[Gr. kirrhos, tawny + -osis]
A chronic disease of the liver characterized by scarring with loss of normal hepatic architecture and areas of ineffective regeneration. Clinical symptoms result from loss of functioning liver cells and increased resistance to blood flow through the liver (portal hypertension).
SYN: SEE: hepatic cirrhosis
SEE: alcoholism; SEE: encephalopathy; SEE: esophageal varix; SEE: hepatic; SEE: liver
Between 0.3% and 1.0% of the U.S. population has cirrhosis of the liver. The disease is responsible for about 100,000 hospitalizations and 32,000 deaths in the U.S. each year.
In the U.S., alcoholism and chronic viral hepatitis (esp. chronic hepatitis B or C infection) are the most common causes of the illness. Other causes are autoimmune (primary biliary cirrhosis), biliary (sclerosing cholangitis), cardiac (caused by right-sided heart failure), nutritional (fatty liver), genetic (alpha-1-antitrypsin deficiency, hemochromatosis, Wilson disease), or toxic (excess exposure to drugs or agents such as vitamin A, carbon tetrachloride, and methotrexate).
SYMPTOMS AND SIGNS
Fatigue and malaise are common, but nonspecific symptoms of the illness. Anorexia, early satiety, dyspepsia, altered bowel habits, and easy bruising and bleeding also are reported often. Alterations in mental status, personality, or behavior (hepatic encephalopathy) are common but vary in severity and may not be noticed initially. Pruritus is reported when significant jaundice is present. Signs of the illness may include ascites; asterixis; bleeding from the gums, nose, or gastroesophageal varices; mousy breath odor; edema; jaundice; and an irregular liver edge with hepatic enlargement (the liver may shrink when complete loss of function is present). Multiple skin findings may include abnormal pigmentation, palmar erythema, spider angiomas, ecchymoses, and dilated abdominal veins. Limited thoracic expansion caused by hepatomegaly or ascites and endocrine changes such as menstrual irregularities, testicular atrophy, gynecomastia, and loss of chest and axillary hair may also be present.
ASCITES CAUSED BY CIRRHOSIS
The likelihood of the disease increases in patients who have abnormal liver function tests (abnormal ratios of alanine aminotransferase to serum aspartate aminotransferease), abnormal coagulation tests (prolongation of prothrombin time or international normalized ratio), and progressively decreasing platelet counts. Cirrhosis is diagnosed by liver biopsy, upper GI endoscopy (the presence of esophageal varices), or measurements of the venous pressures leading into and out of the liver; or noninvasively with radiologic studies such as Doppler ultrasonography, CT or magnetic resonance imaging, a fibroscan test, or an AST/platelet ratio >2.
IMPACT ON HEALTH
Prognosis in cirrhotic patients depends on the Child-Pugh Score (an assessment instrument that accounts for the presence of encephalopathy, ascites, blood coagulation, serum bilirubin, and albumin). Patients with normal Child-Pugh scores (rated “Class A”) can be expected to live between 15 and 20 years. Class C patients have a life expectancy of 1 to 3 years. Class B patients have intermediate life expectancies and are considered to be those most likely to benefit from liver transplantation.
Liver transplantation may be curative, but its use is limited by the number of donor organs available. Shunting procedures to divert blood flow from the hepatic to the systemic circulation may improve portal hypertension and its consequences.
Daily weights are obtained, fluid and electrolyte balance is monitored, and abdominal girth is measured. The ankles, sacrum, and scrotum are also assessed for dependent edema. The stools are inspected for color, amount, and consistency. Stools and vomitus are tested for occult blood. Surface bleeding sites are monitored frequently, and direct pressure is applied to the site if bleeding occurs. The patient is observed for indications of internal bleeding, such as anxiety, epigastric fullness, weakness, and restlessness; and vital signs are monitored as appropriate. Dependent areas are exercised and elevated, and skin breakdown is prevented by eliminating soaps and by using lubricating oils and lotions for bathing. The patient is frequently repositioned. The patient should avoid straining at stool and should use stool softeners as necessary and prescribed. Violent sneezing and nose blowing should also be avoided. A soft toothbrush or sponge stick and an electric razor are used. Aspirin, acetaminophen, or other over-the-counter medications should not be taken without the physician's knowledge. Alcohol or products containing alcohol are prohibited.
Both patient and family may require referral to alcohol cessation and related support groups. Prescribed therapies, including sodium and fluid restriction, dietary modifications, supplemental vitamin therapy, antiemetics, and diuretics, are administered. The patient's response to prescribed therapies is assessed, and he or she is instructed in their use and any adverse reactions. Care is taken to avoid drugs metabolized by the liver, as the cirrhotic liver is increasingly unable to detoxify such substances. A regimen of moderate exercise alternating with periods of rest is prescribed; energy conservation measures are explained; small, frequent, nutritious meals are recommended; and exposure to infections should be avoided. Appropriate safety measures are instituted, esp. if the patient demonstrates hepatic encephalopathy needs to be frequently reoriented to time and place. Salt-poor albumin is administered and paracentesis performed, if prescribed, to control ascites. The patient is physically and psychologically prepared for required medical and surgical procedures.
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