Rhabdomyolysis due to pulsed electric fields

Abstract

High-voltage electrical trauma frequently results in extensive and scattered destruction of skeletal muscle along the current path. The damage is commonly believed to be mediated by heating. Recent experimental and theoretical evidence suggests, however, that the rhabdomyolysis and secondary myoglobin release that occur also can result from electroporation, a purely nonthermal mechanism. Based on the results of a computer simulation of a typical high-voltage electric shock, we have postulated that electroporation contributes substantially to skeletal muscle damage and could be the primary mechanism of damage in some cases of electrical injury. In this study, we determined the threshold field strength and exposure duration required to produce rhabdomyolysis by the electroporation mechanism. The change in the electrical impedance of intact skeletal muscle tissue following the application of short-duration, high-intensity electric field pulses is used as an indicator of membrane damage. Our experiments show that a decrease in impedance magnitude occurs following electric field pulses that exceed threshold values of 60 V/cm magnitude and 1-ms duration. The field strength, pulse duration, and number of pulses are factors that determine the extent of damage. The effect does not depend on excitation-contraction coupling. Electron micrographs confirm structural defects created in the membranes by the applied electric field pulses, and these represent the first clear demonstration of rhabdomyolysis in intact muscle due to electroporation. These results provide compelling evidence in support of our postulate.