👤 General Examination
01. General Appearance & Sensorium
Observe before touching: distress, posture, mobility, speech, work of breathing, body habitus, hygiene, devices and level of consciousness. Describe rather than label.
Begin at the end of the bed; introduce yourself, confirm identity, explain, consent, expose appropriately and preserve dignity. Assess AVPU/GCS when consciousness is impaired.
Classify the finding by distribution, time course and associated systemic clues; use the sign to narrow—not replace—the clinical differential diagnosis.
Describe the physical sign objectively first, then interpret it in the context of history, vital signs and the rest of the examination.
Be ready to demonstrate the technique, define the sign, grade it when a validated grading system exists, and give common plus dangerous causes.
Altered sensorium, severe respiratory distress, shock, active seizure or rapidly evolving focal deficit requires immediate ABC assessment rather than a prolonged routine examination.
Technique → describe → grade/classify → associations → red flags → correlate with the relevant system.
02. Pallor
Reduced visible oxyhaemoglobin in skin/mucosa may reflect anaemia but bedside pallor is not sufficiently accurate to quantify haemoglobin.
Inspect lower palpebral conjunctiva, tongue/oral mucosa and palmar creases in good light; compare with overall complexion.
Classify the finding by distribution, time course and associated systemic clues; use the sign to narrow—not replace—the clinical differential diagnosis.
Describe the physical sign objectively first, then interpret it in the context of history, vital signs and the rest of the examination.
Be ready to demonstrate the technique, define the sign, grade it when a validated grading system exists, and give common plus dangerous causes.
Marked pallor with dyspnoea, syncope, chest pain, haemodynamic compromise or active bleeding needs urgent assessment.
Technique → describe → grade/classify → associations → red flags → correlate with the relevant system.
03. Icterus
Yellow discoloration from hyperbilirubinaemia is best sought in sclera; classify the clinical problem as pre-hepatic, hepatocellular or cholestatic after history/examination.
Inspect sclera in natural light, then skin and oral mucosa. Look for scratch marks, xanthelasma, hepatosplenomegaly and chronic liver disease signs.
Classify the finding by distribution, time course and associated systemic clues; use the sign to narrow—not replace—the clinical differential diagnosis.
Describe the physical sign objectively first, then interpret it in the context of history, vital signs and the rest of the examination.
Be ready to demonstrate the technique, define the sign, grade it when a validated grading system exists, and give common plus dangerous causes.
Jaundice with fever/RUQ pain, encephalopathy, bleeding, hypotension or acute liver failure features is urgent.
Technique → describe → grade/classify → associations → red flags → correlate with the relevant system.
04. Cyanosis
Bluish discoloration reflects increased deoxygenated haemoglobin or abnormal haemoglobin. Central cyanosis involves tongue/mucosa; peripheral cyanosis affects extremities with coolness/low flow.
Inspect tongue and lips for central cyanosis and fingers/toes for peripheral cyanosis; correlate immediately with SpO₂ and cardiorespiratory examination.
Classify the finding by distribution, time course and associated systemic clues; use the sign to narrow—not replace—the clinical differential diagnosis.
Describe the physical sign objectively first, then interpret it in the context of history, vital signs and the rest of the examination.
Be ready to demonstrate the technique, define the sign, grade it when a validated grading system exists, and give common plus dangerous causes.
New central cyanosis, low SpO₂, respiratory distress or altered consciousness is an emergency.
Technique → describe → grade/classify → associations → red flags → correlate with the relevant system.
05. Clubbing
Clubbing is bulbous enlargement of distal digits with loss of the normal nail-fold angle; associations include pulmonary, cardiac and GI/hepatobiliary disease.
Inspect profile, assess nail-bed fluctuation and Schamroth window; look for symmetry and hypertrophic osteoarthropathy.
Classify the finding by distribution, time course and associated systemic clues; use the sign to narrow—not replace—the clinical differential diagnosis.
Describe the physical sign objectively first, then interpret it in the context of history, vital signs and the rest of the examination.
Be ready to demonstrate the technique, define the sign, grade it when a validated grading system exists, and give common plus dangerous causes.
New asymmetric/unilateral clubbing or clubbing with haemoptysis, weight loss or systemic illness warrants focused evaluation.
Technique → describe → grade/classify → associations → red flags → correlate with the relevant system.
06. Edema
Edema results from altered hydrostatic/oncotic pressure, sodium retention, capillary permeability or lymphatic obstruction. Distribution and pitting help narrow cause.
Inspect dependent areas; press firmly over shin/ankle or sacrum and document pitting, symmetry, extent, skin change and associated JVP/ascites.
Classify the finding by distribution, time course and associated systemic clues; use the sign to narrow—not replace—the clinical differential diagnosis.
Describe the physical sign objectively first, then interpret it in the context of history, vital signs and the rest of the examination.
Be ready to demonstrate the technique, define the sign, grade it when a validated grading system exists, and give common plus dangerous causes.
Acute unilateral painful swelling suggests DVT; edema with pulmonary edema, severe oliguria or anasarca needs urgent evaluation.
Technique → describe → grade/classify → associations → red flags → correlate with the relevant system.
07. Lymphadenopathy
Describe nodes by site, size, number, tenderness, consistency, mobility, matting and overlying skin; localised versus generalised distribution guides differential.
Palpate cervical, supraclavicular, axillary and inguinal groups systematically; examine drainage areas and liver/spleen when relevant.
Classify the finding by distribution, time course and associated systemic clues; use the sign to narrow—not replace—the clinical differential diagnosis.
Describe the physical sign objectively first, then interpret it in the context of history, vital signs and the rest of the examination.
Be ready to demonstrate the technique, define the sign, grade it when a validated grading system exists, and give common plus dangerous causes.
Hard fixed supraclavicular nodes, rapidly enlarging nodes, B symptoms or generalized lymphadenopathy require prompt evaluation.
Technique → describe → grade/classify → associations → red flags → correlate with the relevant system.
08. Neck Examination
The neck can reveal thyroid disease, lymphadenopathy, tracheal deviation, venous pressure and vascular clues.
Inspect symmetry/scars/swelling; palpate nodes and thyroid as appropriate; assess tracheal position and carotids carefully.
Classify the finding by distribution, time course and associated systemic clues; use the sign to narrow—not replace—the clinical differential diagnosis.
Describe the physical sign objectively first, then interpret it in the context of history, vital signs and the rest of the examination.
Be ready to demonstrate the technique, define the sign, grade it when a validated grading system exists, and give common plus dangerous causes.
Stridor, rapidly expanding neck swelling, tracheal deviation with respiratory compromise or airway compression is urgent.
Technique → describe → grade/classify → associations → red flags → correlate with the relevant system.
09. Neck Veins & JVP
Position the patient comfortably at about 30–45°, adjusting the angle until venous pulsation is visible. Prefer the right internal jugular vein because it provides a relatively direct column to the right atrium. Use tangential light. Identify JVP by its biphasic/non-palpable character, variation with respiration/posture and ability to obliterate with gentle pressure—unlike the carotid pulse.
