Anatomy & Variants

• Lobar/segmental anatomy: Cantlie’s line (GB fossa → IVC) divides right/left lobes. Couinaud segments I–VIII; I = caudate (separate inflow; drains directly to IVC).
• Portal triad (hepatoduodenal ligament): common bile duct (lateral), portal vein (posterior), proper hepatic artery (medial).
  Pearl: Pringle maneuver (porta clamp) does not stop hepatic vein bleeding.
• Hepatic artery variants (common): replaced RHA off SMA (behind pancreas, posterolateral to CBD); replaced LHA off left gastric (gastrohepatic ligament).
• Venous drainage: three hepatic veins → IVC; middle often joins left before IVC; accessory right hepatic veins common.
• Foramen of Winslow: anterior–portal triad; posterior–IVC; inferior–duodenum; superior–caudate.

Physiology, Bilirubin & Bile

• Synthesis/storage: urea made in liver; stores fat-soluble vitamins + B12. Not synthesized in liver: vWF, factor VIII (endothelium).
• Zone sensitivity: Zone III (centrilobular) most ischemia-sensitive.
• Resection tolerance: up to ~75% of normal liver with adequate function (see FLR below).
• Bilirubin pathway: heme → biliverdin → unconjugated bilirubin → hepatic conjugation → biliary excretion → urobilinogen → urine urobilin.
  • Unconjugated ↑: hemolysis, impaired uptake/conjugation (Gilbert, Crigler–Najjar).
  • Conjugated ↑: secretion/excretion defects (hepatitis, obstruction).
  • Hepatitis labs: very high AST/ALT, modest Alk Phos. Obstruction: very high Alk Phos, modest transaminases.
• Bile composition: bile salts, phospholipids (lecithin), cholesterol, bilirubin, proteins. GB concentrates bile; lecithin emulsifies fat.

Viral Hepatitis

• Acute: avoid surgery; fulminant failure (B, D, E > A, C).
• Chronic risk: B, C, D → chronic hepatitis ± HCC.
• Key: HBV vaccine → anti-HBs only; recovery → anti-HBc + anti-HBs; HCV curable (DAAs). HEV pregnancy: fulminant risk. HBV+HDV: highest mortality.
  Pearl: No biopsy needed for classic HCC imaging + elevated AFP.

Liver Failure, Ascites & Encephalopathy

• Cirrhosis: most common failure; best synthetic marker PT/INR.
• Fulminant failure: ~80% mortality; use King’s criteria for transplant.
• Encephalopathy: triggers—GI bleed, infection (SBP), electrolytes, meds. Tx: lactulose (2–3 stools/day), protein restriction initially (≤70 g/d), consider BCAA; antibiotics only if infection.
• Ascites: portal HTN lymph leak. Tx: Na/fluid restriction, spironolactone, paracentesis with albumin replacement (~1 g/100 mL removed), TIPS if refractory; SBP prophylaxis after SBP or variceal bleed.
• Hepatorenal syndrome: stop diuretics, albumin + vasoconstrictors; definitive = transplant.
• SBP: PMN >250; E. coli common. Tx: 3rd-gen cephalosporin; expect improvement ≤48 h.
  Pearl: Post-partum liver failure + ascites → consider hepatic vein thrombosis.

Portal Hypertension & Varices

• Resistance sites: presinusoidal (schisto, PVT), sinusoidal (cirrhosis), postsinusoidal (Budd–Chiari, constrictive pericarditis/CHF).
• Thresholds: portal (wedged) >10 mmHg significant; rupture ≈ HVPG ≥12 mmHg.
• Collaterals: gastroesophageal, rectal, umbilical.
• Bleed management: resuscitate + antibiotics; airway if needed; octreotide → banding; TIPS if uncontrolled or early rebleed. NSBB for secondary prophylaxis; vasopressin+NTG if necessary.
• Shunts: TIPS (fast, encephalopathy risk); distal splenorenal (Warren) for Child A with bleeding only; partial PV–IVC interposition when TIPS unavailable and ascites predominant.
• Umbilical hernia in ascites: elective repair after ascites control; mesh if clean; no mesh for contaminated/urgent cases; aggressive postop ascites control.
  Pearl: Ascites control best reduces recurrence/complications.

Portal Hypertension – Treatment Map

Hepatic Vascular Disorders

• Budd–Chiari: RUQ pain, hepatosplenomegaly, ascites, failure; polycythemia vera risk. Dx venous-phase imaging/biopsy. Tx: shunt above obstruction; catheter tPA if acute.
• Splenic vein thrombosis: isolated gastric varices; cause pancreatitis; Tx: splenectomy if bleeding.
• Portal vein thrombosis: extrahepatic; hypercoagulable; ascites without failure; varices common (kids: MCC massive hematemesis). Tx: heparin if acute (avoid during active bleed); shunt if needed.

