Abstracts

Rationale: Vagal nerve stimulators (VNS) are used for patients with medically refractory epilepsy who are not candidates for surgical resection. As an implanted electrical device, VNS are inherently susceptible to extraneous electrical interference and subsequent malfunction. We herein report a case of VNS lead malfunction leading to persistent dysphagia.Methods: We present a case of a 60-year-old male with a history of refractory epilepsy with a vagal nerve stimulator inserted in 2006, who was admitted to the hospital for new-onset atrial fibrillation. Chemical cardioversion was initially attempted with diltiazem infusion but was unsuccessful. After being cleared with a TEE for an intracardiac thrombus, he was DC cardioverted to sinus rhythm on the same day. Shortly after the DC cardioversion, the patient developed profound persistent dysphagia and periodic throat irritation, dry hacking cough, and symptomatic bradycardia with heart rate dropping to the 20s. The periodic symptoms remitted soon after placement of a magnet close to the site of his VNS, which resulted in its deactivation. He remained dysphagic. On fluoroscopy for swallow evaluation, the VNS leads could be seen exposed in the soft tissue of the neck. VNS was interrogated and duty cycle was set at on time: 30s; off time: 48s; Output current: 2.25mA; Signal frequency of 20Hz. The periodicity of the throat pain and symptomatic bradycardia appeared to occur at the same intervals as that of the VNS duty cycle.Results: We hypothesize that during DC cardioversion for atrial fibrillation; the VNS generator was shocked leading to a short circuit which caused a burn injury to the left vagus nerve resulting in persistent dysphagia. He then had periodic severe throat pain and symptomatic bradycardia that occurred every minute and corresponded to the VNS duty cycle. We believe this was due to vasovagal responses from the pain caused by the VNS naked lead shocking the neck soft tissue.Conclusions: This case is unique in that there are no recorded cases of DC cardioversion causing VNS dysfunction in the literature. It illustrates the potential of DC cardioversion causing electrical vagal overstimulation, which if not addressed, may be life-threatening. Timely recognition of this phenomenon is critical as the first-line management appears to be deactivation of the malfunctioning VNS.