1. Hydatid Cyst (2016, 30 marks) - full life cycle, WHO classification, all complications, PAIR + surgical options
2. LFT Physiology & Surgical Significance - all liver enzymes, synthetic function tests, Child-Pugh, MELD, patterns per disease
3. Bilirubin Metabolism + Obstructive Jaundice - step-by-step metabolism, comparison table of jaundice types, all biliary drainage techniques (ERCP, PTBD, surgical bypasses)
4. Liver Anatomy + Blunt Trauma (2022, 30 marks) - Couinaud segments, dual blood supply, AAST 2018 grading table, NOM criteria, Damage Control Surgery, Pringle's manoeuvre

Difference Between Build and Nutrition of the Body

BODY BUILD (Body Constitution / Somatotype)

Definition

Basis

• Determined by genetics, sex, age, race, and physical training
• Reflects musculoskeletal development - not dietary intake
• Remains relatively fixed in adulthood (though muscle mass can change with training/disease)

Classification (Sheldon's Somatotypes)

Clinical Grading of Build (Used in Examination)

• Well built - adequate muscle mass, proportionate height and weight, good skeletal development
• Moderately built - average muscle development
• Poorly built - thin bony frame, reduced muscle bulk, low height or disproportionate limbs

What Build Tells You Clinically

• A person can be well-built but malnourished (e.g., an athlete who stops eating properly - frame is preserved but nutrition is poor)
• A person can be poorly built but well-nourished (e.g., a constitutionally thin ectomorph with adequate dietary intake)
• Build gives an idea of baseline muscle mass and surgical reserve
• Relevant pre-operatively: poorly built patients have less physiological reserve

NUTRITION (Nutritional Status)

Definition

Basis

• Determined by dietary intake, absorption, metabolism, and disease state
• Reflects fat stores, protein (muscle) reserves, micronutrient levels, and hydration
• Can change rapidly with illness, surgery, starvation, or supplementation

Classification (Clinical Assessment - SGA Grading)

Clinical Signs of Malnutrition

Nutritional Assessment Tools

Objective Measurements

• BMI = Weight (kg) / Height² (m²): Normal 18.5-24.9; <18.5 = underweight; >30 = obese
• Serum albumin: <3.5 g/dL mild, <2.8 g/dL severe deficiency
• Serum prealbumin: Shorter half-life (2 days) - better marker of acute change
• Serum transferrin, Total lymphocyte count
• Hand-grip dynamometry: Reduced grip strength (<85% of normal for age/sex) = twice the risk of perioperative complications in surgical patients

KEY DIFFERENCES: Build vs. Nutrition

Why Both Matter in Surgery

1. Build determines operative access (e.g., an obese or poorly-built patient may pose technical challenges), physiological reserve, and anaesthetic risk.
2. Nutritional status directly impacts:
   • Wound healing (collagen synthesis requires protein, Vitamin C, zinc)
   • Immune function (T-cell immunity reduced in malnutrition)
   • Anastomotic healing (protein depletion increases leak rate)
   • Drug metabolism and pharmacokinetics
   • Post-operative recovery and complication rates
3. Pre-operative nutritional optimisation (enteral or parenteral nutrition for 7-10 days) is recommended for severely malnourished patients (SGA Grade C) before elective major surgery to reduce morbidity.

Raynaud's Disease and Raynaud's Phenomenon

OVERVIEW / DEFINITION

PATHOPHYSIOLOGY

1. Abnormal blood vessel wall - exaggerated adrenergic receptor sensitivity; endothelial dysfunction with excess endothelin-1 (ET-1) and reduced nitric oxide (NO)
2. Neural control abnormalities - excessive sympathetic vasoconstrictor tone; abnormal central vasodilation response; triggered by cold (reducing core body temp) and emotional stress (catecholamine release)
3. Intravascular factors - platelet activation, oxidative stress, RBC aggregation (cold agglutinins in some cases), cryoglobulinaemia

1. Arterial vasoconstriction → digits turn WHITE (pallor, ischaemia)
2. Postcapillary venular constriction + deoxygenation → digits turn BLUE (cyanosis, anoxia)
3. Rewarming → reactive vasodilation/reperfusion → digits turn RED (hyperaemia, pain/tingling)

