Thermal damage in electrical burns

Even brief 50–60 Hz electric shocks at currents between approximately 100 mA and 4 A carry a significant risk of cardiac fibrillation. Beyond 4 A, that risk is reduced considerably because the myocardium is completely depolarized by current passage; on current interruption and after a few seconds at rest, the heart starts beating again spontaneously. At currents beyond 4 A, however, burns can occur through joule heating due to high voltage, long contact time or both.

In electrical burns, intolerable temperature rise in muscle is the prime cause of tissue necrosis (immediate or delayed) and consequently of limb amputation. Although there is evidence that, in some cases, electric lesions may be morphologically different from thermal lesions, specifically in the appearance of vesicular nuclei, it has not been demonstrated that the necrotic zone in electrical burns extends outside the thermally damaged volume. Perhaps the strongest evidence for the dominant role of thermal damage is that patterns of temperature rise coincide with tissue damage at the anatomical level.

Mechanisms of hyperthermic cell death

Topic factors: thermal stress

By contrast with death from other mechanisms, cell death specifically by hyperthermia is thought to occur rapidly. Mortal heat stress first stops the movement of mitochondria which become pale, swollen and vesiculated. The loss of mitochondrion function is detectable by a vital dye technique monitoring the decrease of its phosphorylation potential. Further, all cellular and intracellular movements cease, cytoplasm and nucleoplasm develop a mottled appearance and both cell and nucleus shrink.