Portal Hypertension

Portal Hypertension

Pathophysiology

Portal hypertension (PHT) occurs when portal venous pressure exceeds 12 mmHg. The most common cause in the developed world is hepatic cirrhosis (alcohol, NAFLD, chronic viral hepatitis), in which fibrosis and regenerative nodules increase hepatic vascular resistance. In cirrhosis, >80% of portal blood may bypass the liver via portosystemic shunts (PSS), markedly impairing hepatic function.

Porto-Systemic Shunts and Varices

When portal pressure rises, blood is forced through pre-existing collateral veins between the portal and systemic venous systems, which dilate into varices:

• Oesophageal varices: left gastric (coronary) vein → azygos vein (systemic). The thin-walled varices in the distal oesophagus are the most dangerous.
• Caput medusae: para-umbilical veins (re-canalised ligamentum teres) → epigastric veins (systemic) → radiating veins around umbilicus.
• Anorectal varices: superior rectal veins (portal) ↔ inferior/middle rectal veins (systemic, drain to IVC).

Variceal rupture: Laplace's law: wall tension T = Pressure × Radius. Thin-walled, high-pressure, large-radius oesophageal varices are prone to rupture, especially triggered by food or retching. Bleeding oesophageal varices have 30–50% mortality per episode. Management: terlipressin (splanchnic vasoconstriction), endoscopic band ligation, TIPS (transjugular intrahepatic portosystemic shunt).

Hepatic Encephalopathy

In cirrhosis with PSS, gut-derived ammonia (from protein catabolism and urease-producing bacteria) bypasses the liver → enters systemic circulation → crosses blood-brain barrier. Astrocytes (the main NH₃-metabolising cells in the brain) convert NH₃ + glutamate → glutamine → accumulates in astrocytes → osmotic swelling → cerebral oedema, astrocyte dysfunction → clinical features: asterixis (flapping tremor), confusion, drowsiness, coma. Precipitants: GI bleed (protein load), high protein diet, constipation, infection, alcohol, sedatives (benzodiazepines), TIPS procedure. Management: lactulose (traps NH₄⁺ in colon by acidifying), rifaximin (reduces urease-producing bacteria), dietary protein moderation.

Ascites

Portal hypertension → increased hydrostatic pressure in splanchnic and hepatic sinusoids + hypoalbuminaemia (reduced hepatic synthesis) → Starling forces favour fluid extravasation into the peritoneal cavity → ascites. Renal Na⁺ and water retention (RAAS activation, reduced renal perfusion) perpetuates fluid accumulation. Management: Na⁺ restriction, spironolactone + furosemide, therapeutic paracentesis, TIPS, liver transplant.