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LIVER - Comprehensive Surgery Answers

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1. LIFE CYCLE OF Echinococcus granulosus AND COMPLICATIONS OF HYDATID CYST OF LIVER (2016, 30 marks)

Life Cycle

• Adult tapeworm (3-5 mm) lives in the small intestine
• Proglottids containing eggs are shed in feces

• Humans ingest eggs via contaminated food/water/soil or direct contact with dogs
• Eggs hatch in the duodenum; oncospheres (hexacanth embryos) penetrate the intestinal wall
• Via portal circulation, they reach the liver (60-70%), lungs (20-30%), and rarely other organs
• In the liver, the oncosphere develops into a hydatid cyst over months to years

Structure of the Hydatid Cyst

1. Pericyst (host-derived) - outer fibrous layer from compressed host tissue
2. Ectocyst (exocyst/laminated membrane) - white, acellular, laminated layer
3. Endocyst (germinal/inner layer) - inner living germinal epithelium that produces daughter cysts, brood capsules, scolices, and hydatid fluid

WHO Classification (Gharbi/WHO-IWGE)

Complications of Hepatic Hydatid Cyst

1. Intrabiliary rupture (most common complication, 10-40%) - bile duct obstruction, cholangitis, jaundice
2. Intraperitoneal rupture - anaphylaxis (release of antigenic hydatid fluid), peritoneal seeding with multiple secondary cysts
3. Secondary bacterial infection - pyogenic abscess formation within the cyst
4. Thoracobiliary fistula - cyst ruptures through diaphragm into bronchus (biliptysis - bile in sputum)
5. Compression effects - Budd-Chiari syndrome, portal hypertension, biliary obstruction
6. Calcification - inactive, calcified cyst (protective but not always sterile)
7. Anaphylactic shock - on spontaneous/traumatic rupture

Treatment of Hydatid Cyst (Recent Trends)

• Percutaneous approach under US guidance
• Scolicidal agent (hypertonic saline 15-20%, 95% ethanol, or 5% povidone-iodine) is injected
• Contraindicated if cyst communicates with biliary tree
• Cover with albendazole 400 mg BD for 4 weeks before and after

• Albendazole 10-15 mg/kg/day (drug of choice) - must be given in cycles (28 days on, 14 days off)
• Mebendazole is alternative but poor bioavailability
• Asymptomatic, inactive (CE4/CE5) cysts can be observed

• Multidisciplinary approach at a tertiary center
• Pericystectomy with omentoplasty - remove pericyst + fill cavity with omentum
• Hepatic segmentectomy - for peripheral cysts
• Marsupialisation - for large/infected cysts (open into peritoneal cavity)
• Laparoscopic approach increasingly used
• Scolicidal agents used intraoperatively; avoid if biliary communication (risk of sclerosing cholangitis)
• Leave asymptomatic/inactive (CE4/CE5) cysts alone with US monitoring

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2. PHYSIOLOGICAL BASE OF LFT - SIGNIFICANCE IN VARIOUS SURGICAL CONDITIONS (Schwartz's 11th Edition)

Tests of Hepatocellular Damage

• Participate in gluconeogenesis (transfer amino groups to ketoglutaric acid)
• AST (SGOT): found in liver, cardiac muscle, skeletal muscle, kidney, brain - less specific
• ALT (SGPT): predominantly in liver - more specific for liver disease
• AST:ALT > 2:1 - alcoholic liver disease
• Mild elevation: NAFLD, chronic viral hepatitis, drug injury
• Moderate elevation: acute viral hepatitis
• Elevation in thousands: ischemic injury, acetaminophen toxicity, fulminant hepatitis
• Poor correlation with severity of fibrosis/cirrhosis

• Produced in liver, bone, placenta, intestine
• Elevated in cholestasis (intrahepatic or extrahepatic obstruction)
• ALP elevation with normal/mildly elevated transaminases = cholestatic pattern

• Highly sensitive for hepatobiliary disease
• Elevated in alcohol use, drug toxicity, cholestasis
• Useful to confirm hepatic origin of elevated ALP

• Total (direct + indirect)
• Conjugated (direct) elevation = cholestasis/hepatocellular disease
• Unconjugated (indirect) elevation = hemolysis or impaired conjugation

