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Introduction on Clinical Examination
https://t.me/med1917
Fig. 1.7: Enterohepatic circulation.
11
systemic disease/general debilitating illness. Pallor
can be seen in nailbed. In iron deficiency anaemia
(Plummer-Vinson syndrome) nails may be brittle/
flat (platynychia)/spoon shaped (koilonychia).
Splinter haemorrhages are seen in nailbed in bacterial
endocarditis and bleeding disorders. Discoloured,
deformed, pitted nails are seen in psoariasis. Hypoalbuminaemia causes whitening of the nailbed—
Te rry’s sign. Onychia is deformity of the nail—seen
in fungal infection or tuberculosis. Specific discolourations are seen in Raynaud’s disease, silver and
mercury poisoning. Ribbing, brittleness, falling of
nails are seen in syringomyelia, leprosy and tabes
dorsalis. Nailbed infarcts are seen in vasculitis due to
SLE or polyarteritis. Onychogryphosis (in toe) is
heaping up of nail and curling over the end of the toe
due to failure of normal sliding mechanism of the nail
and is due to trauma or old age. Ingrowing toe nail is
common in margins of the nail of great toe where
irregular edge of the nail grow beneath the lateral nail
fold due to improper trimming of the nail causing
repeated pain and infection (Figs 1.8A to 1.10B).
A
B
Figs 1.8A and B: Nails should be examined in both hands
and feet (fingers and toes) for change in colour, splinter
haemorrhage, clubbing, pallor, koilonychia and other features.
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A
B
Figs 1.9A and B: Changes in the toe nail also should be
observed. Note the pallor and koilonychia in the toe nails.
SRB’s Clinical Surgery
Clubbing
It is bulbous enlargement of the soft parts of the terminal phalanges with both transverse and longitudinal
curving of the nails. It is due to interstitial oedema and
dilatation of the arterioles and capillaries. There is loss
of normal angle between surface of the nail and the skin
covering the nailbed. When a normal nail is viewed
from side, plane of the nail and the plane of the skin
covering the base of the nailbed form an angle of 130°170° (Lovibond angle). In clubbing tissue hypertrophy
beneath the nailbed makes the base of the nail bulge
upwards distorting the nail growth causing nail to be
curved in both directions. So in clubbing plane of the
nail and plane of the skin covering the nailbed form an
angle which is greater than 180° (Figs 1.11A to D).
Causes: It can be due to pulmonary (Carcinoma
bronchus, lung abscess, bronchiectasis, tuberculosis
with secondary infection); cardiac (cyanotic congenital
heart disease, infective endocarditis); gastrointestinal
(ulcerative colitis, Crohn’s disease, cirrhosis); endocrinal (myxoedema, acromegaly, exophthalmic
ophthalmoplegia—thyroid acropachy ); other causes
(hereditary , idiopathic), unilateral in Pancoast tumour,
subclavian/innominate artery aneurysm: unidigital in
trauma or tophi deposition in Gout, only in upper limbs
in heroin addicts due to chronic obstructive phlebitis.
A
B
Figs 1.10A and B: Note the change in the great toe
nail. It could be onychogryphosis.
Grading:
Grade I: Softening and fluctuation of nailbed;
Grade II: Obliteration of angle of the nailbed with
loss of longitudinal ridges and formation of convexity
from above downwards and side-to-side;
Grade III: Swelling of the subcutaneous tissue over
the base of the nail causing overlying skin tense, shiny
and wet increasing the nail curvature;
Grade IV: Swelling of the fingers occurs in all
dimensions, associated with hypertrophic pulmonary
osteoarthropathy causing pain and swelling of the
hand and radiographic features of subperiosteal new
bone formation.
Disappearance of diamond shaped gap between
nails when fingers are apposed—Schamroth’s sign;
Pathogenesis: Hypoxia leads to opening up of deep
arteriovenous fistulas which increase the perfusion
of the fingers and toes causing its hypertrophy. It may
be due to reduced venous blood ferritin which
escapes oxygenation in the lungs, which after entering
Introduction on Clinical Examination
https://t.me/med1917
C
A
13
B
Figs 1.11A to D: Typical clubbing. In normal individual angle from skin to nail fold is 130 to 170 degree. In
clubbing it is more than 180°. In clubbing both longitudinal and transverse curvatures are increased.
the systemic circulation stimulates dilatation of
arteriovenous anastomosis leading to hypertrophy and
clubbing of terminal phalanx. Pseudoclubbing is seen
in hyperparathyroidism due to undue bone resorption
resulting in disappearance of terminal phalanges
causing telescoping of soft tissues into the terminal
phalanges which appears like clubbing. Nail is not
having curvatures here.
