P284: Neuromuscular effects of stun device discharges

Abstract

Objectives: Stun guns or Electromuscular Incapacitation Devices (EIDs) generate between 25,000 and 250,000 volts and can be discharged continuously for as long as 5-10 minutes. In the US, over 200,000 individuals have been exposed to discharges from the most common type of EID. EIDs are being increasingly used despite a lack of objective laboratory data describing the physiological effects and safety of these devices. An increasing amount of morbidity, and even death, is associated with EID use. To examine this type of electrical injury, we hypothesized that EID discharges will induce acute or delayed cardiac arrhythmia and neuromuscular injury in an animal model. Methods: Using an IACUC approved protocol, from May 2005 through June 2006 in a teaching hospital research setting, 30 Yucatan mini-pigs (24 experimentals and 6 sham controls) were deeply anesthetized with ketamine and xylazine without paralytics. Experimentals were exposed to discharges from an EID (MK-63, Aegis Indus.) over the femoral nerve on the anterior left hind limb for an 80 sec exposure delivered as two 40 sec discharges. EKGs, EMGs, troponin I, CK-MB, potassium, and myoglobin levels were obtained pre-discharge and post-discharge at 5, 15, 30 and 60 min, 24, 48 and 72 hrs (n=6 animals) and 5, 15, and 30 days post discharge (n=6 animals at each time point). Skin, skeletal muscle, and peripheral nerve biopsies were studied bilaterally. Data were compared using one-way ANOVA and paired t-tests. P values < 0.05 were considered significant. Results: No cardiac arrhythmias or sudden deaths were seen in any animals at any time point. No evidence of skeletal muscle damage was detected. No significant changes were seen in troponin I, myoglobin, CK-MB, potassium, or creatinine levels. There were no significant changes in compound muscle action potentials (CMAP). No evidence of conduction block, conduction slowing, or axonal loss were detected on EMG. M-wave latency (Mlat, msec), amplitude (Mamp, mV), area (Marea, mV-msec), and duration (Mdur, msec) were not significantly affected by EID discharge as compared to contralateral or sham controls. F-wave latency (Flat, msec), a sensitive indicator of retrograde nerve conduction and function, was not significantly affected by EID discharge as compared to contralateral or sham controls. The table below indicates mean EMG values from EID-exposed limbs. No significant histological changes were seen at any time point in skeletal muscle or peripheral nerve biopsies although mild skin inflammation was evident. Conclusions: There was no evidence of acute arrhythmia from EID discharge. No clinically significant changes were seen in any of the physiologic parameters measured here at any time point. Neuromuscular function was not significantly altered by the MK-63 discharge. In this animal model, even lengthy MK-63 discharges did not induce muscle or nerve injury as seen using EMG, blood chemistry, or histology. Tabled 1 0 5Ⅎ 15Ⅎ 30Ⅎ 60Ⅎ 24h 48h 72h 5d 15d 30d M lat 1.1 1.3 1.3 1.3 1.3 1.2 1.2 1.2 1.3 1.2 1.1 M amp 17.0 15.7 16.3 16.6 16.3 14.7 16.2 16.4 20.8 20.0 21.5 M area 44.1 41.5 43.0 45.9 44.6 38.1 41.1 39.4 51.2 53.4 50.5 M dur 8.5 7.1 8.4 8.2 8.6 8.3 8.1 7.8 6.2 7.5 6.2 F lat 14.1 13.2 14.3 14.2 14.2 14.0 13.8 13.7 13.9 14.7 13.5 Open table in a new tab