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  • Print publication year: 1992
  • Online publication date: April 2010

10 - The role of arachidonic acid metabolism in the pathogenesis of electrical trauma

from Part III - Tissue responses

Summary

An electrical injury is a unique and thoroughly devastating form of trauma. The clinical pictures following cellular damage due to electrical current comprise more of a syndrome than a specific injury. The syndrome consists of varying degrees of cutaneous burn combined with ‘hidden’ destruction of deep tissue. The electrical insult results in progressive tissue necrosis in excess of the originally apparent trauma, somewhat resembling the injury of crush trauma. Controversy exists as to whether this is a slow manifestation of irreversible muscle damage secondary to the original current passage, or whether it is actively progressive ischaemic necrosis secondary to ongoingmacrovascular or microvascular compromise.

The cause of the controversy is a poor understanding of the pathophysiology. Because the injuries comprise a syndrome, the inciting cellular mechanism(s) for the pathophysiology may be multiple. Historically, the mechanism was thought to be heat. Passage of electric current through a solid conductor results in conversion of electric energy into heat, the joule effect. The amount of heat can be determined by Ohm's Law and the joule effect. Ohm's Law states that the current travelling through tissue is determined by the voltage (V) divided by the resistance (R). Heat production in joules is proportional to the power dissipated multiplied by the duration of contact and is expressed by the equation J = I2RT where J is the heat production, I is the current, R is the tissue resistance, and T is the time of contact. The extent of injury depends on the type of current, the pathway of flow, the local tissue resistance, and the duration of contact.