Identify the highest venous pulsation and measure its vertical height above the sternal angle. Traditionally, >3–4 cm above the sternal angle is considered elevated; interpret with position, technique and clinical context. JVP estimates right atrial pressure and is most valuable when integrated with congestion and perfusion findings.
a wave: right atrial contraction. c wave: early RV systole/tricuspid bulging (often not visible). x descent: atrial relaxation/downward tricuspid movement. v wave: atrial filling against closed tricuspid valve. y descent: atrial emptying after tricuspid opening.
Absent a: atrial fibrillation. Giant a: increased resistance to RV filling (e.g. pulmonary hypertension/tricuspid stenosis). Cannon a: AV dissociation. Prominent v/CV wave: tricuspid regurgitation. Rapid y descent: constrictive physiology/severe TR; slow y: tricuspid stenosis. In tamponade, y descent is classically blunted while x descent may be prominent.
Hepatojugular/abdominojugular reflux: sustained rise in JVP during firm abdominal pressure supports limited right-heart reserve/elevated filling pressure. Kussmaul sign: paradoxical rise or failure of JVP to fall with inspiration; classically associated with constrictive pericarditis, restrictive physiology and RV infarction, among other causes.
Think right-sided/biventricular heart failure, fluid overload, pulmonary hypertension, tricuspid valve disease, constrictive pericarditis, tamponade and SVC-related mimics. Raised JVP with hypotension, chest pain, severe dyspnoea or shock requires urgent evaluation for obstructive/cardiac causes.
Position 30–45° → Right IJV → Identify venous waveform → Measure above sternal angle → a-c-x-v-y → HJR → Kussmaul → Integrate with edema, liver, lungs and cardiac findings.
10. Pulse
Ensure 5 minutes of rest where feasible. Palpate the radial pulse with finger pads, not the thumb. Assess rate, rhythm, volume, character, vessel wall and radio-radial delay. Count 30 seconds ×2 when regular; count a full minute when irregular, very slow/fast or clinically unstable. Compare both radial pulses, then assess radio-femoral delay and relevant central/peripheral pulses.
Adult resting pulse is commonly 60–100/min, but interpret in context. Tachycardia: fever, pain, anxiety, hypovolaemia, anaemia, sepsis, hypoxia, thyrotoxicosis, drugs or arrhythmia. Bradycardia: athletic conditioning, sleep, drugs, hypothyroidism, hypothermia, raised ICP or conduction disease. Regularly irregular rhythms suggest patterned ectopy/AV block; an irregularly irregular pulse strongly suggests atrial fibrillation but requires ECG confirmation.
Low-volume/thready: low stroke volume or shock. Bounding: hyperdynamic circulation. Slow-rising/anacrotic: classically severe aortic stenosis. Collapsing/water-hammer: wide pulse pressure states, classically significant aortic regurgitation. Pulsus bisferiens: selected AR/HOCM patterns. Pulsus alternans: alternating strong/weak beats, suggesting severe LV dysfunction.
Pulse deficit: apical rate exceeds radial rate; assess simultaneously, often in AF. Radio-radial delay: consider proximal arterial obstruction/dissection. Radio-femoral delay: classically coarctation. Pulsus paradoxus: inspiratory fall in systolic BP >10 mmHg; seen in tamponade and severe obstructive airway disease among other settings.
“Pulse is 84/min, regular, normal volume and character, equal bilaterally, with no radio-radial or radio-femoral delay; peripheral pulses are palpable.” State abnormalities precisely rather than saying “pulse normal”.
Very rapid or slow pulse with hypotension, chest pain, syncope, altered sensorium, shock or acute heart failure needs urgent rhythm and haemodynamic assessment. Never diagnose an arrhythmia from pulse palpation alone—confirm with ECG.
Rate → Rhythm → Volume → Character → Vessel wall → Equality → Delays → Peripheral pulses → Special signs.
11. Blood Pressure
Use a validated device and correct cuff: bladder width about 40% of arm circumference and length about 80%. Patient should rest, back supported, feet flat and uncrossed, arm supported at heart level, with no talking. Avoid recent exercise, caffeine or smoking when practical. Measure both arms initially and use the higher-reading arm for subsequent assessment when a consistent difference exists.
Estimate systolic pressure by palpation first to avoid missing an auscultatory gap. Inflate 20–30 mmHg above estimated systolic pressure, then deflate approximately 2–3 mmHg/sec. Korotkoff phase I = systolic BP; phase V (disappearance) = diastolic BP in adults. Record arm, position, cuff size and clinically relevant circumstances.
Do not label chronic hypertension from a single incidental reading unless the clinical situation mandates urgent action. Repeat properly and use home/ambulatory measurements where appropriate. Pulse pressure = SBP − DBP. Mean arterial pressure is approximately DBP + ⅓ pulse pressure at usual heart rates.
When indicated, measure after supine rest and again after standing. A sustained fall of ≥20 mmHg systolic or ≥10 mmHg diastolic within 3 minutes supports orthostatic hypotension. A reproducible inter-arm difference warrants clinical interpretation and may suggest vascular disease depending on magnitude and context.
Narrow pulse pressure: low stroke-volume states such as shock. Wide pulse pressure: may occur in AR, arterial stiffness or hyperdynamic states. Severe BP elevation becomes a hypertensive emergency when accompanied by acute target-organ injury—not because of the number alone.
Wrong cuff size, unsupported arm, talking, crossed legs, rapid deflation and measuring over clothing can distort readings. Hypotension with poor perfusion, or severe hypertension with neurological, cardiac, renal or aortic features, requires urgent evaluation.
Rest → Correct cuff → Arm at heart → Both arms initially → Palpatory SBP → Korotkoff I/V → Repeat → Standing BP when indicated → Interpret with organ perfusion.
12. Respiratory Rate
Observe breathing unobtrusively, ideally while appearing to continue pulse assessment, because awareness can alter the rate. Count chest/abdominal excursions for 60 seconds when irregular; document breaths/min and simultaneously assess pattern, depth, effort and symmetry.
Do not record only a number. Describe rate + rhythm + depth + work of breathing. Look for accessory muscle use, intercostal/suprasternal recession, nasal flaring, inability to speak full sentences, paradoxical breathing and thoraco-abdominal asynchrony.
Tachypnoea may reflect hypoxaemia, fever, pain, acidosis, sepsis, pulmonary/cardiac disease or anxiety. Bradypnoea raises concern for CNS depression, opioids/sedatives, metabolic causes or impending fatigue. Kussmaul breathing: deep laboured breathing with metabolic acidosis. Cheyne–Stokes: crescendo–decrescendo ventilation with apnoeic periods, seen in selected cardiac/neurological states.
Respiratory rate is a sensitive marker of physiological deterioration and is incorporated into early-warning scores. Interpret it with SpO₂, oxygen requirement, mental status, haemodynamics and work of breathing; a “normal” SpO₂ on supplemental oxygen does not exclude serious respiratory failure.
“Respiratory rate is 18/min, regular, normal depth, with no accessory muscle use or thoraco-abdominal paradox.” In illness, add oxygen device/flow and SpO₂.
Marked tachypnoea or bradypnoea, exhaustion, silent chest, cyanosis, altered consciousness, inability to speak, paradoxical breathing or worsening oxygen requirement should prompt immediate ABC assessment.
Rate → Rhythm → Depth → Effort → Symmetry → Pattern → SpO₂/O₂ device → Overall physiology.
