Viral hepatitis fulminant

Managing viral hepatitis involves both prevention and treatment. Prevention of hepatitis A and B (and indirectly for hepatitis D) can be achieved with immune globulin or vaccines. There is no specific pharmacologic treatment for acute viral hepatitis A, B, C, D, or E only supportive care is available. Individuals with mild to moderate symptoms rarely require hospitalization. Occasionally, hospitalization is required in individuals experiencing significant nausea, vomiting, diarrhea, and encephalopathy. Liver transplantation may be required in rare instances if fulminant hepatitis develops. 

There have been reports on the transition from virus-induced acute liver failure to chronic hepatitis. As the final stage of fulminant viral hepatitis (also known as acute liver dystrophy or submassive hepatitic necrosis), a postdystrophic scarred liver ( potato liver ) can develop. (s. fig. 35.14) Cicatricial distortions with a continuing effect, regenerative processes, intrahepatic vascular disorders and hypoxia-related damage lead to the conclusion that a posthepatitic, postdystrophic scarred liver may well be a special form of cirrhosis. 

Feranchak, A.R, Tyson, R.W., Narkewicz, M.R., Karrer, FJM., Sokol, R.J. Fulminant Epstein-Barr viral hepatitis orthotopic liver transplantation and review of the literature. Liver Transpl. Surg. 1998 4 469 -476... 

Very rarely (0.01%), albeit more frequently in elderly patients and people with a compromised immune system (0.1 —1.0%), viral hepatitis A takes a fulminant course. About 1.0% of all cases of fulminant viral hep>afitis are caused by HAV. The survival rate is >90%. (53, 83) (s. pp 377, 433)... 

An indication for an HDV check by means of the anti-HDV search test is given with (7.) an acute intermittent episode of chronic hepatitis B, (2.) an acute HBV infection in risk groups and patients from endemic areas, and (i.) a severe or fulminant course of acute viral hepatitis B. The persistence of anti-HDAg IgM can be considered as a serological risk marker for the development of a chronic form. A titre of >1 1,000 points to chronic hepatitis D. Generally, anti-HDV and HDV RNA are replication markers for an HDV infection. 

Acute episode of a chronic liver disease Fatty liver of pregnancy Fulminant viral hepatitis (371)... 

The packaging of the kava products was unavailable for identification purposes. Liver biopsy revealed active fulminant hepatitis with extensive necrosis and tests for viral hepatitis were negative. She underwent a successful liver transplantation and was able to return to normal activity upon recovery (34). Unfortunately, no information was provided indicating that acetaminophen toxicity had been ruled out, and the observed toxic effect could also have been associated with a large, undiagnosed acetaminophen ingestion. 

Alprostadil also seems to be beneficial in the treatment of some hepatic disorders, with seme promise being shown in patients with fulminant or subfulrninant viral hepatitis (303). In these cases it has also been administered with dinoprostone and the EP, and EP, receptor agonist, misoprostol. 

Hepatitis is a major cause of morbidity and mortality in the United States. Viral hepatitis refers to the clinically important hepatotrophic viruses responsible for hepatitis A (HAV), hepatitis B (HBV), hepatitis C (HCV), delta hepatitis, and hepatitis E. Hepatitis G vims has also been described however, its role in chnical illness is stiU not clear. Viral hepatitis has acute, fulminant, and chronic clinical forms, defined by duration or severity of infection. The clinical, hiochemi-cal, immunoserologic, and histologic features of viral hepatitis follow similar patterns regardless of the virus responsible for the patient s illness. Hepatocellular response to injury and the resulting physical signs and symptoms are nonspecific. 

Liver injury that results in fulminant hepatic necrosis and acute hver failure is relatively rare. Wheu it occurs, death results iu days or weeks in nearly 80% of cases. Any potential hepatotoxic agent (e.g., acetaminophen) can be responsible, although viral hepatitis is the most common cause worldwide, especially HB V (1 % of patieuts with acute hepatitis B develop fuhniuaut hepatitis). " Fulmiuaut hepatitis caused by HAV occasiouaUy occurs acute liver failme caused by HCV is rare. ... 

Patients with fulminant hepatic necrosis typically develop signs and symptoms of viral hepatitis, and then rapidly develop evidence of hepatic failure. The clinical syndrome is usually a 1- to 3-week... 

