Cirrhosis is a chronic degenerative disease in which normal liver cells are damaged and are then replaced by scar tissue.
Cirrhosis changes the structure of the liver and the blood vessels that nourish it. The disease reduces the liver's ability to manufacture proteins and process hormones, nutrients, medications, and poisons.
Cirrhosis gets worse over time and can become potentially life threatening. This disease can cause:
- excessive bleeding (hemorrhage)
- liver cancer
- coma due to accumulated ammonia and body wastes (liver failure)
- sepsis (blood poisoning)
Cirrhosis is the seventh leading cause of disease-related death in the United States. It is the third most common cause of death in adults between the ages of 45 and 65. It is twice as common in men as in women. The disease occurs in more than half of all malnourished chronic alcoholics, and kills about 25,000 people a year. In Asia and Africa, however, most deaths from cirrhosis are due to chronic hepatitis B
Types of cirrhosis
Portal or nutritional cirrhosis is the form of the disease most common in the United States. About 30-50% of all cases of cirrhosis are this type. Nine out of every 10 people who have nutritional cirrhosis have a history of alcoholism
. Portal or nutritional cirrhosis is also called Laënnec's cirrhosis.
Biliary cirrhosis is caused by intrahepatic bile-duct diseases that impede bile flow. Bile is formed in the liver and is carried by ducts to the intestines. Bile then helps digest fats in the intestines. Biliary cirrhosis can scar or block these ducts. It represents 15-20% of all cirrhosis.
Various types of chronic hepatitis, especially hepatitis B and hepatitis C
, can cause postnecrotic cirrhosis. This form of the disease affects up to 40% of all patients who have cirrhosis.
Disorders like the inability to metabolize iron and similar disorders may cause pigment cirrhosis (hemochromatosis
), which accounts for 5-10% of all instances of the disease.
Causes and symptoms
Long-term alcoholism is the primary cause of cirrhosis in the United States. Men and women respond differently to alcohol. Although most men can safely consume two to five drinks a day, one or two drinks a day can cause liver damage in women. Individual tolerance to alcohol varies, but people who drink more and drink more often have a higher risk of developing cirrhosis. In some people, one drink a day can cause liver scarring.
Chronic liver infections, such as hepatitis B and particularly hepatitis C, are commonly linked to cirrhosis. People at high risk of contracting hepatitis B include those exposed to the virus through contact with blood and body fluids. This includes healthcare workers and intravenous (IV) drug users. In the past, people have contracted hepatitis C through blood transfusions. As of 2003, cirrhosis resulting from chronic hepatitis has emerged as a leading cause of death among HIV-positive patients; in Europe, about 30% of HIV-positive patients are coinfected with a hepatitis virus.
Liver injury, reactions to prescription medications, exposure to toxic substances, and repeated episodes of heart failure
with liver congestion can cause cirrhosis. The disorder can also be a result of diseases that run in families (inherited diseases) like:
- a lack of a specific liver enzyme (alpha1-antitrypsin deficiency)
- the absence of a milk-digesting enzyme (galactosemia)
- an inability to convert sugars to energy (glycogen storage disease)
- an absorption deficit in which excess iron is deposited in the liver, pancreas, heart, and other organs (hemochromatosis)
- a disorder characterized by accumulations of copper in the liver, brain, kidneys, and corneas (Wilson's disease)
has recently been recognized as a risk factor in nonalcoholic hepatitis and cirrhosis. Some surgeons are recommending as of 2003 that patients scheduled for weight-reduction surgery have a liver biopsy
to evaluate the possibility of liver damage.
increases a person's risk of developing cirrhosis. In about 10 out of every 100 patients, the cause of cirrhosis cannot be determined. Many people who have cirrhosis do not have any symptoms (often called compensated cirrhosis). Their disease is detected during a routine physical or when tests for an unrelated medical problem are performed. This type of cirrhosis can also be detected when complications occur (decompensated cirrhosis).
