Alcoholic cirrhosis of liver is diffuse fine scaring with loss of liver cells and small regenerating nodules (micronodular)
Pathology With continued alcohol intake, liver cells are destroyed and fibroblasts appear at the site of injury and stimulate collagen formation. Septae of connective tissue appear in the periportal and peri-central zones which eventually connects portal triad and central vein. The remaining liver cells which are surrounded by connective tissue, regenerate and form nodules. Usually, cell loss exceeds regeneration. The liver shrinks and becomes hard and nodular.
Clinical Features It is usually silent in 10 percent of cases. The clinical manifestations are like cirrhosis of liver. Dupuytren’s contracture due to fibrosis of palmar fascia with resulting flexion contracture of the digits and parotid swelling are associated with alcoholism rather than cirrhosis.
Laboratory Tests
- Anemia may occur from GI bleeding, nutritional deficiency (folate and B12 deficiency), hypersplenism, direct bone marrow suppressant effect of alcohol and hemolysis due to acanthoytosis.
- Leucocytosis is usually present. However, leucopenia and thrombocytopenia could occur due to hypersplenism.
- Alkaline phosphatase may be elevated.
- SGOT is high but rarely more than 300 units. Unlike in viral hepatitis where SGPT is higher compared to SGOT, in alcoholic hepatitis SGOT is much higher than SGPT. This is because of greater inhibition of SGPT synthesis by ethanol which may be partially reversed by pyridoxal phosphate.
- Serum prothrombin is prolonged due to reduced synthesis of Vitamin K dependent clotting factors.
- Serum albumin is usually reduced due to impairment in hepatic protein synthesis. Globulins are high due to non-specific stimulation of reticulo-endothelial system. Hyperbilirubinemia may be present due to decompensation.
- Hypomagnesemia and hypophosphatemia may occur due to dietary deficiency. Hypokalemia may occur due to hyperaldosteronism (aldosterone is normally destroyed in liver). Similar to alcoholic hepatitis.
- Elevated blood ammonia may also occur due to impaired liver function and shunting of portal venous blood around the cirrhotic liver.
Prognosis
In milder cases, clinical recovery can occur completely.
Repeated bouts of alcoholic hepatitis may lead to irreversible progressive liver injury, abstinence from alcohol can reduce long term morbidity and mortality. Marked hyperbilirubinemia, elevated creatinine, elevated prothrombin time (more than 1-5 times normal), ascites and encephalopathy are associated with poor short term prognosis. The in-hospital mortality of these patients is more than 50 percent.
Treatment
Bed rest till improvement
Diet: 2000 calories with about 100 gm proteins. Fats and carbohydrates as much as the patient tolerates. Salt is restricted if edema or ascites is present. Supplement Vitamin B complex should be given.
Spironolactone: This is an aldosterone antagonist which antagonizes the effects of excess aldosterone present in cirrhosis due to inadequate elimination of aldosterone by liver. 100 mg per day may be given.
Removal of cause: Withdrawal of alcohol, D-penicillamine for Wilson’s disease, etc.
Corticosteroids and immunosuppressants: This may be helpful in patients with active post-hepatitis cirrhosis.
Treatment of Complications
