Acute Viral Hepatitis At A Glance

An acute viral hepatitis is defined as a diffuse inflammation of the liver caused by specific hepatotropic viruses with different transmission paths and epidemiology. Nonspecific prodrome followed by anorexia, nausea and often fever or pain in the right upper abdomen. Often jaundice typically develops at a time disappear at the other symptoms. Most cases heal spontaneously, but some make a history of chronic hepatitis. Occasionally from acute viral hepatitis, acute liver failure, indicating a fulminant hepatitis develops. Diagnosis is made by analysis of liver function tests and serological tests for the identification of a virus. Promotes good hygiene and general precautions can prevent transmission of viral hepatitis. Some viruses prophylaxis is pre- and postexpositionell possible using vaccines or immunoglobulins. Treatment is generally supportive.

(See also causes of hepatitis, hepatitis B in newborns, hepatitis B virus (HBV) infection in newborns.)

An acute viral hepatitis is defined as a diffuse inflammation of the liver caused by specific hepatotropic viruses with different transmission paths and epidemiology. Nonspecific prodrome followed by anorexia, nausea and often fever or pain in the right upper abdomen. Often jaundice typically develops at a time disappear at the other symptoms. Most cases heal spontaneously, but some make a history of chronic hepatitis. Occasionally from acute viral hepatitis, acute liver failure, indicating a fulminant hepatitis develops. Diagnosis is made by analysis of liver function tests and serological tests for the identification of a virus. Promotes good hygiene and general precautions can prevent transmission of viral hepatitis. Some viruses prophylaxis is pre- and postexpositionell possible using vaccines or immunoglobulins. Treatment is generally supportive. (See also causes of hepatitis;. Hepatitis B in newborns, hepatitis B virus (HBV) infection in newborns) Acute viral hepatitis is a common, worldwide prevalent disease with different causes. All forms have clinical, biochemical and morphological similarities. Liver infections, which are caused by non-specific hepatitis viruses (such. As Epstein-Barr virus, yellow fever and cytomegalovirus), one does not usually referred to as acute viral hepatitis. Etiology known are at least five different hepatitis viruses (see Table: Properties of hepatitis viruses) hepatitis A (HAV) Hepatitis-B (HBV) Hepatitis C (HCV) Hepatitis D (HDV) hepatitis E (HEV) Further, yet unidentified viruses probably also cause acute viral hepatitis. Features of hepatitis viruses characteristic Hepatitis A virus Hepatitis B virus Hepatitis C virus hepatitis D virus hepatitis E virus nucleic acid RNA DNA RNA * RNA Serological diagnosis IgM anti-HA HBsAg Anti-HCV Anti-HDV Anti-HEV main transmission faecal-oral blood blood needle water incubation period (days) 15-45 40-180 20-120 30-180 14-60 epidemics Yes No No No Yes chronicity No Yes Yes Yes No liver cancer No Yes Yes No * Incomplete RNA; requires hepatitis B virus for replication presence. Anti-HCV = antibody against hepatitis C virus, anti-HDV = antibody against hepatitis D virus, anti-HEV = antibody against hepatitis E virus, HBsAg = hepatitis B surface antigen, IgM anti-HAV = IgM antibody to hepatitis A virus. Symptoms and complaints Some manifestations of acute hepatitis virus-specific (see discussion of the different hepatitis viruses), but usually acute infection tend to develop in predictable stages: incubation period: multiply the virus and spreads without symptoms to cause (see Table: Features hepatitis viruses). Prodromal or präikterische phase occur non-specific symptoms such as loss of appetite, malaise, nausea and vomiting, a newly emerged dislike of cigarettes (for smokers), and often fever or pain in the right upper abdomen on. Urticaria and arthralgia are common, especially in HBV infection. Icteric phase: After 3-10 days of urine is dark, followed by jaundice. The systemic symptoms usually regress, and the patient feels better, even though the jaundice increases. The liver is often enlarged and painful on palpation, the liver edges stay soft and smooth. A small splenomegaly occurs in 15-20% of patients. The jaundice has peaked after 1-2 weeks. Recovery phase: During this 2-4 week period faded jaundice. The appetite returns mostly back to first symptomatic week. Acute viral hepatitis is a spontaneous recovery in the majority within 4-8 weeks after the onset of symptoms. A anicteric hepatitis is more