Acute effects of MK63 stun device discharges in miniature swine.

OBJECTIVE: Electromuscular incapacitation (EMI) devices are being used and evaluated by both military and law enforcement agencies. Although the gross muscular response is obvious, physiological responses to these devices are poorly understood. We hypothesized that the intense, repetitive, muscle contractions evoked by EMI devices would cause dose-dependent metabolic acidosis, accompanied by neuromuscular or cardiac injury. METHODS: Using an approved protocol, 26 Yucatan mini-pigs (22 experimental animals and 4 control animals) were anesthetized with ketamine and xylazine. Experimental animals were exposed to MK63 (Aegis Industries, Bellevue, Idaho) discharges over the left anterior hind limb for 10, 20, 40, or 80 seconds. Electrocardiograms, electromyograms, troponin I levels, blood gas values, and electrolyte levels were recorded before and 5, 15, 30, and 60 minutes and 24, 48, and 72 hours after discharge. Skin, muscle, and nerve biopsies were taken from the shocked and contralateral sides. RESULTS: Core body temperature significantly decreased (1.0-1.5 degrees C) in all shocked animals but not in sham-treated control animals. No cardiac dysrhythmias or deaths were seen, and heart rate was unaffected. No clinically significant changes were seen in troponin I, myoglobin, or creatine kinase-MB levels. Central venous blood pH decreased, whereas carbon dioxide pressure and lactate levels increased for 60 minutes after discharge. All values returned to normal by 24 hours after discharge, and no significant histological or electromyographic changes were found. CONCLUSIONS: Changes in blood chemistry were observed but were of little clinical significance, and no neuromuscular damage was detected. Therefore, within the limitations of this model, it appears that EMI can safely be achieved by using this device, even for lengthy periods, without causing significant injury.

Acute effects of TASER X26 discharges in a swine model.

BACKGROUND: Very little objective laboratory data are available describing the physiologic effects of stun guns or electromuscular incapacitation devices (EIDs). Unfortunately, there have been several hundred in-custody deaths, which have been temporally associated with the deployment of these devices. Most of the deaths have been attributed to specific cardiac and metabolic effects. We hypothesized that prolonged EID exposure in a model animal system would induce clinically significant metabolic acidosis and cardiovascular disturbances. METHODS: Using an Institutional Animal Care and Use Committee-approved protocol, 11 standard pigs (6 experimentals and 5 sham controls) were anesthetized with ketamine and xylazine. The experimentals were exposed to two 40-second discharges from an EID (TASER X26, TASER Intl., Scottsdale, AZ) across the torso. Electrocardiograms, blood pressure, troponin I, blood gases, and electrolyte levels were obtained pre-exposure and at 5, 15, 30, and 60 minutes and 24, 48, and 72 hours postdischarge. p values <0.05 were considered significant. RESULTS: Two deaths were observed immediately after TASER exposure from acute onset ventricular fibrillation (VF). In surviving animals, heart rate was significantly increased and significant hypotension was noted. Acid-base status was dramatically affected by the TASER discharge at the 5-minute time point and throughout the 60-minute monitoring period. Five minutes postdischarge, central venous blood pH (6.86 +/- 0.07) decreased from baseline (7.45 +/- 0.02; p = 0.0004). Pco2 (94.5 mm Hg +/- 14.8 mm Hg) was significantly increased from baseline (45.3 mm Hg +/- 2.6 mm Hg) and bicarbonate levels significantly decreased (15.7 mmol/L +/- 1.04 mmol/L) from baseline (30.4 mmol/L +/- 0.7 mmol/L). A large, significant increase in lactate occurred postdischarge (22.1 mmol/L +/- 1.5 mmol/L) from baseline (1.5 mmol/L +/- 0.3 mmol/L). All values returned to normal by 24 hours postdischarge in surviving animals. A minor, nonsignificant increase in troponin I was seen at 24 hours postdischarge (0.052 ng/mL +/- 0.030 ng/mL, mean +/- SEM). CONCLUSIONS: Immediately after the discharge, two deaths occurred because of ventricular fibrillation. In this model of prolonged EID exposure, clinically significant acid-base and cardiovascular disturbances were clearly seen. The severe metabolic and respiratory acidosis seen here suggests the involvement of a primary cardiovascular mechanism.

Neuromuscular effects of stun device discharges.

BACKGROUND: Stun guns or electromuscular incapacitation devices (EMIs) generate between 25,000 and 250,000 V and can be discharged continuously for as long as 5 to 10 min. In the United States, over 200,000 individuals have been exposed to discharges from the most common type of device used. EMI devices 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 EMI device use. To examine this type of electrical injury, we hypothesized that EMI 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 (MK63; Aegis Industries, Bellevue, ID) over the femoral nerve on the anterior left hind limb for an 80 s exposure delivered as two 40 s 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 h (n = 6 animals) and 5, 15, and 30 d 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 analysis of variance 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 (M(lat), ms), amplitude (M(amp), mV), area (M(area), mV-ms), and duration (M(dur), ms) were not significantly affected by MK63 discharge compared with contralateral or sham controls. F-wave latency (F(lat), ms), a sensitive indicator of retrograde nerve conduction and function, was not significantly affected by MK63 discharge compared with contralateral or sham controls. 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 MK63 discharges. No clinically significant changes were seen in any of the physiological parameters measured here at any time point. Neuromuscular function was not significantly altered by the MK63 discharge. In this animal model, even lengthy MK63 discharges did not induce muscle or nerve injury as seen using EMG, blood chemistry, or histology.

Repeated thoracic discharges from a stun device.

BACKGROUND: Little objective laboratory data are available describing the physiologic effects of stun guns or electromuscular incapacitation (EMI) devices, but increasing morbidity and even deaths are associated with their use. We hypothesized that exposure to EMI discharges in a model animal system would induce clinically significant acidosis and cardiac arrhythmia. METHODS: Ten Yucatan mini-pigs, six experimental and four sham controls, were anesthetized with ketamine, xylazine, and glycopyrrolate. Experimental pigs were exposed to two 40-second discharges from an EMI device over the left thorax. Electrocardiograms, troponin I, blood gases, and lactate levels were obtained pre-exposure, at 5, 15, 30, 60 minutes, and at 24, 48, and 72 hours postdischarge. RESULTS: No acute or delayed cardiac arrhythmias were seen. Heart rate was not affected significantly (p>0.05). A subclinical increase in troponin I was seen at 24 hours postdischarge (0.040+/-0.030 ng/mL, p>0.05). Central venous blood pH (7.432+/-0.014) and pCO2 (36.1+/-0.9 mm Hg) were not changed significantly (p>0.05) during the 60-minute postdischarge period. A moderate significant increase in lactate occurred in the 5-minute postdischarge group (4.9+/-0.3 mmol/L, p=0.0179). All blood chemistry and vital signs were normal at 24, 48, and 72 hours postdischarge. CONCLUSIONS: Although significant changes in some parameters were seen, these changes were small and of little clinical significance. Lengthy EMI exposures did not cause extreme acidosis or cardiac arrhythmias. These findings may differ from those seen with other EMI devices because of the unique MK63 waveform characteristics or to specific characteristics of the model systems.