7. CIRRHOSIS

GENERAL CONSIDERATION

     The concept of cirrhosis which evolved during the past few decades includes only those cases in which hepatocellular injury leads to both fibrosis and nodular regeneration throughout the liver. These features delineate cirrhosis as a serious and irreversible disease that is characterized not only by variable degrees of hepatic cell dysfunction but also by portosystemic shunting and portal hypertension. Fibrosis alone, regardless of its severity, is excluded by the previous definition, also excluded by definition are the earlier stages of chronic biliary obstruction and hemochromatosis, neither of which forms regenerating nodules until late.
     An important part of this concept is the realization that the type of cirrhosis
changes with the passage of time in any one patient. Terms such as "portal" and
"postnecrotic" refer not so much to separate disease states with different causes as to stages in the evolution of cirrhosis.
     Attempts to classify cirrhosis on the basis of cause or pathogenesis are usually
unsuccessful when applied to individual patients. Such persons often represent
end-stage cirrhosis, enabling only speculation about the evolutionary process. The use of purely anatomic  and practical classification. One such classification that is currently employed divides cirrhosis into micronodular, mixed, and macronodular
forms. It is important, however, to remember that these are stages of development
rather than separate diseases.
     A. Micronodular cirrhosis is the form in which the regenerating nodulars are no larger than the original lobules, i.e. approximately lmm in diameter or less. It has been suggested that this feature results from the persistence of the offending agent (alcohol), a substance that prevents regenerative growth.
     B. Macronodular cirrhosis is characterized by larger nodulars, which can measure several centimeters in diameter. This form corresponds more or less to postnecrotic cirrhosis but does not necessarily follow episodes of massive necrosis and stromal collapse.
     C. Mixed macro- and micronodular cirrhosis points up the fact that the features of cirrhosis are highly variable and not always easy to classify. In any case, the configuration of the liver is determined by the mixture of liver cell death and regeneration as well as the deposition of fat, iron and fibrosis.
     Finally, it should be emphasized that there does exist a limited relationship
between anatomic types and etiology as well as between anatomic types and prognosis. For example, alcoholics who continue to drink tend to have that form of cirrhosis that remains micronodular for long periods. The presence of fatty micronodular cirrhosis, although not an infallible criterion, is strongly suggestive of chronic alcoholism. On the other hand, liver cell carcinoma not uncommonly arises in macronodular rather than micronodular cirrhosis. Although speculative and subject to dispute, it is possible that this propensity to malignancy is related either to the increased regeneration in macronodular cirrhosis or to the longer period required for the process to develop.
     In traditional Chinese medicine, the condition is thought to be due to liver stasis or invasion of the stomach and spleen by hepatic Qi.
CLINICAL MANIFESTATIONS
     Micronodular cirrhosis may cause no symptoms for long periods both at onset and later in the course (compensated phase). The onset of symptoms may be insidious or less often, abrupt. Weakness, fatigability, and weight loss are common. In advanced cirrhosis, anorexia is usually present and may be extreme with associated nausea and occasional vomiting. Abdominal pain may be present and is related either to hepatic enlargement and stretching of Glisson's capsule or to the presence of ascites. Diarrhea is frequently present, but some patients are constipated. Menstrual abnormalities (usually amenorrhea), impotence, loss of libido, sterility, and painfully enlarged breasts in men (rare) may occur. Hematemesis is the presenting symptom in 15% to 25% of patients.
     In 70% of cases, the liver is enlarged, palpable, firm if not hard, and has a blunt edge. Skin manifestations consist of spider nevi (usually only on the upper half of the body), palmar erythema (mottled redness of the thenar and hypothenar eminences), telangiectases of exposed areas, and evidence of vitamin deficiencies (glossitis and cheilosis). Weight loss, wasting and the appearance of chronic illness are present. Jaundice, usually not an initial sign, is mild at first, increasing in severity during the later stages of the disease. Ascites, pleural effusion, peripheral edema and purpuric lesions are late findings. The precoma state (asterixis, tremor, dysarthrias, delirium and drowsiness) and encephalopathy or coma also reflect the presence of alcoholic hepatitis. The superficial vein of the abdomen and thorax are dilated and reflect the intrahepatic obstruction to portal blood flow.
DIAGNOSIS
     Essentials of diagnosis.
     ?A past history of vital hepatitis, alcohol drink, schistosomiasis, deficient
nutrition.
     ?The liver is enlarged, palpable, firm if not hard, and has a blunt edge.
     ?Blood chemical studies show primarily hepatocellular dysfunction, reflected
by elevations of SGOT (AST), alkaline phosphatase and bilirubin. Serum albumin is
low, whereas gamma globulin is increased.
     ?Liver biopsy shows cirrhosis.
     ?Symptoms and signs of portal hypertension.
TREATMENT
I. Treatment in Western medicine.
     The principles of treatment include abstinence from alcohol and adequate rest,
especially during the acute phase. The diet should be palatable with adequate calories and protein (75 to 100g/d) and in the stage of fluid retention. Sodium and fluid restriction. In the presence of hepatic precoma or coma, protein intake should be low or drastically reduced. Vitamin supplementation is desirable.
     A. Ascites and edema due to sodium retention, hypoproteinemia and portal
hyper