Tests of Synthetic Function

• Liver synthesises ~10 g/day; half-life 15-20 days
• Not useful for acute hepatic dysfunction due to long half-life
• Influenced by nutritional status, renal disease, protein-losing enteropathy
• Hypoalbuminemia = chronic hepatic insufficiency

• Most sensitive indicator of acute hepatic synthetic function
• All clotting factors (except Factor VIII) synthesised exclusively in liver
• INR standardises PT across laboratories
• Prolonged PT in acute liver failure or severe chronic liver disease
• Does NOT correct with Vitamin K in hepatic synthetic failure (unlike Vitamin K deficiency)

• Pure test of liver synthesis (not vitamin K dependent in this context)
• Used in King's College criteria for liver transplantation

Child-Pugh Score (Surgical Risk Assessment)

• Class A (5-6): Well-compensated, safe for major surgery
• Class B (7-9): Significant functional compromise, moderate risk
• Class C (10-15): Decompensated, very high surgical risk

MELD Score (Model for End-Stage Liver Disease)

• MELD = 3.78 x ln[Bilirubin] + 11.2 x ln[INR] + 9.57 x ln[Creatinine] + 6.43
• MELD-Na incorporates sodium: better predictor of 90-day mortality on transplant waitlist
• Used for organ allocation priority for liver transplantation

Significance in Surgical Conditions

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3. METABOLISM OF BILIRUBIN, PATHOPHYSIOLOGY OF JAUNDICE, AND TECHNIQUES OF BILIARY DRAINAGE IN OBSTRUCTIVE JAUNDICE

Bilirubin Metabolism

• 80% from breakdown of senescent RBCs by reticuloendothelial system
• 20% from myoglobin, hepatic heme proteins (cytochromes), ineffective erythropoiesis
• Heme → Biliverdin (by heme oxygenase) → Unconjugated bilirubin (by biliverdin reductase)

• Unconjugated bilirubin (fat-soluble) bound to albumin in plasma (non-filterable by kidney)
• Transported to hepatocytes via OATP1B1/1B3 transporters

• In hepatocyte smooth ER: bilirubin + glucuronic acid (by UDP-glucuronosyltransferase) → bilirubin diglucuronide (conjugated bilirubin - water soluble)

• Conjugated bilirubin excreted into bile via MRP2 transporter (canalicular membrane)
• In intestine: bacterial deconjugation → urobilinogen
  • Most urobilinogen → stercobilin (gives stool brown colour)
  • Small amount reabsorbed (enterohepatic circulation) → urobilinogen in urine
  • Trace amount excreted in urine as urobilin

Types of Jaundice

Pathophysiology of Obstructive Jaundice

• Benign: Choledocholithiasis, strictures (post-op, PSC), pancreatitis, Mirizzi syndrome
• Malignant: Ca head of pancreas, cholangiocarcinoma, ampullary carcinoma, metastatic lymph nodes

1. Renal - renal vasoconstriction, endotoxemia, AKI (hepatorenal-like physiology), bile pigment nephropathy
2. Coagulation - failure of bile-salt-mediated absorption of Vitamin K → deficiency of factors II, VII, IX, X → prolonged PT
3. Immune - impaired Kupffer cell function, endotoxemia from gut, sepsis risk
4. Wound healing - collagen synthesis impaired
5. Nutrition - fat malabsorption (lack of bile salts), steatorrhoea, fat-soluble vitamin deficiency (A, D, E, K)
6. Cardiovascular - splanchnic vasodilation, decreased SVR
7. Hepatocellular - secondary biliary cirrhosis if prolonged

Techniques of Biliary Drainage in Obstructive Jaundice

1. ERCP with sphincterotomy - stone extraction (Dormia basket, balloon catheter), stent placement
2. Endoscopic biliary stenting - plastic stent (short-term) or self-expanding metal stent (SEMS) for malignancy
3. Biliary sphincterotomy - for papillary stenosis, stone clearance

1. Percutaneous Transhepatic Cholangiography (PTC) - delineates biliary anatomy
2. Percutaneous Transhepatic Biliary Drainage (PTBD) - external, internal-external, or internal stenting
3. Used when ERCP fails or anatomy altered (previous surgery)

