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Carbamazepine poisoning

Spencer Greene, MD, MS, FACEP, FACMT
Ayrn O'Connor, MD
Section Editors
Stephen J Traub, MD
Michele M Burns, MD, MPH
Deputy Editor
Jonathan Grayzel, MD, FAAEM


Carbamazepine has been used for many years for the treatment of both partial and generalized seizures, as well as trigeminal neuralgia. It has also been used as a mood stabilizer and for treatment of neuropathic pain syndromes.

In 2014, the American Association of Poison Control Centers reported 3734 toxic exposures to carbamazepine [1]. Of these, 1880 were isolated ingestions. There were no deaths, and 62 patients experienced major toxicity, defined as life-threatening or resulting in significant disability [1].

The toxicology, diagnosis, and management of acute carbamazepine poisoning are discussed here. The clinical use of carbamazepine and chronic complications related to its use are reviewed separately. (See "Overview of the management of epilepsy in adults" and "Seizures and epilepsy in children: Initial treatment and monitoring" and "Antiseizure drugs: Mechanism of action, pharmacology, and adverse effects".)


Carbamazepine interacts with multiple receptors and ion channels. Its therapeutic effect results from binding to sodium channels in their inactivated state, which inhibits neuron depolarization and decreases glutamate release [2]. It is also anticholinergic, a property that is more relative in overdose than the therapeutic setting [3]. (See "Anticholinergic poisoning".)

In carbamazepine toxicity, sodium channel blockade may manifest as cardiovascular toxicity, particularly prolongation of the QRS interval. This conduction abnormality predisposes patients to ventricular arrhythmias and hypotension [4].

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Literature review current through: Oct 2017. | This topic last updated: Sep 19, 2016.
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