The effect of an electronic control device on muscle injury as determined by creatine kinase enzyme

Abstract

The medical literature on the effect of electronic control devices (ECD) on muscle injury is sparse. In this paper, we examine pooled data from five human studies that used creatine kinase (CK) as a marker for muscle injury. CK was measured in five separate studies involving four TASER ECDs with different exposure durations and number of circuits or contact points. Device type, exposure duration, number of circuits or contact points, and CK values at baseline and 24 h after exposure were pooled from these previous studies. Data were analyzed to determine the correlation of CK to duration of exposure, number of contact points, and distance between the probes. The pooled results contained 163 subjects. Seven were withdrawn due to incomplete data, leaving 156 subjects for analysis (median age 36, range 19-67, 93.6% male). 121 (77.6%) subjects had 2 contacts points, 10 (6.4%) had 3 contact points, 18 (11.5%) had 4 contact points, and 7 (4.5%) had 6 contact points. 81 (51.9%) subjects had a 5-s exposure, 64 (41.0%) a 10-s exposure, and, 11 (7.1%) a 30-s exposure. Median baseline CK (145 U/l, IQR 104-217, range 12-1956) did not differ between groups (P = 0.213 for number of contact points, 0.124 for duration). For the number of contacts, the median change in CK for 2 points of contact was 32 (IQR -1 to 1513, range -205 to 1821), for 3 was 1456 (IQR 634-1868, range 101-25452), for 4 was 887 (IQR 285-7481, range -1054 to 7481), and for 6 was 846 (IQR 57-1149, range -8 to 2309), (P < 0.001). For duration, the median change in CK for 5 s was 26.5 (IQR -8 to 109, range -1054 to 2309), for 10 s was 303 (IQR 34.5-1073, range -205 to 25452), and for 30 s was 47 (IQR 23-82, range -140 to 364), (P < 0.001). There was a relationship between the number of points of contact and the change in CK (P < 0.001) but not a relationship between the duration and the change in CK (P = 0.496). The median spread between the probe pairs for our pooled data was 40 cm, with a range from 18 to 70 cm (n = 76). The correlation between the change in CK and spread between the probe pairs was 0.16 at baseline (P = 0.18), and 0.24 at 24 h (P = 0.04) by Spearman's rank correlation. ECD exposure can cause a modest increase in CK. Although we cannot draw conclusions about the individual devices included in this analysis, our findings indicated that multiple contact points or exposures may result in a larger increase in CK, but the duration of the exposure does not appear to have a significant effect on CK. There is a correlation between the distance between the probes and the change in CK.