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Abdominal & Hepatobiliary Surgery: Comprehensive Study Notes

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PART 1 — LIVER

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1.1 Anatomy & Physiology

• Largest organ: 1–1.5 kg, 1.5–2.5% lean body mass
• Dual blood supply: ~20% from hepatic artery (O₂-rich), ~80% from portal vein (nutrient-rich)
• Cell types: Hepatocytes (2/3 of mass), Kupffer cells (fixed macrophages), stellate/Ito cells (fat-storing → activated → fibrosis), endothelial cells, bile ductular cells
• Functional unit: Hepatic acinus (not lobule)
  • Zone 1 (periportal) = around portal tracts — receives oxygenated blood first → phospholipid synthesis, beta-oxidation, gluconeogenesis
  • Zone 3 (centrilobular) = around central veins → most vulnerable to ischemia and toxic injury (acetaminophen, alcohol)
  • Zone 2 = intermediate
• Space of Disse: Between hepatocytes and sinusoidal endothelium — plasma freely contacts hepatocytes here
• Bile flows counter-current to blood (zone 3 → zone 1 → bile ducts)
• — Harrison's Principles of Internal Medicine 22E, p. 2674

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1.2 Bilirubin Metabolism (Biochemistry)

1. RBC hemolysis → Hemoglobin → Heme → Unconjugated (indirect) bilirubin (insoluble, bound to albumin, not excreted in urine)
2. Hepatocyte uptake → conjugated to glucuronic acid → Conjugated (direct) bilirubin (water-soluble)
3. Excreted into bile canaliculi via MRP2 transporter (rate-limiting step is canalicular excretion)
4. In gut: bacterial enzymes → urobilinogen → stercobilin (stool color) / reabsorbed → urobilin (urine)

• Gilbert syndrome: Mild UGT1A1 deficiency → benign unconjugated hyperbilirubinemia, triggered by fasting/illness
• Crigler-Najjar type I: Complete UGT1A1 absence → kernicterus, fatal without liver transplant
• — Harper's Illustrated Biochemistry 32nd Ed, p. 1598; Harrison's, p. 2674

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1.3 Liver Function Tests (LFTs)

• Cholestatic pattern: ↑ ALP > ↑ ALT
• Hepatocellular pattern: ↑ ALT/AST > ↑ ALP
• Bilirubinuria = always conjugated (pathologic), as unconjugated is albumin-bound → cannot be filtered
• — Harrison's, p. 2674; Sabiston Textbook of Surgery

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1.4 Cirrhosis

• Chronic hepatic injury → hepatocyte necrosis → stellate cell activation → TGF-β → collagen deposition → fibrous septa → nodule formation → disrupted vascular architecture → portal hypertension

• Micronodular (<3 mm): Uniform septa and nodules; alcoholic, hemochromatosis
• Macronodular (>3 mm): Varied nodule sizes; post-viral, PBC
• Mixed: Both patterns coexist
• — Schwartz's Principles of Surgery 11th Ed, p. 1390

• Compensated: Often asymptomatic
• Decompensated: Ascites, variceal bleeding, hepatic encephalopathy, jaundice, spontaneous bacterial peritonitis (SBP), hepatorenal syndrome (HRS)
• Signs: Palmar erythema, spider nevi (>5 significant), caput medusae, leukonychia, Dupuytren's contracture, parotid enlargement (alcohol), gynecomastia, testicular atrophy
• — Schwartz's, p. 1390; Harrison's

• 5-year mortality 50% (70% from liver failure)
• 30,000 deaths/year in the US from cirrhosis; additional 10,000–12,000 from HCC
• — Schwartz's, p. 1390

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1.5 Portal Hypertension

1. Esophageal/gastric varices — most deadly complication
2. Ascites — portal HTN + hypoalbuminemia + hyperaldosteronism (RAAS activation)
3. Splenomegaly → hypersplenism (pancytopenia)
4. Hepatic encephalopathy — ammonia accumulation, disrupted urea cycle
5. Hepatorenal syndrome — functional renal failure, extreme vasoconstriction
6. Caput medusae — recanalized umbilical vein → visible abdominal wall collaterals
7. Anorectal varices (≠ hemorrhoids) — present in ~45% of cirrhotic patients

• — Schwartz's, p. 1394

• 30% of compensated, 60% of decompensated cirrhosis have esophageal varices
• 1/3 of patients with varices will bleed
• Each bleed: 20–30% mortality
• Without treatment: 70% rebleed within 2 years

