Unintentional paediatric ingestions of angiotensin converting enzyme inhibitors and angiotensin II receptor antagonists.

AIMS: There is limited information on safety of angiotensin converting enzyme (ACE) inhibitors and angiotensin II (AII) receptor antagonists in unintentional paediatric ingestions. This study was conducted with the aim of developing referral guidelines for poison information centres. METHODS: Calls to the NSW poison information centre from January 2002 to July 2004 regarding paediatric ingestion of ACE inhibitors and AII receptor antagonists were recruited and prospectively followed up. Information collected included: demographics (age, gender, weight), type of exposure (unintentional, therapeutic error), ingested dose and clinical effects. Dose was reported in defined daily doses (DDD) to compare across and within the two drug classes with respect to the normal adult dose. RESULTS: Nineteen cases of paediatric ingestion of ACE inhibitors and AII receptor antagonists were included. The median age was 2 years (Interquartile range (IQR): 20-33 months) and the median dose ingested was 1 DDD (IQR: 1-2). There were nine ACE inhibitor ingestions and 10 AII receptor antagonist ingestions. One of nine children (11%) observed in hospital developed transient hypotension but required no treatment and recovered without complication. This child ingested an ACE inhibitor and ingested >3 DDD. CONCLUSION: Unintentional paediatric ingestions of ACE inhibitors and AII receptor antagonists resulted in the majority of children remaining asymptomatic. ACE inhibitor ingestions under 2 DDD can be observed at home provided the child is asymptomatic and there is a responsible adult to observe the child. The dose required for observation in AII receptor antagonist ingestions is less clear.

Lignocaine and chlorhexidine toxicity in children resulting from mouth paint ingestion: a bottling problem.

BACKGROUND: A pharmaceutical product was marketed in Australia for 'teething' in an almost identical container to a popular paediatric paracetamol preparation. The product contained lignocaine and chlorhexidine. The similarity of the packaging resulted in large number of therapeutic errors in which the 'teething' preparation was given in error for paracetamol. As the exact dose of the erroneously administered mouth paint was known this provided an opportunity for outcome assessment of lignocaine ingestion. METHODS: Calls to two state poison information centres regarding this product were prospectively followed up. Information collected included: demographics, type of exposure, details of the exposure and adverse effects. A systematic review of the literature was used to identify all previous reported cases of lignocaine and chlorhexidine ingestion. RESULTS: There were 28 cases with complete follow up where the product was given in therapeutic errors (10 girls and 18 boys; median age 11 months; range 2 months-4 years). The mean ingested dose of lignocaine was 2.7 mg/kg (standard deviation 1.3 mg) and chlorhexidine was 0.06 mg/kg (standard deviation 0.03 mg). The largest ingested lignocaine dose was 5.9 mg/kg. Two children developed minor symptoms: one vomited twice and the other was reported to have increased salivation and difficulty with solid food for 20 min. No other adverse effects were reported. The literature review suggested that severe effects occurred with doses more than 15 mg/kg. CONCLUSION: No major adverse effects occurred with lignocaine ingestions of less than 6 mg/kg and it would be appropriate to observe these patients at home. Chlorhexidine did not appear to cause clinical effects in this low concentration.