Miguel Álvarez-Montero, Fiorela Dueñas-López, Ramón Pardo-Puras, Begoña de Miguel Lavisier, José Antonio Ruiz Domínguez, Vega Rey-Mauleón, María de Ceano-Vivas, Elena Ramírez, Alberto M Borobia, Mikel Urroz-Elizalde
Reported ingested dose showed only weak correlation with serum paracetamol concentrations, particularly in younger children. These findings suggest that exposure history alone is insufficient for poisoning risk assessment and should be interpreted alongside sampling time and biochemical evaluation.
INTRODUCTION: Paracetamol poisoning is a common cause of paediatric drug toxicity, but contemporary data on incidence trends, management, and predictors of toxicity remain limited. This study will evaluate incidence trends, clinical features, management, and dose-concentration relationships in paediatric patients with paracetamol poisoning.
METHODS: Retrospective cohort study of patients aged ≤16 years evaluated at a tertiary hospital (2015-2025). Cases were identified through serum paracetamol measurements and classified by exposure pattern. Acetylcysteine administration was assessed according to TOXBASE-based institutional criteria. Spearman's correlation between reported dose (mg/kg) and serum concentration was analysed in acute overdoses.
RESULTS: A total of 271 cases were included (114 aged ≤9 years; 157 aged 10-16 years). The incidence of identified cases of suspected paediatric paracetamol poisoning increased from 1.11 to 8.68 cases per 10,000 paediatric inhabitants between 2018 and 2025. Adolescents more frequently had intentional overdoses (96.8% versus 0%), higher reported doses (median 212.7 versus 150 mg/kg), and higher serum paracetamol concentrations (median 59.5 versus 30 mg/L [393.9 versus 198.6 µmol/L]) (P < 0.001). Acetylcysteine was administered in 69.2% of cases and was considered inappropriate in 17% of treated patients, predominantly among younger children. Hepatotoxicity (ALT > 3 × ULN and/or bilirubin > 2 × ULN) occurred in 21.4%, and acute liver failure (according to established paediatric criteria) in 9.2%, without significant differences between age groups. In acute overdoses with serum concentrations measured 4-24 h after ingestion, correlation between reported dose and serum concentration was weak in adolescents (ρ = 0.44; P < 0.001) and very weak in younger children (ρ = 0.28; P = 0.04).
DISCUSSION: Consistent with previous paediatric toxicology studies, exposure patterns differed by age group, with predominantly accidental exposures in younger children and intentional overdoses in adolescents.
CONCLUSION: Reported ingested dose showed only weak correlation with serum paracetamol concentrations, particularly in younger children. These findings suggest that exposure history alone is insufficient for poisoning risk assessment and should be interpreted alongside sampling time and biochemical evaluation.