Early predictors of severe acetaminophen-induced hepatotoxicity in a paediatric population referred to a tertiary paediatric department.

Aim: The data on severe acetaminophen-induced hepatotoxicity in children are very limited. This study explored the dose-response relationship between ingested acetaminophen and hepatotoxicity, the early biochemical and clinical predictors of hepatotoxicity, the impact of early N-acetylcysteine treatment on hepatotoxicity and the incidence of nephrotoxicity.

Methods: We carried out a retrospective case study on 25 children aged 11-16 years with severe acetaminophen poisoning.

Results: Initial biochemical parameters predicted hepatotoxicity, defined as the maximum levels of the international normalised ratio (INR) and alanine aminotransferase (ALT). Significant relationships were found between: (1) the maximal INR and, for example, the initial bilirubin (p = 0.0003) and initial phosphate (p = 0.003), (2) the maximal ALT and, for example, the initial INR (p = 0.0003) and initial creatinine (p = 0.002), (3) the number of prehospital vomiting episodes and, for example, the maximal INR (p = 0.013) and maximum ALT (p = 0.0005) and (4) the time of N-acetylcysteine initiation and, for example, maximum ALT (p = 0.001) and maximum gamma-glutamyl transferase (GGT) (p = 0.007). The incidence of nephrotoxicity was 12%. There was no significant relationship between the amount of ingested acetaminophen and the degree of hepatotoxicity.

Conclusion: Paediatric patients at increased risk of severe hepatotoxicity were identified by early biochemical parameters, prehospital vomiting episodes and latency time before N-acetylcysteine initiation.