• Non-selective β-blockers (propranolol, nadolol, carvedilol): Reduce first bleed by 45%, mortality by 50%
• Endoscopic variceal band ligation (EVBL): Preferred for medium-large varices; every 1–2 weeks until obliteration; EGD at 1–3 months, then q6 months

1. ICU admission, resuscitation → target Hb ~8 g/dL (avoid over-transfusion — increases rebleeding)
2. Vasoactive agents: Octreotide (somatostatin analog) — splanchnic vasoconstriction, reduces portal inflow
3. Antibiotics: Ceftriaxone or norfloxacin (SBP prophylaxis, reduces mortality)
4. Endoscopy within 12 hours: EVBL (preferred) or sclerotherapy
5. Balloon tamponade (Sengstaken-Blakemore tube): Bridge only if refractory — temporary
6. TIPS (Transjugular Intrahepatic Portosystemic Shunt): For refractory bleeding; reduces HVPG; risk of encephalopathy
7. Surgical shunts (last resort in selected patients):
   • Portacaval (side-to-side, end-to-side)
   • Mesocaval
   • Distal splenorenal (Warren shunt) — selective decompression, preserves hepatic portal flow, lower encephalopathy risk

• — Schwartz's, p. 1435–1440

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1.6 Child-Turcotte-Pugh (CTP) Score & MELD

• Class A (5–6): 10% operative mortality
• Class B (7–9): 30% operative mortality
• Class C (10–15): 75–80% operative mortality

• Formula: 3.78×ln(bilirubin) + 11.2×ln(INR) + 9.57×ln(creatinine) + 6.43
• All objective variables; used for liver transplant priority
• — Schwartz's, p. 1311–1320

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1.7 Infections of the Liver

• Most common organism: Klebsiella pneumoniae (especially in diabetics), E. coli, Streptococcus
• Source: Portal pyemia (appendicitis, diverticulitis), biliary infection (most common), hematogenous
• Presentation: Fever, RUQ pain, hepatomegaly; leukocytosis, ↑ ALP
• Imaging: CT/US shows hypoechoic/hypodense lesion
• Treatment: Percutaneous drainage + IV antibiotics (broad-spectrum: piperacillin-tazobactam or metronidazole + cephalosporin); surgical drainage if failed/multiple

• Travel history, young males; "anchovy sauce" pus
• Serology: Anti-amebic antibodies
• Treatment: Metronidazole (drug of choice) → then luminal agent (diloxanide furoate, paromomycin)
• Rarely needs drainage

• Sheep/dog exposure; "double wall" cyst on US/CT; "water lily sign"
• Serology: ELISA
• Treatment: PAIR (Puncture, Aspiration, Injection of scolicidal agent, Re-aspiration) or surgical excision
• Albendazole preoperatively to reduce risk of anaphylaxis from cyst rupture
• NEVER aspirate without prior albendazole (anaphylaxis + peritoneal seeding)

• HBV/HCV → chronic hepatitis → cirrhosis → HCC (major surgical concern)
• — Schwartz's, p. 1599–1603

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1.8 Hepatocellular Carcinoma (HCC)

• CT/MRI: Arterial enhancement + portal venous washout = diagnostic (LI-RADS 5 = HCC)
• AFP >400 ng/mL is highly suggestive
• Biopsy usually avoided (seeding risk); diagnosis by imaging alone is accepted

• BCLC 0/A: Curative — surgical resection or ablation (RFA)
• BCLC B: Intermediate — TACE (transarterial chemoembolization)
• BCLC C: Advanced — Sorafenib (first-line TKI) or lenvatinib/atezolizumab+bevacizumab
• BCLC D: End-stage — best supportive care

• Single tumor ≤5 cm OR ≤3 nodules each ≤3 cm, no vascular invasion, no extrahepatic disease

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PART 2 — BILIARY SYSTEM

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2.1 Anatomy of Biliary Tree

• Contains: Cystic artery (usually from right hepatic artery), Calot's node (lymph node marking cystic artery)
• Critical view of safety must be established during laparoscopic cholecystectomy to prevent bile duct injury

• Replaced/accessory right hepatic artery (20%): Runs through portacaval space, posterior to CBD — palpated during Pringle maneuver
• Short cystic duct → risk of CBD injury
• CBD blood supply at 3 and 9 o'clock positions from gastroduodenal and posterosuperior pancreaticoduodenal arteries
• — Sabiston Textbook of Surgery, p. 1823

