Sections View Full Chapter Figures Tables Videos Annotate Full Chapter Figures Tables Videos Supplementary Content + Download Section PDF Listen ++ For further information, see CMDT Part 16-02: Acute Hepatitis A + Key Features Download Section PDF Listen +++ +++ Essentials of Diagnosis ++ Prodrome of anorexia, nausea, vomiting, malaise, aversion to smoking Fever, enlarged and tender liver, jaundice Normal to low white blood cell count; markedly elevated aminotransferases +++ General Considerations ++ Transmission of hepatitis A virus (HAV) is by the fecal-oral route by either person-to-person contact or ingestion of contaminated food or water The incubation period averages 30 days HAV is excreted in feces for up to 2 weeks before the clinical illness and rarely persists in feces after the first week of illness There is no chronic carrier state +++ Demographics ++ Globally, 15 million people are infected with HAV annually HAV spread is favored by crowding and poor sanitation HAV infection is hyperendemic in developing countries Common source outbreaks result from contaminated water or food In 2017, an outbreak in California and four other states affected a large number of homeless persons and resulted in many deaths HAV has been described as a reemerging food-borne public health threat in Europe Outbreaks have been reported among injection drug users Since introduction of HAV vaccine in the United States in 1995, the incidence rate of HAV infection has declined from 14 to 0.4 per 100,000 population + Clinical Findings Download Section PDF Listen +++ +++ Symptoms and Signs ++ Onset may be abrupt or insidious Malaise, myalgia, arthralgia, easy fatigability, upper respiratory symptoms, and anorexia A distaste for smoking, paralleling anorexia, may occur early Nausea and vomiting are frequent, and diarrhea or constipation may occur Defervescence and a fall in pulse rate often coincide with the onset of jaundice Abdominal pain Usually mild and constant in the right upper quadrant or epigastrium Often aggravated by jarring or exertion Rarely severe enough to simulate cholecystitis Jaundice Never develops in many patients Occurs after 5–10 days but may appear at the same time as the initial symptoms With its onset, prodromal symptoms often worsen, followed by progressive clinical improvement Stools may be acholic Hepatomegaly—rarely marked—is present in over 50% of cases; liver tenderness is usually present Splenomegaly occurs in 15% of patients Soft, enlarged lymph nodes—especially in the cervical or epitrochlear areas—may occur The acute illness usually subsides over 2–3 weeks Complete clinical and laboratory recovery by 9 weeks Clinical, biochemical, and serologic recovery may be followed by one or two relapses, but recovery is the rule A protracted course has been reported to be associated with HLA DRB1*1301 +++ Differential Diagnosis ++ Other viruses that cause hepatitis, particularly hepatitis B and C viruses, as well as Epstein-Barr (infectious mononucleosis) virus, cytomegalovirus, herpes simplex virus, Middle East respiratory syndrome virus, yellow fever virus, influenza virus, Ebola virus, and others Spirochetal diseases, such as leptospirosis and secondary syphilis Brucellosis Rickettsial diseases, such as Q fever Autoimmune hepatitis Drug-induced liver disease Ischemic hepatitis (shock liver) Rarely, metastatic cancer, lymphoma, or leukemia The prodromal phase of viral hepatitis must be distinguished from other infectious disease such as influenza, upper respiratory infections, and the prodromal stages of exanthematous diseases + Diagnosis Download Section PDF Listen +++ +++ Laboratory Tests ++ Antibody to hepatitis A (anti-HAV) appears early in the course of the illness Both IgM and IgG anti-HAV are detectable in serum soon after the onset Peak titers of IgM anti-HAV occur during the first week of clinical disease and usually disappear within 3–6 months Detection of IgM anti-HAV is an excellent test for diagnosing acute hepatitis A (but is not recommended for evaluation of asymptomatic patients with persistent serum aminotransferase elevations) Titers of IgG anti-HAV peak after 1 month of the disease and may persist for years IgG anti-HAV indicates previous exposure to HAV, noninfectivity, and immunity. In