Variceal hemorrhage

Patients with previously stable cirrhosis who develop acute encephalopathy often have an identifiable precipitating event that can account for the increased production and/or decreased elimination of these toxins. Infections, variceal hemorrhage, renal insufficiency, electrolyte abnormalities, and increased dietary protein have all been associated with acute development of HE. 

Sharara AI, Rockey DC. Gastroesophageal variceal hemorrhage. N Engl J Med 2001 345 669-681. 

Garcia-Tsao G Current management of the complications of cirrhosis and portal hypertension Variceal hemorrhage, ascites, and spontaneous bacterial peritonitis. Gastroenterology 2001 120 726-748. 

Clinical improvement or resolution of acute complications, such as variceal bleeding, and resolution of hemodynamic instability for an episode of acute variceal hemorrhage. 

Fig. 21-2 presents an algorithm for the management of variceal hemorrhage. Evidence-based recommendations for selected treatments are presented in Table 21-4. 

FIGURE 21-2. Management of acute variceal hemorrhage. (ABCs, airway, breathing, and circulation TIPS, transjugular intrahepatic portosystemic shunt.)... 

Vasopressin, alone or in combination with nitroglycerin, can no longer be recommended as first-line therapy for the management of variceal hemorrhage. Vasopressin causes nonselective vasoconstriction and can result in hypertension, severe headaches, coronary ischemia, myocardial infarction, and arrhythmias. 

Antibiotic therapy for prevention of SBP should be considered in all patients who are at high risk for this complication (those who experience a prior episode of SBP or variceal hemorrhage, and those with low-protein ascites). 

Several drugs are available that reduce portal pressures. These may be used in the short term for the treatment of active variceal hemorrhage or long term to reduce the risk of hemorrhage. 

Nevens F A critical comparison of drug therapies in currently used therapeutic strategies for variceal hemorrhage. Aliment Pharmacol Ther 2004 20(Suppl 3) 18. 

This patient illustrates a complicated clinical course of oq-antitrypsin deficiency. Our patient had liver disease that presented during infancy and developed into hepatic cirrhosis. He exhibited most of the complications of cirrhosis, including portal hypertension with ascites, hyperammonemia, malnutrition, and variceal hemorrhage. These complications of cirrhosis are not unique to a,-antitrypsin deficiency, but it is important to note the potential severity of the liver disease associated with this condition. 

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