13. Temperature
Record the site and method because oral, axillary, tympanic and rectal readings are not interchangeable. Use a reliable calibrated device and repeat an unexpected value. Core temperature is best approximated by appropriate core-site measurement in critical illness; peripheral methods are more affected by technique and environment.
Body temperature follows circadian variation and is regulated by the hypothalamus. Fever reflects an elevated thermoregulatory set point, commonly from pyrogens; hyperthermia is uncontrolled heat accumulation without a raised set point. This distinction matters because management differs.
Continuous, remittent, intermittent, relapsing and step-ladder descriptions are traditional patterns, but fever pattern alone is rarely diagnostic. More useful bedside information includes duration, rigors, exposures, drugs, immune status, localising symptoms and haemodynamic impact.
Hypothermia is core temperature <35°C and may cause bradycardia, dysrhythmia, coagulopathy and altered sensorium. Hyperthermic syndromes include heat stroke, serotonin syndrome, neuroleptic malignant syndrome and malignant hyperthermia; context and associated neuromuscular/autonomic findings are essential.
Relative bradycardia or pulse–temperature dissociation can occur in selected infections and non-infectious conditions but is not sufficiently specific to diagnose a disease. Fever with rash, meningism, shock, neutropenia or severe immunosuppression deserves urgent focused assessment.
Do not equate absence of fever with absence of infection—elderly, immunocompromised and critically ill patients may be afebrile or hypothermic. Hyperthermia with CNS dysfunction is an emergency; severe hypothermia requires careful handling and monitored rewarming.
Value → Site/method → Confirm → Fever vs hyperthermia → Associated physiology → Focus/source → Red flags.
14. Oxygen Saturation (SpO₂)
Pulse oximetry estimates arterial oxygen saturation but does not measure ventilation or PaCO₂ and can be affected by poor perfusion, motion and dyshemoglobinaemia.
Check waveform/signal quality, warm the extremity if needed and interpret with oxygen delivery, respiratory effort and ABG/VBG when clinically indicated.
Classify the finding by distribution, time course and associated systemic clues; use the sign to narrow—not replace—the clinical differential diagnosis.
Describe the physical sign objectively first, then interpret it in the context of history, vital signs and the rest of the examination.
Be ready to demonstrate the technique, define the sign, grade it when a validated grading system exists, and give common plus dangerous causes.
Low or falling saturation with distress, cyanosis or altered consciousness requires immediate airway/oxygenation assessment.
Technique → describe → grade/classify → associations → red flags → correlate with the relevant system.
15. Hydration & Volume Status
No single sign defines hydration. Integrate intake/losses, mucosa, pulse/BP, capillary refill, JVP, edema, urine output and weight trend.
Inspect mucosa, peripheral perfusion and skin; assess orthostasis/JVP and edema; correlate with urine output and labs.
Classify the finding by distribution, time course and associated systemic clues; use the sign to narrow—not replace—the clinical differential diagnosis.
Describe the physical sign objectively first, then interpret it in the context of history, vital signs and the rest of the examination.
Be ready to demonstrate the technique, define the sign, grade it when a validated grading system exists, and give common plus dangerous causes.
Hypotension, oliguria, delayed refill, altered sensorium or severe electrolyte disturbance suggests significant circulatory/volume compromise.
Technique → describe → grade/classify → associations → red flags → correlate with the relevant system.
16. Nutrition & Body Habitus
Assess weight trajectory, BMI where appropriate, muscle wasting, fat distribution and micronutrient clues rather than appearance alone.
Document height/weight, recent unintentional change, temporal/masseter muscle bulk and functional clues; consider waist circumference when metabolically relevant.
Classify the finding by distribution, time course and associated systemic clues; use the sign to narrow—not replace—the clinical differential diagnosis.
Describe the physical sign objectively first, then interpret it in the context of history, vital signs and the rest of the examination.
Be ready to demonstrate the technique, define the sign, grade it when a validated grading system exists, and give common plus dangerous causes.
Rapid unintentional weight loss, severe wasting, dysphagia or inability to maintain intake warrants prompt assessment.
Technique → describe → grade/classify → associations → red flags → correlate with the relevant system.
17. Skin, Hair & Nails
Skin appendages provide clues to systemic, endocrine, nutritional, hepatic, renal, vascular and connective-tissue disease.
Inspect exposed and relevant covered areas for rash, pigmentation, bruising, ulcers, scars, turgor, hair distribution and nail changes.
Classify the finding by distribution, time course and associated systemic clues; use the sign to narrow—not replace—the clinical differential diagnosis.
Describe the physical sign objectively first, then interpret it in the context of history, vital signs and the rest of the examination.
Be ready to demonstrate the technique, define the sign, grade it when a validated grading system exists, and give common plus dangerous causes.
Non-blanching rash with systemic illness, rapidly spreading skin necrosis, mucosal involvement or severe drug eruption is urgent.
Technique → describe → grade/classify → associations → red flags → correlate with the relevant system.
18. Peripheral Perfusion & Capillary Refill
Perfusion assessment integrates skin temperature, colour, capillary refill, pulse quality, mental state and urine output; CRT alone is imperfect.
Assess centrally and peripherally in appropriate ambient conditions; compare limbs and correlate with BP/lactate when needed.
Classify the finding by distribution, time course and associated systemic clues; use the sign to narrow—not replace—the clinical differential diagnosis.
Describe the physical sign objectively first, then interpret it in the context of history, vital signs and the rest of the examination.
Be ready to demonstrate the technique, define the sign, grade it when a validated grading system exists, and give common plus dangerous causes.
Cool mottled extremities, weak pulses, delayed refill, hypotension or altered mentation suggests shock or critical limb perfusion.
Technique → describe → grade/classify → associations → red flags → correlate with the relevant system.
🩺 Systemic Examination
01. Cardiovascular Examination (CVS)
Positive findings commonly relevant to cardiovascular disease:
- Pulse: tachycardia/bradycardia, irregularly irregular rhythm, low-volume pulse, collapsing pulse or slow-rising pulse depending on the lesion.
- Blood pressure: hypotension in low-output states; hypertension as a major cardiovascular risk factor; pulse-pressure abnormalities may provide additional clues.
- Raised JVP: suggests elevated right-sided filling pressure; assess waveform when possible.
- Pallor: anaemia may aggravate angina or heart failure.
- Central cyanosis: consider severe hypoxaemia or a right-to-left shunt; peripheral cyanosis may occur with poor perfusion.
- Clubbing: consider infective endocarditis or cyanotic congenital heart disease in the appropriate context.
- Pedal/sacral oedema: supports systemic venous congestion, especially with raised JVP.
- Peripheral perfusion: cool extremities, prolonged capillary refill and diaphoresis may indicate low cardiac output.
- Infective endocarditis clues: fever, splinter haemorrhages, Janeway lesions, Osler nodes and conjunctival/palatal petechiae—interpret with the clinical context.
- Other clues: xanthelasma/xanthomas, nicotine staining, malar flush, characteristic facies or surgical scars may point toward risk factors or underlying disease.
Inspection — what to look for: Observe from the end of the bed for breathlessness, orthopnoea, oxygen use, cachexia, cyanosis, scars, pacemaker/ICD bulge and visible precordial activity. Inspect the chest for deformity and the precordium for an unusually prominent or displaced apex impulse. Note raised JVP and peripheral oedema before focusing on the heart.
