fulminant hepatitis

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ful·mi·nant hep·a·ti·tis

severe, rapidly progressive loss of hepatic function due to viral infection or other cause of inflammatory destruction of liver tissue with associated coagulopathy and encephalopathy.
Farlex Partner Medical Dictionary © Farlex 2012


(hep?a-tit'is) [ hepato- + -itis]
Inflammation of the liver, usually caused by exposure to an infectious agent (such as a hepatitis virus), a toxin (such as alcohol), or a drug (such as acetaminophen). The illness may be mild or life-threatening, chronic or acute. Chronic cases may be detected only by the discovery of elevated liver enzymes in the blood. Acute cases are marked by jaundice, hepatic enlargement, and occasional bleeding, altered mental status, and multiple organ system failure. Usually, a history of any type of hepatitis (esp. after age 10), is a contraindication to being a blood donor.


Damage to liver cells is caused by direct injury from the causative agent or indirectly as a result of inflammatory or autoimmune responses. During acute inflammation, the swollen hepatocytes are less able to detoxify drugs; to produce clotting factors, cholesterol, plasma proteins, bile, and glycogen; to store fat-soluble vitamins; or to perform other functions. All of the hepatitis viruses may cause fulminant hepatitis, but hepatitis B and D are the most common causes. Drug overdoses, ingestion of toxins, and shock are also responsible for rapid liver deterioration.

Patient care

Patients are not generally hospitalized unless they experience significant liver damage or complications; the more severely affected need supportive medical and psychological care. Patients at home should be instructed about the nature and course of the illness, its care and treatment, and signs and symptoms of complications. When hepatitis is food-borne, thorough washing of the hands, food handling, and cleaning of dishes and silverware are necessary to prevent transmission to household members. The patient should avoid intimate contact with others until antigen and antibody levels are reduced. The patient is advised to schedule frequent rest periods and to rest between major activities. Diversionary activities should be included to help reduce anxiety. Good nutrition is encouraged (small, high-calorie, low-protein, nutrient-dense, frequent meals, and fluids to 4 qt (4 L)/day). Fluid intake and output, and weight, color, consistency, and frequency of stools should be recorded. The hospitalized patient is assessed for complications (hepatic coma, pneumonia, vascular problems, and pressure ulcers). The patient is advised to avoid alcohol during the period of acute illness and for at least 6 months after recovery. Depression may occur because of the patient’s concerns about the illness, but the depression may also be linked to changes in body chemistry or adverse drug reactions. Hepatitis is the primary reason for liver transplants, and the concerns of potential need and treatment should be explained to the patient. Emotional support and reassurance should be offered to the patient because there may be considerable interference with the patient's habits and lifestyle. See: ; hepatitis A; autoimmune hepatitis; hepatitis E; fulminant hepatitis

hepatitis A

Hepatitis caused by hepatitis A virus (HAV), an RNA virus without an envelope. Because hepatitis A can be contracted through contaminated water or food, young adults and children in institutional settings and travelers in areas with minimal sanitation are at greatest risk for infection; small epidemics have been seen among people eating at restaurants that served contaminated shellfish. The course of the illness is usually mild, although it can be severe; the incubation period is 2 to 6 weeks, the acute stage lasts 2 to 12 weeks, and complete recovery takes weeks to months. The infection affects about 90,000 people every year, about half of whom develop clinically obvious infection. Hepatitis A does not produce a carrier state and does not cause chronic hepatitis. The two antibodies produced in response to hepatitis A antigen serve as markers for infection; one of these, IgG anti-HAV, provides immunity against reinfection. Hepatitis A previously was called infectious hepatitis.


No drugs specifically treat hepatitis A. Immune globulin containing IgG anti-HAV antibodies may be prescribed for family members; it provides passive immunity for 6 to 8 weeks. Preventive education focuses on good personal hygiene, esp. washing of the hands; use of good judgment in choice of food and eating places; and, in some areas of the world, basic sanitation. Hepatitis A vaccine prevents infection either before or immediately after exposure to the virus and is recommended for health care workers, travelers to developing countries, day care workers, people with liver disease, and others at high risk.


