Clinical meaning
Portal hypertension in cirrhosis results from increased intrahepatic resistance (structural: fibrosis, nodular distortion; dynamic: stellate cell contraction from decreased nitric oxide and increased endothelin-1) and increased portal blood flow (splanchnic vasodilation from excessive nitric oxide production in the mesenteric circulation). When the hepatic venous pressure gradient (HVPG) exceeds 10 mmHg, portosystemic collaterals develop at sites of portal-systemic anastomosis: esophageal varices (left gastric vein → esophageal veins), caput medusae (paraumbilical veins), hemorrhoids (superior → inferior rectal veins), and retroperitoneal shunts. Splanchnic vasodilation reduces effective arterial blood volume, triggering RAAS activation, sympathetic nervous system stimulation, and ADH release, causing renal sodium and water retention (ascites) and ultimately hepatorenal syndrome.
Diagnosis & workup
Diagnostics & workup: - HVPG measurement: gold standard; >5 mmHg = portal hypertension; >10 mmHg = clinically significant (variceal formation); >12 mmHg = variceal bleeding risk; >20 mmHg = treatment failure risk - Upper endoscopy: grade varices (small vs large), identify red wale signs (high bleeding risk) - Doppler ultrasound: portal vein diameter (>13 mm suggests portal HTN), flow direction (hepatofugal = reversed flow away from liver) - Platelet count/spleen diameter ratio: <909 has high sensitivity for esophageal varices - Serum-ascites albumin gradient (SAAG): ≥1.1 g/dL confirms portal hypertension as cause of ascites; <1.1 suggests non-portal hypertension cause (malignancy, TB, nephrotic syndrome) - Serum ammonia level: correlates loosely with encephalopathy; trends more useful than single values