Hepatitis A Virus

Presentation

Incubation period is usually 28 days

Prodromal phase of hepatitis (5-7 days with abrupt onset of symptoms)

  • fever
  • malaise
  • muscle and joint pain
  • fatigue
  • nausea and vomiting
  • RUQ pain
  • headache

Icteric phase of hepatitis

  • jaundice
  • pale stools and dark urine if cholestasis is present
  • pruritis
  • fatigue, nausea, vomiting
  • hepatomegaly
  • splenomegaly
  • lymphadenopathy
  • RUQ tenderness

Note: the clinical features of acute hepatitis A are common to all forms of acute viral hepatitis

History

Hepatitis A is transmitted by close contact or via faeces-contaminated food and water

  • Does the patient live in or travelled to an endemic area?
  • Sexual history: Close personal contact with an infected person? Men who have sex with men
  • Exposure to a known food-borne outbreak
  • Drug history: Injecting drug users

Examination

  • jaundice
  • hepatomegaly
  • splenomegaly
  • lymphadenopathy
  • RUQ pain

Note there may be no signs on examination - diagnosis is confirmed using serology

Laboratory investigations

Hepatitis serology

  • Hepatitis A virus immunoglobulin M (HAV-IgM) - marker of acute or recurrent infection
  • Hepatitis A virus immunoglobulin G (HAV-IgG) - marker of previous HVA infection or vaccination

Positive HAV-specific IgM means acute hepatitis A infection is likely.

  • HAV-IgM is detectable about 3 weeks after exposure, increases in titre over 4–6 weeks, then declines to non-detectable levels (generally within 6–12 months of infection).
  • If serology is taken in the first 7–10 days of symptoms, there is a small risk of a false negative result, so serology should be repeated 1–2 weeks later.

If there is a positive HAV-non-specific IgM, repeat the test.

Positive HAV-IgG, this indicates current or past hepatitis A infection, or immunity from previous vaccination.

  • HAV-IgG is detectable 5–10 days after the onset of symptoms and persists, conferring lifelong immunity.

LFTs

  • Alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels may be significantly increased (usually >1000 IU/L).
  • Bilirubin may be elevated (up to 500 micromols/L).
  • Prothrombin time may be prolonged (5 seconds or more suggests hepatic decompensation)

U&Es
Blood urea and creatinine - elevated in renal failure, which is associated with HAV

Clotting screen

  • Prothrombin time - mildly elevated in HAV (11-26 seconds)

Radiological investigations

  • US rarely used but can exclude other diseases

Differential Diagnoses

  • Viral hepatitis caused by other viruses (such as hepatitis B, C, D, and E), Epstein-Barr virus (infectious mononucleosis), or cytomegalovirus (CMV).
  • Alcohol-induced hepatitis.
  • Drug-induced liver disease, such as following paracetamol use.
  • Acute HIV infection.
  • Autoimmune hepatitis.
  • Hepatitis caused by bacteria, such as Leptospirosis and Coxiella burnetii.
  • Granulomatous disorders.
  • Wilson's disease.

Diagnosis

Confirmed infection with hepatitis A is defined by an acute illness and:

  • Jaundice or elevated serum aminotransferase levels and,
  • IgM antibodies to hepatitis A virus

Management

Symptomatic supportive care

Pain relief:

Paracetamol

  • Normal dosages used unless evidence of moderate or severe liver impairment.
  • If serum bilirubin is greater than 300 micromols/L or prothrombin time is greater than 3 seconds, reduce the dosage to a maximum of 1 gram two or three times a day

Ibuprofen

  • A weak opioid (e.g codeine) if liver impairment is mild.
  • Avoid codeine in severe liver impairment due to enhanced sedative effects and reduced drug clearance

Treatment of nausea:

  • Metoclopramide or cyclizine at normal dosages, if liver impairment is mild

Treatment of Pruritis:

  • Simple measures e.g maintaining a cool, well-ventilated environment, wearing loose clothing, and avoiding hot baths or showers
  • Chlorphenamine at normal dosage at night (avoid in severe liver impairment)
  • Ursodeoxycholic acid, colestyramine, or corticosteroids are alternatives

Prior to discharge

Patient lifestyle advice:

  • Avoid alcohol during the acute illness, as this can increase the risk of liver damage.
  • Avoid work, school, or nursery, until no longer infectious (typically 7 days after the onset of jaundice)

Minimize the risk of transmission to partners and contacts. The patient and all close contacts should:

  • Ensure thorough hand washing
  • Ensure good general personal hygiene.
  • Avoid handling food
  • Avoid unprotected sexual intercourse
  • Avoid sharing needles and other drug paraphernalia

Follow up

  • Monitor LFTs and prothrombin time:
  • Check liver function 3–5 days after the diagnosis, then weekly until LFTs start to improve. Monitoring can then be reduced to fortnightly and then monthly until liver function normalizes (usually takes 4–12 weeks).
  • Monitor twice a week in symptomatic or jaundiced patients

Complications

Risk of relapse
Cholestasis (features include severe pruritus, diarrhoea, weight loss, and malabsorption)
Fulminant liver disease

  • Presents with sudden, severe vomiting, irritability and confusion
  • This can lead to coagulopathy and hepatic encephalopathy.
  • Manifests during the first four weeks of illness and is more common in people with concurrent chronic liver disease e.g chronic hepatitis B or C infection
  • It has a mortality rate of 40% without liver transplantation

Prognosis

  • Usually a self-limiting illness which lasts less than 2 months
  • Complete clinical recovery may take up to 6 months after the onset of the illness.
  • Has no long-term sequelae, does not cause chronic liver disease, and has no chronic carrier state.
  • Results in lifelong immunity
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