Clinical manifestations

Presentation and course

	• The medical manifestations of electrical injuries may evolve over minutes to hours and days.
	• Delayed sequelae may occur years following an electrical exposure.

Four categories of neurologic sequelae that could result from electrical trauma categories are:

	(1) immediate and transient, whereby symptoms occur at the time of the incident and remit within hours to days of the incident;
	(2) immediate and prolonged/permanent, whereby symptoms occur at the time of the incident and persist for weeks, months, years, or indefinitely;
	(3) delayed and progressive, whereby symptoms were not present at the time of the incident but appear at some later time and the severity of the symptoms progress; and
	(4) linked or coupled, whereby indirect effects of the incident occur.

An example of immediate and transient sequelae of electrical injuries might be the loss of consciousness or retrograde amnesia. An immediate and prolonged/permanent effect might include a brain hematoma or infarction. The first and second categories are common responses of the body to injury.

The third and fourth categories are less typical and add to the confusing nature of electrical injuries. In the third category, symptoms appear days, months, or even years after the injury and the symptoms intensify over time. Reported cases include movement disorders, demyelinating disorders, and cerebrovascular occlusive disease. Despite numerous reports of delayed sequelae, there has been little progress in the explanation of this phenomenon.

In the fourth category, linked or coupled sequelae are symptoms or conditions that are indirectly related to the exposure to electrical current. For example, because of the force of the current entering and exiting the body, victims often fall, sometimes from excessive heights, and suffer from head injuries. It is particularly challenging for the clinician to separate the effects of the electrical injury from the effects of these secondary injuries.

In nonfatal injuries, the clinical course of survivors can be variable. Opinions differ about the nature and cause of patient symptoms, and the relationship between symptoms and factors like trauma severity, litigation, or premorbid personality. Not all survivors develop physical, cognitive, and emotional difficulties. No consistent relationship has been established between characteristics such as age, injury-related characteristics (eg, voltage, current source, work error), and neuropsychological test performance. Low-voltage electrical injuries usually produce more frequent long-term sequelae than high-voltage injuries.

Neurologic sequelae. The following categories of neurologic sequelae have been reported:

	(1) Peripheral neuropathies
	(2) Seizures or convulsions
	(3) Central nervous system complications such as myelopathy, encephalopathy, cerebral hemorrhage, ischemia, cerebral edema, hydrocephalus, venous thrombosis, rupture of pre-existing vascular malformations, carotid rupture, and intracranial arteriovenous fistula (01; 17; 42; 23). Ischemic stroke in vertebrobasilar territory has been reported as a delayed sequel after electrical injury (22).
	(4) Autonomic nervous system complications such as reflex sympathetic dystrophy
	(5) Movement disorders such as tremors, dystonia, myoclonus, parkinsonism, choreoathetosis, and myokymia
	(6) Cranial nerve dysfunction such as facial nerve palsy. Electrical current injuries predominantly cause pure sensorineural hearing loss and may significantly increase a patient's lifetime risk of vertigo (29).
	(7) Meningitis
	(8) Traumatic brain injury manifestations usually occur from a fall following electrical injury and may vary from mild concussion to more severe symptoms.
	(9) Loss of consciousness
	(10) Headache
	(11) Speech impediment (15)
	(12) Mutism (27)
	(13) Muscular symptoms may include muscle aches, spasm, cramps, and twitches
	(14) A unique combination of brachial plexopathy, partial Horner syndrome, and phrenic nerve palsy secondary to electrical injury has been reported in the literature for the first time (38).
	(15) The first case of reversible bulbar dysfunction with negative MRI following high voltage electrical injury at work has been reported (32). The authors proposed a limited immune-mediated demyelination following electroporation as a possible cause.
	(16) A study of a Canadian database of work-related injuries has shown that dizziness is the most common presenting neurotological feature following electrical injury, whereas other common complaints included tinnitus and imbalance (46). Loss of consciousness or associated head injury had no effect on the clinical presentation in this population.
	(17) Delayed compressive peripheral neuropathy may be caused by scarring from cutaneous burns in patients with electrical injuries. A case of carpal tunnel syndrome following electrical injury has been reported in the absence of severe scarring and likely was caused by other mechanisms, such as direct injuries to the nerve (45).
	(18) In a study on patients with mild cognitive impairment following electrical injury, cerebral blood volume maps showed hypermetabolism in the cerebello-limbic system, but diffuse tensor imaging did not find any microstructural changes, possibly because of a cognitive reserve that protects against deterioration of the condition to dementia (31).
	(19) Low voltage electrical injuries usually present as focal neurologic deficits and are rare, but a case of a 3-year-old boy presented with right facial palsy and hemotympanum after electrical injury (35).

