Cirrhosis and fibrosis
Cirrhosis and fibrosis: Excerpt from Professional Guide to Diseases (Eighth Edition)
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. The prognosis is better in noncirrhotic forms of hepatic fibrosis, which cause minimal hepatic dysfunction and don’t destroy liver cells.
Causes and incidence
These clinical types of cirrhosis reflect its diverse etiology:
❑ Portal, nutritional, or alcoholic (Laennec’s) cirrhosis, the most common type, occurs in 30% to 50% of cirrhotic patients, up to 90% of whom have a history of alcoholism. Liver damage results from malnutrition, especially of dietary protein, and chronic alcohol ingestion. Fibrous tissue forms in portal areas and around central veins.
❑ Biliary cirrhosis (15% to 20% of patients) results from injury or prolonged obstruction.
❑ Postnecrotic (posthepatic) cirrhosis (10% to 30% of patients) stems from various types of hepatitis.
❑ Pigment cirrhosis (5% to 10% of patients) may result from disorders such as hemochromatosis.
❑ Cardiac cirrhosis (rare) refers to liver damage caused by right-sided heart failure.
❑ Idiopathic cirrhosis (about 10% of patients) has no known cause.
Noncirrhotic fibrosis may result from schistosomiasis or congenital hepatic fibrosis or may be idiopathic.
Signs and symptoms
Clinical manifestations of cirrhosis and fibrosis are similar for all types, regardless of the cause. Early indications are vague, but usually include GI signs and symptoms (anorexia, indigestion, nausea, vomiting, constipation, or diarrhea) and a dull abdominal ache. Major and late signs and symptoms develop as a result of hepatic insufficiency and portal hypertension:
❑ Respiratory — pleural effusion and limited thoracic expansion due to abdominal ascites, interfering with efficient gas exchange and leading to hypoxia
❑ Central nervous system — progressive signs or symptoms of hepatic encephalopathy — lethargy, mental changes, slurred speech, asterixis (flapping tremor), peripheral neuritis, paranoia, hallucinations, extreme obtundation, and coma
❑ Hematologic — bleeding tendencies (nosebleeds, easy bruising, and bleeding gums) and anemia
❑ Endocrine — testicular atrophy, menstrual irregularities, gynecomastia, and loss of chest and axillary hair
❑ Skin — severe pruritus, extreme dryness, poor tissue turgor, abnormal pigmentation, spider angiomas, palmar erythema, and possibly jaundice
❑ Hepatic — jaundice, hepatomegaly, ascites, edema of the legs, hepatic encephalopathy, and hepatorenal syndrome comprise the other major effects of full-fledged cirrhosis
❑ Miscellaneous — musty breath, enlarged superficial abdominal veins, muscle atrophy, pain in the right upper abdominal quadrant that worsens when the patient sits up or leans forward, palpable liver or spleen, and temperature of 101° to 103° F (38.3° to 39.4° C). Bleeding from esophageal varices results from portal hypertension.
Diagnosis
CONFIRMING DIAGNOSIS Liver biopsy, the definitive test for cirrhosis, detects destruction and fibrosis of hepatic tissue.
Liver scan shows abnormal thickening and a liver mass. Cholecystography and cholangiography visualize the gallbladder and the biliary duct system, respectively; splenoportal venography visualizes the portal venous system. Percutaneous trans-hepatic cholangiography differentiates extrahepatic from intrahepatic obstructive jaundice and discloses hepatic pathology and the presence of gallstones.
Laboratory findings that are characteristic of cirrhosis include:
❑ decreased white blood cell count, hemoglobin level and hematocrit, albumin, serum electrolyte levels (sodium, potassium, chloride, and magnesium), and cholinesterase
❑ elevated levels of globulin, serum ammonia, total bilirubin, alkaline phosphatase, serum aspartate aminotransferase, serum alanine aminotransferase, and lactate dehydrogenase and increased thymol turbidity
❑ anemia, neutropenia, and thrombocytopenia, characterized by prolonged prothrombin and partial thromboplastin times
❑ deficiencies of folic acid, iron, and vitamins A, B12, C, and K.
Treatment
Treatment is designed to remove or alleviate the underlying cause of cirrhosis or fibrosis, prevent further liver damage, and prevent or treat complications. The patient may benefit from a high-calorie and moderate- to high-protein diet, but developing hepatic encephalopathy mandates restricted protein intake. In addition, sodium is usually restricted to 200 to 500 mg/day and fluids to 1 to 1½ qt (1 to 1.5 L)/day.
If the patient’s condition continues to deteriorate, he may need tube feedings or total parenteral nutrition. He may also need supplemental vitamins — A, B complex, D, and K — to compensate for the liver’s inability to store them and vitamin B12, folic acid, and thiamine for deficiency anemia. Rest, moderate exercise, and avoidance of exposure to infections and toxic agents are essential.
Drug therapy requires special caution because the cirrhotic liver can’t detoxify harmful substances efficiently. When absolutely necessary, vasopressin may be prescribed for esophageal varices, and diuretics may be given for edema. However, diuretics require careful monitoring because fluid and electrolyte imbalance may precipitate hepatic encephalopathy. Encephalopathy is treated with lactulose. Antibiotics are used to decrease intestinal bacteria and reduce ammonia production, which causes encephalopathy. Coagulopathy may be treated with blood products or vitamin K.
Low-protein diets are controversial. They aid in managing acute hepatic encephalopathy but are rarely necessary in chronic conditions because of the underlying protein-calorie malnutrition.
Paracentesis and infusions of salt-poor albumin, in addition to fluid and salt restriction, may alleviate ascites. Surgical procedures include treatment of varices by upper endoscopy with banding or sclerosis, splenectomy, esophagogastric resection, and splenorenal or portacaval anastomosis to relieve portal hypertension. (See Portal hypertension and esophageal varices, page 758, and Circulation in portal hypertension, page 759.)
Alert If cirrhosis progresses and becomes life-threatening, a liver transplant should be considered.
Special considerations
The patient with cirrhosis needs close observation, first-rate supportive care, and sound nutritional counseling.
❑ Check the patient’s skin, gums, stools, and vomitus regularly for bleeding. Apply pressure to injection sites to prevent bleeding. Warn him against taking nonsteroidal anti-inflammatory drugs, straining at stool, and blowing his nose or sneezing too vigorously. Suggest using an electric razor and soft toothbrush.
❑ Observe the patient closely for signs of behavioral or personality changes. Report increasing stupor, lethargy, hallucinations, or neuromuscular dysfunction. Awaken him periodically to determine his level of consciousness. Watch for asterixis, a sign of developing hepatic encephalopathy.
❑ To assess fluid retention, weigh the patient and measure abdominal girth at least daily, inspect his ankles and sacrum for dependent edema, and accurately record intake and output. Carefully evaluate the patient before, during, and after paracentesis; this drastic loss of fluid may induce shock.
❑ To prevent skin breakdown associated with edema and pruritus, avoid using soap when you bathe the patient; instead, use lubricating lotion or moisturizing agents. Handle him gently, and turn and reposition him often to keep his skin intact.
❑ Tell the patient that rest and good nutrition will conserve his energy and decrease metabolic demands on the liver. Urge him to eat frequent, small meals. Stress the need to avoid infections and abstain from alcohol. Refer him to Alcoholics Anonymous, if necessary.
Pictures
Book Source Details
- Book Title: Professional Guide to Diseases (Eighth Edition)
- Author(s): Springhouse
- Year of Publication: 2005
- Copyright Details: Professional Guide to Diseases (Eighth Edition), Copyright © 2005 Lippincott Williams & Wilkins.
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