Symptoms of cirrhosis are usually caused by the loss of functioning liver cells or organ swelling due to scarring. The liver enlarges during the early stages of illness. The palms of the hands turn red and patients may experience:
- dull abdominal pain
- loss of appetite
- weight loss
As the disease progresses, the spleen enlarges and fluid collects in the abdomen (ascites
) and legs (edema
). Spider-like blood vessels appear on the chest and shoulders, and bruising becomes common. Men sometimes lose chest hair. Their breasts may grow and their testicles may shrink. Women may have menstrual irregularities.
Cirrhosis can cause extremely dry skin and intense itching
. The whites of the eyes and the skin may turn yellow (jaundice
), and urine may be dark yellow or brown. Stools may be black or bloody. Sometimes the patient develops persistent high blood pressure due to the scarring (portal hypertension
). This type of hypertension can be life threatening. It can cause veins to enlarge in the stomach and in the tube leading from the mouth to the stomach (esophagus). These enlarged veins are called varices, and they can rupture and bleed massively.
Other symptoms of cirrhosis include:
- bleeding gums
- decreased interest in sex
- fluid in the lungs
- muscle weakness
- musty breath
- painful nerve inflammation (neuritis)
- slurred speech
If the liver loses its ability to remove toxins from the brain, the patient may have additional symptoms. The patient may become forgetful and unresponsive, neglect personal care, have trouble concentrating, and acquire new sleeping habits. These symptoms are related to ammonia intoxication and the failure of the liver to convert ammonia to urea. High protein intake in these patients can also lead to these symptoms.
A patient's medical history can reveal illnesses or lifestyles likely to lead to cirrhosis. Liver changes can be seen during a physical examination
. A doctor who suspects cirrhosis may order blood and urine tests to measure liver function. Because only a small number of healthy cells are needed to carry out essential liver functions, test results may be normal even when cirrhosis is present.
Computed tomography scans
(CT), ultrasound, and other imaging techniques can be used during diagnosis. They can help determine the size of the liver, indicate healthy and scarred areas of the organ, and detect gallstones
. Cirrhosis is sometimes diagnosed during surgery or by examining the liver with a laparoscope. This viewing device is inserted into the patient's body through a tiny incision in the abdomen.
Liver biopsy is usually needed to confirm a diagnosis of cirrhosis. In this procedure, a tissue sample is removed from the liver and is examined under a microscope in order to learn more about the organ.
A newer and less invasive test involves the measurement of hyaluronic acid in the patient's blood serum. As of 2003, however, the serum hyaluronic acid test is most useful in monitoring the progress of liver disease
; it is unlikely to completely replace liver biopsy in the diagnosis of cirrhosis.
The goal of treatment is to cure or reduce the condition causing cirrhosis, prevent or delay disease progression, and prevent or treat complications.
Salt and fluid intake are often limited, and activity is encouraged. A diet high in calories and moderately high in protein can benefit some patients. Tube feedings
or vitamin supplements may be prescribed if the liver continues to deteriorate. Patients are asked not to consume alcohol.
Iron supplements, diuretics
, and antibiotics
may be used for anemia, fluid retention, and ammonia accumulation associated with cirrhosis. Vasoconstrictors are sometimes needed to stop internal bleeding and antiemetics may be prescribed to control nausea.
help the body absorb toxins and accelerate their removal from the digestive tract. Beta blockers
may be prescribed to control cirrhosis-induced portal hypertension. Because the diseased liver can no longer efficiently neutralize harmful substances, medications must be given with caution. Interferon medicines may be used by patients with chronic hepatitis B and hepatitis C to prevent post-hepatic cirrhosis.
Medication that causes scarring can be injected directly into veins to control bleeding from varices in the stomach or esophagus. Varices may require a special surgical procedure called balloon tamponade ligation to stop the bleeding. Surgery may be required to repair disease-related throat damage. It is sometimes necessary to remove diseased portions of the spleen and other organs.
