Cirrhosis
Cirrhosis: Excerpt from Handbook of Diseases
A chronic hepatic disease, cirrhosis is characterized by diffuse destruction and fibrotic regeneration of hepatic cells. As necrotic tissue yields to fibrosis, cirrhosis alters liver structure and normal vasculature, impairs blood and lymph flow and, ultimately, causes hepatic insufficiency. (See Circulation in portal hypertension, page 198.)
Cirrhosis is a serious, irreversible disease that’s the eleventh most common cause of death in the United States. The prognosis is better in noncirrhotic forms of hepatic fibrosis, which cause minimal hepatic dysfunction and don’t destroy liver cells.
Causes
Cirrhosis has various causes, depending on the type.
Hepatocellular disease
Postnecrotic cirrhosis accounts for 10% to 30% of patients and stems from various types of hepatitis (such as types A, B, C, D viral hepatitis) or toxic exposures.
Laënnec’s cirrhosis — also called portal, nutritional, or alcoholic cirrhosis — is the most common type and is commonly caused by hepatitis C. Liver damage results from malnutrition (especially dietary protein) and overuse of alcohol. Fibrous tissue forms in portal areas and around central veins.
Autoimmune disease, such as sarcoidosis and chronic inflammatory bowel disease, may result in cirrhosis.
Cholestatic diseases
Cholestatic diseases include diseases of the biliary tree (biliary cirrhosis resulting from bile duct diseases suppressing bile flow) and sclerosing cholangitis.
Metabolic diseases
Metabolic diseases include disorders such as Wilson’s disease, alpha1-antitrypsin deficiency, and hemochromatosis (pigment cirrhosis).
Other types of cirrhosis
Other types of cirrhosis include Budd-Chiari syndrome, cardiac cirrhosis, and cryptogenic cirrhosis. Cardiac cirrhosis is rare; the liver damage results from right-sided heart failure. Cryptogenic refers to cirrhosis of unknown cause.
Signs and symptoms
Signs and symptoms of cirrhosis and fibrosis are similar for all types, regardless of cause. Early indications are insidious and vague but usually include weakness, fatigue, muscle cramps, weight loss, GI signs and symptoms (anorexia, indigestion, nausea, vomiting, constipation, diarrhea), and abdominal pain (which may be attributed to an enlarged liver).
Major and late signs and symptoms develop as a result of hepatic insufficiency and portal hypertension and include the following:
❑ respiratory — pleural effusion and limited thoracic expansion because of abdominal ascites, interfering with efficient gas exchange and leading to hypoxia
❑ central nervous system — progressive signs and 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, bleeding gums), anemia, and hematemesis
❑ endocrine — testicular atrophy, menstrual irregularities, gynecomastia, loss of chest and axillary hair, loss of libido, and sterility
❑ skin — severe pruritus, extreme dryness, poor tissue turgor, abnormal pigmentation, spider nevi (on upper half of body), palmar erythema, jaundice, and peripheral edema
❑ hepatic — jaundice, hepatomegaly, ascites, edema of the legs, hepatic encephalopathy, and hepatorenal syndrome constitute 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, splenomegaly, and wasting appearance of chronic illness. Fever may be present and usually associated with portal hepatitis, spontaneous bacterial peritonitis, or cholangitis. Bleeding from esophageal and rectal varices results from portal hypertension.
Diagnosis
A liver biopsy, the definitive test for cirrhosis, detects destruction and fibrosis of hepatic tissue. A liver scan shows abnormal thickening and, possibly, a liver mass.
Plain films of the abdomen may reveal hepatic or splenic enlargement. Ultrasonography can aid in the assessment of liver size and the detection of ascites or hepatic enlargement. Doppler ultrasonography is used to evaluate patency of the splenic, portal, and hepatic veins. Computed tomography with I.V. contrast or magnetic resonance imaging with serum alpha-fetoprotein levels can help with further assessment of liver nodules. A biopsy of suspicious liver nodules or masses can be performed to check for cancer. Esophagogastroscopy can be used to detect causes of bleeding in the esophagus, stomach, and proximal duodenum and confirm the presence of varices.
The following laboratory findings are characteristic of cirrhosis:
❑ decreased platelet count, decreased hematocrit, and decreased levels of hemoglobin, albumin, electrolytes (sodium, potassium, chloride, and magnesium), and folate
❑ elevated levels of globulin, serum ammonia, total bilirubin, alkaline phosphatase, serum aspartate aminotransferase, serum alanine aminotransferase, and lactate dehydrogenase
❑ increased thymol turbidity
❑ coagulation abnormalities characterized by prolonged prothrombin and partial thromboplastin times.
Clinical tip The best indications of hepatic function are prothrombin time and cholesterol and albumin levels.
Treatment
The goals of treatment include removing or alleviating the underlying cause of cirrhosis or fibrosis, preventing further liver damage, and preventing or treating complications.