Palpation — what to find: Locate the apex beat and define its intercostal space, relation to the mid-clavicular line and character. A displaced hyperdynamic apex suggests volume overload; a sustained/heaving apex suggests pressure overload. Feel for parasternal heave, palpable P2 and thrills over valve areas. Assess peripheral pulses for rate, rhythm, volume, character, radio-radial/radio-femoral delay where relevant, and correlate the carotid upstroke with systole.
Percussion — limited modern role: Cardiac percussion is not routinely relied upon to define heart size because chest radiography/echocardiography are more accurate. If performed in a traditional bedside examination, an expanded area of cardiac dullness may suggest cardiomegaly, but interpret cautiously.
Auscultation — what to find: Auscultate mitral, tricuspid, pulmonary and aortic areas with diaphragm and bell as appropriate. Define S1/S2 intensity and splitting; identify S3, S4, clicks, opening snap or pericardial rub. For every murmur describe timing, site of maximum intensity, character, grade and radiation, then use manoeuvres deliberately: left lateral position for mitral sounds, sitting forward/end-expiration for aortic regurgitation, and inspiration for right-sided murmurs.
Link pulse character, JVP waveform, apex position/character and heart sounds. For every murmur state timing, site, character, grade, radiation and response to inspiration or dynamic manoeuvres. Build the lesion from the complete pattern rather than from the murmur alone.
Raised JVP + oedema suggests systemic venous congestion; displaced hyperdynamic apex suggests volume overload; sustained apex suggests pressure overload. A slow-rising pulse with an ejection systolic murmur supports aortic stenosis, whereas a collapsing pulse with an early diastolic murmur supports aortic regurgitation.
Always palpate the carotid while timing an uncertain murmur: a systolic murmur coincides with the carotid upstroke. Auscultate again in the left lateral position for mitral sounds and sitting forward in expiration for aortic regurgitation.
“The cardiovascular examination shows…” → haemodynamic state → pulse/BP/JVP → apex → heart sounds/murmur → signs of failure → most likely lesion and severity clues.
Hypotension with chest pain, new severe murmur, pulmonary oedema, syncope with critical aortic stenosis, tamponade physiology or signs of acute aortic syndrome require urgent escalation.
General survey → hands/face → pulse/BP → JVP → precordium → auscultation → dynamic manoeuvres → heart failure signs → peripheral pulses.
First decide timing: systolic, diastolic or continuous. Then describe site of maximum intensity → character → grade → radiation → associated heart sounds → response to manoeuvres.
Aortic stenosis: harsh crescendo–decrescendo ejection systolic murmur, maximal in the aortic area and typically radiating to the carotids. Look for a slow-rising pulse, narrow pulse pressure in severe disease and a sustained apex.
Mitral regurgitation: classically a pansystolic blowing murmur maximal at the apex with radiation toward the axilla; assess for a displaced/hyperdynamic apex when significant chronic volume overload is present.
Tricuspid regurgitation: pansystolic murmur at the left lower sternal border that typically becomes louder with inspiration (Carvallo sign); look for prominent JVP waves and systemic venous congestion.
Ventricular septal defect: classically a harsh pansystolic murmur at the left lower sternal edge, often with a thrill when restrictive. Murmur loudness does not directly measure defect severity.
Aortic regurgitation: high-pitched early diastolic decrescendo murmur, best heard with the patient sitting forward at end-expiration along the left sternal edge. A collapsing pulse and wide pulse pressure support significant AR.
Mitral stenosis: low-pitched mid-diastolic rumble at the apex, best with the bell in the left lateral position; an opening snap and loud S1 may accompany it when valve mobility is preserved.
Dynamic bedside manoeuvres: inspiration tends to augment right-sided murmurs. Standing/Valsalva generally reduces ventricular filling but can intensify hypertrophic obstructive cardiomyopathy; squatting usually has the opposite effect. Use manoeuvres to support—not replace—the complete examination.
Grading: systolic murmurs are commonly graded I–VI. A palpable thrill generally accompanies grade IV or louder. Always document the grade rather than writing only “murmur present.”
JVP: Assess height and waveform, not merely “raised/not raised.” Know prominent a waves, absent a waves in atrial fibrillation, cannon a waves with AV dissociation and prominent v waves in significant tricuspid regurgitation. Test hepatojugular reflux when right-sided congestion is suspected.
Peripheral pulse clues: Compare both radial pulses; assess radio-femoral delay when coarctation is relevant. Know pulsus paradoxus as an exaggerated inspiratory fall in systolic BP and pulsus alternans as alternating strong/weak beats suggesting severe LV dysfunction.
Heart sounds: Learn fixed wide S2 splitting (classically ASD), paradoxical splitting in delayed LV emptying, loud P2 in pulmonary hypertension, and when S3/S4 are clinically meaningful.
Complete the examination: Check lung bases for congestion/effusion, sacral and pedal oedema, hepatomegaly/ascites where indicated, peripheral pulses and relevant scars/devices. In suspected endocarditis, deliberately search peripheral stigmata.
Rapid bedside revision:
- Always correlate the pulse with the heart sounds; an irregularly irregular pulse strongly suggests atrial fibrillation in the appropriate setting.
- A slow-rising, low-volume carotid pulse with an ejection systolic murmur supports significant aortic stenosis.
- A collapsing pulse with a wide pulse pressure and early diastolic murmur supports aortic regurgitation.
- A displaced, hyperdynamic apex suggests volume overload; a sustained/heaving apex suggests pressure overload.
- Raised JVP with peripheral oedema supports systemic venous congestion; JVP is more informative than oedema alone.
- An inspiratory increase in JVP (Kussmaul sign) suggests impaired right-sided filling and should be interpreted in context.
- Right-sided murmurs generally become louder with inspiration; this bedside response can help localise a murmur.
- Mitral stenosis is suggested by a tapping apex, loud S1, opening snap and mid-diastolic rumble at the apex.
- An S3 may indicate volume overload or systolic heart failure in an appropriate adult; an S4 suggests a stiff, poorly compliant ventricle.
- Never describe a murmur only by its name: state timing, site, character, grade, radiation and response to manoeuvres.
- Clubbing in a cardiac patient should prompt consideration of infective endocarditis or cyanotic congenital heart disease rather than uncomplicated heart failure.
- Before concluding that oedema is cardiac, integrate JVP, hepatojugular response, lung findings and the rest of the clinical picture.
02. Respiratory Examination
Positive findings commonly relevant to respiratory disease:
- Respiratory distress: tachypnoea, inability to speak full sentences, accessory-muscle use, intercostal recession or tripod posture indicate increased work of breathing.
- Cyanosis: central cyanosis suggests significant arterial desaturation and requires prompt assessment.
- Clubbing: consider bronchiectasis, lung abscess, lung malignancy, interstitial lung disease or other relevant causes; uncomplicated COPD alone does not usually cause clubbing.
- Hands: nicotine staining may indicate smoking exposure; asterixis can occur with hypercapnia.
- Cachexia/weight loss: may accompany malignancy, tuberculosis or advanced chronic lung disease.