Oedema
It is the collection of fluid in the interstitial spaces
or soft tissues. Oedema will be clinically evident only
when fluid accumulates more than 5 litres. Pitting on
pressure occurs only when circumference of the limb
is increased by 10% (Figs 1.12A and B).
D
Mechanism: Fluid accumulates in the interstitial space
following— Increased capillary permeability like in
acute inflammation (cellulitis); increased capillary
pressure (cardiac failure); decreased osmotic pressure
(hypoproteinaemia); lymphatic block (filariasis).
Pitting on pressure is the cardinal sign of oedema. Using
pulp of the finger/thumb firm pressure is applied for
few seconds over the skin on a bone surface like lower
part of medial aspect of leg just above the malleoli.
Indentation or pitting is seen on releasing the finger.
Slow reaccumulation of fluid in few minutes is
observed. Nonpitting oedema is observed in late stage
of lymphoedema. Oedema is commonly observed in
most dependent part—lower limbs. In bedridden
patient, it may be seen on sacral region. Often limb
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A B
Figs 1.12A and B: (A) Pitting oedema in the leg. (B) Note oedema with multiple ulcers.
SRB’s Clinical Surgery
oedema may also be associated with ascites or pleural
effusion. Oedema can be generalised or localised.
Generalised oedema is called as anasarca. It is due to
cardiac, renal, hepatic or nutritional causes. Localised
oedema is due to cellulitis, lymphatic causes, venous
diseases, pretibial myxoedema of thyrotoxicosis.
Causes may be classified as bilateral (cardiac, renal,
hepatic, IVC obstruction, allergic, nutritional, toxic)
or unilateral (lymphatic, traumatic, infection, metabolic
like gout, DVT/varicose veins, hereditary). In CCF
oedema is in most dependent position—in lower limbs
and is more in evening. In LVF pulmonary oedema
develops earliest and so dyspnoea, basal crepitations,
cough are typical. In pericardial effusion, lower limb
oedema, ascites, hepatomegaly—soft smooth liver,
raised JVP without pulmonary oedema is observed. In
renal cause oedema develops first in eyelids and face,
and then it becomes generalised into legs and ascites.
In hepatic cause like portal hypertension, ascites
develops first due to increased portal pressure and
hypoproteinaemia, and then lower limb oedema
develops. In myxoedema, oedema is nonpitting. Here
oedema over the lateral aspects of the eyelids is typical.
Oedema grading-None (0); asymptomatic, not
requires drug therapy (1); symptomatic requires drug
therapy (2); symptomatic, with limited function, not
responding to therapy (3); anasarca (4).
Visible Veins
Patient should be examined for visible veins. With
normal venous pressure external jugular vein is invisible or just visible for short distance. Raised venous
pressure causes engorgement of external jugular vein.
Bilateral engorgement of external jugular vein/neck
veins may be due to myocardial infarction or intravenous fluid infusion or retrosternal goiter/thoracic
outlet obstruction. Unilateral engorgement of vein is
due to compression by lymph nodes, tumour. In toxic
goiter neck veins may be prominent due to increased
vascularity. In SVC obstruction, inguinoaxillary
veins, chest wall veins, neck veins may be prominent
with flow of blood from above downwards and
through groin veins (across watershed area) to IVC.
In IVC obstruction, veins in the flanks (both sides)
will be prominent, with direction of flow from below
upwards towards axillary vein along inguinoaxillary
vein. Unilateral such flow is observed in unilateral
blockage of common or external iliac vein. IVC
obstruction is classified as—below the renal vein
(standard presentation); at the level of renal vein
(lumbar pain, haematuria, proteinuria); above the
level of renal vein (like Budd-Chiari syndrome).