1. Choledochoduodenostomy - CBD anastomosed side-to-side to duodenum
2. Hepaticojejunostomy (Roux-en-Y) - preferred for hilar strictures/cholangiocarcinoma
3. Choledochojejunostomy - for mid-CBD obstruction
4. Cholecystojejunostomy - palliative bypass for irresectable pancreatic head cancer
5. T-tube drainage - after CBD exploration

• Controversial; selective use (cholangitis, renal failure, very high bilirubin >250 µmol/L preoperatively)
• Reduces operative risk, allows Vitamin K correction

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4. HEPATORENAL SYNDROME (HRS) AND MANAGEMENT (2019, 20 marks)

Definition

Epidemiology

• Occurs in 15-25% of hospitalised patients with cirrhosis
• HRS represents 10-30% of AKI cases in cirrhosis
• Annual frequency: ~8% in cirrhotic patients with ascites (up to 40% in some reports)
• Develops in ~30% of cirrhotics admitted with SBP, 25% with severe alcoholic hepatitis

Pathophysiology (Three-Component Model)

1. Splanchnic arterial vasodilation (hallmark)
   • Portal hypertension → release of NO, CO, glucagon, prostacyclin, adrenomedullin
   • Massive splanchnic vasodilation → decreased effective circulating volume
   • Activates baroreceptors → compensatory activation of RAAS, SNS, ADH
2. Renal vasoconstriction
   • RAAS and SNS activation causes intense renal afferent arteriolar constriction
   • Reduced renal perfusion pressure → decreased GFR
   • Thromboxane A2, leukotrienes, adenosine contribute to renal vasoconstriction
3. Cardiac dysfunction (Cirrhotic cardiomyopathy)
   • Blunted cardiac response fails to compensate for reduced SVR
   • Further worsens effective arterial blood volume

Classification

Diagnosis (ICA Criteria 2019)

• Cirrhosis with ascites OR acute liver failure
• Serum creatinine rise ≥0.3 mg/dL within 48 hours, OR ≥50% rise within 7 days
• No improvement after 48 hours of diuretic withdrawal AND albumin infusion (1 g/kg/day, max 100 g/day)
• Absence of shock
• No nephrotoxic drugs, no obstruction, no intrinsic renal disease (protein <500 mg/day, RBCs <50/HPF, normal ultrasound)

Management

• Albumin infusion with SBP (1.5 g/kg at diagnosis, 1 g/kg at day 3) - prevents HRS
• Prophylactic norfloxacin in advanced cirrhosis with low ascites protein

• Vasoconstrictors (to reverse splanchnic vasodilation):
  • Terlipressin (vasopressin analogue) + albumin: most evidence (first-line in Europe); improves HRS-AKI reversal rates
  • Norepinephrine + albumin: equally effective, cheaper, requires ICU
  • Midodrine + octreotide + albumin: oral option; used where terlipressin unavailable
• Albumin: 20-40 g/day (volume expansion, anti-inflammatory, binds DAMPs)
• TIPS (Transjugular Intrahepatic Portosystemic Shunt): reduces portal pressure, may reverse HRS type 2; limited by encephalopathy risk

• Liver transplantation (LT): only curative treatment; renal function typically recovers post-LT
• Combined liver-kidney transplant if prolonged HRS (>4 weeks) or CKD

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5. MANAGEMENT OF PORTAL HYPERTENSION (2019, 10 marks)

Definition

Classification by site of obstruction

• Pre-sinusoidal extrahepatic: Portal vein thrombosis, Budd-Chiari (sometimes)
• Pre-sinusoidal intrahepatic: Schistosomiasis, primary biliary cholangitis
• Sinusoidal: Cirrhosis (most common in Western world), alcoholic hepatitis
• Post-sinusoidal: Hepatic vein obstruction (Budd-Chiari), veno-occlusive disease

Portosystemic Collaterals (sites of varices)

1. Gastroesophageal junction (most important - oesophageal/gastric varices)
2. Anorectal junction (anorectal varices - not haemorrhoids)
3. Falciform ligament (caput medusae)
4. Retroperitoneal and splenorenal

