Clinical meaning
Esophageal varices develop as a consequence of portal hypertension, most commonly from hepatic cirrhosis. Normal portal venous pressure is 5-10 mmHg; when portal pressure exceeds 10 mmHg (clinically significant portal hypertension), blood is diverted through portosystemic collateral vessels including the submucosal veins of the distal esophagus and gastric fundus. These thin-walled veins dilate progressively under sustained elevated pressure, forming varices. Variceal rupture occurs when wall tension exceeds wall strength, as described by LaPlace's law (wall tension = pressure x radius / wall thickness): as varices enlarge (increasing radius) and their walls thin, the risk of rupture increases dramatically. Portal pressure >12 mmHg (measured as hepatic venous pressure gradient, HVPG) is the threshold for variceal hemorrhage. Variceal bleeding is massive and life-threatening, with mortality rates of 15-20% per episode and 6-week mortality of up to 30% in patients with decompensated cirrhosis. The hemorrhage presents as hematemesis (bright red blood or coffee-ground emesis), melena or hematochezia, and signs of hypovolemic shock (tachycardia, hypotension, altered mental status). Cirrhotic patients are particularly vulnerable because they also have impaired hepatic synthesis of clotting factors (prolonged PT/INR), thrombocytopenia from hypersplenism, and platelet dysfunction, making hemostasis more difficult to achieve.