1. RAYNAUD'S DISEASE (Primary Raynaud's Phenomenon)

Definition

Epidemiology

• Affects 3-5% of the general population (up to 5-15% of young women)
• Strong female predominance (young, premenopausal women)
• Age of onset typically <40 years
• Familial tendency - 30-50% of patients have a first-degree relative with the condition
• More prevalent in cooler climates and in smokers
• Higher prevalence with oestrogen exposure

Clinical Features

• Bilateral involvement of fingers (all fingers, symmetrically)
• Episodes triggered by cold or emotional stress
• Classic triphasic colour change: white → blue → red
• Numbness and tingling during the ischaemic phase; burning pain during hyperaemia
• Peripheral pulses present
• No trophic changes (no ulcers, no gangrene - occurs in <1% of cases)
• No asymmetry
• No systemic symptoms

Diagnostic Criteria (Consensus Criteria for Primary Raynaud's Disease)

1. Normal nailfold capillaroscopy (capillary pattern intact)
2. No physical signs suggesting secondary cause (no sclerodactyly, calcinosis, digital pitting scars, telangiectasias)
3. No history or evidence of connective tissue disease
4. Negative or low-titer ANA (e.g., ≤1:40)
5. Normal Allen test
6. Normal blood chemistry and laboratory tests

Prognosis

• Benign course
• Gangrene extremely rare (<1%)
• 14-37% may eventually progress to a connective tissue disease and be reclassified as secondary (especially if ANA positive, older age at onset, female gender, worsening attacks) - hence follow-up is important

2. RAYNAUD'S PHENOMENON (Secondary Raynaud's)

Definition

Epidemiology

• Occurs in young to middle-aged women but also affects men
• Age of onset often ≥40 years
• Frequently asymmetric or unilateral
• More severe, progressive course

Underlying Causes

• Systemic sclerosis (scleroderma) - most common cause
• Systemic lupus erythematosus (SLE)
• Dermatomyositis / Polymyositis
• Rheumatoid arthritis
• Sjögren's syndrome
• Mixed connective tissue disease (MCTD)

• Thromboangiitis obliterans (Buerger's disease)
• Atherosclerosis
• Arterial embolism

• Hand-arm vibration syndrome ("vibration white finger") - pneumatic drill, jackhammer operators
• Hypothenar hammer syndrome
• Frostbite/cold injury

• Polycythaemia vera
• Cryoglobulinaemia
• Cryofibrinogenaemia
• Cold agglutinins (RBC clumping)
• Multiple myeloma

• Hypothyroidism
• Acromegaly, phaeochromocytoma, carcinoid

• Thoracic outlet syndrome (cervical rib, scalenus anticus syndrome)
• Complex regional pain syndrome (reflex sympathetic dystrophy)
• Subclavian artery disease

• Beta-blockers (including eye drops), ergot preparations
• Bleomycin, cisplatin (chemotherapy)
• Amphetamines, cocaine
• Cyclosporine, interferon-α and -β
• Clonidine, oral contraceptives

• Paraneoplastic (in cancer)
• Hepatitis B antigenemia
• Lead/arsenic poisoning
• Arteriovenous fistula

Clinical Features

• Can be unilateral or bilateral, often asymmetric
• Trophic changes common: digital pitting scars, skin ulceration, gangrene (fingertip necrosis)
• Abnormal Allen test (suggests fixed occlusive disease)
• Signs of underlying disease: sclerodactyly, calcinosis, puffy fingers, telangiectasias, avascular areas on nailfold capillaroscopy
• Systemic symptoms present (of underlying disease)
• Rapid progression of vasospastic attacks
• Abnormal laboratory tests: elevated ANA, elevated ESR, anti-Scl-70, anti-centromere antibodies, etc.

KEY DIFFERENCES: Raynaud's Disease vs. Raynaud's Phenomenon

INVESTIGATIONS

• Full blood count, ESR, CRP
• ANA (antinuclear antibody) - key screening test
• Anti-Scl-70 (topoisomerase-1), anti-centromere antibodies (for scleroderma)
• Complement levels (C3, C4), anti-dsDNA (for SLE)
• Thyroid function tests
• Cryoglobulins, cold agglutinins, serum protein electrophoresis
• Chest X-ray (for thoracic outlet, pulmonary fibrosis)

• Nailfold capillary microscopy (capillaroscopy): GOLD STANDARD for distinguishing primary from secondary; avascular "skip" areas and irregularly dilated capillary loops = secondary (especially scleroderma)
• Allen test: assesses palmar arch patency; abnormal suggests fixed occlusive disease
• Laser Doppler perfusion imaging or Doppler ultrasonography: assesses vascular damage
• Digital thermography / technetium digital blood flow scintigraphy
• Angiography: if fixed obstructive lesion suspected