Liver transplants can benefit patients with advanced cirrhosis. However, the new liver will eventually become diseased unless the underlying cause of cirrhosis is removed. Patients with alcoholic cirrhosis must demonstrate a willingness to stop drinking before being considered suitable transplant candidates.
The incidence of liver cancer
related to cirrhosis in the United States has increased 75% since the early 1990s. Partial surgical removal of the liver in patients with early-stage cancer of the liver appears to be as successful as transplantation, in terms of the 5-year survival rate.
A balanced diet promotes regeneration of healthy liver cells. Eating five or six small meals throughout the day should prevent the sick or bloated feeling patients with cirrhosis often have after eating. Alcohol and caffeine
, which destroy liver cells, should be avoided. So should any foods that upset the stomach. Patients with brain disease associated with cirrhosis should avoid excessive amounts of protein in the diet.
A patient can keep a food diary that describes what was eaten, when it was eaten, and how the patient felt afterwards. This diary can be useful in identifying foods that are hard to digest and in scheduling meals to coincide with the times the patient is most hungry.
Patients who have cirrhosis should weigh themselves every day and notify their doctor of a sudden gain of five pounds or more. A doctor should also be notified if symptoms of cirrhosis appear in anyone who has not been diagnosed with the disease. A doctor should also be notified if a patient diagnosed with cirrhosis:
- vomits blood
- passes black stools
- seems confused or unresponsive
- shows signs of infection (redness, swelling, tenderness, pain)
Alternative treatments for cirrhosis are aimed at promoting the function of healthy liver cells and relieving the symptoms associated with the disease. Several herbal remedies may be helpful to cirrhosis patients. Dandelion (Taraxacum officinale
) and rock-poppy (Chelidonium majus
) may help improve the efficiency of liver cells. Milk thistle extract (Silybum marianum
) may slow disease progression and significantly improve survival rates in alcoholics and other cirrhosis patients. Practitioners of homeopathy and traditional Chinese medicine
can also prescribe treatments that support healthy liver function.
Cirrhosis-related liver damage cannot be reversed, but further damage can be prevented by patients who:
- eat properly
- get enough rest
- do not consume alcohol
- remain free of infection
If the underlying cause of cirrhosis cannot be corrected or removed, scarring will continue. The liver will fail, and the patient will probably die within five years. Patients who stop drinking after being diagnosed with cirrhosis can increase their likelihood of living more than a few years from 40% to 60-70%.
Eliminating alcohol abuse could prevent 75-80% of all cases of cirrhosis.
Other preventive measures include:
- obtaining counseling or other treatment for alcoholism
- taking precautions (practicing safe sex, avoiding dirty needles) to prevent hepatitis
- getting immunizations against hepatitis if a person is in a high-risk group
- receiving appropriate medical treatment quickly when diagnosed with hepatitis B or hepatitis C
- having blood drawn at regular intervals to rid the body of excess iron from hemochromatosis
- using medicines (chelating agents) to rid the body of excess copper from Wilson's disease
- wearing protective clothing and following product directions when using toxic chemicals at work, at home, or in the garden
In 2001, research scientists identified the protein segment and method in which excess tissue grows in diseases like cirrhosis. With further study, the discovery might one day result in an oral or inhalable peptide for those with cirrhosis.
Beers, Mark H., MD, and Robert Berkow, MD. editors. "Cirrhosis." Section 4, Chapter 41 In The Merck Manual of Diagnosis and Therapy. Whitehouse Station, NJ: Merck Research Laboratories, 2004.
Pelletier, Kenneth R., MD. The Best Alternative Medicine, Part II, "CAM Therapies for Specific Conditions: Alcoholism." New York: Simon & Schuster, 2002.
Cha, C. H., L. Ruo, Y. Fong, et al. "Resection of Hepatocellular Carcinoma in Patients Otherwise Eligible for Transplantation." Annals of Surgery 238 (September 2003): 315-321.
Foreman, M. G., D. M. Mannino, and M. Moss. "Cirrhosis as a Risk Factor for Sepsis and Death: Analysis of the National Hospital Discharge Survey." Chest 124 (September 2003): 1016-1020.