Liver Abscesses

• Pyogenic (>80%): right lobe, biliary source common; E. coli #1. Dx aspiration. Tx: CT-guided drain + antibiotics (op if unstable/failure).
• Amebic: solitary right-lobe; travel (Mexico) or ETOH; serology+. Tx: metronidazole (drain only if refractory/rupture).
• Echinococcus: double-walled cyst; don’t aspirate (anaphylaxis). Preop albendazole → careful excision; scolicidal agent; avoid spillage.
• Schistosomiasis: eosinophilia; water exposure; can cause variceal bleeding. Tx: praziquantel + variceal care.

Tumors (Benign & Malignant)

• Hemangioma: most common benign; peripheral→central fill; bright T2; avoid biopsy. Tx: observe (resect if symptomatic). Rare Kasabach–Merritt.
• FNH: women; central scar; Kupffer cells (sulfur colloid uptake). Tx: observe.
• Adenoma: OCPs/anabolics; right lobe; ~10% malignant; bleed risk ↑ if >4–5 cm. Tx: stop OCPs (regress?) → resect if >4 cm/symptomatic/no regression; rupture → embolize then resect.
  Pearl: Sulfur colloid uptake—FNH +, adenoma –.
• HCC: risks HBV/HCV, alcohol cirrhosis, hemochromatosis, A1AT, aflatoxin, PSC; lung = most common mets.
  • Dx: arterial hyperenhancement with portal/delayed washout + ↑AFP → no biopsy.
  • Resection: solitary, no major vascular invasion, adequate function. FLR: no cirrhosis ≥25%; Child A ~30–40%; use PVE if marginal. Margin goal ~1 cm.
  • Transplant: early stage with moderate–severe cirrhosis; Milan: 1 < 5 cm or ≤3 all <3 cm; no macrovascular/extrahepatic spread.
  • Locoregional: ablation (<5 cm), TACE (>5 cm or unresectable), EBRT if not ablation/TACE candidate.
  • Fibrolamellar: young, noncirrhotic; neurotensin marker; better prognosis (recurs often).
• Metastases: far more common than primary (≈20:1). CRC mets resection if adequate FLR → ~35% 5-yr survival.

HCC – Resection vs Transplant vs Bridge

Anatomy & Physiology

• GB position: under segments IV–V. Cystic artery from right hepatic within Calot’s triangle (cystic duct lateral, CHD medial).
• Duct blood supply: longitudinal at 3 & 9 o’clock (retroduodenal GDA medially; right hepatic laterally).
• Normal diameters: CBD ≤6 mm (≤10 mm post-chole); GB wall ≤4 mm; pancreatic duct ≤4 mm.
• Sphincter of Oddi: morphine contracts, glucagon relaxes.
• Ducts of Luschka can leak postop; Rokitansky–Aschoff sinuses with chronic pressure.

Gallstones & Cholecystitis (incl acalculous/emphysematous)

• Stones: ~10% prevalence; most asymptomatic → observe.
  • Cholesterol (US majority): GB stasis/nucleation; mostly in GB.
  • Black pigment: hemolysis/cirrhosis/TPN.
  • Brown pigment (primary CBD): infection (β-glucuronidase); evaluate ampulla/diverticula; many need sphincteroplasty.
• Biliary colic: transient cystic-duct obstruction; resolves 4–6 h → elective chole if stones on US.
• Acute calculous cholecystitis: stones + wall >4 mm/pericholecystic fluid; HIDA most sensitive. Tx: early lap chole if fit; no “cool-off” benefit.
  • Too ill: cholecystostomy → interval chole.
  • Pregnancy: lap chole (prefer 2nd tri), open Hasson entry, low insufflation, left tilt.
  • Cirrhosis: chole once compensated (experienced liver surgeon; correct coagulopathy).
• Acalculous cholecystitis: burns/TPN/trauma/ICU; stasis/ischemia; Tx: chole or percutaneous drain if unstable.
• Emphysematous cholecystitis: diabetics; Clostridium perfringens; urgent source control.

