Cirrhosis is a chronic hepatic disease characterized by diffuse destruction and fibrotic regeneration of hepatic cells. As necrotic tissue yields to fibrosis, this disease alters liver structure and normal vasculature, impairs blood and lymph flow, and ultimately causes hepatic insufficiency.
Cirrhosis is the 10th most common cause of death in the United States and is most common among people ages 45 to 75. Most cases are a result of alcoholism, but toxins, biliary destruction, hepatitis, and a number of metabolic conditions may stimulate the destruction process.
Cirrhosis is sometimes caused by hepatitis, or by eating or drinking harmful chemicals. The most common cause of cirrhosis is drinking too much alcohol. This is called alcoholic cirrhosis.
Women who drink too much alcohol may be at greater risk of developing alcoholic cirrhosis than men who drink too much. If you drink alcohol, you need to tell your family doctor so he or she can check for signs of cirrhosis, especially if you have any of the symptoms listed below.
Signs and Symptoms
Signs and symptoms are similar for all types, regardless of the cause. However, clinical manifestations vary depending on when in the course of the disease the patient seeks treatment.
In the early stage, the patient may experience only vague signs and symptoms, but typically he complains of abdominal pain, diarrhea, fatigue, nausea, and vomiting. Later, as the disease progresses, he may complain of chronic dyspepsia, constipation, pruritus, and weight loss. He may report a tendency for easy bleeding, such as frequent nosebleeds, easy bruising, and bleeding gums.
The history may reveal alcoholism or other diseases or conditions, such as acute viral hepatitis, biliary tract disorders, heart failure, recent blood transfusions, and viral infections.
In a head-to-toe approach, inspection reveals these common signs: telangiectasis on the cheeks; spider angiomas on the face, neck, arms, and trunk; gynecomastia; umbilical hernia; distended, abdominal blood vessels; ascites; testicular atrophy; palmar erythema; clubbed fingers; thigh and leg edema; ecchymosis; and jaundice.
In the early phase of the disease, palpation reveals that the liver is large and firm with a sharp edge. Later, scar tissue causes the liver to decrease in size; at this point, if the liver is palpable, its edge is nodular. Palpation also reveals an enlarged spleen.
A thorough workup consisting of diagnostic and laboratory tests is required to confirm the diagnosis, establish the type of cirrhosis, and pinpoint complications.
Liver biopsy is the definitive test for cirrhosis, revealing hepatic tissue destruction and fibrosis.
Abdominal X-rays show liver size and cysts or gas in the biliary tract or liver; liver calcification; and massive ascites. Computed tomography and liver scans are used to determine liver size, identify liver masses, and visualize hepatic blood flow and obstruction. Esophagogastroduodenoscopy reveals bleeding esophageal varices, stomach irritation or ulceration, and duodenal bleeding and irritation.
Blood studies show elevated levels of liver enzymes (alanine aminotransferase, aspartate aminotransferase, total serum bilirubin, and indirect bilirubin). Total serum albumin and protein levels decrease; prothrombin time is prolonged. Hemoglobin, hematocrit, and serum electrolyte levels decrease. Vitamins A, C, and K are deficient.
Urine and stool studies disclose increased urine levels of bilirubin and urobilinogen; fecal urobilinogen levels decrease.
The goal of therapy is to remove or alleviate the underlying cause of cirrhosis, prevent further liver damage, and prevent or treat complications. Vitamins and nutritional supplements promote healing of damaged hepatic cells and improve the patient's nutritional status. Sodium consumption is usually restricted to 500 mg/day and liquid intake is limited to 1 ,500 ml/day to help manage ascites and edema.
Drug therapy requires special caution because the cirrhotic liver can't detoxify harmful substances efficiently. Antacids may be prescribed to reduce gastric distress and decrease the potential for GI bleeding. Potassium-sparing diuretics, such as furosemide, may be used to reduce ascites and edema. However, diuretics require careful monitoring because fluid and electrolyte imbalance may precipitate hepatic encephalopathy. Vasopressin may be indicated for esophageal varices. Alcohol is prohibited, and sedatives should be avoided.
In patients with ascites, paracentesis may be used as a palliative treatment to relieve abdominal pressure. Surgical intervention may be required to divert ascites into venous circulation; if so, a peritoneovenous shunt is used. Shunt insertion results in weight loss, decreased abdominal girth, increased sodium excretion from the kidneys, and improved urine output.
To control bleeding from esophageal varices or other GI hemorrhage, nonsurgical measures are attempted first. These include gastric intubation and esophageal balloon tamponade. In gastric intubation, a tube is inserted and the stomach is lavaged until the contents are clear. If the bleeding is assessed as a gastric ulcer, antacids and histamine antagonists are administered.
In esophageal balloon tamponade, bleeding vessels are compressed to stanch blood loss from esophageal varices. Several forms of balloon tamponade are available, including the Sengstaken-Blakemore tube method, the esophagogastric tube method, and the Minnesota tube method.
Sclerotherapy is performed if the patient continues to experience repeated hemorrhagic episodes despite conservative treatment. A sclerosing agent is injected into the oozing vessels. This agent traumatizes epithelial tissue, which causes thrombosis and leads to sclerosis. If bleeding from the varices doesn't stop within 2 to 5 minutes, a second injection is given below the bleeding site. Sclerotherapy may also be performed prophylactically on non bleeding varices.
As a last resort, portal-systemic shunts may be used for patients with bleeding esophageal varices and portal hypertension. Surgical shunting procedures decrease portal hypertension by diverting a portion of the portal vein blood flow away from the liver. These procedures are seldom performed because they can result in bleeding, infection, and shunt thrombosis.
Massive hemorrhage requires blood transfusions. To maintain blood pressure, crystalloid or colloid volume expanders are administered until the blood is available.
Although not all cases of cirrhosis are preventable, the following measures can greatly reduce your risk:
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