portalhypertensionrelated

Portal hypertension refers to elevated pressure within the portal venous system, most commonly defined by a hepatic venous pressure gradient above 5 mm Hg, with clinically significant portal hypertension typically exceeding 10 mm Hg. The most frequent cause is cirrhosis from chronic liver disease; other etiologies include portal vein thrombosis, Budd-Chiari syndrome, schistosomiasis, and cardiac conditions that impair portal flow. The pathophysiology involves increased resistance to portal inflow due to liver parenchymal scarring or vascular obstruction, together with splanchnic vasodilation that raises portal inflow. This milieu promotes the development of collateral vessels, esophageal and gastric varices, and fluid accumulation in the abdomen.

Common complications include esophageal and gastric variceal bleeding, ascites, portal hypertensive gastropathy, hypersplenism with splenomegaly, hepatic encephalopathy, and hepatorenal syndrome. Varices arise as collateral channels to bypass high portal pressure, while ascites results from sodium and water retention and reduced oncotic pressure.

Diagnosis combines clinical assessment with imaging and endoscopy. Doppler ultrasound evaluates portal and hepatic blood flow; hepatic venous pressure gradient measurement is the reference standard for quantifying portal hypertension. Endoscopy detects varices and guides treatment. Management aims to reduce portal pressure and address complications: nonselective beta-blockers or endoscopic variceal ligation to prevent variceal bleeding, transjugular intrahepatic portosystemic shunt (TIPS) for refractory cases, diuretics and paracentesis for ascites, antibiotics and albumin for spontaneous bacterial peritonitis, and liver transplantation for eligible patients with advanced disease.

Prognosis varies with liver function and complication burden, emphasizing a multidisciplinary approach and strategies to prevent liver injury and its sequelae.