Management

• Resuscitate: IV access, blood transfusion (Hb target 7-8 g/dL - avoid over-transfusion)
• Pharmacological: IV terlipressin (vasopressin analogue, reduces portal pressure) or somatostatin/octreotide - start immediately on suspicion
• Endoscopic: Variceal band ligation (EVL) - first-line; sclerotherapy if EVL not possible
• Balloon tamponade (Sengstaken-Blakemore tube): bridge to definitive therapy in refractory bleeding
• Antibiotics: IV ceftriaxone (prevent SBP, reduces mortality)
• TIPS: Rescue therapy for failed endoscopic control

• Non-selective beta-blockers (propranolol, carvedilol, nadolol) - reduce cardiac output and portal pressure
• EVL if beta-blockers contraindicated

• Combination of NSBB + EVL (superior to either alone)
• TIPS for failures

• Non-selective shunts: Portocaval (end-to-side, side-to-side), mesocaval, splenorenal
• Selective shunt: Distal splenorenal shunt (Warren shunt) - preserves hepatic portal perfusion
• Devascularisation: Sugiura procedure - oesophageal transection + splenectomy + devascularisation

• Ascites: Diuretics (spironolactone + furosemide), TIPS, LVP + albumin
• Splenomegaly/Hypersplenism: Splenectomy (selective)
• Hepatic encephalopathy: Lactulose, rifaximin, dietary protein adjustment

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6. ANATOMY AND PHYSIOLOGY OF BILE AND SIGNIFICANCE OF LFT IN SURGICAL CONDITIONS (30 marks)

Anatomy of Biliary System

• Right and Left hepatic ducts unite to form the Common Hepatic Duct (CHD)
• CHD + Cystic duct = Common Bile Duct (CBD) (8-10 cm long, 6 mm normal diameter)
• CBD passes behind the first part of duodenum, through the head of pancreas, opens at Ampulla of Vater with the pancreatic duct
• Ampulla controlled by Sphincter of Oddi

Physiology of Bile

• 600-1000 mL/day produced by hepatocytes (canalicular bile) and cholangiocytes (ductal bile)
• Stored and concentrated (10-20x) in gallbladder

• Water (97%), bile salts (0.7%), phospholipids (lecithin 0.2%), cholesterol, conjugated bilirubin, electrolytes, proteins

• Primary bile acids: Cholic acid and chenodeoxycholic acid (synthesised from cholesterol)
• Conjugated with glycine or taurine → bile salts
• Secondary bile acids: Deoxycholate, lithocholate (formed by bacterial action in colon)
• Enterohepatic circulation: 95% reabsorbed in terminal ileum; total pool circulates 6-10x/day

1. Fat digestion and absorption - emulsification of fats, micelle formation for fat-soluble vitamins
2. Cholesterol excretion - only route for cholesterol elimination from body
3. Bilirubin excretion
4. Alkalinisation of duodenum - neutralises gastric acid
5. Drug and toxin excretion
6. Antibacterial - bile salts inhibit bacterial overgrowth

• Secretin (from S cells of duodenum): stimulates ductal bicarbonate secretion (most potent stimulator)
• Cholecystokinin (CCK): contracts gallbladder, relaxes Sphincter of Oddi
• Vagal stimulation: enhances bile flow
• Somatostatin: inhibits bile secretion

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7. ANATOMY OF LIVER, SEGMENTS, AND MANAGEMENT OF BLUNT LIVER TRAUMA (2022, 30 marks)

Surgical Anatomy of the Liver

• Right lobe (Segments V-VIII): Right portal pedicle
• Left lobe (Segments I-IV): Left portal pedicle
• Caudate lobe (Segment I): Receives portal blood from both sides; drains directly into IVC
• Hepatic veins divide liver into 4 sectors between the segments

• Left: Segments I, II, III, IVa, IVb
• Right: Segments V, VI, VII, VIII

• Hepatic artery (25% blood flow, 50% oxygen) - from celiac axis via common hepatic artery
• Portal vein (75% blood flow, 50% oxygen) - formed by superior mesenteric + splenic veins behind neck of pancreas
• Dual blood supply provides protection from ischaemia

• Left, Middle (most important surgically), Right
• Drain into IVC just below diaphragm

