Massive overdose with controlled-release carbamazepine resulting in delayed peak serum concentrations and life-threatening toxicity.
Massive overdose with controlled-release carbamazepine resulting in delayed peak serum concentrations and life-threatening toxicity.
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DOI：
10.1046/j.1442-2026.2002.00290.x
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发表时间：
2002-03-01
期刊：
影响因子：
--
通讯作者：
Dowsett, Robert P
中科院分区：
文献类型：
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作者：
Graudins, Andis;Peden, Guy;Dowsett, Robert P
简介：据报告，过量服用卡马西平速释制剂后的血清峰浓度在摄入后2天内出现。我们报告的情况下，中毒与卡马西平控制释放导致的峰值水平postingesthes.Case报告：一名31岁的女性出现后，怀疑多药过量。她的血流动力学稳定，格拉斯哥昏迷量表评分为3分，并在急诊室接受气管插管。入院时给予单剂量活性炭，患者神经系统状态逐渐改善。入院后24 h进入重症监护室进行定性尿液药物筛查，结果显示苯二氮卓类药物和卡马西平。此时血清卡马西平浓度为66 μ mol/L（治疗浓度17-42 μ mol/L）。发现了使用控释卡马西平的治疗史。开始重复剂量活性炭和全肠灌洗，但耐受性差。血清卡马西平水平持续升高，由于肠梗阻的存在，停止胃肠道去污。到第4天，血清卡马西平浓度达到峰值196 μ mol/L。这与昏迷、全身性间歇性癫痫发作和低血压有关。由于存在终末器官毒性和胃肠道净化失败，开始进行活性炭血液灌流。血液灌流1小时后，血清卡马西平浓度从176 μ mol/L降至106 μ mol/L，此时患者可发出声音并能服从命令。她证实摄入300 Tegretol-CR（200毫克）拔管，出院后没有长期的后遗症。结论：未识别的中毒与控释卡马西平有可能产生显着的延迟卡马西平毒性和延迟峰值血清卡马西平浓度。这可能比以前报道的速释卡马西平制剂发生的时间晚得多。
INTRODUCTION: 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 micromol/L (therapeutic 17-42 micromol/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 micromol/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 micromol/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.