- Lymphadenopathy: cervical/supraclavicular nodes may be important in infection or malignancy.
- Pedal oedema/raised JVP: may suggest cor pulmonale or concomitant right-heart failure.
- Face/voice: ptosis, miosis, facial swelling, hoarseness or stridor can provide important clues to intrathoracic pathology.
- Oxygen/devices: note oxygen delivery, inhalers, nebulisers, sputum pot, drains or NIV support before beginning the chest examination.
Inspection — what to look for: Assess respiratory rate, rhythm and effort before touching the patient. Look for tachypnoea, accessory-muscle use, intercostal recession, pursed-lip breathing, inability to speak full sentences, cyanosis, chest deformity and asymmetry. Compare movement of both hemithoraces and note scars, sinuses, dilated veins, chest drains or oxygen devices. A visibly lagging side suggests reduced expansion on that side.
Palpation — what to find: Check tracheal position first when major unilateral disease is suspected. Compare chest expansion bilaterally; reduced unilateral expansion occurs with pleural effusion, pneumothorax, collapse or consolidation, while bilateral reduction is common in obstructive/restrictive disease. Assess tactile vocal fremitus when useful: it tends to increase over consolidation and decrease when pleural fluid or air separates lung from chest wall. Palpate for tenderness, masses and cervical/supraclavicular nodes.
Percussion — what to find: Percuss corresponding areas side-to-side. Dullness supports consolidation or collapse; stony dullness strongly suggests pleural effusion; hyper-resonance suggests excess air such as pneumothorax or marked hyperinflation. Assess diaphragmatic level/excursion selectively rather than mechanically in every patient.
Auscultation — what to find: Compare symmetrical zones while the patient breathes through an open mouth. Decide whether breath sounds are vesicular, diminished/absent or bronchial. Bronchial breathing over peripheral lung supports consolidation when the bronchus remains patent. Listen for wheeze, fine/coarse crackles, pleural rub and other added sounds. Test vocal resonance when indicated: increased resonance/bronchophony supports consolidation, whereas reduced transmission favours pleural effusion or pneumothorax.
Consolidation tends to produce dull percussion, bronchial breathing and increased vocal resonance. Pleural effusion gives stony dullness with reduced breath sounds/resonance. Pneumothorax produces hyper-resonance and reduced breath sounds; obstruction commonly produces prolonged expiration and wheeze.
Think in four bedside patterns: air-space disease, pleural disease, airway obstruction and diffuse interstitial disease. Localise an abnormality first, then decide which pattern best explains the combination of inspection, palpation, percussion and auscultation.
Compare identical points side-to-side rather than completing one hemithorax first. In a breathless patient, count respiratory rate before touching the patient so voluntary control does not alter it.
State respiratory distress and oxygen requirement first, then trachea/chest movement, percussion, breath sounds, added sounds and vocal resonance, followed by the likely anatomical pattern.
Silent chest, severe hypoxaemia, exhaustion, altered sensorium, unilateral absent breath sounds with haemodynamic compromise or stridor are immediate danger signs.
End of bed → hands/face → neck/trachea → inspect → palpate → percuss → auscultate → vocal resonance → posterior bases → oedema/DVT clues when relevant.
Wheeze: A continuous musical sound caused by narrowed airways. Polyphonic wheeze suggests widespread airway narrowing, classically asthma/COPD; a monophonic localized wheeze raises concern for focal large-airway obstruction.
Fine crackles: Brief, discontinuous, usually late-inspiratory sounds. Fine basal “Velcro-like” crackles suggest interstitial fibrosis; fine basal crackles may also occur with pulmonary oedema.
Coarse crackles: Lower-pitched, bubbling discontinuous sounds produced by secretions or opening of larger airways; consider bronchiectasis, pneumonia or secretion-filled airways. Note whether they change after coughing.
Pleural friction rub: A superficial grating/creaking sound from inflamed pleural surfaces, usually heard in inspiration and expiration and localized to an area of pleuritic pain. It does not usually clear with coughing.
Stridor: A harsh, predominantly inspiratory upper-airway sound. Treat significant stridor as a potential airway emergency rather than merely an auscultatory finding.
Squawk: A short inspiratory musical sound, sometimes associated with small-airway involvement such as hypersensitivity pneumonitis; interpret with the overall clinical context.
Must describe: timing (inspiratory/expiratory), pitch, location, extent, symmetry and whether the sound changes after coughing. Never document only “added sounds present.”
Vocal tests: Understand vocal resonance, bronchophony and whispering pectoriloquy as manifestations of increased sound transmission through consolidated lung; transmission falls with pleural fluid or pneumothorax.
Trachea and mediastinum: Always interpret displacement with volume: lesions that push (large effusion/tension pneumothorax) tend to move it away, whereas major collapse/fibrosis can pull it toward the affected side.
Chest expansion: Document symmetry and whether restriction is unilateral or bilateral. Hyperinflation may reduce bilateral expansion; focal pleural/parenchymal disease often creates asymmetry.
Complete the examination: Examine cervical/supraclavicular nodes, assess legs for DVT when pulmonary embolism is plausible, and look for cor pulmonale (JVP/oedema). Peak flow or oxygen saturation may complement—but never replace—the physical examination.
Rapid bedside revision:
- Tracheal deviation away from the affected side suggests a large pleural effusion or tension pneumothorax; deviation toward it may occur with major volume loss.
- Stony dull percussion with reduced breath sounds and reduced vocal resonance is the classic bedside pattern of pleural effusion.
- Hyper-resonance with markedly reduced/absent breath sounds suggests pneumothorax; tension physiology is an emergency diagnosis.
- Dull percussion, bronchial breathing and increased vocal resonance together strongly support lung consolidation.
- Reduced chest expansion should be interpreted as unilateral or bilateral; the distribution narrows the differential.
- Fine late-inspiratory crackles at the bases are important in interstitial lung disease and pulmonary oedema, but the whole clinical pattern matters.
- Polyphonic wheeze suggests widespread airway narrowing; a fixed monophonic wheeze can suggest focal large-airway obstruction.
- Clubbing is not a usual feature of uncomplicated COPD—look for bronchiectasis, malignancy, interstitial disease or another cause.
- Asterixis in a drowsy patient with chronic lung disease can be a clue to hypercapnia, but it is not specific.
- Always document respiratory rate and work of breathing; they may reveal deterioration before auscultatory signs become dramatic.
- Bronchial breathing requires patent airways transmitting sound through abnormal peripheral lung; it is not synonymous with every opacity.
- Compare corresponding areas side-to-side during palpation, percussion and auscultation; asymmetry is often more informative than an isolated finding.
03. CNS Examination
Positive findings commonly relevant to neurological disease:
- Consciousness and behaviour: altered GCS, confusion, agitation, drowsiness or abnormal behaviour may immediately localise severity rather than diagnosis.
- Orientation and speech: disorientation, dysarthria, aphasia or abnormal voice should be identified early.
- Posture and spontaneous movement: hemiplegic posture, abnormal limb positioning, tremor, chorea, dystonia, myoclonus or fasciculations may guide localisation.
- Gait: hemiplegic, spastic, ataxic, parkinsonian, waddling or high-stepping patterns provide valuable localisation clues.
