2 point discrimination?
Use 2 pins. Place one or two of them on the pulp of the index finger and ask the patient to
determine if one or two stimuli were applied. Determine the minimum distance at which 2 points
were discriminated.
Cortical sensation:
Point localisation of tactile stimuli.
Stereognosis of objects like pen top, coin, key, Etc
Graphaesthesia of any common symbol like C, P... etc
Calculating skills
Primitive reflexes like Glabellar tap, Pointing reflex, Grasp reflex (Absent in normal individuals)
Arm drift test by asking the patient to outstretch the limbs and close his eyes and watch for any drift.
Any apraxias
Apraxia : Disorder of a learnt motor act in the absence of weakness, incoordination, sensory loss or failure
to comprehend the commands. It is seen in the lesions of the dominant parietal or the corpus callosum. It is
tested by asking the patient to use object or to make or imitate certain movements. Eg. The patient is
given a
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matchbox and is asked to strike it. He may fail to open the box or may fail to take out the matchstick, to
strike it or may actually fail to recognise which end to strike.
Coordination:
Finger nose test: Ask the patient to hold one arm outstretched and with the tip of the index finger to
alternatively touch the tip of the nose and then the examiners finger tip. Examine for speed,
smoothness and accuracy.
Dysdiadochokinesia: Rapid alternating movements of pronation and supination.
Heel shin test: Ask the patient to raise one leg at the hip and place the heel of the flexed leg on the
contralateral knee and to run the heel down the surface of the tibial shaft towards the ankle and then
back again
Heel toe test of gait: Ask the patient to walk in a straight line so that the heel of one foot comes
directly in contact with toes of the other foot. The rear foot is the advanced so that its heel is then
placed in front of the contralateral toes. Observe the gait and the tendency to stagger to one side.
Romberg's test: Ask the patient to stand with his feet close together and eyes open. After he has
stabilized ask him to close his eyes. If the sign is positive the patient sways and may even fall down. It
is seen in the lesions of the posterior column, wherein there is position sense loss of lower limbs in
diseases like tabes dorsalis, subacute combined degeneration and sensory polymeuropathies. The
patient stabilises when he opens his eyes. Even in cerebellar diseases the patient sways but he even
sways when the eyes are open.
Gait:
Gait is assessed by asking the patient to walk for a short distance and observe him. Observe whether he
needs any help? If yes,how much of help? Whether his stride is normal? Whether he sways/ waddles?
Whether he drags his legs? Whether he walks on a broad base and whether the arm swing is normal.
Abnormalities of gait manifest in conditions causing weakness of muscles, alteration of muscle tone, Loss
of coordination, deformities of musculoskeletal system and pain during movement
Types of gait:
Spastic gait: The patient walks with his legs stiffy held together the pelvis tilting from side to side and
toes scraping the floor. It is seen in bilateral pyramidal disease like subacute combined degeneration of
spinal cord and syringomyelia.
Hemiplegic gait (circumduction gait): The patient walks with the affected lower limb dragged stiffly
and in a semicircular fashion, the foot scrapping the floor and the pelvis tilting sideward. There is no
arm swinging in the affected side. It is seen in unilateral pyramidal lesions and upper motor neurone
lesions.
Scissoring gait: The patient with the legs close to each other or crossing each other. It is seen in
adductor muscle spasticity due to cerebral diplegia.
Festinant gait: The patient walks with his body bent forward and the limbs partially flexed. The steps
are short, rapid and shuffling. There is no arm swinging and he cannot stop immediately when asked to
do so. It is seen in Parkinsonism, cerebral arteriosclerosis and Wilson's disease.
Cerebellar ataxic gait: The patient walks on a broad based swaying from one side to another
uncertainly like a drunkard. It is seen in cerebellar lesions.
Sensory ataxic gait: The patient walks on the broad base raising the leg high and stamping it suddenly
on the floor with a loud noise. It is seen in sensory loss of lower limbs in disease like tabes dorsalis and
polyneuropathy.

