Paediatrics chapters
Acute hepatitis in children
Acute inflammation of the liver in children: the hepatitis viruses and other causes, the prodrome and icteric phase, how to read liver tests and hepatitis serology, who needs admission, and prevention by hygiene and vaccines.
- Acute hepatitis is inflammation and necrosis of the liver; in children the main causes are the hepatotropic viruses: A and E (faeco-oral, acute only) and B, C, D (blood, sexual, perinatal; can become chronic), plus EBV, CMV, drugs, Wilson disease and autoimmune hepatitis.
- After a prodrome of fever, anorexia, nausea and abdominal pain, the child develops jaundice, dark urine, pale stools and a tender liver; ALT and AST rise 15 to 20 times, and the prothrombin time is the best guide to severity.
- Diagnose with IgM anti-HAV (hepatitis A) and HBsAg + IgM anti-HBc (acute hepatitis B); treatment is supportive; admit for persistent vomiting, dehydration, prolonged PT or encephalopathy; prevent with hand washing, safe water, HAV and HBV vaccines and HBIG for babies of HBsAg-positive mothers.
On this page
Overview
Acute hepatitis means inflammation and necrosis of the liver of recent onset. In Pakistani children the commonest cause is hepatitis A, spread by contaminated food and water, and most children recover fully. The key exam skills are choosing and reading the serology, recognising the child who is sliding into acute liver failure, and knowing the prevention (hygiene, vaccines, HBIG).
Aetiology
| Group | Causes |
|---|---|
| Hepatotropic viruses | HAV, HBV, HCV, HDV, HEV (and HGV) |
| Other viruses | EBV, CMV, herpes simplex, varicella, adenovirus, enteroviruses |
| Bacteria and parasites | Sepsis (E. coli), leptospirosis, typhoid, amoebic and pyogenic liver abscess |
| Drugs and toxins | Paracetamol, isoniazid, valproate, phenytoin, carbamazepine, poisonous mushrooms |
| Metabolic | Wilson disease (over 3 years), galactosaemia, tyrosinaemia, alpha-1 antitrypsin deficiency |
| Autoimmune | Autoimmune hepatitis |
| Other | Shock, hypoxia (ischaemic hepatitis), biliary disease |
Hepatitis viruses at a glance
| Virus | Genome | Spread | Incubation | Chronic infection | Notes |
|---|---|---|---|---|---|
| HAV | RNA (picornavirus) | Faeco-oral | 15 to 30 days (Nelson) | Never | Commonest in children; mostly silent in young children |
| HBV | DNA (hepadnavirus) | Blood, sexual, perinatal | 60 to 180 days | 90% if perinatal, 5 to 10% in adults | Risk of cirrhosis and hepatocellular carcinoma |
| HCV | RNA (flavivirus) | Blood, transfusion, perinatal | 30 to 60 days (Nelson) | About 85% | Few symptoms; no vaccine |
| HDV | Defective RNA | Like HBV | With HBV | Common | Needs HBsAg to replicate |
| HEV | RNA | Faeco-oral (water) | 35 to 60 days | No | High mortality in pregnancy; outbreaks after rains |
"Vowels (A, E) hit the Bowels": faeco-oral and never chronic. B, C, D go through blood and can become chronic.
Pathophysiology (brief)
- Hepatotropic viruses infect hepatocytes; injury is largely due to the immune response against infected cells.
- Hepatocyte damage releases ALT and AST; swelling and bile duct injury cause cholestasis (raised conjugated bilirubin, ALP).
- Severe necrosis lowers synthesis of clotting factors (prolonged PT), albumin and glucose, and failure to clear ammonia leads to encephalopathy.
Clinical features
Phases
| Phase | Features |
|---|---|
| Incubation | No symptoms |
| Prodrome (pre-icteric), about 1 week | Fever, anorexia, nausea, vomiting, malaise, headache, right upper quadrant discomfort; dislike of food |
| Icteric | Jaundice, dark urine, pale stools, tender hepatomegaly; prodromal symptoms often improve as jaundice appears; splenomegaly and posterior cervical nodes in some |
| Recovery | Bilirubin and enzymes normalise over 6 to 8 weeks |
- Anicteric or silent infection is common in young children with HAV; Akbar notes fewer than 5% of HAV infections cause recognisable illness.
