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Accidental paracetamol overdosing and fulminant hepatic failure in children
F K Miles1, R Kamath, S F Dorney
1Department of Gastroenterology, Royal Alexandra Hospital for Children, Sydney, NSW.
Insights
Accidental paracetamol overdose can cause severe liver failure in children. Key signs include high transaminase levels and liver synthetic failure disproportionate to bilirubin levels, aiding early diagnosis and treatment.
Area of Science:
- Pediatric Hepatology
- Toxicology
- Gastroenterology
Background:
- Fulminant hepatic failure (FHF) in children necessitates accurate diagnosis of underlying causes.
- Distinguishing paracetamol (acetaminophen) overdose as a cause of FHF is critical for management.
Purpose of the Study:
- To identify clinical features that help diagnose liver failure caused by accidental paracetamol overdose in children.
- To compare the clinical presentation of paracetamol-induced liver failure with other causes.
Main Methods:
- Retrospective review of medical records of pediatric patients admitted with FHF between 1985 and 1998.
- Analysis of paracetamol's contribution to liver failure, other risk factors, and clinical features.
Main Results:
- Eight of 18 FHF patients had accidental paracetamol hepatotoxicity; three others had paracetamol as a major contributor.
- Paracetamol-induced liver failure cases presented with prodromal illness, encephalopathy, coagulopathy, very high transaminases, and disproportionately low bilirubin.
- Hypoglycemia was noted in five patients; end-stage liver failure occurred in 4/11 paracetamol cases versus 7/7 in others.
Conclusions:
- Accidental paracetamol overdose is a significant cause of FHF in pediatric patients.
- Clinical presentation of high transaminases and liver synthetic failure out of proportion to bilirubin suggests paracetamol toxicity.
- Early identification of paracetamol-induced liver failure is crucial for potential recovery with supportive care.
Objective:
To delineate clinical characteristics useful for identifying children with liver failure due to accidental paracetamol overdose.
Design:
Retrospective review of medical records of all patients admitted from 1985 to 1998 with fulminant hepatic failure.
Setting:
Royal Alexandra Hospital for Children, a tertiary referral centre for paediatric liver transplantation.
Main Outcome Measures:
Contribution of paracetamol to liver failure; other risk factors for liver failure; comparison of clinical features of paracetamol group and others.
Results:
18 patients were identified. Eight were considered to have accidental paracetamol hepatotoxicity. In a further three, other risk factors were present but paracetamol was considered a major contributor to liver failure. The seven remaining patients had other risk factors for liver failure. Patients with paracetamol-induced liver failure usually had an acute prodromal illness with prolonged fasting and, at presentation, had encephalopathy, coagulopathy, very high transaminase levels, but disproportionately low total bilirubin levels. Five patients had hypoglycaemia. End-stage liver failure occurred in 4/11 of the paracetamol group compared with 7/7 of the others.
Conclusion:
Accidental paracetamol overdose is associated with fulminant hepatic failure in infants and children. Patients present with high transaminase levels and liver synthetic failure out of proportion to the level of serum bilirubin. Prompt identification of such patients is important as many recover with supportive therapy.