Hepatitis A is transmitted by fecal-oral contact. To prevent the spread of the disease, those infected should not be involved in food preparation.

acute anicteric hepatitis

Hepatitis marked by slight fever, gastrointestinal upset, and anorexia but without jaundice.

alcoholic hepatitis

Destruction of large numbers of hepatocytes due to excessive ingestion of alcohol. Fever, jaundice, altered mental status, and enlargement of the liver are common findings. It can be treated with abstinence, corticosteroids, pentoxifylline, and supportive therapy.

amebic hepatitis

A syndrome marked by a tender, enlarged liver; pain over the liver; fever; and leukocytosis in a patient with amebic colitis. This term is a misnomer because the liver changes are not due to an infestation of that organ with amebae but are a part of the nonspecific reaction to the infection in the intestinal tract. Nevertheless, a liver abscess will occasionally develop, and the walls of the abscess will contain amebae.


Metronidazole plus iodoquinol, or chloroquine phosphate plus either emetine or dehydroemetine are used to treat amebic hepatitis. These latter two drugs are toxic and should be given only if their course can be carefully observed with a cardiac monitor. The drugs should not be given to a patient who has cardiac disease or is pregnant. Needle aspiration of the abscess may be needed.

autoimmune hepatitis

Persistent hepatic inflammation and necrosis, in the setting of hypergammaglobulinemia and autoantibodies and in the absence of other common causes of liver injury.

hepatitis B

Injury to liver cells caused by hepatitis B virus (HBV), a double-stranded DNA virus. It may appear as an asymptomatic, acute, chronic, or fulminant infection. Acute infection often is marked by jaundice, nausea and vomiting, joint pains, rashes, and marked elevations in serum liver function tests. Chronic infection typically is asymptomatic and may be detected only by blood tests until it causes late complications (cirrhosis, portal hypertension, or hepatocellular carcinoma). Fulminant hepatitis B infection occurs when the patient suffers hepatic encephalopathy within 8 weeks of the onset of the disease.

The virus is transmitted by exposure to the blood or body fluids of an infected person. The incubation period is approximately 2 to 6 months. Acute infection usually resolves in less than 6 months. When HBV surface antigen does not clear from the blood within 6 months, chronic hepatitis is said to have developed. Each year in the U.S., about 300,000 people are infected with HBV. Worldwide, chronic hepatitis affects about 300 million people.

Those at greatest risk for infection include intravenous drug abusers, people with multiple sex partners, men who have sex with men, infants born of HBV-infected mothers, and health care workers. Blood banks now routinely screen for HBV antigens, which has greatly reduced the transmission of infection by transfusion.


People who have not been vaccinated against HBV and receive a needlestick or have mucous membrane contact with blood or other body secretions should contact their occupational health department. Hepatitis B virus immune globulin (HBIg) can be given to provide temporary protection.

Antigens and Antibodies

The primary antigenic markers used to diagnose hepatitis B infection include the following: 1. hepatitis B surface antigen (HBsAg), the first marker to appear in the blood. It is sometimes detected before serum levels of hepatic enzymes rise; 2. hepatitis Be antigen (HBeAg) and hepatitis B DNA, markers of active viral replication and high infectivity; and 3. Hepatitis B core antibodies (antibodies against the core antigen of hepatitis B), which indicate infection of a patient with HBV. IgM antibodies against the core antigen (IgM anti-HBc) are present early in the course of infection and may sometimes be the only detectable evidence of an acute infection. IgG antibodies against the core antigen (anti-HBc) are present in any patient infected with the virus, either acutely or at some time in the past.

Protective IgG antibodies to the HB surface antigen (HBsAB), which develop late in the disease, persist for life and protect against reinfection. As hepatitis B surface antibody levels rise, HBsAg levels fall, indicating resolution of acute infection. Antibodies against hepatitis B core antigen and hepatitis Be antigen are not protective. Approx. 5% to 10% of patients develop chronic infection.


Hepatitis B vaccine, which contains the HB surface antigen, provides active immunity and is recommended for those at increased risk (children, health care workers, hemodialysis patients, intravenous drug abusers). All pregnant women should be screened for infection. Hepatitis B immune globulin, which contains antibodies against hepatitis HBV, provides passive immunity to those who have not been vaccinated and are exposed to the virus.


