Synopsis
Recognise enterically acquired hepatitis A and E, stabilise severe acute hepatitis, interpret time-dependent virology, control transmission, and protect exposed or vulnerable people.
- HAV spreads mainly through faeco-oral exposure; HEV acquired in the UK is commonly zoonotic and linked to undercooked pork, offal, wild boar or game.
- Both usually cause an acute hepatitic illness with malaise, nausea, anorexia, dark urine, pale stools, pruritus and jaundice, but infection may be asymptomatic.
- HAV never becomes chronic; HEV can persist in transplant recipients and other immunosuppressed people and may cause rapid fibrosis.
Key red flags
Confusion, drowsiness, asterixis or behavioural change with acute hepatitis is encephalopathy until proved otherwise and needs emergency liver-centre discussion.
New confusion, low glucose, bruising, rising INR, acidosis or renal dysfunction identifies acute liver failure rather than uncomplicated hepatitis.
Investigation priorities
Identify hepatic failure and complications before virological classification.
Management branches
A patient presents with jaundice, dark urine or a markedly hepatitic blood-test pattern.
- Assess ABCDE, cognition and hydration, then obtain bedside glucose, INR, renal function, acid-base status and a complete medication and toxin history.
- Treat hypoglycaemia immediately, stop non-essential hepatotoxic agents and provide cautious fluid, antiemetic and electrolyte support according to clinical state.
The patient is stable enough for cause-directed acute-hepatitis investigation.
Key medicines
Hepatitis A vaccine for post-exposure prophylaxisGive one age-appropriate intramuscular dose as soon as possible and within the current UKHSA contact window, then complete the product-specific course if ongoing protection is indicated.
Human normal immunoglobulin for selected HAV contactsArrange the exact intramuscular product dose through the health-protection and Green Book pathway as soon as possible; do not substitute a locally remembered volume.