View Abstract

A7283 - Hypoglossal Nerve Stimulator Dysfunction Following Cardioversion
Author Block: D. S. Imanirad1, K. Calero2; 1Internal Medicine, University Of South Florida College of Medicine, Tampa, FL, United States, 2Pulmonary, Tampa General Hosp, Tampa, FL, United States.
Introduction: Obstructive sleep apnea (OSA) has been associated with daytime somnolence, metabolic syndrome, hypertension, other cardiovascular morbidity and all-cause mortality. Continuous Positive Airway Pressure (CPAP) is the standard treatment for OSA, although adherence is around 70%. The implantable hypoglossal nerve stimulating (HNS) device has been used in patients with difficulty tolerating CPAP. It has shown to improve OSA by improving collapse of the velopharynx in the upper airway during sleep. The HNS pulse generator is generally on the right side of the body to preserve the left side for potential cardiac pacemakers and defibrillators. Several studies show positive result in concomitant use of HNS and other devices, such as an implantable cardiac defibrillator (ICD). Other studies have demonstrated implantable device malfunctions such as neuromodulating devices following use of cardioverter defibrillator devices. Here, we present a case which reveals impaired functionality of an implantable HNS in a patient with obstructive sleep apnea following use of Automated External Defibrillator (AED). To our knowledge there is no report in the literature regarding use of AED and its impact on an upper airway implantable pulse generator (IPG).
Case: 71-year-old male with history of severe OSA with apnea-hypopnea index of 57 and low O2 saturation of 77% refractory to CPAP use, septoplasty, inferior turbinate reduction and expansion pharyngoplasty who underwent HNS placement with low O2 saturation improvement to 83%, and AHI of 58. The patient presented following a motor vehicle collision causing closed fracture of tenth thoracic vertebra and right hemothorax. Prior to surgical correction, patient developed hypoxic respiratory failure followed by Atrial fibrillation with rapid ventricular response and cardiogenic shock. He was cardioverted twice until stabilized. Following this event, patient noticed that his IPG device was no longer functional. Upon multiple HNS interrogations, the device was found to be permanently non-functional. Patient was re-evaluated and is currently in process of arranging replacement of the device but until then agreed to use his CPAP.
Conclusion: Possible unfamiliarity of medical staff with the existence of the upper airway stimulator device as well as the urgent need for use of an AED may lead to overlooking the impact of external electrical defibrillator on other implantable pulse generator(s). Further study is needed to demonstrate protection of upper airway stimulating devices at the time of cardioverting patients with such existing devices.