Neuro-urological electrical injuries. These may occur secondary to spinal cord or brain trauma or as independent consequences of electrical shock (47). The main urological functions that can be affected secondary to an electrical injury are lower urinary tract function, erectile function, and renal function:

	1. Lower urinary tract symptoms must be estimated in electrical trauma patients, and if present, clinical and laboratory investigation (urodynamic and imaging studies) should follow.
		a. Overactive bladder: This is the result of the dyssynergy between detrusor and detrusor sphincter combined with high detrusor pressure and can be responsible for lower or upper urinary tract infections, upper urinary tract dilatation, and renal failure. Suprapontine cerebral lesions or cervical and thoracic myelopathy secondary to electrical injury can induce this syndrome.
		b. Underactive bladder: This appears with urinary retention and voiding dysfunction and can also induce urological complications. Cerebral or spinal lesions between the pontine micturition center in the brainstem and the sacral micturition center in the sacral spinal cord are the usual causes. Underactive bladder is the most common sequel of myelopathy secondary to electrical injury.
	2. Erectile dysfunction
		a. Due to high-voltage injuries without recognized neurologic injury (severe penile trauma, penile amputation).
		b. Due to spinal cord injury. Myelopathy after high-voltage electrical injury or lightning injury can occur as a direct injury in any spinal cord level (39), and it can also occur secondary to indirect spinal cord damage such as spinal fractures due to fall, mainly of the thoracic vertebrae. Renal electrical injury requiring hemofiltration is associated with a highly-increased mortality.

Neuropsychological symptoms. These may include memory disturbance, increased emotional sensitivity, insomnia, unusual anxiety, reduced attention span/loss of concentration, personality changes, fear of electricity, and inability to cope. Some of the neuropsychological symptoms are compatible with the current diagnosis of post-traumatic stress disorder (PTSD), which has an estimated prevalence of 7.6% in a retrospective study of 311 cases of occupational electrical injuries (34). PTSD is characterized by intrusive thoughts, nightmares and flashbacks of past traumatic events, avoidance of reminders of trauma, hypervigilance, and sleep disturbance, all of which lead to considerable social, occupational, and interpersonal dysfunction. A diagnosis of PTSD is made for patients older than 6 years of age who meet all the DSM-5 criteria for the syndrome (02).

Nonelectrical effects in electrical events. With higher power density and smaller, more compact spaces, there is an increased risk of damage from explosive effects with characteristics of closed blast injury.

For example, the potential ignition of 1 MW is roughly equivalent to the potential ignition of 1 stick of dynamite. One stick of dynamite is roughly one-third pound of TNT equivalent. A 100 MW scenario can be represented as loaded with 100 sticks of dynamite. Or, a 300 MW scenario can be represented as loaded with 100 pounds of TNT. An electrical exposure scenario in a closed space creates the possibility of closed blast effects; at a pole top in a vacant field, the space is more like an open area might be in a free blast scenario. Blast can result in tissue destruction from shrapnel, confined space air contamination, acoustic or pressure effects, and acceleration-deceleration forces. Traumatic brain injury can occur with intact skull. When a patient’s neurologic presentation is consistent with blunt force or blast injury after an electrical event, consideration should be given to the possibility of exposure to an electrical explosion scenario complicating an electrical shock.

