Major complications of cirrhosis include ascites, spontaneous bacterial peritonitis, hepatic encephalopathy, portal hypertension, variceal bleeding, and hepatorenal syndrome. Diagnostic studies on ascitic fluid should include a differential leukocyte count, total protein level, a serum-ascites albumin gradient, and fluid cultures. Therapy consists of sodium restriction, diuretics, and complete abstention from alcohol. Patients with ascitic fluid polymorphonuclear leukocyte counts of 250 cells per [mm.sup.3] or greater should receive empiric prophylaxis against spontaneous bacterial peritonitis with cefotaxime and albumin. Patients who survive an episode of spontaneous bacterial peritonitis should receive long-term prophylaxis with norfloxacin or trimethoprim/sulfamethoxazole. Patients with gastrointestinal hemorrhage and cirrhosis should receive norfloxacin or trimethoprim/sulfamethoxazole twice daily for seven days. Treatment of hepatic encephalopathy is directed toward improving mental status levels with lactulose; protein restriction is no longer recommended. Patients with cirrhosis and evidence of gastrointestinal bleeding should undergo upper endoscopy to evaluate for varices. Endoscopic banding is the standard treatment, but sclerotherapy with vasoconstrictors (e.g., octreotide) also may be used. Prophylaxis with propranolol is recommended in patients with cirrhosis once varices have been identified. Transjugular intrahepatic portosystemic shunt has been effective in reducing portal hypertension and improving symptoms of hepatorenal syndrome, and can reduce gastrointestinal bleeding in patients with refractory variceal hemorrhage. When medical therapy for treatment of cirrhosis has failed, liver transplantation should be considered. Survival rates in transplant recipients have improved as a result of advances in immunosuppression and proper risk stratification using the Model for End-Stage Liver Disease and Child-Turcotte-Pugh scoring systems.
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Long Island Technology Briefs: September 30, 2005
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Part I of this two-part series outlines the diagnosis and evaluation of cirrhosis and chronic liver failure. (1) This article, part II, discusses complications and treatment. Major complications of cirrhosis include ascites, spontaneous bacterial peritonitis, hepatic encephalopathy, portal hypertension, variceal bleeding, and hepatorenal syndrome.
Ascites
Ascites is defined as the pathologic accumulation of fluid in the peritoneal cavity. Approximately 85 percent of patients with ascites have cirrhosis, and the remaining 15 percent have a nonhepatic cause of fluid retention. (2,3) The American Association for the Study of Liver Diseases recommends a diagnostic abdominal paracentesis be performed and ascitic fluid obtained from patients with clinically evident ascites. (3) Paracentesis with ascitic fluid culture in blood culture bottles should be performed before the initiation of antibiotics to determine a true infection.
The initial laboratory investigation of ascitic fluid should include a differential leukocyte count, a total protein level, and a serum-ascites albumin gradient (SAAG). The SAAG is a useful prognosticator of portal pressure; it is calculated by subtracting the ascitic albumin concentration from the serum albumin concentration obtained on the same day. (4) If the SAAG is 1. lorazepam. 1 g per dL (11 g per L) or greater, there is a high likelihood of portal hypertension; if it is less than 1.1 g per dL, other causes of ascites should be explored, including peritoneal carcinomatosis, tuberculous peritonitis, and pancreatic ascites (Figure 1 (2)). (2,5) The ascitic fluid total protein level typically has been used in defining ascitic fluid as transudative (protein content less than 2.5 g per dL [25 g per L]) or exudative (protein content of 2.5 g per dL or greater) and to help identify patients at higher risk of developing spontaneous bacterial peritonitis. However, this method is flawed because many patients with spontaneous bacterial peritonitis, in which ascitic fluid is infected, have a low rather than high ascitic fluid total protein level, and many fluid samples from patients with portal hypertension secondary to heart failure have a high rather than the expected low ascitic fluid total protein level. (6)
First-line treatment of patients with cirrhotic ascites consists of sodium restriction (i.e., no more than 2,000 mg per day) and diuretics (e.g., oral spironolactone [Aldactone], furosemide [Lasix]), as well as complete abstention from alcohol (Table 1 (3,7-10)). (3) Fluid restriction is unnecessary unless serum sodium is less than 120 to 125 mEq per L (120 to 125 mmol per L). Patients who are sensitive to diuretics should be treated with sodium restriction and oral diuretics rather than with serial paracenteses, unless the ascites is refractory to these therapies or infection is suspected. (3) Postparacentesis albumin infusion is unnecessary for a single paracentesis of less than 4 to 5 L, but for large-volume paracenteses, an albumin infusion of 8 to 10 g per liter of fluid removed can be considered. (3) Referral for liver transplantation should be expedited for patients with refractory ascites. Transjugular intrahepatic portosystemic shunt (TIPS) should be considered in patients with refractory ascites who may require a transplant, whereas a peritoneovenous shunt should be considered in patients with refractory ascites who are not candidates for paracenteses, transplant, or TIPS. (3)