Caput medusae is visible dilated veins radiating
from umbilicus, seen in portal hypertension (Figs
1.13A to 1.14B).
Introduction on Clinical Examination
https://t.me/med1917
15
A
C
Figs 1.13A to D: Superior vena caval obstruction causing dilated veins in the chest wall. Note the
direction of flow from above downwards towards lower abdomen and to inferior vena cava.
B
D
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A
SRB’s Clinical Surgery
tachycardia. ‘c’ wave is due to carotid artery impact into
jugular vein and right ventricular systole. ‘x’ wave is
due to fall in right atrial pressure and atrial relaxation.
It is absent in tricuspid regurgitation. It is prominent
in constrictive pericarditis. ‘v’ wave is due to right atrial
filling. Giant v wave is seen in tricuspid regurgitation.
‘y’ wave is due to opening of tricuspid valve causing
rapid inflow of blood from right atrium into the right
ventricle. Rapid y descent occurs in constrictive
pericarditis, heart failure and tricuspid regurgitation.
Jugular venous pressure is 3-4 cm of water. It is
elevated in cardiac tamponade, right ventricular failure,
tricuspid stenosis, increased blood volume, asthma,
emphysema, SVC obstruction. It is reduced in shock,
dehydration. During normal inspiration, intrathoracic
pressure falls and venous blood flow to thorax increases
causing inspiratory collapse of jugular venous pressure.
In constrictive pericarditis when intrapericardial pressure rises, there will be paradoxical increase in jugular
venous pressure during inspiration—Kussmaul’ s sign.
B
Figs 1.14A and B: Dilatation of abdominal veins including
inguinoaxillary vein and bilateral varicose veins in a patient
with IVC obstruction.
Jugular Venous Pulse (JVP)
Normal JVP has got 3 positive waves a, c and v and
2 negative waves x and y. ‘a’ wave is due right atrial
contraction (Fig. 1.15). It is absent in atrial fibrillation;
prominent in tricuspid/pulmonary stenosis. Cannon a
wave is seen in complete heart block, ventricular
Fig. 1.15: Normal jugular venous pulse-waves.
Pulse Means Arterial Pulse
Pulse is an ideal indicator of severity of many
diseases. It is increased in sepsis, severe pain, shock,
fever, toxic thyroid. It is also altered in all cardiac
conditions. Rate (count the pulse); rhythm (regularity); tension and force; character; condition of
arterial wall should be noted. Pulse felt usually is
radial pulse (against head of the radius) but when
indicated, other pulses in the body also should be
examined. It is felt using three fingers-index, middle
and ring. Ring finger is kept distally to obliterate the
retrograde pressure transmission; middle finger is
over to feel the pulse; index finger is kept proximally
to control and fix the artery to reduce the blood flow
while checking the vessel wall thickness. Pulse is
counted for full one minute. Counting for few seconds
and multiplying is wrong. Normal pulse has got a
Introduction on Clinical Examination
https://t.me/med1917
small anacrotic wave in the upstroke (which is not
felt), a big tidal percussion wave which is felt (Fig.
1.16). During downstroke there is a dicrotic notch
with a dicrotic wave (both are not felt). Anacrotic
wave pulse is felt in severe aortic stenosis. Pulsus
bisferiens is rapid rising, twice beating waves in the
systole of the pulse; felt in idiopathic hypertrophic
subaortic stenosis, severe aortic incompetence with
mitral stenosis. Dicrotic pulse is twice beating pulse
with initial normal percussion wave of systole and
eventual abnormal prominent dicrotic wave in
diastole. It is seen in reduced peripheral resistance
like CCF, cardiac tamponade, typhoid fever. Pulsus
alterans is alternate strong and weak beats; due to
alternate contractions of the cardiac muscle; seen in
left ventricular failure, toxic myocarditis. Pulsus
paradoxus—During inspiration there is increased
venous return to right atrium; lung expansion causes
pooling of blood in the pulmonary vessels causing
decreased venous return to left atrium and ventricle.