Higuchi, H., and G. J. Gores. "Mechanisms of Liver Injury: An Overview." Current Molecular Medicine 3 (September 2003): 483-490.
Kamath, B. M., and D. A. Piccoli. "Heritable Disorders of the Bile Ducts." Gastroenterology Clinics of North America 32 (September 2003): 857-875.
"Management of Alcoholic Hepatitis." Drug Therapy Bulletin 41 (July 2003): 49-52.
Moretto, M., C. Kupski, C. C. Mottin, et al. "Hepatic Steatosis in Patients Undergoing Bariatric Surgery and Its Relationship to Body Mass Index and Co-Morbidities." Obesity Surgery 13 (August 2003): 622-624.
"Peptides: Peptide Critical to Cirrhosis Development." Drug Discovery and Technology News 4, no. 11 (November 2001).
Phillips, M. G., V. R. Preedy, and R. D. Hughes. "Assessment of Prognosis in Alcoholic Liver Disease: Can Serum Hyaluronate Replace Liver Biopsy?" European Journal of Gastroenterology and Hepatology 15 (September 2003): 941-944.
Ristig, M., H. Drechsler, J. Crippin, et al. "Management of Chronic Hepatitis B in an HIV-Positive Patient with 3TC-Resistant Hepatitis B Virus." AIDS Patient Care and STDs 17 (September 2003): 439-442.
American Liver Foundation. 1425 Pompton Ave., Cedar Grove, NJ 07009. (800) 223-0179. http://www.liverfoundation.org.
United Network for Organ Sharing. 1100 Boulders Parkway, Suite 500, P.O. Box 13770, Richmond, VA 23225-8770. (804) 330-8500. http://www.unos.org.
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK). Cirrhosis of the Liver. April 200 [cited October 2002]. http://www.niddk.nih.gov/health/digest/pubs/cirrhosi/cirrhosi.htm.
a liver disease (actually a group of chronic diseases) characterized by loss of the normal microscopic lobular architecture and regenerative replacement of necrotic parenchymal tissue with fibrous bands of connective tissue that eventually constrict and partition the organ into irregular nodules. It has a lengthy latent period, usually followed by the sudden appearance of abdominal pain and swelling, hematemesis, dependent edema, or jaundice. In advanced stages, ascites, pronounced jaundice, portal hypertension, and central nervous system disorders, which may end in hepatic coma
, become prominent. adj., adj
. The signs and symptoms are manifestations of interference with the major functions of the liver: (1) the storage and release of blood to maintain adequate circulating volume, (2) the metabolism of nutrients and the detoxification of poisons absorbed from the intestines, (3) the regulation of fluid and electrolyte balance, and (4) production of clotting factors.
The patient with alcoholic cirrhosis (Laënnec's cirrhosis
) may be admitted to the hospital with acute alcoholic hepatitis, marked by fever and dehydration. Prominent spider angiomas and redness of the palms of the hands (palmar erythema) are usually present. delirium tremens
may be a difficult problem during the early phase of hospitalization. Data from liver function tests usually show elevated transaminase levels, elevated bilirubin levels, and decreased values for albumin and clotting factors. (See also alcoholism
Continued fluid and electrolyte imbalances and inefficient metabolism of nutrients produce ascites, hypoglycemia, and hypoproteinemia. Obstruction to the return of blood from the portal system causes increased pressure within the veins of the esophagus and stomach. These engorged vessels are subject to rupture with subsequent hemorrhage that is abetted by clotting disorders. jaundice
develops as a result of biliary obstruction.
Neurological symptoms begin with subtle changes in mental acuity, mild memory loss, poor reasoning ability, and irritability. Tremor of the outstretched hands (asterixis) is common. These symptoms become more severe and may eventually progress to delirium, suicidal tendencies, and coma.
