Hepatitis A
Exam Tips
- Infectivity is highest before jaundice appears, so contact history in the 2 weeks pre-icterus is high yield for OSCE stations.
- Anti-HAV IgM can be false positive (especially in older adults); interpret with timing, IgG pattern, LFTs, and exposure risk.
- A negative early serology (first few days of symptoms) does not exclude HAV; repeat testing if suspicion remains high.
- HAV does not cause chronic hepatitis or chronic carrier state, which helps distinguish it from HBV/HCV in viva questions.
- Red flags needing urgent admission: rising INR/prolonged PT, encephalopathy, hypoglycaemia, worsening jaundice, intractable vomiting/dehydration.
- See Figure: classic phase progression of acute HAV (incubation -> prodromal -> icteric -> convalescent) and timeline of stool viral shedding versus jaundice onset.
Definition
Hepatitis A is an acute infectious hepatitis caused by hepatitis A virus (HAV), a non-enveloped positive-sense RNA hepatovirus transmitted mainly by the faeco-oral route. It typically causes a self-limiting inflammatory liver illness with prodromal, icteric, and recovery phases, and unlike hepatitis B or C it does not produce chronic carrier state or chronic hepatitis.
Pathophysiology
After ingestion, HAV crosses the gut, enters portal blood, and reaches the liver where it replicates in hepatocytes and Kupffer cells. Liver injury is predominantly immune mediated (host T-cell and inflammatory response) rather than directly cytopathic viral destruction, producing marked transaminitis and cholestatic features in some patients. Virus is excreted in bile and shed heavily in stool, with peak infectivity in the 2 weeks before jaundice; shedding then declines but may persist longer in children and immunocompromised people. The illness classically progresses through incubation (about 15-50 days, mean about 28), prodromal, icteric, and convalescent phases, with lifelong IgG-mediated immunity after recovery.
Risk Factors
- Travel to high/intermediate endemic regions (especially VFR travellers, long-stay travellers, poor sanitation exposure)
- Close household/contact exposure to a confirmed case
- Men who have sex with men, particularly oro-anal exposure and multiple partners
- Injecting drug use or sharing contaminated drug paraphernalia
- Consumption of contaminated food/water (for example undercooked shellfish, frozen berries, leafy vegetables, unsafe ice)
- Occupational exposure (sewage workers, laboratory staff handling HAV, staff in large residential institutions, primate handlers)
- Clotting factor disorders receiving blood products (rare modern risk)
- Chronic liver disease (higher risk of severe outcomes if infected)
Clinical Features
Symptoms
- Prodrome: fatigue, malaise, myalgia/arthralgia, low-grade fever
- Anorexia, nausea, vomiting, right upper quadrant discomfort
- Icteric phase: jaundice, dark urine, pale stools, pruritus
- Headache, diarrhoea or constipation, occasional urticarial-type symptoms
- Convalescent phase: prolonged fatigue and reduced appetite
Signs
- Tender hepatomegaly
- Right upper quadrant tenderness
- Jaundice/scleral icterus
- Less common splenomegaly
- Occasional cervical lymphadenopathy or rash
- Features of severe disease if present: encephalopathy, bruising/bleeding, dehydration
Investigations
Management
Lifestyle Modifications
- Supportive care: oral hydration, rest, small frequent meals, avoid alcohol until clinical and biochemical recovery
- Strict hand hygiene and toilet hygiene; avoid preparing food for others while infectious
- Public health notification and contact tracing via UKHSA/local health protection team
- Avoid sex likely to involve faeco-oral exposure until no longer infectious and advised by public health
- Safety-net urgently for confusion, worsening jaundice, bleeding, persistent vomiting, reduced urine output, or drowsiness
Pharmacological Treatment
Symptom control (supportive)
- Paracetamol 500 mg-1 g orally every 4-6 hours when required (maximum 4 g/day; consider lower maximum such as 2-3 g/day in frail/low body weight or significant liver impairment)
- Ondansetron 4-8 mg orally/IV every 8-12 hours when required for significant nausea/vomiting
- Chlorphenamine 4 mg orally every 4-6 hours (maximum 24 mg/day) for itch
- Colestyramine 4 g orally once or twice daily, titrated up to 16 g/day in divided doses for cholestatic pruritus
No routine antiviral therapy for HAV. Avoid unnecessary hepatotoxic drugs and review all prescribed/OTC medicines. Use antiemetics and antipruritics pragmatically based on severity and hydration status.
Prevention in exposed/high-risk groups
- Inactivated hepatitis A vaccine: adult dose 1 mL IM as soon as possible after exposure (follow product schedule for booster, commonly at 6-12 months)
- Human normal immunoglobulin (HNIG) IM may be used for selected contacts at higher risk of severe disease or poor vaccine response, according to UKHSA protocols
Post-exposure prophylaxis is time-sensitive and should be arranged with public health specialists. Check contraindications to IM injection (for example severe thrombocytopenia/anticoagulation risk) and vaccine allergy history.
Complications
- Relapsing hepatitis A (typically 3-12 weeks after initial illness)
- Fulminant hepatic failure with coagulopathy and encephalopathy (rare, but life-threatening)
- Prolonged cholestatic hepatitis with severe pruritus
- Acalculous cholecystitis or pancreatitis (rare)
- Haematological/immune complications (for example aplastic anaemia, autoimmune haemolysis, thrombocytopenia)
- Neurological complications (for example Guillain-Barre syndrome, post-viral encephalitis, transverse myelitis)
- Acute kidney injury (rare)
- Preterm labour risk if infection occurs in later pregnancy
Prognosis
Prognosis is generally excellent: around 85% recover within 3 months and almost all within 6 months, with lifelong immunity after clearance. Severity rises with age and with pre-existing chronic liver disease; death is uncommon in the UK but risk increases markedly if fulminant liver failure develops.
Sources & References
🏥BMJ Best Practice(5)
✅NICE Guidelines(1)
- Hepatitis A[overview]
📖Textbook References(8)
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1833)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1493)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1506)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1833)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1506)[context]
- Oxford Handbook of Clinical Diagnosis (Huw Llewelyn, Hock Aun Ang, Keir Lewis etc.) (Z-Library).pdf(pp. 317)[context]
- [Oxford Medical Handbooks] Ian Wilkinson, Tim Raine, Kate Wiles, Anna Goodhart, Catriona Ha - Oxford Handbook of Clinical Medicine (2017, Oxford University Press) - libgen.li.pdf(pp. 292, 293)[context]
- [Williams, Bailey and Love's Short Practice of Surgery] Norman Williams, Christopher Bulstrode, P Ronan O'Connell - Bailey & Love's Short Practice of Surgery 26E (2013, CRC Press) - libgen.li.pdf(pp. 1096, 1097)[context]