- Hepatitis B may begin with an immune-complex prodrome: urticaria, rash, arthritis (Nelson).
Extrahepatic features
| Virus | Extrahepatic features |
|---|---|
| HAV | Guillain-Barré syndrome, post-viral encephalitis, interstitial nephritis, autoimmune haemolytic anaemia |
| HBV | Glomerulonephritis, polyarteritis nodosa, macular or maculopapular rash, arthritis, aplastic anaemia, Guillain-Barré syndrome |
Laboratory interpretation
Liver tests
| Test | Meaning |
|---|---|
| ALT, AST | Hepatocyte injury; rise 15 to 20 times normal in acute viral hepatitis |
| Bilirubin (total and direct) | Both conjugated and unconjugated rise |
| ALP, GGT | Degree of cholestasis |
| Prothrombin time / INR | Best predictor of severe injury and progression to liver failure |
| Albumin, glucose | Low albumin and hypoglycaemia are bad signs |
| Ammonia | Raised in encephalopathy |
The height of ALT does not predict outcome. A rising PT/INR, falling liver size, hypoglycaemia or drowsiness means acute liver failure.
Hepatitis A serology
- IgM anti-HAV: acute infection (appears with symptoms, persists about 4 to 6 months).
- IgG anti-HAV: past infection or vaccination; lifelong immunity.
- No carrier state; virus shedding in stool largely stops by the time jaundice appears; children are infectious for about a week after jaundice begins (Akbar).
Hepatitis B serology
| Marker | Meaning |
|---|---|
| HBsAg | First marker; present in acute or chronic infection; over 6 months = chronic |
| HBeAg | Active replication, high infectivity |
| HBV DNA (PCR) | Viral replication |
| IgM anti-HBc | Acute infection; only marker in the window period |
| IgG anti-HBc | Past or chronic infection |
| Anti-HBe | Lower infectivity |
| Anti-HBs | Immunity (recovery or vaccine) |
| Pattern | HBsAg | IgM anti-HBc | IgG anti-HBc | Anti-HBs |
|---|---|---|---|---|
| Acute infection | + | + | − | − |
| Window period | − | + | − | − |
| Chronic infection | + (over 6 months) | − | + | − |
| Resolved infection | − | − | + | + |
| Vaccinated | − | − | − | + |
Anti-HBs with negative anti-HBc means vaccination, not past infection.
Other serology
- HCV: anti-HCV (exposure, not protective) and HCV RNA by PCR (active infection). Maternal anti-HCV can cross the placenta, so antibody cannot confirm infection in infants for the first months (Akbar: up to 15 months).
- HDV: anti-HDV with HBsAg.
- HEV: anti-HEV.
Differential diagnosis
- Other infections: EBV (infectious mononucleosis), CMV, varicella, herpes simplex, adenovirus, leptospirosis, E. coli sepsis
- Drug-induced hepatitis (paracetamol, isoniazid, valproate)
- Wilson disease and autoimmune hepatitis (always consider in a child over 3 with unexplained hepatitis)
- Haemolysis (unconjugated jaundice, normal ALT)
- Biliary obstruction: cholecystitis, choledochal cyst, gallstones
- Pancreatitis, viral enteritis
Management
Supportive (most children)
- Care at home with rest, adequate fluids and a nutritious diet with enough calories.
- Avoid hepatotoxic drugs and sedatives; avoid unnecessary paracetamol in high doses and elective surgery during the illness.
- Corticosteroids are not used in acute viral hepatitis (Akbar notes they are contraindicated in HBV).
- Hygiene: hand washing, safe disposal of stool and nappies (HAV, HEV); avoid sharing blood-contaminated items (HBV, HCV).
- Prolonged cholestasis: fat-soluble vitamins (A, D, E, K) and relief of itching.
Indications for admission (Nelson, Akbar)
- Persistent vomiting and dehydration, unable to take oral fluids
- Prolonged prothrombin time or bleeding
- Any sign of encephalopathy: drowsiness, confusion, irritability, behaviour change
- Hypoglycaemia, deepening jaundice, ascites, shrinking liver
- Very young infants, underlying chronic liver disease, or uncertain diagnosis
Refer to a liver centre
- Signs of acute liver failure (INR rising, encephalopathy): consider liver transplantation.
