Book contents
- Frontmatter
- Contents
- Contributors
- Preface
- Acknowledgements
- Part I Introduction
- Part II Clinical manifestations and management
- Part III Tissue responses
- 10 The role of arachidonic acid metabolism in the pathogenesis of electrical trauma
- 11 Thermal damage: mechanisms, patterns and detection in electrical burns
- 12 Evaluation of electrical burn injury using an electrical impedance technique
- 13 Impedance spectroscopy: the measurement of electrical impedance of biological materials
- 14 Analysis of heat injury to the upper extremity of electrical shock victims: a theoretical model
- Part IV Biophysical mechanisms of cellular injury
- Index
11 - Thermal damage: mechanisms, patterns and detection in electrical burns
from Part III - Tissue responses
Published online by Cambridge University Press: 08 April 2010
- Frontmatter
- Contents
- Contributors
- Preface
- Acknowledgements
- Part I Introduction
- Part II Clinical manifestations and management
- Part III Tissue responses
- 10 The role of arachidonic acid metabolism in the pathogenesis of electrical trauma
- 11 Thermal damage: mechanisms, patterns and detection in electrical burns
- 12 Evaluation of electrical burn injury using an electrical impedance technique
- 13 Impedance spectroscopy: the measurement of electrical impedance of biological materials
- 14 Analysis of heat injury to the upper extremity of electrical shock victims: a theoretical model
- Part IV Biophysical mechanisms of cellular injury
- Index
Summary
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.
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- Information
- Electrical TraumaThe Pathophysiology, Manifestations and Clinical Management, pp. 189 - 215Publisher: Cambridge University PressPrint publication year: 1992
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