. The major goals of treatment for the patient with cirrhosis are: (1) to maintain liver function at its current level and prevent further deterioration of the organ, (2) to maintain electrolytes within normal limits, (3) to maintain sufficient respiratory function, (4) to prevent or resolve gastrointestinal bleeding, and (5) to provide adequate nutritional intake and a positive nitrogen balance.
Since there is no cure for cirrhosis, supportive measures are instituted to help the liver rebuild and repair its damaged cells. Prevention of further deterioration of the cells is accomplished by removing the primary cause; for example, restriction of the intake of alcohol or other toxic agent, treatment of infection, and providing an adequate nutritional intake; supplemental vitamins are often prescribed.
Severe blood loss is compensated for by transfusions of whole blood. Excessive bleeding from esophageal varices may necessitate insertion of a Sengstaken-Blakemore tube. This device has three channels: one for inflation of the esophageal balloon, one for inflation of the gastric balloon, and a third for aspiration of stomach contents.
Relief of portal hypertension sometimes is accomplished by a surgical procedure called a portacaval shunt. The portal vein is surgically connected to the inferior vena cava to allow drainage of excessive amounts of blood from the portal system to the general circulation. A similar procedure called the splenorenal shunt involves connecting the splenic vein to the renal vein.
Removal of fluid from the abdominal cavity (abdominal paracentesis
) may be necessary to relieve respiratory embarrassment or pressure on the abdominal organs caused by ascites. A more permanent resolution of the problem of chronic ascites is surgical creation of a peritoneovenous shunt
and coma can be precipitated by any of a number of factors, including gastrointestinal bleeding, fluid and electrolyte and acid-base imbalances, intercurrent infection and fever, administration of analgesics and sedatives that are central nervous system depressants, and increased dietary protein intake.
Patients with chronic hepatic encephalopathy
are placed on a protein-restricted diet. An antibiotic may be prescribed to reduce bacterial flora in the intestine. Surgical removal of all or part of the bacteria-laden colon is an alternative treatment, but the surgical risk is high in these chronically ill patients.
. In view of the many functions of the liver, it is essential that a thorough assessment of the patient be done to identify specific problems before a plan of care is developed. Among the problems likely to be associated with cirrhosis are self-care deficit related to low energy level due to inadequate metabolism of carbohydrates; fluid volume excess, especially ascites; potential for impairment of skin integrity related to edema, jaundice, and itching; electrolyte imbalance related to poor storage of minerals; alteration in comfort; tendency to bleed excessively related to deficits of vitamin K and prothrombin and the presence of esophageal varices; potential for infection related to decreased levels of gamma globulins and dysfunction of phagocytic Kupffer cells; impaired gas exchange related to pressure against the lungs by ascitic fluid; potential for injury related to altered levels of consciousness; alteration in nutrition related to indigestion, nausea, inability of liver cells to metabolize food elements, or confusion and depression; and diarrhea related to diminished bile production and decreased tolerance to fatty acids.
Patients in the advanced stages of cirrhosis require periodic and thorough monitoring to detect blood loss in the form of hematemesis, tarry stools, bleeding gums, frequent and heavy nosebleeds, and bruising. In order to evaluate fluid status the fluid intake and output and daily weight are measured and recorded.
Dietary restrictions and prohibition of alcohol may result in noncompliance in some patients. Education must include the purpose of these restrictions, the expected effect and dosage of medications that have been prescribed, and the importance of adequate nutrition, rest, and preservation of independence within the patient's capabilities. Compliance may be improved by enhancing the patient's self-esteem, emphasizing personal strengths, encouraging the use of available community resources such as alcoholics anonymous
if alcoholism is a problem, and providing for active participation of the patient and family in planning and implementing some aspects of care.
acholangic cirrhosis a liver disorder affecting children up to 12 years of age, due to complete or partial agenesis of the intrahepatic, intralobular bile ducts, with manifestations similar to those seen in obstructive biliary cirrhosis.
atrophic cirrhosis cirrhosis in which the liver is decreased in size; it may be seen in the alcoholic, but is more common in posthepatic or postnecrotic cirrhosis.