Choledocholithiasis, Cholangitis & Obstruction (ERCP/MRCP/IOC)

• Strong suspicion (stone on imaging, cholangitis, bili >3, dilated CBD ≥6–7 mm): pre-op ERCP for clearance (IOC/lap CBD exploration if ERCP unavailable).
• Moderate suspicion (abnl LFTs, mild bili ↑, gallstone pancreatitis without cholangitis): MRCP or IOC (ERCP if obstruction confirmed).
• Low suspicion: proceed to chole without further testing.
• IOC stone: flush + glucagon (×2 max); transcystic exploration if feasible; otherwise lap CBD exploration or post-op ERCP per resources.
• Cholangitis: Charcot triad ± Reynolds pentad. Tx: fluids + antibiotics → emergent ERCP with sphincterotomy/extraction; PTC if ERCP fails; perform chole before discharge.
  Pearl: Normal GGT has very high NPV for choledocholithiasis.
• RYGB anatomy: if GB present → chole + intra-op CBD exploration; if GB absent → double-balloon ERCP or lap transgastric ERCP.

Choledocholithiasis – Workup Summary

Bile Duct Injury & Stricture

• Etiology: most after lap chole; excess cephalad fundus retraction/misidentification.
• Intra-op troubleshooting: if hepatic ducts don’t fill on IOC → withdraw catheter, flush, Trendelenburg; convert to open if injury suspected.
• Partial (<50%) CBD injury: possible primary repair; otherwise hepaticojejunostomy (HJ) (do not try to reach duodenum).
• Post-op bile leak: drain collection; if bilious → ERCP + sphincterotomy/stent (cystic stump/small injuries/Luschka).
• Complete transection: PTC to decompress → HJ (≤7 d: immediate if feasible; >7 d: delay 6–8 wk to allow tissue maturation).
• Benign late stricture: ischemia after chole most common; MRCP roadmap; durable repair = choledochojejunostomy (after excluding malignancy).

Benign GB (Polyps, Adenomyomatosis, Cholesterolosis)

• Polyps management:
  • ≤5 mm: observe.
  • 6–9 mm: annual US; operate if high-risk (stones, symptoms, sessile, rapid growth, infundibular polyp, wall abnormality, age >50).
  • ≥10–18 mm: lap chole.
  • >18 mm: treat as GB cancer.
• Adenomyomatosis (RA sinuses): not premalignant; chole if symptomatic.
• Cholesterolosis: speckled mucosa; ceftriaxone can cause sludge/jaundice.
• Prophylactic chole: consider in transplant or RYGB candidates with stones.

Gallbladder Polyp – Management Algorithm

*High-risk features: gallstones, symptoms, sessile morphology, rapid growth, infundibular location, wall abnormality, age >50.

Malignancy & Choledochal Cysts

• Gallbladder adenocarcinoma: RFs—stones (#1), polyps ≥10 mm, porcelain GB (risk lower than once thought), typhoid, PSC/IBD; liver most common metastasis.
  • Incidental T1a (lamina propria): chole only.
  • ≥T1b (muscularis): chole + wedge of IVb/V + portal LND; extend for margins. No port-site excision.
• Cholangiocarcinoma: intrahepatic or extrahepatic; RFs—PSC, choledochal cysts, stones, liver flukes, HBV/HCV.
  • Dx: MRCP/contrast MRI ± laparoscopy; resect if no distant or prohibitive nodal disease (avoid SMA/celiac nodes in extrahepatic disease).
  • Hilar (Klatskin): often unresectable; distal → Whipple. Transplant not for multifocal cholangio.
• Choledochal cysts (Todani): majority extrahepatic; malignant potential ~15%.
  • I: excision + HJ. II: diverticulum excision ± Roux. III: transduodenal excision or sphincteroplasty. IVa: hepatic resection + biliary reconstruction. IVb: excision + HJ. V (Caroli): transplant (partial resection if localized).

Cholestatic Diseases (PSC / PBC)

• PSC: men; UC association; multifocal strictures; pruritus/jaundice; risks—cirrhosis, cholangiocarcinoma. Tx: cholestyramine/UDCA symptom control; dilations/stents PRN; transplant for failure.
• PBC: women; antimitochondrial Ab+; cholestasis → portal HTN. Tx: UDCA ± cholestyramine; transplant for failure.

Special Situations & Hemobilia

• Gallstone ileus: cholecystoenteric fistula → SBO (IC valve common). Tx: proximal enterotomy and stone extraction; avoid same-setting chole + fistula takedown.
• Post-lap chole shock: early = hemorrhage (cystic-artery clip); late = septic shock from clipped CBD → cholangitis.
• Pneumobilia: prior ERCP/sphincterotomy most common; also gallstone ileus/infection.
• Hemobilia: hepatic artery–bile duct fistula (trauma, PTC). UGIB with blood from ampulla; Tx: angioembolization.