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Quick Test posted on 5.11.11:
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Liver Failure
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Hepatic cirrhosis remains a major public health problem worldwide, with and annual mortality of approximately 23,000 per year in the United States alone. The incidence of cirrhosis is increasing, due in large measure to hepatitis C, and at present is the third-most common cause of death in men in the fifth decade of life.
Alcohol abuse remains the leading cause of cirrhosis in most Western countries. Alcohol exerts direct toxic effects on the liver that are magnified in the presence of protein and other dietary deficiencies that are often present. Even still, cirrhosis develops in a small minority of patients who abuse alcohol. Alcohol induces a specific cytochrome P450 in the liver (ie, P450 2E1) that participates in its metabolism to acetaldehyde, which has a number of deleterious effects, including antibody formation, decreased DNA repair, enzyme inactivation, and alterations in microtubules, mitochondria, and plasma membranes. Acetaldehyde also promotes glutathione depletion, free radical-mediated toxicity, lipid peroxidation, and hepatic collagen synthesis. Hepatic steatosis and alcoholic hepatitis are stages of alcoholic liver injury that may precede cirrhosis. Alcoholic hyalin, a glycoprotein, accumulates in centrilobular hepatocytes of patients with alcoholic hepatitis. There is some evidence that immunologic responses to alcoholic hyalin may be important in the pathogenesis of cirrhosis.
Collagen deposition in cirrhosis results from increased fibroblastic activity as well as from repair following hepatocellular injury and necrosis. The ultimate result is a liver containing regenerative nodules and connective tissue septa linking portal fields with central canals.
The natural history of cirrhosis is difficult to predict. Once the diagnosis has been established, up to 30% of patients die within a year from hepatic failure or complications of portal hypertension, of which bleeding esophageal varices is the most feared. In newly diagnosed cirrhotics, the chances of dying within the subsequent 2–3 years are influenced by the status of liver function (as reflected by the Child-Pugh classification), the presence of varices, and the portal pressure. A group of cirrhotics with varices followed by the Boston Interhospital Liver Group experienced a 1-year death rate of 66%. Cirrhotics without varices may benefit substantially by abstaining from alcohol. Bleeding episodes occur in up to 40% of all patients with cirrhosis, and the initial episode of variceal hemorrhage is fatal in 50% or more. At least two thirds of those who survive their initial hemorrhage will bleed again, and the risk of dying from the second is similarly high. It is principally for such patients that portal decompressive procedures are recommended.
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| Table 24–4. Measures to Control Acute Bleeding from Esophageal Varices. |
| Medical |
| 1. Vasopressin, terlipressin |
| 2. Somatostatin analogues |
| Mechanical |
| 3. Balloon tamponade |
| Interventional, nonsurgical |
| 4. Endoscopic sclerotherapy |
| 5. Transhepatic embolization and sclerotherapy |
| Surgical |
| 6. Emergency portasystemic shunts |
| 7. Esophageal transection and reanastomosis |
| 8. Esophagogastric devascularization |
| 9. Suture ligation of varices |
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