Blunt Liver Trauma

• Primary survey: ATLS protocol (Airway, Breathing, Circulation, Disability, Exposure)
• FAST scan (Focused Assessment with Sonography for Trauma): rapid bedside assessment for free fluid
• CT abdomen with IV contrast (haemodynamically stable patients): gold standard - grades injury, identifies active extravasation, defines vascular injuries
• Diagnostic Peritoneal Lavage (DPL): largely replaced by FAST and CT

• Success rate: 80-90% for Grades I-III; even Grade IV-V increasingly managed non-operatively
• Prerequisites: haemodynamic stability, no peritonism, no other indication for laparotomy
• ICU monitoring, serial abdominal examinations, serial Hb
• Angioembolisation: for contrast blush (active arterial bleeding) on CT - highly effective
• Follow-up CT at 24-48 hours if any deterioration

• Damage Control Surgery (DCS): for exsanguinating patients
  1. Control haemorrhage (perihepatic packing, manual compression)
  2. Control contamination (not a priority in liver trauma)
  3. Temporary closure (vacuum dressing)
  4. ICU resuscitation (correct lethal triad: hypothermia, acidosis, coagulopathy)
  5. Return to OR in 24-48 hours for definitive repair
• Specific techniques:
  • Pringle manoeuvre (hepatoduodenal ligament clamping): reduces inflow; safe for up to 60 minutes
  • Simple suture hepatorrhaphy
  • Argon beam coagulation, topical haemostatic agents (oxidised cellulose, fibrin glue)
  • Hepatotomy with direct vessel ligation
  • Hepatic resection (debridement resection) for devitalised tissue
  • For juxtahepatic venous injuries: atriocaval shunt, total hepatic vascular isolation

• Bile leak/biloma, haemobilia, hepatic artery pseudoaneurysm
• Post-traumatic abscess, delayed haemorrhage
• Hepatic necrosis, bile duct stricture

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8. INDICATIONS AND TECHNIQUES OF LIVER RESECTION (2018 marks)

Indications

• Primary liver tumours: Hepatocellular carcinoma (HCC), cholangiocarcinoma (intrahepatic)
• Metastatic liver disease: Colorectal liver metastases (most common indication in Western world), neuroendocrine tumour metastases
• Gallbladder carcinoma with liver involvement

• Symptomatic hepatic adenoma (>5 cm, or in women on OCP), haemangioma (symptomatic), FNH (rarely)
• Hydatid cyst (pericystectomy/segmentectomy)
• Hepatic abscess (pyogenic, rarely needed)
• Liver donor hepatectomy for living donor liver transplantation

Pre-operative Assessment

• Child-Pugh score, MELD score (assessment of hepatic reserve)
• Future Liver Remnant (FLR) volumetry on CT: minimum FLR >20% in normal liver; >30-40% in cirrhotic liver
• Portal vein embolisation (PVE): induces hypertrophy of FLR when it is inadequate; performed 4-6 weeks before surgery
• Liver biopsy: to assess for fibrosis/cirrhosis
• Intraoperative ultrasound: gold standard for identifying additional lesions

Hepatic Segments and Resection Types

Operative Technique

1. Patient positioning: Supine, right side elevated 30°
2. Incision: Rooftop (bilateral subcostal) or Mercedes incision
3. Intraoperative USS: identify lesions, define margins
4. Liver mobilisation: divide falciform, coronary, triangular ligaments
5. Hilar dissection: Pringle's hepatoduodenal control
6. Hepatic vein control: isolate and control hepatic veins before parenchymal transection
7. Parenchymal transection techniques:
   • CUSA (Cavitron Ultrasonic Surgical Aspirator): gold standard - fragments and aspirates parenchyma while preserving vessels
   • Waterjet dissection
   • Radiofrequency-assisted (Habib device)
   • Clamp-crush technique
8. Haemostasis: Argon beam coagulation, bipolar diathermy, Pringle's manoeuvre, fibrin glue
9. Biliary closure: suture biliary radicles to prevent bile leak
10. Drain placement: Blake's drain near cut surface

ALPPS (Associating Liver Partition and Portal Vein Ligation for Staged Hepatectomy)

• Two-stage procedure: Stage 1 - in situ liver splitting + right PVL → rapid hypertrophy of FLR in 1-2 weeks; Stage 2 - completion hepatectomy
• For cases where FLR too small for one-stage resection
• Higher morbidity than conventional two-stage approach; used selectively

