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Outpatient management of cirrhosis.

Cirrhosis is an advanced stage of liver disease caused by a variety of insults to hepatic parenchyma including infections, autoimmune processes, genetic disorders and toxins. It is characterized by extensive fibrosis with nodule formation and interruption of normal hepatic blood flow. The major complications of cirrhosis are ascites, gastroesophageal varices-related bleeding, hepatic encephalopathy, hepatorenal syndrome and hepatocellular carcinoma (HCC). Therefore, ultimate treatment of decompensated cirrhosis is liver transplantation. Hence, cirrhotics with the above complications should be referred to a hepatologist at a liver transplant center for transplant evaluation and possible listing for liver transplant. Some of the complications such as variceal bleeding and refractory ascites require hospitalization and inpatient treatment, but many of the complications can be managed on an outpatient basis. Proper outpatient care decreases the number of hospitalizations leading to decreased morbidity and mortality until the patient receives liver transplant. Cirrhotics without any complications are usually managed by screening for HCC and periodic measurement of liver tests, including coagulation profiles, until the development of complications. Abstinence from alcohol is imperative even if the cirrhosis is not a result of alcohol. Other hepatotoxins and nonsteroidal anti-inflammatory drugs should also be avoided. Acetaminophen up to 2 g/d may safely be used in most cirrhotics for pain control. Ascites is the most common complication of cirrhosis, which is the result of portal hypertension. There is no evidence that fluid removal improves survival, but patients feel better and it may also protect against bacterial infection of ascitic fluid. It also decreases the amount of energy wasted in heating the fluid and reduces the risk of cellulites and chances of hernia formation or diaphragmatic rupture associated with tense ascites. The dietary sodium restriction and diuretics with a goal weight loss of 0.5kg/d-1 kg/d (if peripheral edema is present) is the usual treatment. Higher weight loss may lead to an increased intravascular volume loss since the absorptive capacity of the peritoneal membrane is about 300 to 500cc/d. Small bowel dysmotility and bacterial overgrowth have been documented to be related to spontaneous bacterial peritonitis (SBP). A recent study has shown that the addition of a prokinetic agent, cisapride, to the prophylactic regimen of norfloxacin reduces the incidence of SBP in highrisk cirrhosis patients. However, safety, efficacy and longterm data on cisapride among cirrhotic patients are lacking. Therefore, due to potential cardiotoxicity, the prophylactic use of cisapride for SBP is not recommended at present time. Cirrhotics who develop SBP should be admitted to the hospital and treated with IV antibiotics and albumin since addition of albumin decreases the short-term mortality-related renal insufficiency. Hypokalemia should be avoided since it can increase renal ammonia production and precipitate hepatic encephalopathy. Variceal bleeding is the major cause of morbidity and mortality in patients with liver cirrhosis. Each episode of bleeding carries a 30% risk of mortality. In cirrhosis, elevated portal pressure results from a combination of increased portal inflow due to splanchnic arteriolar vasodilatation and elevated resistance to outflow through distorted hepatic sinusoids. Varices develop in response to portal hypertension to decompress the portal vein and return blood to systemic circulation. All patients with cirrhosis should undergo diagnostic endoscopy to document the presence of varices and to determine their risk of variceal hemorrhage. Propranolol or nadolol can be recommended for primary prophylaxis of variceal bleeding. Multiple studies have shown that endoscopic variceal ligation (EVL) is as good as nonselective -blockers for primary prophylaxis of esophageal variceal bleeding without having an increased risk for complications. However, EVL has been recommended for high-risk patients who are intolerant to -blocker therapy due to side effects such as dizziness, hypotension, fatigue, sexual dysfunction, bronchoconstriction and heart failure, considering the invasive nature of EVL. Furthermore, whether there is a benefit of adding -blockers to patients who have undergone EVL for primary prophylaxis has not been well studied, but EVL may be considered in high risk patients who can tolerate -blocker therapy. Hepatic encephalopathy (HE) results from portosystemic venous shunting. In addition to accumulation of ammonia, various other mechanisms such as the production of false neurotransmitters, activation of central -aminobutyric acid– benzodiazepine receptors by ligands of endogenous origin, altered cerebral metabolism, zinc deficiency, deposition of manganese in the basal ganglia and disturbed activity of Na / K ATPase, have been implicated in the pathogenesis of HE. Management of HE includes treatment of the precipitating cause and oral lactulose titrated to produce 2 to 3 bowel movements per day. Currently, rifaximin is often used for HE in cirrhotics who are intolerant to lactulose due to an From the Department of Internal Medicine, Weiss Memorial Hospital, and the Section of Gastroenterology, Department of Medicine, Center for Liver Diseases, The University of Chicago, Chicago, IL.