- Facies: facial asymmetry, reduced expression, ptosis or other characteristic appearances may suggest cranial-nerve, neuromuscular or extrapyramidal disease.
- Muscle bulk: focal/generalised wasting, hypertrophy or fasciculation may indicate lower motor neuron, muscle or chronic neurological disease.
- Skin and neurocutaneous clues: café-au-lait macules, neurofibromas, hypopigmented macules, vascular lesions, scars or pressure sores may be relevant.
- Autonomic/trophic clues: abnormal sweating, postural BP fall, bladder clues, trophic ulcers or altered skin texture may accompany autonomic/peripheral nerve disease.
- Meningism/raised ICP warning signs: fever, neck stiffness, persistent vomiting, severe headache, papilloedema or deteriorating consciousness demand urgent assessment.
1. Higher mental functions: Begin with level of consciousness and behaviour. Assess orientation to time, place and person, attention, memory and language. When indicated examine speech, naming, repetition, comprehension, reading/writing, calculation, praxis, neglect and frontal-lobe functions. The pattern should help distinguish global encephalopathy from a focal cortical deficit.
2. Cranial nerves: Examine CN I selectively; then visual acuity and fields, pupils and fundus, ocular movements, facial sensation and corneal reflex when indicated, muscles of mastication, facial symmetry/movements, hearing, palate and phonation, shoulder shrug/head turn, and tongue. Interpret abnormalities anatomically—for example UMN versus LMN facial weakness, ocular-motor palsy, bulbar weakness or multiple cranial neuropathies.
3. Motor system: Inspect posture, involuntary movements, fasciculations and muscle bulk. Assess tone, then power systematically using the MRC scale and compare sides. Look for pronator drift when appropriate. Integrate bulk + tone + power + reflexes + plantar response to decide whether the pattern is UMN, LMN, neuromuscular-junction or primary muscle disease.
4. Reflexes: Test relevant deep tendon reflexes symmetrically and grade them. Assess superficial reflexes when clinically useful and plantar responses routinely in a complete motor examination. Hyperreflexia, clonus and an extensor plantar response support corticospinal involvement; depressed reflexes suggest peripheral nerve/root/anterior horn involvement depending on distribution.
5. Sensory system: Test light touch and pinprick first when appropriate, then vibration and joint-position sense. Map any deficit rather than simply recording “reduced sensation.” Determine whether the pattern is peripheral nerve, dermatomal, stocking-glove, sensory level, hemibody, cortical or dissociated. Test cortical sensory functions such as stereognosis and graphesthesia only when primary sensation is sufficiently intact.
6. Coordination and cerebellar signs: Assess finger–nose and heel–shin testing, rapid alternating movements and rebound where appropriate. Look for intention tremor, dysmetria, dysdiadochokinesia, nystagmus and scanning/dysarthric speech. Distinguish true cerebellar incoordination from weakness or sensory ataxia.
7. Gait and station: Observe initiation, base, stride, arm swing, turning and balance. Perform tandem gait, heel/toe walking and Romberg testing when safe and relevant. Recognise characteristic hemiplegic, spastic, ataxic, sensory, parkinsonian, waddling and high-stepping patterns.
8. Meningeal and special signs: In the appropriate presentation assess neck stiffness and other meningeal signs. Add disease-directed tests—e.g. extrapyramidal signs, fatigability, autonomic examination, spine examination or peripheral nerve examination—rather than applying every special test to every patient.
9. Localisation before diagnosis: Finish by stating the neurological syndrome and anatomical localisation: cortex, subcortex, brainstem, cerebellum, spinal cord, anterior horn cell, root, plexus, peripheral nerve, neuromuscular junction or muscle. Only then construct the likely aetiological differential.
Ask whether the lesion is cortical, subcortical, brainstem, cerebellar, spinal cord, root, plexus, peripheral nerve, neuromuscular junction or muscle. For weakness, use tone, power, reflexes and plantar response to separate upper from lower motor neuron patterns.
Hemiparesis suggests a lesion above the cervical cord; crossed cranial nerve and limb findings suggest brainstem disease; a sensory level suggests spinal cord disease; glove-and-stocking loss suggests polyneuropathy; proximal weakness with preserved sensation suggests myopathy.
Do not start by naming a disease. Describe the neurological deficit, localise anatomically, then discuss likely causes. This makes the examination reproducible and dramatically improves viva answers.
“The patient is conscious/oriented…” → cranial nerves → motor findings with UMN/LMN pattern → sensory distribution → coordination/gait → anatomical localisation → likely differential.
New focal deficit, rapidly falling GCS, status epilepticus, acute flaccid paralysis with respiratory weakness, meningism with sepsis, or features of raised intracranial pressure require urgent assessment.
Mental state → cranial nerves → tone → power → reflexes → plantar → sensation → coordination → gait → localisation → differential.
Neurological localisation framework: Ask whether findings are unilateral/bilateral, proximal/distal, upper/lower limb predominant and whether sensory, sphincter, cranial-nerve or higher-function involvement accompanies weakness.
Spinal cord syndromes: A sensory level, bilateral long-tract signs and sphincter dysfunction strongly favour cord disease. In acute cord lesions, early spinal shock may temporarily produce flaccidity and absent reflexes before UMN signs emerge.
Peripheral localisation: Distinguish root disease (dermatomal pain/sensory loss with myotomal weakness), mononeuropathy, plexopathy and length-dependent polyneuropathy. Map findings rather than using the vague term “neuropathy.”
Movement disorders: Describe tremor by rest/postural/action components and observe rigidity, bradykinesia, chorea, dystonia or myoclonus rather than grouping all involuntary movement together.
Complete the examination: Examine fundus when raised ICP/vascular disease is relevant, assess spine and peripheral nerves when localisation requires it, and add autonomic or cognitive testing selectively. End every case with syndrome → site → side/level → likely pathology → differential.
Rapid bedside revision:
- Localise before naming the disease: decide whether the lesion is cortical, brainstem, cerebellar, spinal, root, peripheral nerve, NMJ or muscle.
- UMN weakness is supported by increased tone, hyperreflexia, clonus and an extensor plantar response; LMN disease tends toward wasting, fasciculation, hypotonia and reduced reflexes.
- Pronator drift is a sensitive bedside clue to subtle pyramidal weakness when the patient can cooperate.
- Forehead sparing in facial weakness supports a supranuclear lesion, whereas complete ipsilateral facial weakness suggests a peripheral facial nerve lesion.
- A sensory level on the trunk strongly points toward spinal cord pathology and should be mapped carefully.
- Loss of vibration/joint position with a positive Romberg suggests sensory ataxia; Romberg is not primarily a test of cerebellar function.
- Cerebellar lesions produce ipsilateral limb incoordination; weakness must be excluded before calling a test dysmetric.
- Hyperreflexia alone is not enough to diagnose an UMN lesion—interpret reflexes with tone, power, plantar response and symmetry.
- Fatigable weakness with relatively preserved sensation should raise suspicion of a neuromuscular-junction disorder.
- Proximal weakness with preserved sensation suggests a myopathic pattern, whereas distal weakness is common in many peripheral neuropathies.
- Language disturbance (aphasia) implies dominant cortical network dysfunction; dysarthria is a motor-speech problem and does not itself imply aphasia.