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Waddling gait: The patient walks on a broad base with his body waddling from side to side his shoulders
thrown back and the abdomen forwards. It is seen in congenital dislocation of the hips, muscular
dystrophies, etc
Trendelenberg gait: It is a type of waddling gait seen in bilateral disease of the hip joints.
Signs Meningial irritation:
1. Neck stiffness:
In meningial irritation neck flexion causes pain in the posterior part of neck.
2. Kerning sign:
Put the patient in supine position and passively extend the patient's knee when the hip is fully flexed. In
patient with meningial irritation affecting the lower part of the spinal subarachanoid space this movement
causes pain and spasm of hamstrings.
EXAMINATION OF THE OTHER SYSTEMS
Cardiovascular Systems: To rule out cardiac causes of embolism and routine.
Respiratory system: To rule out pulmonary TB when meningitis is suspected and as a routine.
Per Abdomen: To rule out abdominal causes of encephalitis and Ca metastases.

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Anaemia
SYMPTOMATOLOGY

Fatigue, tiredness, lassitude and generalized muscular weakness. These are the most common and
often the earliest symptoms of anemia.
Symptoms related to the CVS like dyspnoea on exertion, palpitations, anginapectoris
(especially in the elderly), intermittent claudication (especially in those with atherosclerosis) etc..
Symptoms related to the CNS like faintness, giddiness, headache, roaring and banging in the
ears,tinnitus,spots before the eyes, lack of concentration and drowsiness. In cases of severe anaemia
.there can be clouding of consiousnes, numbness, coldness, tingling of the hands and feet. Etc.
Menstrual disturbances like amenorrhoea, menorrhagia is more usually a cause of anemia
Symptoms related to the GIT like anorexia, fatulence,nausea,constipation, distension and pain
abdomen
Prolonged fever
Burning and soarness of the tongue
Pica
Dysphagia (Plummer Vinson Syndrome)
Jaundice Hemolytic anemia)
Bleeding manifestations (if anaemia is associated with thrombocytopenia or leukemia
SYMPTOM ANALYSIS
Elaborate on the above symptoms enquiring about their presence, onset, duration, progress and
associated symptoms
The symptoms due to anaemia depend partly on the severity and partly on how rapidly the anaemia
develops
Hemolytic anaemias due to red cell defects present very early in life.

Apart from describing the presenting symptoms enquire about the following:
History of blood loss like hematemesis, malaena, bleeding from menorrhagia, metrorrhagia,
epistaxis, hematuria, hemoptysis. etc
History of Trauma
History of passing worms in stools
History of acid peptic disease
History of easy bruisability, prolonged bleeding after trivial injuries and bleeding from more than one
site
History of loss of appetite and weight loss
History of dysphagia, regurgitation & dyspepsia
History of abdominal pain, diarrhoea and constipation
History of jaundice, recurrent jaundice
History of bone pain, arthritis, arthralgia
History of fever, night sweats
History of exposure to metal dusts, solvent fumes, lead etc. either in occupation or residence,
History of ingestion of caustic material
History suggestive of liver disease
History of exacerbations of any of the above symptoms by a precipitating factor
For example: episodes of paroxysmal cold hemoglobinuria are precipitated by cold climate
History of paraesthaesiae difficulty in walking
History of nocturnal polyuria
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PAST HISTORY:
History of recurrent pain abdomen, jaundice etc
History of recurrent bleeding manifestations
History of previous blood transfusions and the need for those transfusions
History of drug intake like chloramphenicol, alkylating agents, antionvulsants, OCPs. etc.
History surgeries like gastrectomy, ileal resection. Etc
History of exposure to radiation
History of previous anemia diagnosis, treatment and response to treatment.
FAMILY HISTORY:
History of similar complaints among the family members
History of recurrent jaundice, intrauterine and childhood death
PERSONAL HISTORY:
Diet- Whether vegetarian or non-vegetarian, whether his daily food constitutes all essential dietic
constituents.
Appetite- If there is any loss of appetite, enquire about the cause.
Sleep- Whether disturbed? If yes, what is the cause?
Any habits like alcohol intake, smoking etc. If so since when and what is the quantity of intake?
Bowel and bladder movements.
MENSTRUAL HISTORY:
Enquire into the age of menarche, the frequency of cycles, the duration of flow ,the quantity of flow (assess
by the number of diapers she changes everyday, usually 3-4 diapers are used), any clots, history of
dysmenorrhoea and any tiredness during the menses
GENERAL PHYSICAL EXAMINATION
Do a complete physical examination and emphasise on the following aspects
Build and nutrition
Pallor /icterus/pedal edema/koilonychia
Pulse,BP, temperature, JVP, and respiratory rate (collapsing pulse is seen in severe anemia due to
high volume output)
Skin- for colour, texture, petechiae, ecchymoses and scratch marks
Nails- for brittleness, pallor, longitudinal ridging and koilonychias
Conjunctiva and sclera- for pallor icterus and haemorrhage
Mouth-Circumoral pigmentation
Mucous membranes- pallor, petechiae,pigmented patches
Gums-any bleeding, hypertrophy
Tongue- any redness or atrophy of papillae

