Varices, particularly esophageal varices, are one of the end results of portal hypertension.
- Fibrosis and regenerative nodules cause impedance to splanchnic flow through the liver and lead to formation of portosystemic collaterals, particularly with the gastric and esophageal venous systems.
- Rupture of the high-pressure collaterals that are formed is a highly lethal and feared complication of portal hypertension.
- Portal hypertension is diagnosed by measurement of the wedged hepatic venous pressure (WHVP). Patients with esophageal varices can be expected to have HVPGs of at least 10 to 12 mm Hg.
- Esophagogastroduodenoscopy is the gold-standard procedure for diagnosing varices.
- The presence of varices correlates with the severity of underlying liver disease.
- Nonselective β-blockers reduce portal pressure by two mechanisms: a decrease in cardiac output (β-1) and splanchnic vasoconstriction (β-2).
- Acute variceal bleed should be managed with a combination of volume resuscitation, correction of severe coagulopathy, pharmacologic manipulation of portal pressure, and endoscopic variceal ligation.
- Although the temptation to vigorously volume resuscitate and completely correct all coagulation abnormalities can be overwhelming in this setting, it should be resisted.
- Resistant or early recurrent variceal bleeding occurs in about 10% to 20% of patients. A measured HVPG >20 mm Hg is a risk factor for failure of standard therapy.