2.2 Physiology of Bile

• CCK (cholecystokinin): Released by intestinal mucosa → gallbladder contraction + sphincter of Oddi relaxation
• Secretin: Stimulates bile flow (bicarbonate-rich) from cholangiocytes
• Vagal stimulation: Promotes bile secretion

• — Sabiston, p. 1820–1623

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2.3 Cholelithiasis (Gallstones)

1. Supersaturation: ↑ Cholesterol secretion or ↓ bile salts/phospholipids
2. Nucleation: Gallbladder stasis + mucin glycoproteins → crystal nucleation
3. Growth: Stagnant bile in gallbladder

• — Sabiston, p. 1634

• Asymptomatic cholelithiasis → 2% per year become symptomatic → prophylactic cholecystectomy not indicated (except porcelain gallbladder with mucosal calcification, sickle cell, immunosuppressed)
• Biliary colic: RUQ/epigastric pain after fatty meal, radiates to right shoulder/back; 30–60 min duration; no fever/leukocytosis
• Acute cholecystitis: Persistent colic >6 hours + fever + Murphy's sign + leukocytosis → stone impacted in cystic duct
• Choledocholithiasis: Stone in CBD → obstructive jaundice ± Charcot's triad
• Cholangitis: Charcot's triad / Reynold's pentad
• Gallstone pancreatitis: Stone at ampulla → pancreatic duct obstruction

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2.4 Acute Cholecystitis

• RUQ pain >6 hours, fever, nausea/vomiting
• Murphy's sign: Pain/arrest of inspiration on palpation of RUQ (gallbladder presses against examiner's fingers during inspiration)
• Leukocytosis (WBC 10,000–15,000)

• USS: Wall thickening (>3 mm), pericholecystic fluid, stone in gallbladder, sonographic Murphy's sign — most sensitive
• HIDA scan: Gold standard if USS inconclusive (non-filling of gallbladder)
• CT: If complications (perforation, gangrene) suspected

• Grade I (mild): Healthy patient, mild local inflammation
• Grade II (moderate): WBC >18,000, symptom duration >72h, pericholecystic fluid, local abscess
• Grade III (severe): Organ dysfunction (CV, neurologic, respiratory, renal, hepatic, hematologic)

• Grade I: Early laparoscopic cholecystectomy within 24–72 hours (reduces conversion rate, shorter hospital stay)
• Grade II: Early LC if feasible; gallbladder drainage (percutaneous cholecystostomy) if unfit
• Grade III: Organ support, drainage; interval cholecystectomy after stabilization
• IV antibiotics: Cephalosporins ± metronidazole; or piperacillin-tazobactam for severe

• Empyema (pus in GB)
• Gangrene → perforation (peritonitis)
• Mirizzi syndrome: Stone in Hartmann's pouch → extrinsic compression of CHD
• Cholecystoenteric fistula → Gallstone ileus (stone >2.5 cm passes into small bowel → obstruction at ileocecal valve; Rigler's triad on AXR: pneumobilia, SBO, stone visible)

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2.5 Choledocholithiasis & Cholangitis

• Presentation: Obstructive jaundice (conjugated ↑), pale stool, dark urine, pruritus, ↑ALP/GGT >↑AST/ALT
• Investigations: MRCP (non-invasive, 95% sensitivity) → confirms diagnosis; ERCP = diagnostic + therapeutic
• Management: ERCP + sphincterotomy + stone extraction (laparoscopic CBD exploration as alternative)
• Pre-op assessment for concomitant CBD stones during cholecystectomy: IOC (intraoperative cholangiography)

• Charcot's triad: Fever + jaundice + RUQ pain (all 3 in 50–70%)
• Reynolds' pentad (severe/suppurative): Charcot's triad + hypotension + altered consciousness
• Organisms: E. coli (most common), Klebsiella, Enterococcus, Bacteroides, Clostridium
• Management:
  1. IV resuscitation + broad-spectrum antibiotics (piperacillin-tazobactam, or carbapenem if severe)
  2. Urgent biliary decompression: ERCP (preferred) or PTBD (percutaneous transhepatic biliary drainage)
  3. Treat underlying cause

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2.6 Jaundice: Surgical Approach

• CBD stone — most common surgical cause
• Periampullary carcinoma — pancreatic head (Courvoisier's sign: palpable painless gallbladder in jaundiced patient → suggests malignancy not stone)
• Cholangiocarcinoma (Klatskin tumor at hilum)
• Strictures — post-cholecystectomy, PSC
• Mirizzi syndrome

