NEUROMUSCULAR EFFECTS OF STUN DEVICE DISCHARGES Daniel J. Valentino MD,1,2 Robert J. Walter PhD,1,2 Andrew J. Dennis DO,1,2 Kimberly Nagy MD,1,2 Michele M. Loor MD,1,2 Jerry Winners BS,1 Faran Bokhari MD,1,2 Dorion Wiley MD,1,2 Azher Merchant BS,2 Kimberly Joseph MD,1,2 and Roxanne Roberts MD1,2 1 Department of Trauma, Stroger Hospital of Cook County, Chicago, IL 60612 Department of General Surgery, Rush University Medical Center, Chicago, IL 60612
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Mean myoglobin levels (Figure 3) were not significantly affected. MK-63 discharge had limited effects on EMG responses:
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Figure 5. M-wave CMAP area for femoral nerve seen during the 30 day time course. Mwave area showed no significant changes (oneway, ANOVA p>0.05) during the 72 hr postdischarge period but rose gradually from mean values of 40.6±2.7 and 39.4±3.1 mV-msec to 54.8 and 53.4 mV-msec during the long-term follow-up for the control and experimental limbs, respectively.
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M-wave CMAP latency (Figure 4) was not affected in the shocked or the contralateral control limb.
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No significant changes were noted in M-wave CMAP amplitude. M-wave CMAP area (Figure 5) showed no significant changes during the 72 hr postdischarge period. Mean F-wave CMAP latency (Figure 6) was not significantly affected. No significant histological changes were seen (Figure 7).
Figure 6 F-Wave Latency 17
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Figure 2 Heart Rate
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Figure 6. F-wave CMAP latency for femoral nerve seen during the 30 day time course. Mean F-wave latency decreased by 7-14% in the experimental and contralateral control limbs at the 5 min time point, but this difference was not significant. F-wave latency was similar in both limbs at all time points studied (one-way ANOVA p>0.05).
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Figure 2. Heart rate before EID discharge and during the 30 day time course after EID discharge. Heart rate was not significantly affected by MK63 discharges in the 60 min postdischarge period or in the subsequent time points (one-way ANOVA, p>0.05).
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Figure 7. Skin, skeletal muscle and peripheral nerve biopsies
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Figure 3 Myoglobin Concentration
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The effects and safety of these discharges on living organisms are poorly understood and their ability to induce neuromuscular injury is not known.
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MK-63 discharge did not significantly affect serum electrolyte levels. Neither potassium nor creatinine values exceeded normal levels at any time point.
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More than 100 fatalities from cardiac arrest have occurred during the 2001-2004 period that were associated with EID use in the US.
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No evidence of acute arrhythmia or myocardial injury was found. Mean CK-MB and TnI levels were not significantly affected by MK-63 discharge (one-way ANOVA p>0.05).
INTRODUCTION 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 used.
Figure 5 M-Wave Area
Heart rate (Figure 2) and blood pressure were not significantly affected by MK-63 discharge.
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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.
Figure 4. M-wave CMAP latency for femoral nerve seen during the 30 day time course. M-wave latency was not significantly affected in the shocked limb or the contralateral control limb. No significant differences were seen between sham controls and experimental animals (one-way ANOVA, p>0.05).
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Figure 1. E-Pod and MK-63 lab simulator. The e-pod was placed over the left anterior thigh inferior to the inguinal ligament and discharges were administered with the electrodes oriented parallel to the femur and thus to the muscle fibers of the underlying rectus femoris and vastus medialis muscles for 80 sec.
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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 used increasingly 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.
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Figure 4 M-Wave Latency
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Figure 3. Myoglobin concentrations seen during the 30 day time course. Mean myoglobin levels in both groups fluctuated somewhat over the time course, but did not change significantly relative to the baseline for each group or each other (oneway ANOVA and t-tests, p>0.05).
Figure 7. At 72 hrs post-discharge, no effect was evident on skeletal muscle (rectus femoris) or peripheral nerve (femoral). Occasionally, minor highly localized inflammatory changes in skin were seen at site of discharge.
CONCLUSIONS No evidence of acute or delayed cardiac arrhythmia or neuromuscular injury was seen in this swine model. No skeletal or cardiac muscle damage was seen biochemically or histologically. This study shows that even lengthy discharges from the MK-63 do not cause significant injury.
