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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.


TABLE 157-1Causes of Cirrhosis


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.

Laboratory Findings

Anemia (microcytic due to blood loss, macrocytic due to folate deficiency; hemolytic called Zieve’s syndrome), pancytopenia (hypersplenism), prolonged PT, rarely overt DIC; hyponatremia, hypokalemic alkalosis, glucose disturbances, hypoalbuminemia.


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) (see Table 157-2 and Chaps. 44, 45, and 158).

TABLE 157-2Complications of Cirrhosis
TABLE 157-3Child-Pugh Classification of Cirrhosis

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