the United States, about 30% of the population have serologic evidence of previous infection The white blood cell count is normal to low, especially in the preicteric phase. Large atypical lymphocytes may occasionally be seen Mild proteinuria is common, and bilirubinuria often precedes the appearance of jaundice Strikingly elevated serum alanine or aspartate aminotransferases occur early, followed by elevations of bilirubin and alkaline phosphatase; in a small number of patients, the latter persist after aminotransferase levels have normalized Cholestasis is occasionally marked + Treatment Download Section PDF Listen +++ +++ Medications ++ If nausea and vomiting are pronounced or if oral intake is substantially decreased, intravenous 10% glucose is indicated Small doses of oxazepam are safe, since its metabolism is not hepatic; morphine sulfate should be avoided Corticosteroids have no benefit in patients with viral hepatitis, including those with acute liver failure +++ Therapeutic Procedures ++ Bed rest is recommended only for marked symptoms Dietary management consists of palatable meals as tolerated, without overfeeding; breakfast is usually best tolerated Strenuous physical exertion, alcohol, and hepatotoxic agents should be avoided + Outcome Download Section PDF Listen +++ +++ Complications ++ Acute liver failure due to hepatitis A is uncommon; the frequency is increased when hepatitis A occurs in a patient with chronic hepatitis C Other occasional extrahepatic complications include Acute kidney injury Arthritis Vasculitis Acute pancreatitis Aplastic anemia Variety of neurologic manifestations +++ Prognosis ++ Generally, clinical recovery is complete in 9 weeks Hepatitis A does not cause chronic liver disease, though it may persist for up to 1 year, and clinical and biochemical relapses may occur before full recovery The mortality rate is < 1%, with a higher rate in older adults than in younger persons +++ Prevention ++ Strict isolation is not necessary, but hand washing after bowel movements is required Thorough hand washing by anyone who may contact contaminated utensils, bedding, or clothing is essential +++ Immune globulin ++ Give to all close (eg, household) personal contacts and consider giving it to persons who consume food prepared by an infected food handler The recommended dose, 0.02 mL/kg intramuscularly, is protective if administered during incubation +++ Vaccination ++ Two effective inactivated hepatitis A vaccines are recommended for Persons living in or traveling to endemic areas (including military personnel) Patients with chronic liver disease on diagnosis Persons with clotting-factor disorders who are treated with factor concentrates Men who have sex with men Animal handlers Illicit drug users Sewage workers Food handlers Close personal contacts of international adoptees Children and caregivers in day care centers and institutions HAV vaccine is effective in the prevention of secondary spread to household contacts of primary cases The recommended dose for adults 1 mL (1440 ELISA units) of Havrix (GlaxoSmithKline) or 1 mL (50 units) of Vaqta (Merck) intramuscularly Follow with a booster dose at 6–18 months A combined hepatitis A and B vaccine (Twinrix, GlaxoSmithKline) is available +++ When to Admit ++ Encephalopathy is present INR > 1.6 The patient is unable to maintain hydration + References Download Section PDF Listen +++ + +Barrett CE et al. Impact of public health interventions on drinking water-associated outbreaks of hepatitis A—United States, 1971–2017. MMWR Morb Mortal Wkly Rep. 2019 Sep 6;68(35):766–70. [PubMed: 31487277] + +Centers for Disease Control and Prevention (CDC). 2017—Outbreaks of hepatitis A in multiple states among people who are homeless and people who use drugs. https://www.cdc.gov/hepatitis/outbreaks/2017March-hepatitisA.htm + +Foster MA et al. Increase in hepatitis A virus infections—United States, 2013–2018. MMWR Morb Mortal Wkly Rep. 2019 May 10;68(18):413–15. [PubMed: 31071072] + +Lemon SM et al. Type A viral hepatitis: a summary and update on the molecular virology, epidemiology, pathogenesis and prevention. J Hepatol. 2018 Jan;68(1):167–84. [PubMed: 28887164] + +Linder KA et al. JAMA patient page. Hepatitis A. JAMA. 2017 Dec 19;318(23):2393. [PubMed: 29094153]