Paediatrics: Acute hepatitis

Acute hepatitis

Viral causes

Hepatitis A (HAV)

Incubation 2–6wks, faecal–oral transmission.

Hepatitis B (HBV) 

Incubation 6wks to 6mths. Endemic in the Far East and

Africa. Infection may be transmitted from:

•   Blood products.

•   IV drug abuse, contaminated needles, or syringes.

•   Sexual intercourse.

•   Close direct contact (e.g. intrafamilial, health workers).

•   Vertical (may cause fulminant hepatitis).

Hepatitis C (HCV) 

Incubation 2wks to 6mths. Transmission is as for HBV. Usually causes a mild severity acute illness or is asymptomatic. HCV rarely causes acute hepatitis.

Hepatitis E 

Faecal–oral transmission, endemic in India.

Hepatitis D 

Requires previous HBV infection.

Hepatitis G 

Parenteral transmission.

Other organisms 

Can cause hepatitis as part of systemic infection: Epstein– Barr virus (EBV, common in adolescents, only 40% have hepatitis); TORCH organisms (neonatal hepatitis); HIV; CMV (immune-compromised); Listeria.

Other causes

•   Poisons and drugs: e.g. paracetamol, isoniazid, halothane.

•   Metabolic disease: e.g. Wilson’s disease, tyrosinaemia type I.

•   Autoimmune hepatitis: May present with acute hepatitis.

•   Reye’s syndrome: a rare, acute encephalopathic illness associated with aspirin therapy and microvesicular fatty infiltration of the liver.

•   Prodrome: (nausea, vomiting, hypoglycaemia, abdominal pain) occurs 2–3 days before onset of jaundice or abnormal LFT.

Presentation

Acute fulminant hepatic failure (encephalopathy and coagulopathy) may rarely occur. Many infections are asymptomatic, particularly HAV and HCV. There are many presentations which include:

•   fever;

•   fatigue;

•   malaise;

•   anorexia;

•   nausea;

•   arthralgia;

•   right upper quadrant abdominal pain;

•   jaundice +/– hepatomegaly;

•   splenomegaly;

•   adenopathy;

urticaria.

Investigations

• LFT: ‘rise’bilirubin >20mg/L; ‘rise’AST/ALT (× 2–100).

• ‘falls’ Blood glucose (especially in Reye’s syndrome).

• Viral serology (IgM antibodies), viral PCR (HCV), EBV heterophil antibodies (Monospot or Paul–Bunnell). Blood culture if appropriate.

• Paracetamol level or halothane antibodies, if relevant.

·Serum immunoglobulin, complement (C3, C4), positive autoimmune antibodies (anti-smooth muscle, anti-mitochondrial, and/or anti-liver and kidney microsomal) in autoimmune hepatitis.

·Serum copper/caeruloplasmin, 24hr urinary copper (Wilson’s disease).

• Urinary succinylacetone (tyrosinaemia type I).

Management

Usually none is required, except support and rest.

• Alcohol avoidance in teenagers.

• There is no place for antivirals unless the child is immune-compromised.

• Fulminant hepatitis requires referral to a specialist unit for intensive care management and possible liver transplantation.

• Reye’s syndrome: maintain blood glucose >4mmol/L; prevent sepsis; provide intensive care support.

Prognosis

• Acute hepatitis is usually self-limiting.

• Mortality after fulminant hepatitis is 730% if both cerebral oedema and renal failure are absent, 770% if both are present without liver transplant.

• There is a long-term risk of:

o chronic hepatitis (HAV 0%; HBV 5–10%; HCV 785%);

o cirrhosis;

o hepatocellular carcinoma (HBV and HCV);

o glomerulonephritis (circulating immune-complexes).

Prevention

Active immunization exists for both HAV and HBV. Within 24hr after an infectious contact, infection may be prevented by giving pooled serum immunoglobulin for HAV and CMV, or specific HBV serum immunoglob-ulin for HBV.