TREATMENT

Conservative (Both Primary and Secondary)

• Cold avoidance - avoid cold exposure to extremities AND core body (whole body warming)
• Warm gloves, layered clothing
• Smoking cessation - absolutely imperative (nicotine causes vasoconstriction)
• Avoid precipitating drugs (beta-blockers, ergot, etc.)
• Biofeedback techniques - for stress-triggered attacks
• "Windmill" manoeuvre - swinging the affected arm in a wide circle from the shoulder can abort an acute attack

Pharmacological Treatment (Both Types)

• Nifedipine (prolonged-release) or amlodipine - most widely used
• Reduce frequency and severity of attacks; ~2/3 of patients respond
• Cochrane review: 1.72 fewer attacks/week vs placebo (modest but clinically meaningful)

• Sildenafil (Viagra) - reduces Raynaud severity score, frequency, and duration; improves digital ulcer healing
• Now considered second-line agents of choice

• Losartan (angiotensin receptor blocker) - shown superior to nifedipine in one RCT for frequency and severity
• SSRIs (fluoxetine, ketanserin) - useful in refractory cases
• Topical nitroglycerin (MQX-503) - improves skin blood flow topically without systemic side effects
• Statins (atorvastatin) - in scleroderma-associated Raynaud; reduces vascular injury markers
• IV prostacyclin (iloprost) - for severe digital ischaemia in secondary Raynaud; given as inpatient infusion
• IV N-acetylcysteine (biweekly) - shown effective in reducing attacks
• ACE inhibitors - NOT recommended (failed to show benefit in RCTs)

• IV iloprost (prostacyclin analogue) infusion
• Endothelin-1 receptor antagonist (bosentan) - reduces new digital ulcers in scleroderma
• Anticoagulation if thrombosis present

Surgical Treatment

• Digital sympathectomy (periarterial sympathectomy) - considered in severe refractory cases; strips adventitia from digital arteries to eliminate adrenergic supply
• Botulinum toxin (Botox) injection near the neurovascular bundle - improves digital perfusion; emerging evidence
• Cervical sympathectomy - largely abandoned due to temporary benefit only and high relapse rate; also risk of Horner's syndrome
• Treat underlying cause in secondary Raynaud (e.g., cervical rib resection for thoracic outlet syndrome)

RAYNAUD'S PHENOMENON AS A PREDICTOR OF SYSTEMIC DISEASE

• Raynaud's may be the first manifestation of systemic sclerosis, SLE, or other CTD - appearing years before other features
• 14-37% of patients initially labelled as primary Raynaud's will eventually develop a connective tissue disease (mean 4.8 years)
• Predictors of progression to CTD: positive ANA, older age at onset, female gender, worsening attacks, abnormal nailfold capillaroscopy
• Sequential nailfold capillaroscopy + autoantibody testing can predict development of systemic sclerosis

Intermittent Claudication

DEFINITION

• Brought on by walking (or exercise)
• Reliably reproduced at approximately the same walking distance (claudication distance)
• Relieved by rest (standing or sitting) within 5 minutes
• Not present on the first step (distinguishes it from osteoarthritis/musculoskeletal causes)

AETIOLOGY AND PATHOPHYSIOLOGY

Underlying Cause

Pathophysiology

• At rest, blood flow through a stenosed artery is sufficient to meet resting muscle oxygen demand
• During exercise, muscle oxygen demand increases 10-20 fold
• The stenosed/occluded artery cannot increase blood flow to meet this demand
• Muscle shifts to anaerobic metabolism → lactic acid accumulation
• Lactic acidosis in the muscle → cramp-like pain, weakness
• On resting, demand falls below supply → lactic acid cleared → pain resolves within 5 minutes
• Pain is not present at rest (differentiates IC from rest pain/critical limb ischaemia)

Common Atherosclerotic Risk Factors

• Smoking (most important - present in >75% of PAD patients)
• Diabetes mellitus
• Hypertension
• Hyperlipidaemia / dyslipidaemia
• Increasing age
• Male sex
• Positive family history
• Obesity, sedentary lifestyle

ANATOMICAL LEVELS AND CLINICAL CORRELATION

Leriche's Syndrome

1. Buttock claudication (ischaemia via internal iliac/hypogastric artery)
2. Erectile impotence (internal iliac artery insufficiency)
3. Absent femoral pulses bilaterally

