Electric current can induce immediate cardiac dysrhythmias, respiratory arrest, and seizures. Current that traverses the chest vertically (hand to foot or head to toe) or horizontally (hand to hand) can produce arrhythmias and respiratory arrest.
Fatalities due to asystole or ventricular fibrillation usually occur prior to arrival in the ED.5 Asymptomatic patients with normal ECGs on arrival to the hospital do not develop later dysrhythmias after low-voltage (<1000 V) injuries.9,10,11,12,13 However, nerve and deep-muscle injuries are relatively common following contact with voltages >400 V. Therefore, carefully examine for peripheral nervous system and CNS function and burns, and check for elevated serum creatine phosphokinase.
CNS, SPINAL CORD, AND PERIPHERAL NERVOUS SYSTEM INJURY
Neurologic impairment is common in electrical injuries, occurring in approximately 50% of patients with high-voltage injuries.2 Nerve tissue has the lowest resistance in the body, encouraging electrical passage through these tissues and causing associated damage. Given the multisystem dysfunction present in many electrical injury patients, document a neurologic exam, if possible, before intubation and sedation.
Electrocution can result in a broad range of CNS dysfunction. Transient loss of consciousness is common and may be followed by seizures. Victims may be confused and agitated or deeply comatose and require airway protection. Patients may also demonstrate focal neurologic deficits such as quadriplegia, hemiplegia, aphasia, or visual disturbances. Obtain head and cervical spine CT to rule out traumatic etiologies for these deficits; MRI may be necessary for purely electrical damage. Electrical injury can cause blindness14 due to occipital lobe injury as well as direct injury to the optic nerve.15,16 Neurologic deficits may be transient, but survivors may have persistent difficulties with attention, working memory, and learning.17
Spinal cord injury can occur in up to 8% of high-voltage electrical injuries.18 Spinal cord injuries can be the result of compressive vertebral fractures, sometimes at multiple levels.19 However, damage can also occur due to purely electrical damage without fractures, through direct cellular damage as well as vascular injury.20 With electrical trauma, initial spinal cord MRI results do not necessarily correlate with prognosis. MRI findings may be normal in electrical trauma patients with permanent spinal cord injury,21,22,23 although newer MRI imaging protocols may detect abnormalities silent on standard MRI.24 With mechanical trauma, emergency MRI after spinal cord injury provides accurate prognostic information regarding neurologic function.
Neurologic deterioration can occur days to months after the initial injury25,26,27 and generally has incomplete resolution. There is a motor predominance in deficit in most of these cases. Delayed onset of spinal cord dysfunction may be due to progressive vascular injury (especially to the spinal artery branch supplying the anterior horn cells) or delayed cell membrane damage via the cumulative effect of free radicals (electroporation), leading to progressive demyelination.21,28 The clinical features may take the form of transverse myelitis, amyotrophic lateral sclerosis, or a Guillain-Barré–like illness.29
Peripheral nerve injuries often involve the hands after the individual touches a power source. Paresthesias may be immediate and transient or delayed in onset, appearing up to 2 years after injury.2,30 Extensive peripheral nerve damage may occur with minimal thermal injury. Electrical contact with the palm produces median or ulnar neuropathy more often than radial nerve injury.31 Brachial plexus lesions have also been reported. Persistent symptoms related to peripheral nerve damage can occur despite normal results on nerve conduction studies.32
Cutaneous burns are often seen at the electrical contact areas (often referred to as entry and exit wounds in the case of DC current, or contact wounds in the case of AC current). Many seriously injured patients have burns on either the arm or skull, paired with burns on the feet. Burns are typically painless, gray to yellow, depressed areas. Most patients with burns from electrical injury need admission and care by a burn specialist. See chapter 216 for detailed discussion of management of cutaneous burns.
Fractures may be caused by tetanic muscle contractions or associated falls. Fractures may be missed on initial assessment due to altered mental status and the overall severity of systemic illness. A comprehensive tertiary survey should be performed when clinically feasible to detect orthopedic injuries. Although fractures are more likely to result from high-voltage injury, fractures of the wrist, forearm, humerus, femoral necks, shoulders, and scapulae have been reported from exposure to household voltages (120 to 220 V AC) without associated trauma.7,33,34 Posterior shoulder dislocations are commonly seen with electrical injury.
VASCULAR AND MUSCLE INJURY
Vascular and muscle injuries occur most commonly in the setting of high-voltage injury, such as power line contact. Electric current passing along peripheral arteries may cause early spasm and persistent deficits in endothelial and smooth muscle function,35 as well as subsequent thrombosis, stenosis, or aneurysm formation. Because of concomitant vascular and muscular destruction, patients with high-voltage shocks are at significant risk for development of compartment syndrome, even if the contact (or arcing) lasted <1 second. Compartment syndrome has also been noted in patients with injuries from 120 V AC or higher who sustain contact for longer than a few seconds. Patients typically exhibit ongoing muscle pain with movement.6
Contact with >1000 V, prehospital cardiac arrest, crush injury, and full-thickness skin burns are associated with significant tissue damage requiring surgical intervention. Fasciotomy and amputation are frequent sequelae of high-voltage injuries, occurring in 29% and 41% of patients in one study.36 High-voltage electrical injury is associated with rapid loss of body fluids into the areas of tissue damage, requiring aggressive resuscitation.
Thermal injury or tissue necrosis from electric current can cause a variety of coagulation disorders. Low-grade disseminated intravascular coagulation may be a result of hypoxia, vascular stasis, rhabdomyolysis, and release of procoagulants from damaged tissue. Transient coagulopathies have also been reported with high-voltage injury, including acquired, transient factor X deficiency.37 Electrical injury may unmask underlying vascular injury and has been reported in association with ischemic stroke at low voltage.38
Electric arcs in the industrial environment or near a power line can produce a strong blast pressure, similar to those seen in other types of explosions.39 Cognitive complaints following blast injury may resemble those that result from moderate mechanical head trauma. Mechanisms of brain injury include mechanical trauma related to the blast and arterial air emboli associated with blast-related alveolar disruption (see chapter 7, "Bomb, Blast, and Crush Injuries").
Chemical toxins such as ozone can be produced by coronas and arcs. Acute effects of ozone exposure include mucous membrane irritation, temporarily reduced pulmonary function, and pulmonary hemorrhage and edema. Fires and explosions associated with electric incidents may lead to inhalation of carbon monoxide and other toxic substances.
Electrical shock can cause a wide range of ocular trauma, most commonly to the cornea (epithelial erosion/defect, keratitis, scarring), as well as uveitis, retinal detachment, macular edema, optic nerve damage, and intraocular bleeding and thrombosis.15,40,41 Obtain a full ophthalmologic evaluation for any electric shock patient with an ocular complaint to document related injury. Cataract formation has been described weeks to years after electrical injury to head, neck, or upper chest.7 Cataracts have also occurred after electric arc or flash burns.
The auditory system may be damaged by current or by hemorrhage in the tympanic membrane, middle ear, cochlea, cochlear duct, and vestibular apparatus. Delayed complications include mastoiditis, sinus thrombosis, meningitis, and brain abscess. Hearing loss may be immediate or develop later as a result of complications. Hearing should be briefly checked in the ED, with follow-up formal testing arranged for any patient who appears to have a deficit.
Pain due to bowel perforation and intra-abdominal hemorrhage may be attributed to more obvious coexisting injuries.42 There are reports in the literature of lethal intra-abdominal injuries from electric current that were found only at autopsy. Ileus may develop in association with spinal cord injury.