Approach

Post-exposure prophylaxis for both the patient and close contacts of the patient should not be delayed while waiting for test results if reasonable clinical certainty exists about the probability of infection.

History

Thorough history can highlight relatively significant risk factors, including living in an endemic area, close personal contact with an infected person, men who have sex with men, travel to high-risk areas, drug use, known foodborne or waterborne outbreak, and homelessness.[1][24]​​​ In about one third of reported cases, no risk factor is identified.[16]

History should also assess risk or history of other liver diseases such as hepatitis B and hepatitis C virus infections and/or cirrhosis, as concomitant acute hepatitis A virus (HAV) infection in these circumstances has a higher risk for progression to HAV acute liver failure.

Symptoms and signs

The incubation period averages 28 days (range 15-50 days).​[1]

Most infections in children aged <6 years are asymptomatic; possible symptoms include fever, nausea, anorexia, and malaise.[7]

In adults and older children, clinical course can be divided into pre-icteric phase and icteric phase. The pre-icteric phase lasts 5-7 days characterised by abrupt onset of nausea, vomiting, abdominal pain, fever, malaise, fatigue, and headache.[2][22] ​​Relatively less common symptoms include arthralgias, myalgias, diarrhoea, constipation, cough, pruritus, and urticaria.[22]

Physical signs may include right upper quadrant pain with tender hepatomegaly, splenomegaly, posterior cervical lymphadenopathy, evanescent rash, and bradycardia.[21][22]

Within a few days to 1 week the icteric phase begins with dark urine, acholic stools, and jaundice.[2][21]​​ With the onset of jaundice the pre-icteric phase symptoms usually diminish. Jaundice peaks typically at 2 weeks. Jaundice is uncommon in young children.[1][7]

Prolonged disease or acute liver failure

A minority of people (10% to 20%) have a prolonged or relapsing course. After initial infection, there is a remission with partial or complete resolution of symptoms and abnormal liver tests. Relapse typically occurs within 3 weeks and is milder than the initial infection. Immune-mediated manifestations (purpura, arthralgia, nephritis) may occur.[36] A prolonged course can last several months with persistent fever, pruritus, diarrhoea, jaundice, weight loss, and malabsorption.[22][23]

Acute liver failure occurs in <1% of patients, and is characterised by worsening jaundice, coagulopathy, and encephalopathy, due to severe impairment of hepatic functions, or severe necrosis of hepatocytes in absence of pre-existing chronic liver disease.[37][38] An excessive host immune response has been implicated.[38][39]

Diagnostic tests

Serum liver enzymes and bilirubin can be ordered as soon as clinical symptoms begin.[21][22] Transaminase levels may reach more than 10,000 units/L, although there is a little correlation between level and disease severity. The serum alanine aminotransferase (ALT) is commonly higher than the serum aspartate aminotransferase (AST). While alkaline phosphatase level is usually elevated minimally, the bilirubin level is usually elevated to about 85.5 to 171.0 micromol/L (5-10 mg/dL).[40]

Blood urea, serum creatinine, and prothrombin time (PT) may also be measured at baseline. Acute kidney injury has been reported in patients with HAV.[41] Patients with acute liver failure typically have a prolonged PT.

Immunoglobulin M (IgM) anti-HAV test should be ordered when patient is symptomatic or HAV is suspected.[1]​ IgM anti-HAV and IgG anti-HAV tests can be ordered concurrently. Serum IgM anti-HAV antibodies are usually positive 5-10 days before onset of symptoms, peak during the acute or early convalescent phase of the disease, and decline to undetectable levels over 6 months.[1]​​[23][24]

Laboratory findings should be correlated with clinical features. Some asymptomatic patients may have previous HAV infection with prolonged presence of IgM anti-HAV. False-positive laboratory results and asymptomatic infection are both possible (more common in children aged younger than 6 years).[42] IgG anti-HAV remains detectable for decades.

Reverse-transcriptase polymerase chain reaction to detect HAV RNA in stool, body fluids, serum, and liver tissue is available. It is rarely necessary but may be considered to detect very early cases or if HAV-IgM results are inconclusive.[7]​​

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