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 2010, the American Association of Poison Control Centers reported 4282 toxic exposures to carbamazepine . Of these, 2248 were reportedly isolated ingestions. Among the 1489 patients who sought treatment, there was one death and 538 patients who experienced moderate or major toxicity .
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 "Overview of the treatment of seizures and epileptic syndromes in children" and "Pharmacology of antiepileptic drugs".)
PHARMACOLOGY AND CELLULAR TOXICOLOGY
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 . It is also anticholinergic, a property that is more relative in overdose than the therapeutic setting . (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 .