SYSTEMIC EXAMINATION
Examination of the abdomen: Look for hepatomegaly, splenomegaly, tenderness, mass ascites
scars of previous surgeries etc.
Examination the CVS: emphasise on BP,Cervical venous hum, pulse (water hawwer pulse),
hyperdynamic precordium, is S1 loud? Any murmurs? (In severe anemia any ejection systolic
murmur is heard. This is best heard over the pulmonary area because pulmonary valve is the most
superficial valve of the heart) & any signs of cardiac dilatation or cardiac failure
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Examination of the Respiratory system: Look for any crepitations (due to pulmonary edema following
heart failure as a result of severe anaemia), any signs of chronic lung disease (can cause anaemia)etc
Examination of the CNS: Do a detailed examination to rule out peripheral neuritis, subacute combined
degeneration of the spinal cord, etc. (which occur in megaloblastic anameia).
PR examination: To rule out haemorrhoids, ca rectum. Etc.
Tourniquet test: Do it when there are signs or symptoms suggestive of bleeding tendency.
How to do it?
Tie the cuff of the sphygmonanometer to the arm of the patient and rise the pressure upto
20-40Hg
above the systolic blood pressure of the patient, If the patient is suffering from any bleeding diathesis,
minute petechial haemorrhages will be seen in the part of the limb distal to the cuff.
Some important aspects of Anaemia:
Definition of anemia: It is a state of reduced oxygen carrying capacity of the blood either due to
decreased haemoglobin or due to red cell count or both for that particular age, sex and race.
Normal red cell values
Red cell count
1. Men--- 5.5+/- 1.0 x 1012/I
2. Women --- 4.8 +/- 1.0 x 1012/I
Hb:
1. Men 15.5 +/- 2.5 g/dl
2. Women 14.0+/- 2.5 g/dl
Packed cell volume (PCV; hemotocrit)
1. Men0.47+/-0.07
2. Women -0.42+/- 0.05
Mean corpuscular volume (MCV): 85 +/-9fl
Mean corpuscular haemoglobin (MCH]: 29.5 +/- 2.5pg
Mean corpuscular haemoglobin concentration (MCHC):33 +/- 2g/dl
Recticulocytes: 0.2-2.0%
How to arrive at a dignosis?
Pallor with koilonychia goes in favour of iron deficiency anemia
Pallor with icterus goes in favour of hemolytic anaemia.
Pallor with hepatosplenomegaly suggests myelodysplasias.
Pallor with splenomegaly hints to investigate for malaria
Severe anemia without hepatosplenomegaly suggests aplastic anemia.
Circumoral, oral mucous membrane and knuckle pigmentations suggest megaloblastic anaemia.
Soreness of the tongue ,angular stomatitis, bald tongue suggest iron deficiency. They are also seen in
vit B12 deficiency.
Paraesthesia and numbness go in favour of vit B12 deficiency.
Pallor associated with bleeding tendencies, bony pains suggests associated thrombocytopenia or
leukemia
Anaemia during pregnancy is usually due to iron deficieny.
Pallor and pedal edema associated with ascites hints at anaemia with hypoproteinemia.
Plummer Vinson syndrome: This occurs in long standing iron deficiency. The characteristic features are
iron deficiency anemia, glossitis, koilonychia and postcricoid web resulting in dysphagia.
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