Citation

Sanford A, Gamelli RL. Handb. Clin. Neurol. 2014; 120: 981-986.

Affiliation

Department of Surgery, Loyola University Medical Center, Maywood, IL, USA. Electronic address: rgamell@lumc.edu.

Copyright

(Copyright © 2014, Elsevier Publishing)

DOI

10.1016/B978-0-7020-4087-0.00065-6

PMID

24365365

Abstract

Electrical burns are classified as either high voltage (1000 volts and higher) or low voltage (<1000 volts). The typical injury with a high-voltage electrical contact is one where subcutaneous fat, muscles, and even bones are injured. Lower voltages may have lesser injuries. The electrical current has the potential to injure via three mechanisms: injury caused by current flow, an arc injury as the current passes from source to an object, and a flame injury caused by ignition of material in the local environment. Different tissues also have different resistance to the conduction of electricity. Voltage, current (amperage), type of current (alternating or direct), path of current flow across the body, duration of contact, and individual susceptibility all determine what final injury will occur. Devitalized tissue must be evaluated and debrided. Ocular cataracts may develop over time following electrical injury. Lightning strikes may conduct millions of volts of electricity, yet the effects can range from minimal cutaneous injuries to significant injury comparable to a high-voltage industrial accident. Lightning strikes commonly result in cardiorespiratory arrest, for which CPR is effective when begun promptly. Neurologic complications from electrical and lightning injuries are highly variable and may present early or late (up to 2 years) after the injury. The prognosis for electricity-related neurologic injuries is generally better than for other types of traumatic causes, suggesting a conservative approach with serial neurologic examinations after an initial CT scan to rule out correctable causes. One of the most common complications of electrical injury is a cardiac dysrhythmia. Because of the potential for large volumes of muscle loss and the release of myoglobin, the presence of heme pigments in the urine must be evaluated promptly. Presence of these products of breakdown of myoglobin and hemoglobin puts the injured at risk for acute renal failure and must be treated. The exact mechanism of nerve injury has not been explained, but both direct injury by electrical current overload or a vascular cause receive the most attention. Because electrical injuries carry both externally visible cutaneous injuries and possible hidden musculoskeletal damage, conventional burn resuscitation formulas based on body surface area injured may not provide enough fluid to maintain urine output. Damaged muscle resulting in swelling within the investing fascia of an extremity may result in compartment syndromes, requiring further attention. If myoglobin has been detected in the urine, treatment is aggressive volume resuscitation and possibly alkalinization of the urine or mannitol is given IV push to minimize pigment precipitation in the renal tubules. Approximately 15% of electrical burn victims also sustain traumatic injuries. This is because of falls from height or being thrown against an object. The tetanic contractions that result from exposure to electrical injury cause imbalance in flexor versus extensor muscles, with the flexor groups being stronger. Not only is the victim unable to release from the electrical contact, but they are at risk for fracture of bones from this prolonged muscular contracture. Neurologic and psychological symptoms were the most common sequelae of electrical and lightning injuries. Many of these symptoms are nonspecific, and they often do not appear until several months after the injury. A full neurologic examination must be performed on admission, documenting initial presentation and at any change in symptoms. Electrical injuries can have devastating consequences. Prevention of electrical injuries is clearly the preferable strategy for treatment.

Language: en