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9. LIVER TRANSPLANTATION - INDICATIONS AND BASIC PRINCIPLES (2018, 20 marks)

Indications

• Acetaminophen-induced: pH <7.3 OR INR >6.5 + Creatinine >3.4 mg/dL + Grade III-IV encephalopathy
• Non-acetaminophen: INR >6.5 OR any 3 of: Age <10 or >40; aetiology (NANB hepatitis, drug-induced, Wilson's); jaundice to encephalopathy >7 days; INR >3.5; bilirubin >300 µmol/L

• Cirrhosis: alcoholic, viral (Hep B, C), autoimmune, cryptogenic, NASH
• Listed when MELD ≥15 (benefit of transplant outweighs risk)

• Primary biliary cholangitis (PBC), Primary sclerosing cholangitis (PSC)
• Wilson's disease, Haemochromatosis, Alpha-1 antitrypsin deficiency
• Budd-Chiari syndrome
• HCC within Milan criteria: Single lesion ≤5 cm OR up to 3 lesions all ≤3 cm, no vascular invasion, no extrahepatic disease

• Absolute: Active sepsis outside biliary tract, extrahepatic malignancy, active substance abuse (alcohol <6 months abstinence), advanced cardiopulmonary disease, HIV with AIDS
• Relative: Portal vein thrombosis (relative), prior abdominal surgery, obesity

Basic Principles of Liver Transplantation

• Deceased Donor (Donation after Brain Death - DBD; Donation after Circulatory Death - DCD)
• Living Donor Liver Transplantation (LDLT): Right lobe (60-65% liver volume) or left lateral segment (for paediatric recipient)

• Divide hepatic hilum (HA, PV, CBD)
• Divide hepatic veins (bicaval) or preserve IVC (piggyback technique)

1. Suprahepatic IVC anastomosis (or piggyback anastomosis to hepatic veins)
2. Infrahepatic IVC anastomosis (classic) - or plication in piggyback
3. Portal vein anastomosis (end-to-end)
4. Hepatic artery anastomosis (Carrel patch technique)
5. Biliary reconstruction: Duct-to-duct (choledochocholedochostomy) preferred; Roux-en-Y hepaticojejunostomy if size mismatch or PSC

• Calcineurin inhibitors (Tacrolimus - first-line, or Cyclosporine)
• Antiproliferatives: Mycophenolate mofetil (MMF)
• Corticosteroids: Prednisolone (tapering)
• mTOR inhibitors (Sirolimus/Everolimus): Used in HCC patients post-LT

• Early: Primary non-function, hepatic artery thrombosis (most feared early complication), PV thrombosis, biliary leak, rejection
• Late: Biliary stricture, chronic rejection, recurrence of disease, malignancy (immunosuppression-related)

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10. HOW WILL YOU ARRIVE AT DIAGNOSIS IN CASE OF HAEMATEMESIS (2018, 30 marks)

Definition

History

• Character of vomit (bright red = active; coffee-ground = slower)
• Volume, number of episodes
• Associated symptoms: melena, haematochezia (massive bleed), abdominal pain, jaundice
• Risk factors: alcohol intake (varices, Mallory-Weiss, alcoholic gastritis), NSAID/aspirin use (peptic ulcer), prior episodes, known liver disease, anticoagulants

Examination

• Haemodynamic assessment: pulse, BP, capillary refill, respiratory rate
  • Tachycardia + hypotension = > 1000 mL blood loss (Class III/IV)
• Stigmata of liver disease: jaundice, spider naevi, leukonychia, palmar erythema, gynaecomastia, caput medusae, splenomegaly, ascites → suggests variceal bleed

Resuscitation FIRST (before diagnosis)

• Two large-bore IV cannulae (14G), O negative blood if needed
• IV fluid resuscitation (crystalloid initially)
• Blood: FBC, coagulation, LFT, renal, X-match 4-6 units
• FFP for INR >1.5; Platelet transfusion if <50

Risk Stratification

• Urea, Hb, Systolic BP, pulse, melena, syncope, liver disease, heart failure
• Score 0 = can be managed outpatient; ≥6 = high risk, urgent endoscopy

• Age, shock, comorbidity, diagnosis, stigmata of recent haemorrhage
• Score ≥8 = high mortality risk