CLINICAL FEATURES

Symptoms

• Cramp-like or aching pain in the affected muscle group
• Brought on by walking; onset at a predictable, reproducible distance
• Relieved completely by resting in any position (standing or sitting) within 5 minutes
• Claudication distance - distance walked before pain begins; varies minimally day-to-day
• Claudication distance decreases with: faster walking, uphill walking, carrying heavy loads, anaemia, cold weather, cardiorespiratory disease
• As disease progresses, claudication distance shortens further → eventually rest pain develops

Signs (Examination Findings)

• Reduced or absent pulses at and distal to the level of disease
• Femoral, popliteal, posterior tibial, dorsalis pedis pulses assessed bilaterally
• Arterial bruits (over aorta, iliacs, femorals) indicate turbulent flow through stenosis

• Loss of skin hair on foot and lower leg
• Thickened, brittle nails
• Thin, shiny skin
• Pallor on elevation (Buerger's test) and rubor on dependency
• Muscle wasting
• Delayed capillary refill

• Elevate the leg to 45° - note angle at which the leg becomes pale (normal: no pallor up to 90°; significant ischaemia: pallor at <20°)
• On dependency, reactive hyperaemia occurs; venous guttering present before filling

CLASSIFICATION OF PERIPHERAL ARTERIAL DISEASE

Fontaine Classification (Clinical)

Rutherford Classification (Clinical + Objective Data)

INVESTIGATIONS

First-Line: Ankle-Brachial Index (ABI)

• Simplest and most important non-invasive test
• Method: Systolic BP recorded at both ankles (posterior tibial + dorsalis pedis) and both brachial arteries using a handheld Doppler probe; ABI = highest ankle pressure ÷ highest brachial pressure
• Interpretation:

• Exercise ABI: In mild PAD, resting ABI may be normal; ABI drops significantly after walking → confirms exercise-induced claudication
• Toe-Brachial Index (TBI): Used when ABI is falsely elevated; normal TBI ≥0.7; absolute toe pressure >30 mmHg needed for wound healing (>40 mmHg in diabetics)

Segmental Limb Pressures

• BP measured at thigh, calf, and ankle levels
• A gradient of >20 mmHg between levels indicates significant occlusive disease at that segment
• Helps localise the level of disease

Duplex Ultrasonography

• First-line imaging; non-invasive, no contrast
• Identifies site, length, and severity of stenosis/occlusion
• Waveform analysis (monophasic = severe disease; triphasic = normal)

CT Angiography (CTA)

• High-resolution 3D imaging of aorta → pedal vessels
• Gold standard for surgical planning pre-revascularisation
• Defines anatomy for bypass/endovascular planning
• Limitation: contrast nephrotoxicity, radiation

MR Angiography (MRA)

• No radiation, no nephrotoxic contrast (gadolinium)
• Good quality images, but expensive, time-intensive
• May overestimate stenosis degree (limitation)

Digital Subtraction Angiography (DSA)

• Invasive gold standard for imaging
• Best for infrainguinal (tibial) disease and when endovascular intervention is planned simultaneously
• Allows direct measurement of pressures and intervention in the same sitting

DIFFERENTIAL DIAGNOSIS: VASCULAR vs. NEUROGENIC CLAUDICATION

• Osteoarthritis of hip/knee - pain from the first step; relieved by sitting only
• Venous claudication - bursting pain from venous hypertension; worse with dependency; history of DVT/varicose veins
• Compartment syndrome - pain with exertion, tight tense compartment; associated with trauma
• Muscle cramps - nocturnal, resolve with stretching

MANAGEMENT

Conservative (all IC patients - first line)

• Smoking cessation - single most effective intervention; slows progression, reduces cardiovascular mortality significantly
• Statins - all PAD patients should be on statin therapy (mortality benefit + vascular remodelling); high-intensity preferred
• Antiplatelets - aspirin (75-150 mg/day) or clopidogrel for all PAD patients; reduce cardiovascular events (MI, stroke, vascular death)
• Tight glycaemic control (diabetes)
• Antihypertensives (ACE inhibitors/ARBs preferred)
• Lipid control (LDL <70 mg/dL target)

