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 ||Download (.pdf) TABLE 157-1 Causes of Cirrhosis
|Alcoholism ||Cardiac cirrhosis |
|Chronic viral hepatitis ||Inherited metabolic liver disease |
| Hepatitis B || Hemochromatosis |
| Hepatitis C || Wilson’s disease |
|Autoimmune hepatitis || α1-Antitrypsin deficiency |
|Nonalcoholic steatohepatitis || Cystic fibrosis |
|Biliary cirrhosis ||Cryptogenic cirrhosis |
| Primary biliary cholangitis || |
| Primary sclerosing cholangitis || |
| Autoimmune cholangiopathy || |
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.
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 ||Download (.pdf) TABLE 157-2 Complications of Cirrhosis
|Portal hypertension ||Coagulopathy |
| Gastroesophageal varices || Factor deficiency |
| Portal hypertensive gastropathy || Fibrinolysis |
| Splenomegaly, hypersplenism || Thrombocytopenia |
| Ascites ||Bone disease |
| Spontaneous bacterial peritonitis || Osteopenia |
|Hepatorenal syndrome || Osteoporosis |
| Type 1 || Osteomalacia |
| Type 2 ||Hematologic abnormalities |
|Hepatic encephalopathy || Anemia |
|Hepatopulmonary syndrome || Hemolysis |
|Portopulmonary hypertension || Thrombocytopenia |
|Malnutrition || Neutropenia |
TABLE 157-3Child-Pugh Classification of Cirrhosis ||Download (.pdf) TABLE 157-3 Child-Pugh Classification of Cirrhosis
| ||POINTS TOWARD TOTAL SCORE |
|FACTOR ||UNITS ||1 ||2 ||3 |
|Serum bilirubin ||µmol/L ||<34 ||34–51 ||>51 |
| ||mg/dL ||<2.0 ||2.0–3.0 ||>3.0 |
|Serum albumin ||g/L ||>35 ||30–35 ||<30 |
| ||g/dL ||>3.5 ||3.0–3.5 ||<3.0 |
|Prothrombin time ||seconds prolonged ||<4 ||4–6 ||>6 |
| ||INRa ||<1.7 ||1.7–2.3 ||>2.3 |
|Ascites || ||None ||Easily controlled ||Poorly controlled |