It causes decreased left ventricular output and arterial
pressure during inspiration by 3-10 mm Hg. When
this fall in systolic pressure is exaggerated more than
10 mm Hg, it is called as pulsus paradoxus. It is seen
in SVC obstruction, airway obstruction, asthma,
pericardial effusion. In immobile thoracic cage pulsus
paradoxus does not exists. Pulsus bigeminus with
coupling occurs in atrioventricular block. Thready
pulse is rapid, small waved pulse seen in shock,
cardiac diseases. Waterhammer pulse is large boun-
ding pulse with a forcible jerk, disappearing quickly.
It is due to sudden fall in peripheral resistance;
seen in thyrotoxicosis, AV fistula, beriberi, aortic
regurgitation, PDA. Tachycardia means increased
pulse rate more than 100/minute. Bradycardia
(Greek-slow) is decreased pulse rate less than 60/
minute.
Fig. 1.16: Normal arterial pulse wave.
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Blood Pressure (BP)
BP is essential part of the general examination in all
cases. It gives the idea about the general condition
of the patient along with other parameters. BP is
lateral pressure exerted by the column of blood on
the walls of the arteries. Systolic pressure is due to
stroke volume of the heart and stiffness of vessels.
It is the maximum pressure produced during (cardiac
cycle) systole. Diastolic pressure is due to peripheral
resistance. BP varies in phases of respiration. It is
the minimum pressure exerted during cardiac cycle
(diastole). It is related to emotion, exercise, smoking,
alcohol, tobacco, meals, temperature, anxiousness,
circadian rhythm, age, race, obesity, etc. BP is
recorded by indirect method. Riva Rocci invented
sphygmomanometer. It contains mercury manometer,
cuff and air pump. Russian surgeon Korotkoff
originated the method of placing of stethoscope over
cubital fossa to hear sounds of brachial artery.
Procedure of taking BP should be meticulous. Patient
should be explained about the procedure. Patient
should be on rest for 5 minutes prior to checking BP.
Patient should avoid exertion or meals 30 minutes
prior to checking BP. Clothing of the arm should be
removed or kept as it is without folding (folding may
cause constriction band). Width of the inflatable
bladder cuff should be about 40% of the upper arm
circumference (12-14 cm width in average adult);
length of the inflatable bladder should be 80% of
upper arm circumference, almost long enough to
encircle the arm. Standard commonly used is 12 ×
23 cm size. In the thigh 18 × 24 cm is used. In obese,
12 × 35 cm sized cuff is used. In children smaller
sized cuff (width 3 cm in infants; 8 cm in children)
is used. Bladder of the BP cuff should encircle the
arm completely; center of the bladder cuff should be
over brachial artery; ideally rubber tubes should be
placed on the inferior aspect in the line of the brachial
artery (eventhough tubes are commonly placed
superiorly to make stethoscope placement over
cubital fossa easier); though bell of stethoscope gives
better sound; diaphragm of the stethoscope is
commonly used due to its ability to cover wider area
and easier to secure. Usual position is supine lying
down with arm supported to heart level. In sitting/
standing position arm should be horizontal at 4th
intercostals space of the sternum. If arm is not
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supported, arm with isometric contraction will elevate
the diastolic BP by 10%. In normal individual, there
is not much difference in BP in standing, sitting or
lying down positions. BP in right arm is higher by
up to 10 mm Hg; if BP is higher by more than 10
mm Hg then it should be analyzed carefully. Repeat
inflations of cuff will raise the systolic and diastolic
BP and give false readings. So cuff should be inflated
rapidly and deflated early and completely; further
repeat readings are taken with a gap of 15 seconds.
Phases in BP measurement: Phase I: Appearance of
faint clear tapping sound which gradually increases in
intensity; Phase II: Softening or swishing sounds;
Phase III: Return of sharper crisper sounds; Phase IV:
Soft, blowing, muffling of sounds; Phase V : Disappearance of sounds completely. Phase I is systolic BP;
Phase V is diastolic BP. Hypertension is persistent
raised systolic (above 140 mm Hg) or diastolic (above
90 mm Hg) BP. It is sustained elevation of systemic
arterial pressure. It could be—essential HT; renal;
vascular; endocrinal; neurological; haematological.
Hypotension is diminished BP (systolic pressure less
than 90 mm Hg). It could be due to—postural, cardiac,
endocrinal like Addison’s disease; tuberculosis,
malignancy, dehydration, shock, haemorrhage, hypovolaemia, anaemia, anorexia nervosa.