- In an acutely altered patient, stabilisation and reversible causes such as glucose disturbance take priority over an exhaustive neurological examination.
04. Gastrointestinal / Abdominal Examination
Positive findings commonly relevant to gastrointestinal and hepatobiliary disease:
- Pallor: consider chronic GI blood loss, malnutrition or chronic disease.
- Icterus: inspect sclera in good light; jaundice directs assessment toward hepatocellular, cholestatic or haemolytic causes.
- Hydration and nutrition: dry mucosa, reduced skin turgor, muscle wasting, low BMI or cachexia may indicate fluid loss, malabsorption, malignancy or chronic disease.
- Clubbing: may occur with inflammatory bowel disease, chronic liver disease or selected GI malignancies.
- Lymphadenopathy: especially supraclavicular nodes, may provide a clue to intra-abdominal malignancy or infection.
- Pedal oedema: consider hypoalbuminaemia, portal hypertension or associated cardiac/renal disease.
- Chronic liver disease stigmata: spider naevi, palmar erythema, leukonychia, bruising, parotid enlargement, gynaecomastia, testicular atrophy and loss of body hair where relevant.
- Portal hypertension/decompensation clues: ascites, abdominal-wall collaterals, splenomegaly-associated signs, oedema and hepatic encephalopathy.
- Pruritus/scratch marks: can support cholestasis in the appropriate clinical setting.
- Hands: asterixis may suggest hepatic encephalopathy but is not specific to liver disease.
Inspection — what to look for: Inspect from the end of the bed and tangentially with adequate exposure. Note abdominal contour and symmetry, distension, visible masses, scars, striae, sinuses, stomas, dilated superficial veins, hernias and skin changes. Look specifically for visible peristalsis or pulsation. Observe movement with respiration and inspect the umbilicus. In suspected chronic liver disease, integrate peripheral stigmata rather than treating the abdomen in isolation.
Palpation — what to find: Ask about pain and start away from it. Light palpation assesses tenderness, guarding and superficial masses; deep palpation defines deeper masses and organ enlargement. Characterise any mass by site, size, surface, edge, consistency, tenderness, mobility, pulsatility and movement with respiration. Palpate liver and spleen systematically, assess kidneys by bimanual palpation/ballotment where indicated, and use targeted signs such as Murphy's sign or rebound/peritonism only when clinically appropriate.
Percussion — what to find: Map liver dullness when relevant and percuss the spleen selectively. Generalised tympany accompanies gas-filled bowel; focal or shifting dullness may indicate fluid or a mass. For suspected ascites, test shifting dullness; fluid thrill is more useful with larger-volume ascites. Percussion can also help distinguish a gas-filled bowel loop from a solid/fluid-filled structure.
Auscultation — what to find: Listen before prolonged palpation when bowel sounds are diagnostically important. Describe bowel sounds cautiously rather than labeling obstruction from a brief listen alone; prolonged assessment may be needed before calling them absent. Listen for arterial bruits when vascular disease is suspected and for a venous hum in selected portal-hypertension contexts. Always interpret auscultation alongside pain, distension, vomiting, peritonism and imaging—not in isolation.
Distinguish tenderness from guarding and rigidity; define any mass by site, size, surface, consistency, mobility, movement with respiration and pulsatility. Characterise hepatomegaly and splenomegaly rather than simply recording that the organ is enlarged.
Ascites + splenomegaly + dilated abdominal veins suggests portal hypertension; tender hepatomegaly may occur with congestion or inflammation; shifting dullness supports free intraperitoneal fluid; peritonism changes the examination from routine assessment to urgent surgical evaluation.
Ask where pain is worst and palpate that area last. Warm your hands and watch the patient’s face during palpation; involuntary guarding is easier to recognise when attention is not focused on the examiner’s hand.
General/peripheral signs → abdominal contour and scars → tenderness/mass → liver/spleen → ascites → bowel sounds when relevant → rectal/groin examination if indicated → clinical syndrome.
Rigid abdomen, rebound/percussion tenderness with systemic toxicity, pulsatile expansile mass, GI bleeding with shock, incarcerated hernia or rapidly worsening abdominal pain require urgent escalation.
Hands/eyes/mouth → inspect → auscultate if needed → percuss → light palpation → deep palpation → liver/spleen/kidneys → ascites → targeted signs.
Liver — standard palpation: Position the patient supine with the head supported and knees relaxed. Place your right hand flat in the right iliac fossa/right lower quadrant, fingers parallel to the right costal margin. Ask the patient to take slow deep breaths and advance the hand progressively upward after each expiration until the descending liver edge meets the fingertips during inspiration. If palpable, describe distance below costal margin, edge, surface, consistency, tenderness and pulsatility.
Liver — alternative methods: Hooking technique can help in obese patients: stand near the right shoulder, hook the fingertips beneath the right costal margin and ask for deep inspiration. Bimanual palpation supports the lower right chest posteriorly with the left hand while the right hand palpates anteriorly. Confirm suspected enlargement with percussion/liver span rather than relying on a palpable edge alone.
Spleen — standard palpation: Begin in the right iliac fossa because a markedly enlarged spleen may extend diagonally across the abdomen. Palpate toward the left hypochondrium while the patient inspires deeply. If not felt, roll the patient slightly onto the right side and repeat. Describe size, edge/notch, surface, consistency, tenderness and movement with respiration. A splenic notch and inability to get above the mass support splenomegaly.
Kidney — bimanual palpation: Place one hand posteriorly in the renal angle and the other anteriorly below the costal margin. During inspiration, press the hands toward each other to capture the descending kidney. Assess size, surface, consistency, tenderness and mobility. The lower pole of a normal right kidney may occasionally be palpable in a thin person.
Kidney — ballotment: With the anterior hand maintained over the renal area, use the posterior fingers to give a brief upward push; a mobile enlarged kidney may be felt to strike the anterior hand and return. A renal mass is typically ballotable and one may be able to get above it, helping distinguish it from splenomegaly.
Key differentiation: An enlarged spleen moves inferomedially with inspiration, may have a notch and usually cannot be palpated above; an enlarged kidney is more posterior, ballotable, generally lacks a notch and may permit the examiner to get above it.
Abdominal mass: Always describe site, size, shape, surface, edge, consistency, tenderness, mobility, movement with respiration, pulsatility and whether you can get above/below it. This disciplined description often narrows the organ of origin.
Ascites: Combine flank fullness, percussion and shifting dullness. In tense ascites, organ palpation may require dipping techniques. Remember that bedside signs are less sensitive for small-volume fluid.
Portal hypertension: Deliberately seek splenomegaly, ascites, abdominal-wall collaterals and relevant chronic liver disease signs. Mental-state change/asterixis may indicate encephalopathy in the appropriate context.
Hernial orifices and rectal examination: Include them when the presentation requires them—particularly obstruction, GI bleeding, altered bowel habit, pelvic/rectal pathology or an unexplained abdominal mass. Explain and obtain consent before intimate examination.
Complete the examination: Examine supraclavicular nodes, chest for pleural effusion/metastatic clues, and relevant cardiovascular/systemic findings. A good abdominal examination extends beyond the abdomen.
Rapid bedside revision:
- Always inspect before palpating; abdominal contour, scars, distension, veins, stomas and visible movement can immediately redirect the examination.