1. LFTs (↑ Conjugated bilirubin, ↑ ALP/GGT)
2. USS (first-line: shows dilated ducts, gallstones)
3. CT abdomen (tumor, mass)
4. MRCP (best non-invasive for biliary anatomy)
5. ERCP (if intervention needed)
6. PTC/PTBD (if ERCP failed)

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2.7 Cholangiocarcinoma

• Intrahepatic (10%): Within liver parenchyma; treated like HCC
• Perihilar/Klatskin tumor (60–70%): At hepatic duct bifurcation; Bismuth-Corlette classification
• Distal (20–30%): At CBD near ampulla

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2.8 Choledochal Cysts

• Type I (50–80%): CBD dilation (most common) — cystic (Ic) or fusiform (If)
• Type II (2%): CBD diverticulum
• Type III (1–4%): Choledochocele (intramural duodenal CBD dilation)
• Type IV (15–35%): Intra- + extrahepatic duct involvement
• Type V = Caroli disease: Intrahepatic duct dilation only

• — Sabiston, p. 2693

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PART 3 — PANCREAS

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3.1 Anatomy & Physiology

• Retroperitoneal; four parts: Head (in C-loop of duodenum), neck, body, tail (touches spleen)
• Duct of Wirsung (main): Joins CBD at ampulla of Vater → sphincter of Oddi
• Duct of Santorini (accessory): Opens separately at minor papilla
• Pancreas divisum: Failure of dorsal and ventral pancreatic buds to fuse (most common congenital anomaly); most pass dorsal duct drainage through minor papilla — risk of pancreatitis

• Acinar cells → digestive enzymes: lipase, amylase, trypsinogen, chymotrypsinogen, elastase, phospholipase A2
• Ductal cells → bicarbonate-rich fluid (secretin-stimulated)
• Trypsinogen → Trypsin activated by enterokinase in duodenum → activates all other zymogens (cascade)
• Premature activation → acute pancreatitis

• α cells: Glucagon
• β cells: Insulin (most numerous)
• δ cells: Somatostatin
• PP cells: Pancreatic polypeptide

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3.2 Acute Pancreatitis

• Gallstones (40–50%) — stone at ampulla
• Ethanol (30–35%)
• Trauma (ERCP, post-surgical)
• Steroids
• Mumps (viral)
• Autoimmune (IgG4)
• Scorpion sting
• Hypertriglyceridemia (>1000 mg/dL), Hypercalcemia
• ERCP-related
• Drugs (azathioprine, valproate, thiazides, tetracyclines)

• Epigastric pain radiating to back (boring, constant)
• Nausea, vomiting
• Fever, tachycardia
• Cullen's sign: Periumbilical ecchymosis (hemorrhagic pancreatitis)
• Grey-Turner's sign: Flank ecchymosis (hemorrhagic pancreatitis)

• Serum lipase >3× ULN (more specific than amylase)
• Amylase rises faster but normalizes faster
• US (for gallstones + biliary dilation)
• CT with contrast (after 48–72 hours if no improvement — assess necrosis)

• Mild: No organ failure, no local complications
• Moderate-severe: Transient organ failure (<48h) OR local complications (peripancreatic fluid, necrosis)
• Severe: Persistent organ failure (>48h)

• Grades A–E based on peripancreatic inflammation + % gland necrosis

1. Aggressive IV fluid resuscitation (Lactated Ringer's preferred over NS — lower risk of acidosis and complications)
2. Analgesia (opioids, NSAIDs)
3. Nil by mouth initially → early enteral feeding via nasojejunal tube (superior to TPN)
4. Antibiotics: NOT prophylactically; only for proven infected necrosis
5. ERCP within 24–72 hours if gallstone + cholangitis/biliary obstruction
6. Cholecystectomy before discharge (gallstone pancreatitis) — prevents recurrence

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3.3 Chronic Pancreatitis

• Recurrent/chronic epigastric pain radiating to back; relieved by sitting forward (knee-chest position)
• Exocrine insufficiency: Steatorrhea (fat malabsorption), weight loss; when >90% gland destroyed
• Endocrine insufficiency: Type 3c diabetes (pancreatogenic)
• Calcifications on AXR/CT ("chain of lakes" duct dilation on MRCP)