Respiration
Tachypnoea is rapid breathing seen in fever, shock,
hypoxia, acidosis, tetany, hysteria. Gradual deepening
of respiration alternating with short periods of apnoea
is called as Cheyne-Stokes respiration.
Fever/Rise in Temperature
Normal body temperature is balance between heat
gain and loss maintained by hypothalamus. It is the
temperature of viscera and body tissues. Normal
temperature is 36.7°C-37.5°C (98 to 99°F-98.6°F).
A diurnal variation of 1°C is normal; lowest
temperature is during morning 2-4 AM highest being
in afternoon. Fever is increase in body temperature
more than 1°C or more than the maximum range.
Hypothermia is 35°C/95°F or below; subnormal
temperature is 35°-36.7°C/95°-97°F; normal is
36.7-37.5°C/98° to 99°F (98.6°F); mild fever is
37.2°-37.8°C/99°-100°F; moderate fever is 37.8°-
SRB’s Clinical Surgery
39.4°C/100°-103°F; high fever is 39.4°-40.5°C/103°105°F hyperpyrexia is more than 40.1°C/106°F.
Types of fever:
Continuous fever: Fever persists throughout the day
and does not fluctuate more than 1°C in 24 hours. It is
seen in pneumonia, urinary infection, endocarditis.
Remittent fever: Fever is above normal throughout
the day but there is fluctuation of more than 1°C in
24 hours. Intermittent fever—temperature is present
only few hours a day and reaches to normal. It is
observed in malaria, Kala azar . When fever develops
daily, it is called as quotidian; when fever develops
on alternate days it is called as tertian; when it occurs
every third day it is called as quartan.
Pel-Ebstein fever: Recurrent bouts of fever and
afebrile periods occur at regular alternations. Fever
rises for 3 days, remains high for 3 days, remits in
3 days and goes for an afebrile period of 9 days to
develop fever again in the same manner. It observed
in brucellosis; earlier also thought to be due to
Hodgkin’s lymphoma.
Fever with chills is sensation of cold with fever. Rigor
is profound chill with piloerection (gooseflesh) with
teeth shattering and shivering (Fig. 1.17). Pyrexia
Unknown Origin (PUO) is defined as—fever more
than 101°F; more than 3 weeks of duration; failure
to reach into a diagnosis even after one week of
inpatient investigation.
Causes for fever: Infective (bacterial, viral, fungal,
parasitic); neoplastic; vascular (myocardial infarction,
pulmonary embolism, pontine/subarachnoid haemorrhage); traumatic; collagen diseases; endocrinal;
metabolic (Gout, acidosis); haemolytic.
Grading of fever: None (0); 38-39°C (1); 39.1-40° (2);
> 40° for 24 hours (3).
Tongue
Tongue may be large called as macroglossis. It is
seen in lymphangioma, haemangioma, acromegaly,
myxoedema, critinism, amyloidosis. T ongue tremor is
observed in thyrotoxicosis (primary). It is checked with
tongue kept inside the oral cavity. If tongue is protruded,
tongue twitchings may mimic tremor. Tongue is bright
red in colour normally—due to rich blood supply
through capillary network. Pallor is seen in anaemia,
Introduction on Clinical Examination
https://t.me/med1917
Fig. 1.17: Different types of fever.
19
haemorrhage. Discolouration can occur after coloured
food intake, tobacco chewing, Addison’ s disease, iron
tablets intake. Central cyanosis is observed in tongue.
Tongue is moist normally; dry tongue suggests
dehydration, shock. Dry brown tongue is a feature of
uraemia, intestinal obstruction. Mouth dryness is
graded as normal (0); mild (1); moderate (2). Furring
of tongue is seen in smokers, stomatitis, and poor oral
hygiene. Black hairy tongue is seen in fungal infection.
Bald tongue is due to atrophy of papillae. It is seen in
iron deficiency anaemia, vitamin B12 deficiency . Curdy
coating is seen in candidiasis infection. Leukoplakia
as a whitish opaque thickened epithelium may be seen;
it is often associated with superficial glossitis.