Investigations

• OGD (Oesophago-gastroduodenoscopy): GOLD STANDARD - diagnostic AND therapeutic; within 24 hours (within 12 hours in massive bleed/suspected varices)
• FBC: Hb, platelets
• Coagulation: PT, APTT, INR
• LFTs, renal function
• Blood group and crossmatch
• ABG (for acid-base in shocked patient)

Causes and Endoscopic Findings

• Ia - Spurting haemorrhage (highest rebleed risk ~90%)
• Ib - Oozing haemorrhage
• IIa - Visible vessel (non-bleeding)
• IIb - Adherent clot
• IIc - Haematin on ulcer base
• III - Clean base (lowest risk ~5%)

Management of Variceal Bleed

Management of Non-variceal (Peptic Ulcer) Bleed

• IV PPI (omeprazole 80 mg bolus + 8 mg/hr infusion) for 72 hours
• Endoscopic therapy: dual therapy (injection of 1:10,000 adrenaline + clips/thermocoagulation) for Forrest Ia, Ib, IIa
• Repeat endoscopy if rebleeding
• Angioembolisation: for recurrent haemorrhage after 2 failed endoscopies
• Surgery (under-running of ulcer ± oversewing ± vagotomy) for failure of all above

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11. OPERATIVE TECHNIQUE FOR LEFT LOBE HEPATIC RESECTION (2018, 20 marks)

Indications

• Left-sided HCC, cholangiocarcinoma, metastases in segments II, III, IV
• Living donor left lateral segment donation

Pre-operative preparation

• Volumetric CT to assess FLR (adequate if right lobe + caudate = >40% in cirrhosis)
• PFTs, cardiac evaluation, optimise nutrition
• Cross-match 4 units blood; FFP available

Operative Steps: Left Hemihepatectomy (Segments I, II, III, IV)

1. Position: Supine, right side slightly elevated
2. Incision: Mercedes (midline + bilateral subcostal) or extended right subcostal (rooftop)
3. Exploration: Confirm resectability; check peritoneal cavity for metastases; intraoperative USS
4. Liver mobilisation:
   • Divide falciform ligament
   • Divide left triangular and left coronary ligaments
   • Expose left hepatic vein, left portion of middle hepatic vein
5. Hilar dissection:
   • Isolate left hepatic artery (branch of proper hepatic artery) - ligate and divide
   • Isolate left portal vein - ligate and divide
   • Left bile duct identified but divided after parenchymal transection
6. Ischaemic demarcation: After vascular division, line of demarcation appears on liver surface along Cantlie's line
7. Hepatic vein control: Left hepatic vein identified and controlled (divide before or during parenchymal transection)
8. Parenchymal transection along Cantlie's line (principal scissura):
   • Using CUSA (preferred) or clamp-crush technique
   • Pringle's manoeuvre (clamp hepatoduodenal ligament) to reduce blood loss
   • Secure biliary radicles with sutures (not clips) as you progress
   • Middle hepatic vein branches from left lobe must be managed
9. Left hepatic vein division: staple or oversew
10. Haemostasis: Argon beam, bipolar diathermy, fibrin glue, bolster sutures
11. Biliary check: Inject saline into cystic duct stump to check for leaks
12. Drain placement: Closed suction drain near cut surface
13. Closure: Mass closure with PDS

Left Lateral Sectionectomy (Segments II + III)

• Simpler procedure, less morbidity
• Falciform ligament divided, left triangular ligament mobilised
• Parenchymal transection to the left of the falciform ligament
• Left lateral pedicle (portal + arterial + biliary) divided and secured

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SUMMARY TABLE - Topics by Weightage

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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

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Difference Between Build and Nutrition of the Body

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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

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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

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KEY DIFFERENCES: Build vs. Nutrition

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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.

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Raynaud's Disease and Raynaud's Phenomenon

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OVERVIEW / DEFINITION

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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)

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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

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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.

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

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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

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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)

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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

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Intermittent Claudication

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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)

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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

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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

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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

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CLASSIFICATION OF PERIPHERAL ARTERIAL DISEASE

Fontaine Classification (Clinical)

Rutherford Classification (Clinical + Objective Data)

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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

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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

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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

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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

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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)

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