- Start palpation away from pain and watch the patient's face; involuntary guarding/rigidity is more concerning for peritoneal irritation than voluntary tensing.
- A palpable liver edge is not automatically hepatomegaly—interpret its position with percussion, span, consistency, surface and clinical context.
- Splenomegaly typically enlarges inferomedially, may have a palpable notch and is not usually possible to get above on examination.
- Shifting dullness is a useful bedside sign of ascites; very small fluid volumes may not be clinically detectable.
- Caput medusae/dilated abdominal veins should be interpreted with venous flow direction and other evidence of portal hypertension or caval obstruction.
- Courvoisier's sign describes a palpable non-tender gallbladder with jaundice and raises concern for malignant distal biliary obstruction; it is not absolute.
- Murphy's sign supports acute cholecystitis in the right clinical setting but should not replace imaging and laboratory assessment.
- A pulsatile abdominal mass must be approached cautiously; expansile pulsation raises concern for an abdominal aortic aneurysm.
- Absent bowel sounds should not be declared after a few seconds of listening; clinical context and adequate auscultation matter.
- Chronic liver disease is a systemic examination—hands, face, chest, abdomen, mental state and oedema all contribute.
- Peritonism, haemodynamic instability, GI bleeding or a suspected ruptured aneurysm are red flags that take priority over completing an elaborate routine examination.
05. Locomotor Examination
Positive findings commonly relevant to locomotor and rheumatological disease:
- General appearance: fever, weight loss, cachexia or systemic illness may suggest infection, inflammatory disease or malignancy.
- Posture and gait: antalgic gait, deformity, reduced arm swing, abnormal spinal posture or use of walking aids should be noted before examining individual joints.
- Hands and nails: joint deformities, swelling, muscle wasting, nail pitting, onycholysis, splinter haemorrhages or periungual changes can provide diagnostic clues.
- Skin: psoriasis, malar/discoid rash, Gottron papules, heliotrope rash, sclerodactyly, ulcers, livedo or nodules may indicate systemic rheumatological disease.
- Rheumatoid clues: rheumatoid nodules, typical hand/foot deformities and muscle wasting support established inflammatory arthritis.
- Eyes and mouth: conjunctival/uveal inflammation, dry eyes, dry mouth or oral ulcers may indicate extra-articular systemic disease.
- Lymphadenopathy: may occur with systemic inflammatory disease, infection or malignancy and should not be overlooked.
- Muscle bulk: proximal wasting or weakness may suggest inflammatory myopathy, disuse or neurological disease.
- Extra-articular organ clues: respiratory, cardiovascular, renal or neurological findings may be part of a multisystem rheumatological disorder.
Inspection — what to look for: Observe gait, posture and functional movement before examining a joint. Compare both sides for swelling, erythema, deformity, muscle wasting, scars, nodules and abnormal alignment. At a joint, decide whether swelling appears intra-articular or periarticular and look for fixed deformity. Examine relevant skin and nails for rheumatological clues and inspect the joint above and below when indicated.
Palpation — what to find: Assess temperature with the dorsum of the hand, then localise tenderness precisely. Define swelling—soft tissue, synovial thickening, effusion or bony enlargement—and look for fluctuation when appropriate. Palpate joint lines, tendons, entheses and bony landmarks according to the region. Assess crepitus during movement and perform neurovascular examination when trauma, deformity or compression is possible.
Percussion — selective orthopaedic role: Routine joint examination does not require classical percussion. Use percussion only for a specific question—for example spinal percussion tenderness when vertebral pathology is suspected or transmitted-impact tests in selected bone/joint assessments. Do not manufacture a percussion finding simply to complete IPPA.
Auscultation — generally not routine: Auscultation has little role in standard locomotor examination. Rarely, a bruit over a swelling may suggest a vascular lesion and should change subsequent handling/investigation. The core examination instead proceeds through Look → Feel → Move → Function, documenting active and passive range, pain, restriction, instability and relevant special tests.
Decide whether pathology is articular, periarticular, muscular, neurological or referred. Inflammatory disease is suggested by warmth, swelling and prolonged morning stiffness; mechanical disease more often worsens with use and has less overt inflammation.
Restriction of both active and passive movement favours joint pathology; active movement restricted more than passive suggests muscle/tendon disease. True synovitis is soft/boggy and warm, whereas bony enlargement is hard and more typical of chronic degenerative change.
Functional testing often reveals disability better than isolated range-of-motion measurements. Ask the patient to demonstrate a task relevant to the joint—walking, gripping, reaching overhead or rising from a chair.
Site and symmetry → swelling/deformity → warmth/tenderness → active/passive range → special tests only when indicated → function → neurovascular status → likely articular pattern.
An acutely hot swollen joint is septic arthritis until adequately excluded. Neurovascular compromise after injury, compartment syndrome features or an unstable spine are emergencies.
Look → feel → move → function → special tests → joint above/below → neurovascular examination → compare sides.
GALS screen: For a rapid musculoskeletal screen use Gait, Arms, Legs, Spine, preceded by three functional questions about pain/stiffness, dressing and stairs. Follow abnormalities with a regional examination.
Regional examination: Use Look → Feel → Move → Function → Special tests. Compare active and passive range and always relate a special test to a specific suspected structure; indiscriminate special testing creates false positives.
Inflammatory vs mechanical: Inflammatory disease tends toward prolonged morning stiffness, warmth/swelling and improvement with activity; mechanical pain more often worsens with use and has shorter stiffness. These are patterns, not absolute rules.
Spine: Inspect alignment, assess movement and neurological status when indicated. Back pain with major trauma, fever, cancer history, progressive neurological deficit, saddle anaesthesia or bladder/bowel dysfunction requires urgent evaluation.
Complete the examination: Search for extra-articular clues in skin, nails, eyes and other systems, and document distal neurovascular status after trauma. Functional limitation should be recorded alongside physical signs.
Rapid bedside revision:
- Use Look → Feel → Move → Function rather than forcing a classical IPPA sequence onto joints.
- Compare both sides and examine the joint above and below when the pathology may extend beyond one articulation.
- Active movement limited more than passive movement often suggests muscle/tendon or pain-related dysfunction; restriction of both may indicate joint pathology.
- A hot, acutely swollen monoarthritis is septic arthritis until adequately excluded, especially with fever or systemic illness.
- True joint swelling should be distinguished from periarticular soft-tissue swelling, bursitis, tendon disease and bony enlargement.
- Morning stiffness lasting a prolonged period supports inflammatory arthritis, whereas brief stiffness after rest is more typical of mechanical disease.
- Crepitus alone does not establish osteoarthritis; combine it with pain pattern, bony enlargement and restricted movement.
- Rheumatoid arthritis commonly produces symmetrical inflammatory small-joint disease; established deformities reflect chronic structural damage.
- Psoriasis, nail pitting, dactylitis and enthesitis are important clues to psoriatic/spondyloarthritic disease.
- Always assess neurovascular status after significant limb trauma, dislocation or deformity and document it before and after intervention.
- Proximal muscle weakness should prompt consideration of myopathy and systemic disease rather than assuming a primary joint disorder.
- Functional assessment—walking, grip, rising from a chair or performing a task—often reveals disability that isolated range-of-motion measurements miss.