common than the icteric form of hepatitis in patients with HCV infection and in children with HAV infection. It typically manifests as a small flu-like illness. In some patients observed recurrent hepatitis, which is characterized by recurrent disease manifestations during the recovery phase. Manifestations of cholestasis may develop during the icteric phase (the so-called cholestatic hepatitis), usually it disappears spontaneously. If they persist, they cause prolonged jaundice, elevated alkaline phosphatase, and pruritus, despite the general regression of inflammation. Diagnostic liver function tests (AST and ALT increased disproportionately compared to the alkaline phosphatase, usually with hyperbilirubinemia) serological tests PT / INR measurement initial diagnosis of acute viral hepatitis are Acute hepatitis must first of other diseases that cause similar symptoms, distinguished Viral. In the prodromal phase, the hepatitis is not different from many non-specific viral diseases and is therefore difficult to diagnose. In anicteric patients who due to risk factors, there is a hepatitis suspicion initially non-specific liver function tests incl. Transaminases, bilirubin and alkaline phosphatase be determined. In general, the suspected acute hepatitis only during the icteric phase is collected. Therefore, the differential diagnosis of acute hepatitis should be delimited from other diseases that cause jaundice (Simplified approach to diagnostic potential acute viral hepatitis.). Acute hepatitis can be added from other diseases that cause jaundice, delimited by the sharp increase in the transaminases ALT and AST (typically ? 400 IU / l) Alanine aminotransferase (ALT) is typically higher than the aspartate aminotransferase (AST), but the absolute values ??correlate poorly with clinical severity. The levels rise early in the prodromal phase to reach its peak before jaundice is maximum and then decrease slowly during the recovery phase. One of bilirubin in the urine precedes jaundice usually. The hyperbilirubinemia is less pronounced in acute viral hepatitis and its differentiation has no clinical benefit. The alkaline phosphatase is usually raised only moderately large increases raise suspicion of extrahepatic cholestasis close and cause imaging techniques (e.g., as ultrasonography). A liver biopsy is generally not necessary as long as the diagnosis is uncertain. If the laboratory findings have acute hepatitis suspect, especially with an increase in ALT and AST to> 1000 I.E./l, prothrombin time and INR should be determined. Disease manifestations such as portosystemic encephalopathy, a bleeding diathesis or an extension of the INR raise suspicion of acute liver failure and near point to a fulminant hepatitis. If the suspected acute hepatitis is, you must first diagnose the underlying cause. An appropriate exposure history may be the only indication of a drug-induced or toxic hepatitis. The history should also uncover risk factors for viral hepatitis. Sore throat in the prodromal phase and a general lymph node enlargement can be more reminiscent of an infectious mononucleosis as a viral hepatitis. An alcoholic hepatitis is suspected in a drinking history in rather slowly developing symptoms and existence of spider nevi or other signs of chronic alcohol abuse or chronic liver disease). The aminotransferase levels exceed even in severe cases rarely 300 I.E./l. In contrast to viral hepatitis, AST is typically higher than the ALT, although this difference alone is not a reliable criterion for distinguishing the two diseases. In unclear situations can be distinguished on the basis of a liver biopsy usually between alcoholic and viral hepatitis. Simplified diagnostic approach to potential acute viral hepatitis. * Additional laboratory tests for hepatitis A (see Table: hepatitis A SerologieHepatitis-bRefer table: hepatitis B serology *) and hepatitis C (see Table: hepatitis C serology). Anti-HCV = antibody against hepatitis C virus, HBsAg = hepatitis B surface antigen, IgM anti-HAV = IgM antibodies to hepatitis A virus. Serology in patients with findings that have an acute viral hepatitis suggest the following tests to screen for hepatitis viruses A, B and C are carried out: IgM antibody to HAV (IgM anti-HAV) hepatitis B surface antigen (HBsAg) IgM antibody to hepatitis B core (anti-HBc IgM) antibody to HCV (anti-HCV) positive test results are further serological tests to differentiate an acute from a past or chronic infection appears (see table: hepatitis a serology, hepatitis