• Pain: Analgesics, celiac plexus block, pancreatic enzyme supplements (reduce CCK stimulus)
• Exocrine insufficiency: Oral pancreatic enzymes (pancrelipase) + fat-soluble vitamin supplementation
• Endocrine: Insulin therapy
• Surgical options: Puestow procedure (longitudinal pancreaticojejunostomy), Frey procedure, Beger procedure, total pancreatectomy + islet autotransplantation (TP-IAT) for refractory pain

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3.4 Pancreatic Cancer (Ductal Adenocarcinoma)

• KRAS mutation (90%)
• CDKN2A (p16) loss (85%)
• TP53 mutation (75%)
• SMAD4/DPC4 loss (55%)
• Precursor lesion: PanIN (Pancreatic Intraepithelial Neoplasia) → adenocarcinoma

• Head tumors: Painless obstructive jaundice (Courvoisier's sign), pale stool, dark urine, weight loss
• Body/tail tumors: Late presentation, pain (retroperitoneal invasion), weight loss
• New-onset diabetes, deep vein thrombosis (Trousseau's sign)
• Trousseau's syndrome: Migratory thrombophlebitis in occult malignancy

• CT pancreas protocol (triple-phase): Best for staging and resectability
• CA 19-9 (tumor marker; sialyl-Lewis A antigen); elevated in ~80% — not diagnostic alone
• EUS + FNA for tissue diagnosis in unresectable disease
• MRCP for ductal anatomy

• Resectable: No arterial involvement, ≤180° portal/SMV involvement
• Borderline resectable: 180–360° of SMA/CA, >180° portal/SMV → neoadjuvant chemotherapy first
• Unresectable/locally advanced: >360° encasement of SMA/CA, aorta involvement, distant mets

• Whipple procedure (pancreaticoduodenectomy): Head/periampullary tumors — resects pancreatic head, duodenum, distal CBD, gallbladder, part of stomach (classical) or pylorus-preserving (PPPD)
• Distal pancreatectomy + splenectomy: Body/tail tumors

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PART 4 — GI TRACT (Surgical Emergencies)

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4.1 Acute Appendicitis

• Starts as periumbilical pain → migrates to RIF (McBurney's point) over hours
• Anorexia, nausea, vomiting (after pain onset)
• Low-grade fever, tachycardia
• Signs:
  • McBurney's sign: Tenderness at McBurney's point (1/3 from ASIS to umbilicus)
  • Rovsing's sign: RIF pain on palpation of LIF (indicates peritoneal irritation)
  • Psoas sign: Pain on extension of right hip (retrocecal appendix)
  • Obturator sign: Pain on internal rotation of flexed right hip (pelvic appendix)
  • Guarding, rebound tenderness

• WBC ↑ (leukocytosis with left shift)
• CRP elevated
• Urinalysis (sterile pyuria possible — adjacent inflammation)
• USS: First-line in children, pregnant women; non-compressible appendix >6 mm
• CT abdomen/pelvis (contrast): Most accurate (>95%); visualization of appendix, perforation, collections

• Migratory RIF pain (1), Anorexia (1), Nausea/vomiting (1), Tenderness RIF (2), Rebound tenderness (1), Elevated temp (1), Leukocytosis (2), Shift to left (1) = max 10
• ≥7: High likelihood → surgery; 5–6: observe; ≤4: Low likelihood

• Laparoscopic appendicectomy (gold standard): IV antibiotics (co-amoxiclav or cefuroxime + metronidazole) perioperatively
• Open (if laparoscopy unavailable or dense adhesions)
• Perforated with abscess: IV antibiotics ± percutaneous drainage → interval appendicectomy at 6–8 weeks
• Antibiotics alone (non-operative): Selected uncomplicated appendicitis (recent RCTs support — ~20% recurrence within 5 years)

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4.2 Bowel Obstruction

• Adhesions (most common, 60%): Post-operative
• Hernia (15–20%): Inguinal, femoral, umbilical — always suspect in patient with no previous surgery
• Tumor (small bowel relatively rare)
• Intussusception, Crohn's, volvulus, gallstone ileus

• Simple: No vascular compromise
• Strangulated: Vascular compromise → urgent surgery (fever, tachycardia, peritonism, ↑ lactate, ↑ CRP, ↑ WBC)
• Closed loop: Both ends obstructed → rapid distension → highest perforation risk (caecum most vulnerable in LBO — thin-walled, right-sided)

• Colicky abdominal pain (central, intermittent)
• Vomiting (bilious/feculent depending on level)
• Distension
• Constipation/obstipation (complete); diarrhea early (proximal SBO)
• High-pitched tinkling bowel sounds → later silent (ileus/peritonitis)

