Introduction

Rhabdomyolysis is a characteristic clinical feature of electrical trauma. The release of large quantities of myoglobin into the intravascular space and the frequent localization of technetium-99 in skeletal muscle are common manifestations. It was this attribute of electrical trauma victims that caused several experienced clinicians to liken electrical trauma to the mechanical crush injury in its clinical manifestations. More than a decade later, the pathogenic mechanisms responsible for rhabdomyolysis following electrical trauma have yet to be specifically identified by clinical studies. While heat generation by the passage of electrical current (joule heating) has commonly been believed to be the only mediator of tissue injury, over the past few decades considerable evidence has accrued suggesting that other nonthermal mechanisms may be important.

In many cases of electrical trauma, particularly when the duration of electrical contact is short, heating is predictably insignificant in some regions in the current path where skeletal muscle damage is common (see Chapter 14). This information has been the motivation to postulate that in these instances cell membrane rupture due to the induced transmembrane potential may be the important mechanism of cellular damage. This chapter describes the rationale for the hypothesis and details the results of experiments designed to test its validity.

For a given applied electric field, the magnitude of the induced transmembrane potential imposed by the field depends on the cell size and orientation in the field.