biliary cirrhosis cirrhosis caused by obstruction or infection of the major extra- or intrahepatic bile ducts (except in primary biliary cirrhosis). It is marked by jaundice, abdominal pain, steatorrhea, and enlargement of the liver and spleen.
cirrhosis in which liver cells are infiltrated with fat (triglyceride), the infiltration usually being due to alcohol ingestion; see laënnec's cirrhosis
cirrhosis associated with chronic alcoholism
. In the early stages, liver enlargement may reflect fatty infiltration of liver cells (fatty cirrhosis) with necrosis and inflammation due to acute alcohol injury; progressive fibrosis extending from portal areas separates uniform small regeneration nodules. Some attribute the condition to a nutritional deficiency associated with alcoholism and others to chronic exposure to alcohol as a hepatotoxin. Called also alcoholic cirrhosis
macronodular cirrhosis morphological changes that cause the liver to become small and shrunken.
micronodular cirrhosis morphological changes in the liver resulting in an enlarged liver.
mixed cirrhosis morphological changes in the diseased liver that represent both the micronodular and macronodular patterns.
posthepatic cirrhosis cirrhosis (usually macronodular) resulting as a sequel to acute hepatitis.
postnecrotic cirrhosis cirrhosis following submassive necrosis of the liver (subacute yellow atrophy) due to toxic or viral hepatitis.
primary biliary cirrhosis
a rare form of biliary cirrhosis
of unknown etiology, occurring without obstruction or infection of the major bile ducts, sometimes developing after the administration of such drugs as chlorpromazine and arsenicals. Affecting chiefly middle-aged women, it is characterized by chronic cholestasis with pruritus, jaundice, and hypercholesterolemia with xanthomas, and malabsorption.
secondary biliary cirrhosis cirrhosis resulting from chronic bile obstruction due to congenital atresia or stricture.
cirrhosis (si-ro'sis) [Gr. kirrhos, tawny + -osis]
ASCITES CAUSED BY CIRRHOSIS
A chronic disease of the liver characterized by scarring of the liver 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). See: alcoholism
; esophageal varix
In the U.S., alcoholism and chronic viral hepatitis are the most common causes of the illness. Other causes are autoimmune (primary biliary cirrhosis), biliary (sclerosing cholangitis), cardiac (due to right-sided heart failure), nutritional (e.g., 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).
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 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. See: illustration
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, and the patient is 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.
Cirrhosis resulting from chronic liver damage by alcoholism. Approx. 20% of chronic alcoholics develop cirrhosis.
Cirrhosis in which the liver is decreased in size.
Cirrhosis marked by prolonged jaundice due to chronic retention of bile and inflammation of bile ducts. See: obstructive biliary cirrhosis; primary biliary cirrhosis
Passive congestion of the liver caused by right-sided heart failure, ultimately resulting in hepatic scarring and failure. Synonym: congestive hepatopathy
An inflammation of the peritoneal coat of the liver. Synonym: perihepatitis
Cirrhosis in which connective tissue hyperplasia causes the liver to be greatly enlarged.
End-stage scarring of the liver without ongoing inflammation. It is one of the patterns of cirrhosis of the liver that may be seen on liver biopsy.
Cirrhosis occurring in childhood as a result of protein malnutrition. See: kwashiorkor
Laënnec cirrhosis See: Laënnec, René
Cirrhosis resulting from metabolic disease such as hemochromatosis, glycogen storage disease, or Wilson disease.
obstructive biliary cirrhosis
Cirrhosis resulting from obstruction of the common duct by a stone or tumor.
primary biliary cirrhosis
A rare, progressive form of cirrhosis usually occurring in middle-aged women, marked by jaundice, pruritus, fatigue, and autoimmune destruction of the small bile ducts.
Cirrhosis occurring in tertiary syphilis, in which gummas form in the liver and cause coarse lobulation on healing.
Cirrhosis resulting from infestation with hepatobiliary parasites, esp. blood flukes of the genus Schistosoma or liver flukes, e.g., Clonorchis sinensis.