• AXR: Central dilated loops + valvulae conniventes (SBO); no gas in colon
• CT abdomen: Gold standard — identifies cause, level, strangulation (e.g., whirl sign in volvulus, mesenteric ischemia)

• IV fluids + NG tube decompression + catheter (monitor UO)
• Conservative for uncomplicated adhesional SBO: NBM, NG, IVF, 24–48h observation; water-soluble contrast study (Gastrografin) both diagnostic + therapeutic
• Urgent surgery if: Strangulation signs, complete obstruction not resolving, hernia, worsening

• Causes: Carcinoma (most common), volvulus (sigmoid most common), diverticular stricture
• Caecal dilation >12 cm = impending perforation → urgent decompression
• Sigmoid volvulus: AXR "coffee bean sign" → endoscopic decompression (recurrence risk high → elective sigmoidectomy)
• Caecal volvulus: More acute, surgical emergency (caecostomy or right hemicolectomy)

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4.3 Peritonitis

• Occurs in cirrhosis/ascites; monomicrobial (E. coli, Klebsiella)
• Diagnosis: Ascitic fluid PMN >250 cells/mm³
• Treatment: Cefotaxime 2g IV q8h × 5 days; albumin IV on day 1 and 3 (reduces HRS)
• Prophylaxis: Norfloxacin or ciprofloxacin in high-risk cirrhotic patients

• Due to visceral perforation (appendix, peptic ulcer, bowel)
• Presentation: Acute abdomen, board-like rigidity, absent bowel sounds, shock
• Features: Guarding (voluntary) → rigidity (involuntary) → rebound tenderness (peritoneal sign)
• Erect CXR: Free air under diaphragm (perforation)
• Management: Immediate resuscitation + broad-spectrum antibiotics + emergency laparotomy (or laparoscopy if stable)

• Gram-negative: E. coli, Klebsiella, Proteus
• Anaerobes: Bacteroides fragilis
• Gram-positive: Streptococcus, Staphylococcus

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4.4 Peptic Ulcer Disease (Surgical Complications)

1. Perforation: Emergency — Graham patch repair (omental patch); if H. pylori + → treat post-operatively
2. Hemorrhage: Endoscopy first (adrenaline injection, clipping, thermocoagulation); surgery if fails (Billroth II or oversewing of vessel — gastroduodenal artery for posterior DU)
3. Obstruction (pyloric stenosis): Balloon dilation (endoscopic) vs. surgery (gastrojejunostomy)

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PART 5 — PHARMACOLOGY & MEDICINE

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5.1 Drugs Used in Hepatic/Biliary Disease

• SVR (Sustained Virological Response = cure) >95% with modern DAAs

• Ursodeoxycholic acid (UDCA): Reduces biliary cholesterol saturation; used for small (<5 mm) radiolucent stones in unfit patients; also primary biliary cholangitis (PBC) treatment; slow + stones recur after stopping

• Pancrelipase (Creon): Oral porcine pancreatic enzymes; must be taken with meals; enteric-coated; use with PPI (protect from acid degradation)

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5.2 Key Microbiology for Abdominal Surgery

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5.3 Key Pathology Findings

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5.4 Important Clinical Syndromes & Eponyms

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5.5 Hepatorenal Syndrome (HRS)

• HRS-AKI (Type 1): Rapid, doubling of creatinine >2.5 mg/dL in <2 weeks; precipitated by SBP; poor prognosis
• HRS-CKD (Type 2): Slow, gradual renal impairment; refractory ascites

• Terlipressin + Albumin (first-line, best evidence)
• Midodrine + Octreotide + Albumin (alternative)
• TIPS: Bridge to transplant
• Liver transplantation: Only curative treatment

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5.6 Hepatic Encephalopathy

• Grade 0: No abnormality
• Grade I: Trivial lack of awareness, euphoria/anxiety, shortened attention span
• Grade II: Lethargy, disorientation for time, obvious personality change, asterixis
• Grade III: Somnolence but arousable, gross disorientation, asterixis
• Grade IV: Coma (no response to verbal/painful stimuli)

1. Identify + treat precipitant
2. Lactulose 30–60 mL BD–TDS → 2–3 soft stools/day
3. Rifaximin 550 mg BD (reduces recurrence)
4. Protein restriction no longer recommended — adequate protein intake 1.2–1.5 g/kg/day

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