• Supervised exercise therapy - FIRST-LINE treatment for IC (before any intervention)
• Structured programme: walking to near-maximum pain, then rest, then repeat; 30-60 min sessions, 3 times/week for ≥3 months
• Improves claudication distance by promoting collateral development, improving muscle metabolism
• Superior to unsupervised exercise
• A systematic review of 10 RCTs (1087 patients) found supervised exercise equivalent to endovascular revascularisation in functional performance improvement
• Medicare-reimbursed in the USA
• Goal: improve claudication distance and functional quality of life

Pharmacological

• Phosphodiesterase-3 inhibitor → inhibits platelet aggregation + dilates limb arterioles
• Increases claudication distance by ~40-60%
• Contraindicated in heart failure (all PDE3 inhibitors)
• Dose: 100 mg BD
• Considered standard pharmacological treatment for IC

• Haemorrheological agent - improves red cell deformability, reduces blood viscosity
• Modest benefit; less effective than cilostazol; rarely used as first choice

• Aspirin, clopidogrel - reduce cardiovascular events but do not improve walking distance directly

• ACE inhibitors (ramipril) may have modest benefit on walking distance beyond BP lowering
• Statins improve claudication symptoms in addition to cardiovascular protection

Interventional (after failure of conservative + pharmacological therapy)

• IC that is lifestyle-limiting after ≥3 months of supervised exercise + medical therapy
• Anatomically favourable lesion
• Low-risk patient
• Short claudication distance (<200 m) significantly impairing quality of life (SVS 2022 Guidelines: revascularisation only after exercise + medical therapy failure)

• Percutaneous Transluminal Angioplasty (PTA): balloon dilation of stenosis/occlusion
• Stenting: primary stenting for aortoiliac disease (excellent results); selective stenting for femoropopliteal
• TASC A/B lesions: endovascular approach preferred (short, focal disease)
• Common iliac/external iliac disease: balloon-expandable stents - excellent long-term patency (~80-90% at 5 years)
• Common femoral artery: stenting discouraged due to flexion point; open endarterectomy + patch preferred

• TASC C/D lesions: surgical bypass preferred (long, complex, occlusive disease)
• Aorto-bifemoral bypass (aortobifemoral bypass graft - ABFG): gold standard for aortoiliac disease; uses bifurcated Dacron/PTFE graft; 5-year patency ~90%
• Axillo-bifemoral bypass: for high-risk patients unfit for aortic surgery (extra-anatomic)
• Femoro-popliteal bypass: for SFA disease; autologous great saphenous vein preferred; above-knee popliteal - PTFE acceptable; below-knee popliteal - vein mandatory
• Femoro-distal bypass: for tibial/peroneal disease
• Endarterectomy: for common femoral artery disease; direct removal of plaque ± patch angioplasty

• Hybrid procedure for combined femoral + iliac disease
• Combines open common femoral endarterectomy with endovascular iliac stenting in the same sitting

PROGNOSIS

• IC is a marker of systemic atherosclerosis - not just a limb problem
• 5-year risk of limb amputation: ~5% (relatively low)
• 5-year life expectancy: 75-80% (mortality mainly from MI and stroke)
• Patients with symptomatic PAD have a 25% risk of cardiovascular mortality within 5 years
• 20-30% of IC patients will develop symptoms severe enough to warrant intervention
• ~75-80% of IC patients will maintain their current level of function or decline slowly with optimal medical management

• Stable / slow progression in most
• ~10-15% progress to critical limb ischaemia
• Rest pain and gangrene (Chronic Limb-Threatening Ischaemia / CLTI): 5-year mortality >50% and high amputation risk

SUMMARY: KEY POINTS FOR EXAMINATIONS

1. IC = anaerobic muscle metabolism from inadequate arterial perfusion during exercise
2. Pain is one level below the obstruction: SFA disease → calf claudication (70% of cases)
3. Leriche's syndrome = buttock claudication + impotence + absent femoral pulses (aortoiliac occlusion)
4. First investigation: ABI (<0.9 = PAD confirmed)
5. Supervised exercise therapy is the cornerstone of treatment
6. Cilostazol - only licensed drug for IC (PDE3 inhibitor; contraindicated in heart failure)
7. Revascularisation only after failure of exercise + medical therapy in lifestyle-limiting IC
8. Distinguishing IC from neurogenic claudication: vascular IC relieved by standing; neurogenic requires sitting/flexion
9. All PAD patients need statins + antiplatelet + smoking cessation regardless of limb symptoms (cardiovascular risk reduction)
10. Prognosis: low limb loss risk (5% at 5 years) but high cardiovascular mortality (25% at 5 years)