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ESSENTIAL CONCEPTS
Either nonselective β-blockers or esophageal variceal ligation are first-line treatment for primary prophylaxis of variceal hemorrhage in patients with medium to large esophageal and high-risk small varices.
Endoscopic variceal ligation (EVL) is an alternative to pharmacologic therapy for patients intolerant to β-blockers.
Management of acute variceal hemorrhage includes resuscitation to conservative PRBC transfusion thresholds, antibiotic prophylaxis, use of vasoactive agents, and endoscopic treatment with band ligation. Early transjugular intrahepatic portosystemic shunt (TIPS) should be considered for high-risk patients.
Balloon tamponade or an esophageal stent can be used as a bridge to TIPS or surgical shunt therapy.
The combination of a nonselective β-blocker and esophageal variceal ligation is first-line treatment for prevention of recurrent variceal hemorrhage.
Hepatic venous pressure gradient (HVPG) measurements aid in prognosis and therapy.
TIPS, surgical shunt procedures, or liver transplantation are treatment options for patients who do not respond to medical therapy.
Gastric varices that are cardiofundal in location (isolated gastric varices Type I and gastroesophageal varices Type II) are best treated with endoscopic ultrasound (EUS) guided injection therapy with hemostatic coils and/or cyanoacrylate glue or direct endoscopic injection with glue. Gastroesophageal varices Type I (esophageal varices extending into the lesser curvature) can be treated as esophageal varices (banding ligation) or injection therapy.
TIPS is the preferred rescue procedure for uncontrolled variceal bleeding and can be first-line therapy for high-risk patients.
Portal hypertensive gastropathy (PHG) is usually mild to moderate and bleeding can be chronic or acute.
Chronic bleeding from PHG is treated with β-blockers or TIPS based on the severity of hemorrhage.
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General Considerations
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Chronic liver disease and cirrhosis are among the leading causes of mortality in the United States. Cirrhosis is further defined into two clinically important categories: compensated and decompensated cirrhosis. The distinction between these two stages reflects the presence or absence of cirrhosis complications resulting from clinically significant portal hypertension (defined by a HVPG of ≥10 mm Hg). The main decompensating events of cirrhosis are development of ascites, hepatic encephalopathy or variceal hemorrhage. Portal hypertension and its consequences are progressively debilitating complications of cirrhosis (Table 47–1). Variceal hemorrhage, spontaneous bacterial peritonitis, and the hepatorenal syndrome are chiefly responsible for the high morbidity and mortality rates in patients with cirrhosis.
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