Chronic HBV and HCV
Treated by specialists (interferon or oral antivirals for HBV; antiviral combinations for HCV). Children with chronic HBV or HCV should be vaccinated against HAV (and HBV for HCV) and screened for liver cancer and cirrhosis.
Complications and prognosis
| Outcome | Notes |
|---|---|
| Full recovery | Usual with HAV (about 95% in Akbar) and HEV in children |
| Fulminant hepatitis / acute liver failure | Rare (well under 1% of acute viral hepatitis); HBV with HDV co-infection and HEV in pregnancy are higher risk |
| Relapsing or cholestatic HAV | Prolonged jaundice and itching, eventually resolves |
| Chronic hepatitis | HBV, HCV, HDV only; can lead to cirrhosis and hepatocellular carcinoma |
| Aplastic anaemia | Rare after hepatitis |
The younger the child at HBV infection, the higher the chance of chronic carriage: about 90% in infancy, about 30% at 1 to 5 years, 5 to 10% in adults.
Prevention
Hygiene
- Safe drinking water, sanitation, hand washing, food hygiene (HAV, HEV).
- Screening blood donors, sterile needles and equipment (HBV, HCV).
Hepatitis A
- HAV vaccine (inactivated, intramuscular, two doses 6 to 12 months apart) from about 12 months to 2 years of age.
- After exposure: vaccine (preferred from 12 months) or immunoglobulin 0.02 mL/kg IM (under 12 months or immunocompromised), within 2 weeks.
Hepatitis B
- Universal infant vaccination, starting at birth; it is part of Pakistan's EPI (check the current national schedule, as it can change).
- Baby of an HBsAg-positive mother: give HBIG 0.5 mL together with the first HBV vaccine dose, within the first 12 hours, then complete the vaccine course; check the infant's HBsAg and anti-HBs status at about 9 to 15 months (Nelson). Vaccine plus HBIG prevents about 99% of vertical transmission (Nelson).
- Mother's status unknown: vaccine within 12 hours; give HBIG as soon as she is found positive (no later than 1 week).
- Breastfeeding is not contraindicated.
Hepatitis C and E
- No vaccine for HCV; prevention is by safe blood and injection practice.
- HEV: safe water; protect pregnant women.
Expect: HAV as the commonest cause in children and IgM anti-HAV for diagnosis; A and E faeco-oral and never chronic; HBV serology patterns (HBsAg first, IgM anti-HBc in the window period, anti-HBs alone after vaccine, HBeAg for infectivity); age and chronicity of HBV (90% if perinatal); prothrombin time as the best severity marker; indications for admission (vomiting, dehydration, prolonged PT, encephalopathy); no steroids in acute viral hepatitis; HEV danger in pregnancy; and newborn prophylaxis with vaccine plus HBIG within 12 hours.
Quick revision
- HAV commonest; faeco-oral; IgM anti-HAV; no carrier state.
- A and E: faeco-oral, acute only; B, C, D: blood-borne, chronic possible.
- Prodrome then jaundice, dark urine, pale stools, tender liver; ALT 15 to 20 times normal.
- PT/INR is the best severity guide; hypoglycaemia and drowsiness = liver failure.
- HBsAg first marker; IgM anti-HBc acute and window; anti-HBs = immunity.
- HBV chronic in 90% after perinatal infection.
- Supportive care; admit for vomiting, dehydration, prolonged PT, encephalopathy.
- Newborn of HBsAg-positive mother: vaccine plus HBIG 0.5 mL, both inside the first 12 hours.
Written by The House Job from standard references (Basis of Paediatrics by Pervez Akbar; Nelson Essentials of Paediatrics).
FAQ
Which single test confirms hepatitis A?
IgM antibody to hepatitis A virus (IgM anti-HAV), which is positive from the start of symptoms for several months.
What does a positive anti-HBs with negative anti-HBc mean?
The child is immune because of vaccination, not because of past infection.
When should a child with jaundice from hepatitis be admitted?
If there is persistent vomiting, dehydration, a prolonged prothrombin time, bleeding, low blood sugar or any change in behaviour or consciousness.
Can a mother with hepatitis B breastfeed?
Yes, provided the baby has received hepatitis B vaccine and HBIG at birth.