Electrical injuries account for only 3-5% of all burn admissions. Low-voltage burns most commonly involve the oral commissure in infants and toddlers due to suckling on the female end of live extension cords or biting electrical cords. These low-voltage injuries cause little tissue destruction and are best managed conservatively with intraoral splinting. A significant late complication may be hemorrhage from the labial artery.
On the other hand, high-voltage electrical injuries are classified as major burns due to associated massive tissue damage. On average, high-voltage cutaneous involvement is only 10-15% BSA, but this visible injury is only a small portion of the overall tissue destruction. The human body serves as a volume conductor to electricity. Current flow is therefore concentrated in the extremities by their narrowing. Since bone has the highest resistance to electrical current, conduction through bone produces the greatest amount of heat. For this reason, damage to muscle by electricity is greatest at tendonous attachments and periosteal regions. Massive muscle destruction causes myoglobinemia. Precipitation of myoglobin in the renal tubules can produce acute tubal necrosis and acute renal failure. In addition, high-voltage electrical burns are commonly associated with dislocations, fractures, vertebral injuries, myocardial damage, neurologic sequelae, and intra-abdominal injuries due in part to concomitant trauma. The most common cause of early mortality is cardiopulmonary arrest due to induced fibrillation.
Treatment of the high-voltage electrical victim should include prompt initiation of aggressive fluid resuscitation, serial assessment of distal vascular integrity, and urgent surgical intervention for fasciotomies and muscle compartment explorations. If the urine is rose-pigmented from haemochromogens, the urine output should be maintained at 100-125 ml/hr (1-2 ml/kg/hr) in adults, or twice the normal hourly rate in infants and young children, until gross pigment is cleared. The urine can be alkalized by IV administration of sodium bicarbonate to help prevent myoglobin precipitation. In severe injuries, IV mannitol (12.5 gm in an adult) is given in addition to aggressive fluid replacement to help promote an osmotic diuresis. Early use of other diuretics is contraindicated. Development of compartment syndromes should be anticipated. Deeper muscle groups sustain the greatest injury. Intraoperative exploration, decompression, and debridement is an essential part of early treatment. Serial technetium-99m stannous pyrophosphate muscle scans can be useful in assisting determination of progressive muscle damage.
Initial assessment of high-voltage patients would also include a careful neurologic examination, cardiac evaluation, and a skeletal survey. Vertebral fractures are frequent due to falls or forceful muscular contractions. All patients should have an electrocardiogram and serum CPK-MB determinations. In the patients without history of unconsciousness or cardiac arrest who have normal EKG's and myocardial isoenzymes, routine cardiac monitoring is not needed. Two-thirds of patients will have early neurological changes on initial exam, although long-term neurologic complications are rare. Late formation of cataracts following major electrical injuries has been documented.
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