- Causes
- Clinical Manifestations
- Diagnostic Studies
- Complications
- Alcoholic Liver Disease
- Fatty Liver
- Alcoholic Hepatitis
- Other Metabolic Consequences of Alcoholism
- Adverse Prognostic Factors
Cirrhosis is defined histopathologically and has a variety of causes, clinical features, and complications. In cirrhosis, there is the development of liver fibrosis to the point that there is architectural distortion with the formation of regenerative nodules, which results in decreased liver function.
May be absent, with cirrhosis being incidentally found at surgery.
Anorexia, nausea, vomiting, diarrhea, vague RUQ pain, fatigue, weakness, fever, jaundice, amenorrhea, impotence, infertility.
Spider angiomas, palmar erythema, jaundice, scleral icterus, parotid and lacrimal gland enlargement, clubbing, Dupuytren's contracture, gynecomastia, testicular atrophy, hepatosplenomegaly, ascites, gastrointestinal bleeding (e.g., varices), hepatic encephalopathy.
Depends on clinical setting. Serum: HBsAg, anti-HBc, anti-HBs, anti-HCV, anti-HDV, Fe, total iron-binding capacity, ferritin, antimitochondrial antibody (AMA), smooth-muscle antibody (SMA), anti-liver/kidney microsomal (anti-LKM) antibody, ANA, ceruloplasmin, α1 antitrypsin (and phenotyping); abdominal ultrasound with Doppler study, CT or MRI (may show cirrhotic liver, splenomegaly, collaterals, venous thrombosis). Definitive diagnosis often depends on liver biopsy (percutaneous, transjugular, or open).
The Child-Pugh scoring system has been used to predict the severity of cirrhosis and the risk of complications (Table 157-3 Child-Pugh Classification of Cirrhosis) (see Table 157-2 Complications of Cirrhosis and Chaps. 44 Jaundice and Evaluation of Liver Function, 45 Ascites, and 158 Portal Hypertension).
Excessive alcohol use can cause fatty liver, alcoholic hepatitis, cirrhosis. Alcoholic cirrhosis accounts for about 40% of the deaths due to cirrhosis. History of excessive alcohol use often denied. Severe forms (hepatitis, cirrhosis) associated with ingestion of 160 g/d for 10-20 years; women more susceptible than men and develop advanced liver disease with less alcohol intake. Hepatitis B and C may be cofactors in the development of liver disease. Malnutrition may contribute to development of cirrhosis.
Often presents as asymptomatic hepatomegaly and mild elevations in biochemical liver tests. Reverses on withdrawal of ethanol; does not lead to cirrhosis.
Clinical presentation ranges from asymptomatic to severe liver failure with jaundice, ascites, GI bleeding, and encephalopathy. Typically anorexia, nausea, vomiting, fever, jaundice, tender hepatomegaly. Occasional cholestatic picture mimicking biliary obstruction. Aspartate aminotransferase (AST) usually <400 U/L and more than twofold higher than alanine aminotransferase (ALT). Bilirubin and WBC may be elevated. Diagnosis defined by liver biopsy findings: hepatocyte swelling, alcoholic hyaline (Mallory-Denk bodies), infiltration of PMNs, necrosis of hepatocytes, pericentral venular fibrosis.
Other Metabolic Consequences of Alcoholism 
Increased NADH/NAD ratio leads to lactic acidemia, ketoacidosis, hyperuricemia, hypoglycemia, hypomagnesemia, hypophosphatemia. Also mitochondrial dysfunction, induction of microsomal enzymes resulting in altered drug metabolism, lipid peroxidation leading to membrane damage, hypermetabolic state; many features of alcoholic hepatitis are attributable to toxic effects of acetaldehyde and cytokines (interleukins 1 and 6, and TNF, released because of impaired detoxification of endotoxin).
Critically ill pts with alcoholic hepatitis have 30-day mortality rates >50%. Severe alcoholic hepatitis characterized by PT >5 × above control, bilirubin >137 µmol/L (>8 mg/dL), hypoalbuminemia, azotemia. A discriminant function can be calculated as 4.6 × (pt's PT in seconds) (control PT in seconds) + serum bilirubin (mg/dL). Values ≥32 are associated with poor prognosis. A Model for End-Stage Liver Disease (MELD) score > 21 is also associated with significant mortality in alcoholic hepatitis. Ascites, variceal hemorrhage, encephalopathy, hepatorenal syndrome predict a poor prognosis.
| TREATMENT | ||
Alcoholic Liver DiseaseAbstinence is essential; 8500- to 12,500-kJ (2000- to 3000-kcal) diet with 1 g/kg protein (less if encephalopathy). Daily multivitamin, thiamine 100 mg, folic acid 1 mg. Correct potassium, magnesium, and phosphate deficiencies. Transfusions of packed red cells, plasma as necessary. Monitor glucose (hypoglycemia in severe liver disease). Pts with severe alcoholic hepatitis defined as a discriminant function >32 or MELD >20 should be given prednisone 40 mg/d or prednisolone 32 mg/d PO for 4 weeks followed by a taper. In one trial pentoxifylline demonstrated improved survival, primarily due to a decrease in hepatorenal syndrome but subsequent trials failed to find increased benefit with use of this agent. Liver transplantation may be an option in carefully selected pts with end-stage cirrhosis. |