Pappas SC. Fulminant viral hepatitis. Gastroenterol Clin North Am 1995 24 161-173. 

Karvountzis GG, Redeker AG, Peters RL (1974) Long-term follow-up studies of patients surviving fulminant viral hepatitis. Gastroenterology 67 870-877... 

Torre D, Zeroli C, Giola M, Ferrario G, Fieri GP, Bonetta G, Tambini R (1994) Serum levels of interleukin-1 alpha, interleukin-1 beta, interleukin-6, and tumor necrosis factor in patients with acute viral hepatitis. Clin Infect Dis 18 194 Tsuji H, Harada A, Mukaida N, Nakanuma Y, Bluethmann H, Kaneko S, Yamakawa K, Nakamura S-1, Kobayashi K-I, Matsushima K (1997) Tumor necrosis factor receptor p55 is essential for intrahepatic granuloma formation and hepatocellular apoptosis in a murine model of bacterium-induced fulminant hepatitis. Infect Immun 65 1892-1898... 

Acute fulminant hepatic failure has not been an important condition which has been treated to date with liver transplantation . This apparently paradoxical situation obtains because such patients rapidly deteriorate and consideration of transplantation as a therapeutic option usually is initiated only after advanced coma has occurred. In such case, brain edema leading to herniation usually occurs before an appropriate donor can be identified and transplantation can be accomplished. Moreover, the likelihood of recurrent infection in cases of fulminant viral hepatitis would seem to be great and therefore not warrant the procedure. 

Adverse reactions may include acneiform eruptions allergic dermatitis arthropathy multiple cases of cholestatic and fulminant hepatitis drowsiness fatigue headache hepatotoxicity resembling viral or alcoholic hepatitis impotence metallic or garlic-like aftertaste peripheral neuropathy polyneuritis optic or retrobulbar neuritis restlessness occasional skin eruptions. 

Fulminant liver failure results from massive necrosis of liver tissue. Diminution of mental function results, and this often leads to coma. The body undergoes a buildup of toxic products, alteration of its acid balance, and a decrease in cerebral blood flow. Impaired blood coagulation and intestinal bleeding occur as well. Other malfunctions and diseases of the liver include viral infections and alcoholic hepatitis. In 1999, of the 14,707 individuals on a waiting list for transplants, 4,498 received transplants and 1,709 died while waiting. As of February 2002, 18,434 people awaited liver transplants. 

Hepatitis B virus (HBV) is a member of the Hepadnaviridae family and of the genus Orthohepadnavirus [15]. HBV causes chronic, acute, and fulminate hepatitis and is still a major health issue, with hundreds of millions of individuals infected despite the development of a number of efficacious vaccines [120]. HBV first assembles the capsid around the RNA pregenome and reverse transcriptase. On assembly, the pregenome is retrotranscribed [121] and the nucleocapsid is enveloped by portions of the host cellular membrane and viral glycoprotein. There are two sizes of HBV, composed of 90 or 120 capsid protein dimers in a T=3 or T=4 icosahedral arrangement, respectively [122, 123]. 

A 6-year-old boy sustained pelvic injuries and a femoral fracture. The first anesthetic he received consisted of thiopental, suxamethonium, isoflurane, and nitrous oxide. He also received two units of blood. He subsequently underwent four halothane anesthetics over 6 weeks for dilatation of a urethral stricture. Two days after the last anesthetic he was noted to be jaundiced. He had a negative viral screen but was positive for antitrifluoroacetyl IgG antibodies. He developed fulminant hepatic failure with grade 2 hepatic encephalopathy and underwent an auxiliary Uver transplantation 24 days after his last exposure to halothane. He died of septicemia 18 days later. Both at autopsy and on a previous hepatobiliary scan he was noted to have had extensive native Uver regeneration. 

The important uses of laboratory tests in acute hepatitis are to identify individuals with fulminant hepatic failure, document recovery, and determine clearance of any infectious agents. The most important tests in determining extent of injury are not plasma activities of cytosolic enzymes, but evidence of impaired liver function. The most important indicator of prognosis in acute hepatitis is impairment in synthetic functions of which PT is a widely accepted indicator. In acute viral or alcoholic hepatitis, PT more than 15... 

---