All patients with acute hepatitis must be observed until the acute liver injury resolves.

Abstract

Ahmed and Keeffe point out that only a few basic viral diagnostic tests are indicated for the initial evaluation of patients presenting with acute hepatitis. This is in consideration that hepatitis A and B account for three fourths of cases of acute viral hepatitis in the United States. The presence of hepatitis A or B is sometimes heralded by arthralgias, nephritis, or urticaria, which can provide useful diagnostic clues.1,2 Hepatitis C should be considered in patients with a known blood exposure, but only a fraction of persons with hepatitis C have acute jaundice or other recognizable symptoms. Furthermore, when symptoms occur with acute hepatitis C, the development of hepatitis C antibodies is often delayed several weeks after the onset of symptoms. The use of viral diagnostic tests other than the basic tests for hepatitis A and B can be guided by epidemiologic risk factors.3 A large number of viruses and other infectious agents occasionally cause hepatitis, sometimes as part of a multisystem illness such as infectious mononucleosis or Hantavirus infection. Hepatitis E is a form of acute viral hepatitis found in the Indian subcontinent and occasionally in Latin America.4 In a patient without a pertinent travel history or a history of immunosuppression, it is usually not useful to pursue these less common diagnoses. Not all patients presenting with acute elevation of aminotransferase levels have viral hepatitis. Many other serious, treatable conditions can masquerade as viral hepatitis. A hepatic drug reaction can be lethal if the offending agent is not stopped. Acetaminophen can cause intentional or unintentional hepatotoxicity, especially in persons with high alcohol consumption.5 Ischemic liver injury can be caused by an abrupt decrease in cardiac output, especially when combined with hepatic venous congestion. This can occur unobserved when a patient with serious valvular or myocardial disease has arrhythmia during sleep. Acute obstruction of the common bile duct by a gallstone can cause the aminotransferase levels to rise for a day or two to more than 1,000 U/L. This can be especially confusing because the alkaline phosphatase level may take several days to rise, and imaging studies may not initially show bile duct dilatation. If the initial evaluation of a patient with greatly elevated aminotransferase levels is negative for viral hepatitis, then other less common causes of acute hepatitis, such as autoimmune hepatitis or Wilson disease,6 should be considered. If the initial clinical evaluation and a basic laboratory evaluation for hepatitis A and B do not reveal a diagnosis, then it may not be possible to reach one. Further laboratory evaluation may be guided by the clinical course. For any patient who appears ill with acute hepatitis, the prothrombin time should be measured, and an assessment should be done for hepatic encephalopathy. Regardless of the cause, any evidence of encephalopathy or a substantially prolonged prothrombin time should prompt hospital admission and close follow-up. Also, any patient with acute hepatitis, regardless of the cause, needs to be observed until the acute liver injury resolves.