No drug therapy is available that controls acute HBV infection, and treatment for this phase of the illness is supportive. Interferon-alfa has been effective in some patients with chronic infection. Antiviral drugs such as adefovir, entecavir, and lamivudine are used to treat chronic hepatitis B infections.

hepatitis C

A chronic blood-borne infection believed to affect roughly 3,200,000 people in the U.S. Hepatitis C (formerly known as non-A, non-B hepatitis) is caused by a single-stranded RNA virus transmitted from person to person by exposure to blood or body fluids. In the past it was the most common form of hepatitis transmitted by transfusions of blood or blood products and by organ transplantation.

About 30,000 to 40,000 new cases occur each year in the U.S., most of which result from needle sharing during intravenous drug abuse. A smaller number of infections are acquired as a result of exposure to tainted blood at work, e.g., in health care. About 6% of cases are the result of the transmission of the virus from mother to child during childbirth. Tattooing, body piercing, and cocaine snorting are associated with some cases. Sexual transmission of the virus seems rare. Long-term infection develops in 55% to 85% of those infected, and 5% to 20% develop cirrhosis over 20 to 30 years. Chronic hepatitis C infection has become the preeminent cause of cirrhosis, liver cancer, and death from liver failure in the U.S. The incubation period is usually 6 to 12 weeks, although it can be longer, and the acute phase lasts approx. 4 weeks. Signs and symptoms of acute infection are often milder than those of hepatitis A and B.

Infection with hepatitis C virus (HCV) is usually identified (often years after exposure) when an asymptomatic person is found to have repeatedly elevated liver enzymes on routine blood tests. Antibodies to HCV or HCV RNA in the blood confirm the infection. Antibody production is stimulated by HCV RNA, but antibodies against HCV do not destroy the virus or provide immunity.

Patient care

Antiviral agents such as pegylated alpha interferon in combination with ribavirin and boceprevir may cure hepatitis C if given for prolonged courses (about 24 to 48 weeks, depending on the viral genotype). Genotype 1, the type most often found in the U.S., responds to treatment about 30% of the time. Genotypes 2 and 3 respond to combination therapy more than 60% of the time. The treatment can cause significant side effects, including high fevers, chills, malaise, muscle aches, and other flulike symptoms. Prevention of hepatitis C in health care professionals stresses using safely engineered sharps, providing safe sharps disposal, limiting contact with blood and body fluids, and properly sterilizing instruments. Public health teaching regarding prevention for the general public includes use of properly sterilized instruments for body piercing, single-use needles for tattooing, and avoiding needle sharing and taking advantage of needle-replacement programs (for intravenous drug users). Health care providers can provide invaluable education to affected patients by giving them written and verbal information on high-risk behavior, including the need to avoid needle sharing by users of intravenous drugs, having unprotected sex, or drinking alcohol. Regular consumption of alcohol increases the risk of liver cancer dramatically for a person with HCV.

Other recommendations for people infected with hepatitis C are summarized in the following list: 1. do not donate blood, blood products, tissue, or semen; 2. avoid sharing cosmetic items or personal grooming items that may be contaminated by blood, e.g., toothbrushes or razors; 3. do not use over-the-counter, herbal, or prescription medications unless they have been approved by a knowledgeable health care provider; and 4. get vaccinations for hepatitis A and B to avoid additional viral insults to the liver.

Community support groups and Internet-based resources may help those infected to learn more about disease management, e.g., http://www.liverfoundation.org. Regular professional care may help optimize health and well-being.

chronic hepatitis

Hepatic inflammatory and necrotic changes that continue for more than 6 months. The most common causes are hepatitis B, C, and D viruses. Chronic liver inflammation may also result from abuse of alcohol or other drugs, exposure to toxic chemicals, fatty infiltration of the liver, or autoimmune processes. Patients may be asymptomatic or present with only elevated serum transaminase levels, fatigue, anorexia, malaise, or mild jaundice. In other patients, the disease actively progresses, eventually leading to cirrhosis and death. Depending on the underlying cause, corticosteroids, interferons, or antiviral agents such as ribavirin may be used to manage chronic hepatitis. In alcoholic patients, abstinence from alcohol may allow the liver to heal.