Congenital fissuring can occur with irregular folds.
Fissuring may also be a presentation of carcinoma of
tongue. Lozenge shaped loss of papillae and fissuring
is seen in midline in front of the foramen caecum.
Lingual thyroid may be seen posteriorly in midline.
Inability to protrude tongue is seen in ankyloglossia
in tongue tie, advanced carcinoma tongue infiltrating
the genioglossus muscle. While protruding tongue may
deviate towards same side in hypoglossal nerve palsy.
Hiccup
It is spasmodic contraction of diaphragm. It is commonly idiopathic which subsides on its own. Post-
operative hiccup is common. It is due to increased
abdominal pressure, pushing the diaphragm upwards.
There may be paralytic ileus, gastric dilatation, and
intestinal obstruction. Peritonitis involving diaphragmatic surface can cause hiccup. Renal failure causes
hiccup.
Crepitus
It is crackling or grating sensation felt on palpation
of subcutaneous tissue or joint or bone. Crackling
sensation is felt when air is under the palpating
fingers. Pockets of air moves in between separated
subcutaneous or soft tissues causing crackling feel.
Grating sensation is felt in bone or joint as crepitus.
Types
Crepitus in subcutaneous (surgical) emphysema: It
is crackling sensation felt with gentle pressure under
examining fingers similar to a palpating horse hair
mattress. It can often be heard by placing a stethoscope
over the surface. Subcutaneous emphysema is better
felt (often seen as bull neck) in neck, shoulder and
chest wall. Causes of subcutaneous emphysema are—
traumatic (Fracture ribs, laryngeal injury, tracheostomy, fracture skull with air sinus like frontal sinus
injury); after surgery air may get trapped in the
subcutaneous plane prior to closure of skin, after
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SRB’s Clinical Surgery
laparoscopic surgery; infective (in gas gangrene); after
oesophageal rupture (Boerhaave’s syndrome—here
mediastinal emphysema, subcutaneous emphysema,
shock, toxicity occurs).
Crepitus of tenosynovitis: It is seen in de Quervain’s
tenosynovitis. Here hand is laid upon arm above the
wrist, and the patient is asked to close and open the
hand. Crepitus is felt at the junction of extensor pollicis
brevis and abductor pollicis longus crossing the
extensor carpi radialis longus and brevis. Crepitus of
bursitis is felt when lining is rough or contains loose
fibrinous particles.
Joint crepitus: It is felt when af fected joint passively
moved by one hand, and by placing other hand over
the suspected joint. It can be—fine, even crepitations
of chronic and subacute joint diseases; coarse, irregular
crepitations of osteoarthritis; a click due to loose body
or displaced cartilage. Bone crepitus is elicited over
the fracture segments of the bone when two fragments
are moved against each other. A grating sensation is
typical. But this should be elicited with utmost
gentleness; only when radiological doubt exists.
Crepitus is an unmistakable, diagnostic sign of
fracture.
Fig. 1.18: Drug induced allergic rashes
on the back extensively involved.
Skin Changes and Eruptions (Figs 1.18 to 1.22)
Macule: It is not raised above the skin; there is
alteration in colour of skin; it is seen but not felt;
capillary naevi or erythema blanch on pressure,
purpuric macules do not blanch on pressure. Macules
can be generalised; as seen in typhoid, syphilis,
purpura; localised type is called as roseolar.
Papule: It is raised tiny nodule; usually of few mm in
size; it may be epidermal or dermal; seen in measles,
chickenpox, smallpox, drugs like sulfonamides,
occasionally in tuberculosis, sarcoidosis.
Vesicles: They are small blisters; elevations from
epidermis containing clear or milk like fluid within;
seen in chickenpox, smallpox, herpes.
Pustules: They are epidermal elevations containing
pus; due to bacterial like streptococcal infection.
Granule is projection of < 2 cm in size. Nodule is large
usually solid projection from the skin of more than
2 cm in size.
Fig. 1.19: Alopecia scalp developed after
chemotherapy.
Wheal: It is elevated patch on the skin with centre paler
than the periphery; it is oedematous elevation with
itching; seen in allergical conditions.
Café au lait spots: They are coffee brown coloured
patches in the skin; more than 5 in number with each
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