Rare but real: Unusual manifestations of hepatitis A

Introduction

Globally, the incidence of new hepatitis A infections is observed to be 1.5 million per year. Hepatitis A virus (HAV) usually causes jaundice but may be complicated by cholestatic or relapsing hepatitis, autoimmune hepatitis, fulminant hepatic failure, or acute kidney injury. Extra-hepatic presentations, though rare, include anaemia, pancreatitis, neuritis, pleural and pericardial effusions, and myocarditis. Here, we present two rare paediatric manifestations: complete heart block with pleural effusion and acute pancreatitis.

Case report 1

A 6-year old boy, immunised according to national schedule, presented with abdominal pain, anorexia, and vomiting for 2 days. There was no drug ingestion, fast breathing, rash, chest pain, and dizziness. He was icteric and lethargic, with a bradycardia of 51/min and had hepatomegaly but normal heart sounds. An electrocardiogram (ECG) showed complete heart block (Fig. 1). Laboratory results revealed bilirubin 54.72 µmol/L, aspartate transaminase (AST) 1428 IU/L, alanine transaminase (ALT) 3372 IU/L, a normal coagulogram, and renal profile.

On the second day, he developed tachypnoea with bilateral pleural effusions. Repeat ECG showed Mobitz type I block. HAV immunoglobulin M (IgM) was positive; other infectious and autoimmune markers (Leptospira and Scrub IgM, hepatitis B surface antigen (HBsAg), anti- hepatitis C virus (HCV), hepatitis E, Epstein–Barr virus, parvovirus serology, widal, blood, and urine cultures) were negative. He was managed conservatively without pacing. By the sixth day, bilirubin and liver enzymes normalised, and at 1 month, heart rate improved to 86/min. The child was diagnosed as acute hepatitis A with heart block and bilateral pleural effusions.

Case report 2

A 10-year old unimmunised boy presented with progressive jaundice, acute abdominal pain radiating to the back, vomiting, and fever. There was no history of drug or toxin intake, altered sleep–wake cycle, or bleeding from any site. He was icteric, with abdominal tenderness and guarding.

Investigations revealed bilirubin 56.4 µmol/L, AST 172 IU/L, ALT 500 IU/L, international normalised ratio (INR) 1.72, and markedly elevated amylase (631 IU/L) and lipase (4045 IU/L). Ultrasound showed a bulky pancreas with hypoechoic areas, no gallstones or choledochal cyst were observed, and HAV immunoglobulin M (IgM) was positive.

The child was diagnosed as acute hepatitis A with pancreatitis. He was managed with intravenous (IV) fluids, proton pump inhibitors, antibiotics: cefotaxime at 50 mg/kg/dose thrice daily for 14 days and metronidazole at 30 mg/kg/dose thrice daily for 10 days. Computed tomography abdomen revealed walled-off pancreatic necrosis with peri-pancreatic collection (Fig. 2). Enzymes improved gradually and feeding was resumed. He recovered well and was discharged after 14 days with normalised liver function.

Discussion

Hepatitis A is a vaccine-preventable disease. The Advisory Committee on Immunization Practices (ACIP), Centre for Disease control (CDC), USA recommends two vaccine doses for children aged 12–23 months, 6 months apart. However, in India, the vaccine is not part of the national immunisation schedule at present. ¹

Extra-hepatic complications of HAV include dermatologic signs (urticarial or maculopapular rashes), renal complications (acute kidney injury, glomerulonephritis), haematologic conditions (autoimmune haemolytic anaemia, aplastic anaemia, thrombocytopenia), musculoskeletal issues (reactive arthritis), neurologic involvement (Guillain–Barré syndrome, mononeuritis), pleural or pericardial effusions, and vasculitic syndromes such as polyarteritis nodosa and cryoglobulinaemia. Cardiac involvement presenting as myocarditis, conduction abnormalities, and bradyarrhythmia have been reported in the past.^2–5 However, a complete heart block with pleural effusion in the absence of hypotension is an exceptional finding. The mechanism remains unclear, though it is speculated that elevated bilirubin and bile salts may depress sinoatrial node activity, leading to arrhythmias. ⁶ Pancreatic involvement in viral hepatitis, though uncommon, was first proposed by Lisney in 1944. ⁷ The pathogenesis may involve direct cytopathic injury to pancreatic acinar cells or an immune-mediated response.^7,8 Jain et al. observed pancreatitis in 5.65% of patients with viral hepatitis, though only a few were HAV-related. ⁹ Our case progressed to walled-off necrosis but improved with supportive therapy.

(P.S. Ref 7 mentions Lisney's contribution and also describes possible pathogenesis).

Conclusion

This case series underscores two rare but serious extra-hepatic manifestations of hepatitis A in children – complete heart block and acute pancreatitis. While HAV is typically self-limiting, clinicians must remain alert to these unusual complications. Cardiac evaluation is warranted in children with bradyarrhythmias, and pancreatitis should be suspected in those with severe abdominal pain during hepatitis. Timely HAV serology, an ECG, and pancreatic enzyme testing ensure prompt diagnosis, without the need of unnecessary interventions. These cases strongly advocate for inclusion of hepatitis A vaccine in India's universal immunisation programme to reduce preventable morbidity.

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Figure 1.

Complete heart block, Mobitz type I (second-degree) heart block.

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Figure 2.

CT scan of abdomen. Image 1 showing bulky pancreas with peri-pancreatic collection. Image 2 showing walled-off pancreatic necrosis with residual peri-pancreatic collection (pseudo sac). CT: computed tomography.