hepatitis D

A form of hepatitis caused by the hepatitis delta virus (HDV). It is considered a defective virus because it can produce infection only when hepatitis B virus (HBV) is present and therefore can be prevented through hepatitis B vaccination. It is rare in the U.S. In healthy people, coinfection with HDV and HBV usually causes acute disease and recovery with immunity. In patients with chronic hepatitis B, it may produce severe acute disease or, more commonly, chronic progressive disease that may lead to cirrhosis. Mortality is approx. 10%. Hepatitis D antigens (HDV RNA) are found in the blood and liver and stimulate production of an antibody that is present only briefly during early acute infection. HDV is also sometimes referred to as delta hepatitis. See: hepatitis B


Because hepatitis D only occurs in people already infected with hepatitis B, vaccination against hepatitis B helps prevent the spread of this virus.

hepatitis E

A form of hepatitis similar to hepatitis A, occurring primarily in regions with contaminated water supplies or in travelers returning from abroad. It is caused by an RNA virus that produces acute infection only.

fulminant hepatitis

Acute liver failure.

hypoxic hepatitis

Ischemic hepatitis.

infectious hepatitis

A term formerly used for hepatitis A virus infection.

ischemic hepatitis

Acute, severe liver injury that results from an episode of hypotension, typically in someone with underlying heart or lung disease. This type of hepatitis may result in bleeding, encephalopathy, coma, or death. Synonym: hypoxic hepatitis

Lábrea hepatitis

Santa Marta hepatitis.

rapidly recurrent cholestatic hepatitis C

, recurrent cholestatic hepatitis
Hepatitis C infection occurring in a patient's transplanted liver shortly after organ transplantation. The disease causes early damage to the grafted organ and carries a poor prognosis.

Santa Marta hepatitis

Fulminant hepatitis due to coinfection with hepatitis B and hepatitis D.
Synonym: Lábrea hepatitis

serum hepatitis

A term formerly used for HBV infection.

toxic hepatitis

Inflammation of the liver caused by the ingestion or absorption of toxins or drugs into the body. Included in the great number of agents known to be able to cause this type of hepatitis are common drugs and chemicals (such as halothane, isoniazid, anabolic steroids, carbon tetrachloride, trichlorethylene) used in either the treatment of disease or in the workplace.
Medical Dictionary, © 2009 Farlex and Partners
References in periodicals archive ?
Suppl Table 2: top 55 candidate nucleotides associated with fulminant hepatitis B.
describe the case of a 54-year-old female presenting with fulminant hepatitis 29 days following the initiation of crizotinib therapy [6].
Arai, "The third case of fulminant hepatitis associated with "Kitami/ Abashiri strain" of hepatitis E virus genotype 4," Kanzo, vol.
Pacheco-Moreira et al., "Fulminant hepatitis failure in adults and children from a public hospital in Rio de Janeiro, Brazil," Brazilian Journal of Infectious Diseases, vol.
Rebuilding the balance of STAT-1 and STAT3 signalings by fusaruside, a cerebroside compound, for the treatment of T-cell-mediated fulminant hepatitis in mice.
It was unable to judge the causality relationship between the HBV reactivation and bortezomib, and the patient died from fulminant hepatitis. In a study of Singapore, a HBV reactive case was reported 4 months after the bortezomib and dexamethasone treatment.
(12) Co-infection usually results in an acute self-limited illness with increasing risk of fulminant hepatitis, whereas super-infection generally causes severe and rapidly progressive liver disease that often leads to end-stage liver disease including cirrhosis and hepatocellular carcinoma.
Association of a precore genomic variant of hepatitis B virus with fulminant hepatitis. Hepatology 1991; 14: 219-222, doi: 10.1002/hep.1840140203.
Stopping HBV-active ART can lead to a rapid rise in HBV replication, leading to symptoms that can range from subclinical to fulminant hepatitis, and may mimic acute HBV infection.
Hepatitis E has variable clinical presentations and ranges from asymptomatic carriers to fulminant hepatitis. As one would expect clinical manifestations to some extent depend on the predominant genotype.
However studies carried out in India Iran Africa and Middle East has found the higher incidence of fulminant hepatitis in pregnancy.