Dietary measures
The patient may benefit from a high-calorie and moderate- to high-protein diet, but if the patient develops hepatic encephalopathy, protein intake must be restricted. In addition, sodium is usually restricted to 400 to 800 mg/day; fluids, to 1,000 to 1,500 ml/day.
If the patient’s condition continues to deteriorate, he may need tube feedings or hyperalimentation. Other supportive measures include supplemental vitamins — A, B complex, D, and K — to compensate for the liver’s inability to store them and vitamin B, folic acid, and thiamine for deficiency anemia. Rest, moderate exercise, and avoidance of exposure to infections and toxic agents are essential.
Drug therapy
With cirrhosis, drug therapy requires special caution because the cirrhotic liver can’t detoxify harmful substances efficiently. Alcohol is prohibited; sedatives should be avoided or prescribed with great care. Acetaminophen is especially hepatotoxic, particularly when combined with alcohol.
When absolutely necessary, an antiemetic, such as trimethobenzamide or benzquinamide, may be given for nausea; vasopressin, for esophageal varices; and a diuretic, such as furosemide or spironolactone, for edema. However, if the patient receives a diuretic, careful monitoring is necessary; fluid and electrolyte imbalance may precipitate hepatic encephalopathy.
Vitamin K may be given for bleeding tendencies due to hypoprothrombinemia. Transfusion of blood and fresh frozen plasma may also be necessary.
A beta-adrenergic blocker may be given to decrease pressure from varices.
Lactulose may be given orally or rectally to reduce a high ammonia level. If lactulose therapy alone is inadequate, neomycin may be used.
Other treatment
Paracentesis and infusions of salt-poor albumin may alleviate ascites. Surgical procedures include ligation of varices, splenectomy, esophagogastric resection, and splenorenal or portacaval anastomosis to relieve portal hypertension.
Clinical tip Transjugular intrahepatic portosystemic shunt is an alternative to surgical shunting in patients with variceal bleeding refractory to standard therapy. It’s also helpful in patients with severe ascites. The technique involves insertion of an expandable metal shunt between a branch of the hepatic vein and portal vein over a catheter inserted via the jugular vein. This is usually a bridging mechanism to control variceal bleeding or ascites until liver transplantation can be performed.
Hepatorenal and hepatopulmonary syndromes may occur. Treatment is ineffective except in patients who are acceptable candidates for liver transplantation.
Special considerations
❑ Check skin, gums, stool, and vomitus regularly for bleeding. Apply pressure to injection sites to prevent bleeding. Warn the patient against taking aspirin, straining during defecation, and blowing his nose or sneezing too vigorously. Suggest using an electric razor and a soft toothbrush.
Clinical tip Assess the patient for internal bleeding as well as for overt signs of external bleeding.
❑ Observe the patient closely for signs and symptoms of behavioral or personality changes — especially increasing stupor, lethargy, hallucinations, and neuromuscular dysfunction — which may indicate increasing ammonia levels. Arouse the patient periodically to determine his level of consciousness. Watch for asterixis, a sign of developing hepatic encephalopathy.
❑ Monitor ammonia levels to determine effectiveness of lactulose therapy.
❑ To assess fluid retention, weigh the patient and measure his abdominal girth daily, inspect the 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 bathing the patient; instead, use lubricating lotion or another moisturizer. Handle the patient gently, and turn and reposition him often to keep skin intact.
❑ Tell the patient that rest and good nutrition will conserve energy and decrease metabolic demands on the liver. Encourage frequent, small meals. Stress the need to avoid infections and abstain from alcohol.
❑ Support the family during this difficult time, and refer the patient to support groups and Alcoholics Anonymous as indicated.
Pictures
Book Source Details
- Book Title: Handbook of Diseases
- Author(s): Springhouse
- Year of Publication: 2003
- Copyright Details: Handbook of Diseases, Copyright © 2003 Lippincott Williams & Wilkins.
More About Primary biliary cirrhosis
More Medical Textbooks Online about Primary biliary cirrhosis
Review other book chapters online related to Primary biliary cirrhosis:
Medical Books Excerpts
- ASCITES
- "Algorithmic Diagnosis of Symptoms and Signs" (2003)
- [ read ]
- Ascites
- "In A Page: Pediatric Signs and Symptoms" (2007)
- [ read ]
- Ascites
- "A Pocket Manual of Differential Diagnosis" (1999)
- [ read ]
- Ascites
- "The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter" (2000)
- [ read ]
Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.
|
|
More About This Book:
Title: Handbook of Diseases
Authors: Springhouse
Publisher: Lippincott Williams & Wilkins
Copyright: 2003
ISBN: 1-58255-266-5
|
|
» Next page: Cirrhosis (The 5-Minute Pediatric Consult)
Rate This Website
What do you think about the features of this website?
Take our user survey and have your say:
Website User Survey
Medical Tools & Articles:
Next articles:
Tools & Services:
Medical Articles:
Forums & Message Boards
- Ask or answer a question at the Boards:
