Hepatitis A
Acute self-limiting viral hepatitis caused by hepatitis A virus (HAV), transmitted via faecal-oral route. Notifiable disease. No chronic state. Supportive management; prevention through vaccination and hygiene.
Key Facts
Faecal-oral transmission: contaminated food/water, close contact, MSM, travel to endemic areas Incubation period: 15-50 days (average 28 days); most infectious 2 weeks before to 1 week after jaundice onset Clinical: often subclinical in children; adults: prodromal illness → jaundice → recovery over 2-6 weeks; NO chronic hepatitis Diagnosis: anti-HAV IgM (acute infection); anti-HAV IgG (past infection/immunity) Fulminant hepatic failure: rare (<0.5% overall; higher in pre-existing liver disease and elderly — up to 1-2%) Prevention: HAV vaccine (Havrix/Vaqta — 2 doses, 0 and 6-12 months); post-exposure prophylaxis (vaccine within 14 days); notifiable disease in UK
Overview
Key Facts
Hepatitis A is an acute, self-limiting liver infection that does not cause chronic hepatitis. It is a notifiable disease in the UK. Prevention through vaccination and public health measures is the primary strategy.
Epidemiology
~350 cases per year in the UK (most travel-associated). Endemic in Sub-Saharan Africa, South/Southeast Asia, Central America. UK is low-endemicity — most adults are susceptible. Outbreaks occur in MSM communities, people who inject drugs, and institutional settings.
Aetiology
- Hepatitis A virus (HAV): non-enveloped RNA virus (Picornaviridae family)
- Transmission: faecal-oral — contaminated food (shellfish, salad), water, person-to-person (household, sexual contact), blood-borne (rare)
- Risk groups: travellers to endemic areas, MSM, PWID, household contacts, occupational (sewage workers)
Pathophysiology
HAV replicates in hepatocytes. Liver damage is primarily immune-mediated (CD8+ T-cell response) rather than direct viral cytopathic effect. The inflammatory response causes hepatocyte necrosis and cholestasis. Viral shedding in stool begins 1-2 weeks before symptom onset and peaks around jaundice onset — hence transmission occurs before diagnosis. Complete viral clearance occurs and there is no chronic carrier state.
Clinical Presentation
Prodromal Phase (1-2 weeks)
- Malaise, fatigue, anorexia, nausea
- Low-grade fever, myalgia
- RUQ discomfort
Icteric Phase (2-6 weeks)
- Jaundice (dark urine, pale stools, pruritus)
- Hepatomegaly (tender)
- Prodromal symptoms often improve as jaundice appears
- Splenomegaly (~15%)
Recovery Phase
- Gradual resolution over weeks to months
- Fatigue may persist for months
Atypical Presentations
- Subclinical/anicteric: common in children (<6 years — 70% asymptomatic)
- Cholestatic hepatitis: prolonged jaundice (>3 months) — good prognosis
- Relapsing hepatitis: symptoms recur after apparent recovery (~10%)
- Fulminant hepatic failure: rare (<0.5%) but potentially fatal; more common in elderly and those with pre-existing liver disease
Red Flags
- Encephalopathy (confusion, asterixis) — fulminant failure
- INR >1.5 with rising bilirubin
- Rapidly shrinking liver size
- Renal failure
Differential Diagnosis
| Diagnosis | Key Features | Investigation |
|---|---|---|
| Hepatitis B (acute) | Risk factors (IVDU, sexual, endemic), HBsAg | HBsAg, anti-HBc IgM |
| Hepatitis E | Similar presentation, UK autochthonous (pork) | Anti-HEV IgM, HEV RNA |
| EBV hepatitis | Pharyngitis, lymphadenopathy, splenomegaly | EBV VCA IgM, monospot |
| CMV hepatitis | Immunosuppressed, or mononucleosis-like illness | CMV IgM, CMV PCR |
| Drug-induced liver injury | Temporal relationship to drug | Drug history |
| Autoimmune hepatitis | Raised IgG, autoantibodies | ANA, SMA, IgG |
| Biliary obstruction | Obstructive LFT pattern, dilated ducts | USS, MRCP |
Diagnosis / Investigation
Bedside
- History: travel, food exposure, contacts, sexual history, occupation
Bloods
- Anti-HAV IgM: diagnostic of acute infection (positive for up to 6 months)
- Anti-HAV IgG: indicates past infection or vaccination (lifelong immunity)
- LFTs: markedly raised ALT/AST (often >1000 IU/L); raised bilirubin; ALP variably raised
- INR/PT: normal in most; raised in severe/fulminant disease (poor prognostic sign)
- FBC: mild lymphopaenia, sometimes leucopaenia
- U&Es: renal function (hepatorenal syndrome in fulminant)
Imaging
- USS abdomen: exclude biliary obstruction; may show hepatomegaly
Special Tests
- HAV RNA (PCR): confirms viraemia; rarely needed clinically (IgM sufficient)
- Liver biopsy: NOT routinely indicated; shows portal and periportal inflammation with hepatocyte necrosis
- King's College Criteria: for assessing need for liver transplant in fulminant failure
Management
Non-pharmacological
- Supportive care: rest, adequate hydration, avoid alcohol, avoid hepatotoxic drugs
- Infection control: handwashing, food hygiene; infectious until 7 days after jaundice onset
- Notify PHE: HAV is a notifiable disease under the Health Protection (Notification) Regulations 2010
- Contact tracing: household and sexual contacts
Pharmacological
- No specific antiviral treatment for hepatitis A
- Symptomatic relief: anti-emetics (cyclizine, ondansetron), cholestyramine for pruritus, paracetamol for pain (avoid if severe liver impairment)
- Post-exposure prophylaxis: HAV vaccine within 14 days of exposure for close contacts (effective if given early); ± immunoglobulin (HNIG) if immunosuppressed or chronic liver disease
Surgical/Interventional
- Liver transplantation: for fulminant hepatic failure meeting King's College Criteria (very rare)
Referral Criteria
- Hepatology referral if: INR >1.5, encephalopathy, worsening liver function, prolonged cholestasis
- Public health notification: mandatory for all cases
- Liver transplant centre: if fulminant hepatitis
Prognosis
Hepatitis A is self-limiting in >99% of cases. No chronic hepatitis, no carrier state. Complete recovery with lifelong immunity. Fulminant hepatic failure occurs in <0.5% overall but ~1-2% in those >50 years or with pre-existing liver disease. Mortality from fulminant HAV is ~50% without transplant. Cholestatic and relapsing variants have good prognosis. Return to normal activities typically within 2-6 weeks.
Other Relevant Information
Hepatitis A Serology Interpretation
| Marker | Acute Infection | Past Infection/Immunity | Vaccinated |
|---|---|---|---|
| Anti-HAV IgM | Positive | Negative | Negative |
| Anti-HAV IgG | Positive (late) | Positive | Positive |
| HAV RNA | Positive | Negative | Negative |
HAV Vaccination
| Indication | Regimen |
|---|---|
| Travel to endemic areas | Havrix: 2 doses (0 and 6-12 months) |
| MSM | 2-dose schedule |
| Chronic liver disease | 2-dose schedule |
| PWID | 2-dose schedule |
| Post-exposure prophylaxis | Single dose within 14 days of exposure |
| Occupational (sewage workers) | 2-dose schedule |