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Senior Fellow, Toxicology, New York University/Bellevue Hospital & New York City Poison Control Center, 455 First Avenue, Room 123, New York, New York 10016, fax 212/447-8223, onyxhawk{at}gmail.com
Emergency Medicine Resident, Beth Israel Medical Center, New York, NY
Director, New York City Poison Control Center
Published Online, December 19, 2007. www.theannals.com, DOI 10.1345/aph.1K162a
In therapeutic doses, the extended-release formulation of carbamazepine produces a peak serum concentration at about 12-24 hours postingestion.2,3 Following overdose, however, the peak may be delayed up to 106 hours.4 This is consistent with the case reported by Lurie et al., in which the peak serum concentration was reached at approximately 65 hours. The half-life in patients who are naïve to the drug averages 35 hours.3 Yet, when calculated from the data presented in this case, the apparent elimination half-life of carbamazepine was 12.3 hours. This significant reduction in the expected half-life can only be attributed to enhanced elimination from activated charcoal and is entirely consistent with demonstrable clinical improvement following the use of multiple doses of activated charcoal (MDAC) in patients with carbamazepine poisoning.5 As such, a strong argument can be made for the benefit of activated charcoal in the case presented.
The rebound in carbamazepine serum concentrations described is probably due to the large amount of drug ingested (20 g), with continued gastrointestinal absorption. A similar rebound effect occurred in a previously reported case in which both activated charcoal was used and whole bowel irrigation was performed following the ingestion of 34 grams of carbamazepine.4 Either the uncommon possibility of a pharmacobezoar4 or an unproven adverse interaction between polyethylene glycol and activated charcoal binding sites may provide alternative hypotheses for the rebound.6,7 However, given the patient's cabamazepine concentration and the maximal absorptive capacity of charcoal, the simple fact that most of the ingested drug remained free in the gastrointestinal tract is sufficient to predict some amount of rebound.
We agree that hemoperfusion can rapidly decrease carbamazepine serum concentrations4 and is an important adjunct in severe overdoses. However, considering the limitations, limited availability of hemoperfusion, and the actual data presented in this case, we still believe that MDAC has a role in the management of patients with carbamazepine overdose, given that both experimental and clinical data demonstrate a substantial reduction in the elimination half-life.
References
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