B serology * and hepatitis C serology). When a suspect for HBV infection serology the e antigen (HBeAg) and anti-HBe are tested to determine the prognosis of the disease and establish an antiviral treatment for hepatitis B. If the serologically diagnosed HBV infection is severe, anti-HDV should be determined. the patient has recently been in a corresponding endemic area should be tested for IgM antibodies against HEV (IgM anti-HEV) when the test available steht.Biopsie A biopsy is not usually necessary, but if it is carried out, shows they usually have a similar histopathology, regardless of the specific virus: patchy cell output acidophile hepatocellular necrosis mononuclear inflammatory infiltrate histological evidence of regeneration, the preservation of Retikulinnetzwerks Sometimes you can (caused by densely packed HBsAg HBV infection due to the presence of Milchglashepatozyten in plasma) and detected by specific immunological staining of viral components. However, these findings are in acute HBV infection unusual and are more common in chronic infection. HCV infection can sometimes be suspected because of fine morphological clues. Liver biopsy may be helpful in prognosis in the case of acute hepatitis, but is not carried out as a rule solely for this question. Usually there is a complete histological regeneration, unless extensive Brückennekrosen have all acini destroyed (so-called bridging necrosis). However, most patients show a complete regression with Brückennekrosen, in some cases, chronic hepatitis develops. Treatment Supportive treatment No specific treatment softens the course of acute viral hepatitis. Alcohol should be avoided because it increases the liver damage. Restrictions in diet or physical activity incl. The often prescribed bed rest have no scientific basis. Most patients can resume safe to work after the jaundice has subsided, even if the transaminases are still increased. In the cholestatic hepatitis, the administration of cholestyramine can be 8 g p.o. 1 to 2 times reduce the itching daily. The presence of a viral hepatitis is reportable. Prevention Because all forms of treatment have only a limited effect, prevention is of great importance. General measures A good personal hygiene is the risk of transmission down, especially the fecal-oral transmission as HAV and HEV. Blood and other body fluids (eg. As saliva, seminal fluid) from patients with acute HBV and HCV, as well as the stool of patients with hepatitis A must be considered as infectious. Protective measures are recommended, but isolation of patients is of little help to prevent HAV spread and has no value in HBV or HCV infection. The risk of post-transfusion hepatitis is minimized by avoiding unnecessary transfusions and all blood donors are tested for HBsAg and anti-HCV. This screening has the incidence of post-transfusion hepatitis to about 1: 100,000 units transfused blood components reduziert.Immunprophylaxe The immunoprophylaxis consists of an active immunization using vaccines and passive immunization. Vaccines for hepatitis A and hepatitis B are available in the US. Routine vaccination against hepatitis A and B is recommended in the US for all children and adults at high risk (see Adult Immunization Schedule). A vaccine against hepatitis E is available in some countries outside the US immediately. prevent standard immunoglobulins or reduce the severity of HAV infection and should be administered by the patient to family members and close contacts. can HBIG hepatitis B immunoglobulin probably an infection does not prevent, but it prevents or mitigates the clinical picture. Vaccines for immune prophylaxis of HCV or HDV not exist. The prevention of HBV infection also means an HDV prevention. The ability of HCV to change its genome complicates vaccine development. Summary The transmission paths are fecal-oral route for hepatitis A and parenterally or via the blood for hepatitis-B and -C. Hepatitis-B and -C predispose to chronic hepatitis and liver cancer, unlike hepatitis-A. Patients with acute viral hepatitis may be anicteric or even asymptomatic. It should be performed viral serological tests (IgM anti-HAV, HBsAg, anti-HCV) if the clinical findings are consistent with acute viral hepatitis and AST and ALT are greatly increased compared to the alkaline phosphatase. Treatment is supportive. Routine vaccination against hepatitis A and B is recommended in the US for all children and adults at high risk.

Health Life Media Team

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