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Wiley InterScience | ||
 Emergency MedicineVolume 14 Issue 1, Pages 89 - 94 Published Online: 26 May 2002 © 2004 Australasian College for Emergency Medicine and Australasian Society for Emergency Medicine.
Abstract | References | Full Text: HTML, PDF (Size: 201K) | Related Articles | Citation Tracking  TOXICOLOGY Massive overdose with controlled-release carbamazepine resulting in delayed peak serum concentrations and life-threatening toxicity Andis Graudins, MB BS, FACEM, Consultant Toxicologist and Staff Specialist in Emergency Medicine; Guy Peden, MB BS, Registrar; Robert P Dowsett, BM MS, FACEM, Consultant Toxicologist and Director of Emergency Medicine. Copyright 2002 Blackwell Science Asia Pty Ltd KEYWORDS anticonvulsants • carbamazepine • haemoperfusion • poisoning ABSTRACTIntroduction:Peak serum levels following overdose with immediate-release formulations of carbamazepine have been reported to occur up to 2 days postingestion. We report a case of poisoning with carbamazepine controlled-release resulting in peak levels 96 h postingestion. Case Reports:A 31-year-old female presented following a suspected polypharmacy overdose. She was haemodynamically stable with a Glasgow Coma Scale score of 3 and was endotracheally intubated in the emergency department. A single-dose of activated charcoal was administered on admission and her neurological status improved gradually. Results of qualitative urine drug screen available 24 h postadmission to the intensive care department revealed benzodiazepines and carbamazepine. The serum carbamazepine concentration at this time was 66 µmol/L (therapeutic 17–42 µmol/L). A history of therapy with controlled-release carbamazepine was discovered. Repeat-dose activated charcoal and whole-bowel irrigation were commenced, but poorly tolerated. Serum carbamazepine levels continued to rise and gastrointestinal tract decontamination was ceased due to the presence of an ileus. By day 4, the serum carbamazepine concentration peaked at 196 µmol/L. This was associated with coma, generalized intermittent seizure activity and hypotension. Charcoal haemoperfusion was commenced due the presence of end-organ toxicity and failed gastrointestinal tract decontamination. Serum carbamazepine concentrations fell from 176 to 106 µmol/L after 1 h of haemoperfusion and the patient was rousable to voice and could obey commands at this time. She confirmed ingestion of 300 Tegretol-CR® (200 mg) on extubation and was discharged without long-term sequelae. Conclusion:Unrecognized poisoning with controlled-release carbamazepine has the potential to produce significant delayed carbamazepine toxicity and delayed peak serum carbamazepine concentrations. This may occur much later than previously reported with immediate-release carbamazepine preparations. Accepted: 28 September 2001; |  |