Prognosis and complications

Survival from electrical injury can be associated with significant functional impairment. In a landmark retrospective study of employees of a national electrical energy company, the electrical trauma survival experience during 1970 to 1989 was reviewed for a workforce between 100,000 to 120,000 (18). Electrical burns affected 2080 workers. Of these, 515 patients, or 25%, were noted to have postinjury complications, including: 63% burn related, with amputations in 5%; 18% neuropsychiatric; 12% sensory; 5% orthopedic; and 1% cardiovascular. Sense organ disorders included vision-related changes due to conjunctivitis, keratitis, and cataracts; auditory sequelae, with conductive or sensorineural hearing loss, tinnitus, and vertigo; and anosmia. In 59 of the 515 patients, disability was considered serious, with impairment rating from 31% to 100%.

Neurologic complications of electrical injury. CNS complications are well recognized, causing an increased risk of morbidity, whereas peripheral nervous system complications and neurologic, cognitive, and psychological abnormalities are less predictable after electrical injuries. Delayed neurologic sequelae include hydrocephalus, cerebral venous thrombosis, and amyotrophic lateral sclerosis and usually carry a great risk for permanent disability (47). However, a case of acute-onset quadriplegia following high-voltage electrical injury, with no radiographic abnormalities, regained partial sensorimotor function 2 months after the injury (14).

Cases of postelectrocution delayed onset of visual symptoms have been reported where MRI showed bilaterally symmetrical diffusion restriction in parietal and occipital areas and improvement followed intravenous steroids (08; 30). Treatment with intravenous steroids resulted in remarkable improvement in symptoms.

Osteoporosis has been described as a complication of electrical skin burns and is explained by prolonged dysfunction of sympathetic nervous system, which may result in bone metabolism derangement even after the acute phase of electrical burn (37). Linking of high voltage electrical injuries to greater physical morbidity, as measured by total body surface burned, total days in intensive care, and hospital length of stay have been traditionally used as predictor of outcome in electrical injury, but functional outcome including neuropsychological sequelae has been found to be similar between disparate levels of voltage-induced electrical injury. As a corollary to this comprehensive approach, multidisciplinary burn-care teams should equally consider high-voltage and low-voltage electrical injuries when predicting neuropsychiatric sequelae and final functional outcomes. Burn care teams might, thus, treat electrical injuries as continuum of traumatic stresses that affect patients regardless of voltage (09).

Clinical vignette

A 29-year old male was referred to the emergency room because of electrocution. He had grasped the end of a live electrical cable with his right hand. He received a severe electrical shock throwing him 2 meters backward, he lost consciousness without seizures, according to witnesses, and immediately afterward reported limited motion and numbness of his right extremities. An emergency room evaluation that day found no objective abnormality apart from 2 small electrical burns on his right hand and foot. Twenty days later, neurologic evaluation revealed very limited voluntary and passive movement of the right leg, which caused an inability to flex the knee. Both voluntary and passive movements resulted in excruciating pain and tremor of the right lower limb. Examination revealed intact mental status.

Cranial nerves were intact. Motor examination of the other 3 limbs was normal. He received diazepam and carbamazepine with no response. Botulinum toxin type A administration was considered painful and was not tolerated by the patient. Three years later his right leg was markedly extended at the knee and every attempt to flex it caused coarse tremor and painful muscle contractions of the whole limb. Atrophy of the right quadriceps was noticed. He was trying to walk with the leg always extended to avoid tremor and pain. His situation remained unchanged throughout many years, but he did not stop working as an office clerk.

He had no previous medical problems. There was no history of head trauma, systemic diseases, or exposure to neuroleptic drugs. Family history of movement disorders was also negative. Routine laboratory tests and brain and spinal MRI were unremarkable. Nerve conduction studies were normal. EMG recordings did not show neuropathic or myopathic changes but did reveal that: (1) knee flexion produced continuous muscle fiber activity of high frequency simultaneously in agonist and antagonist muscles of the right limbs. At the same time, a painful lower limb muscle spasm was observed. The above patterns, indicative of dystonia, were stable for several minutes; (2) immediately afterward, a 10-Hz bursting pattern of motor unit action potentials with high amplitude and separated by relative silence was observed; it was produced in an alternating fashion between flexors and extensors of the right upper and lower extremity. This activity with tremor morphology was accompanied by a high range tremor of 3 to 4 minutes duration only in the lower-right extremity; (3) another spontaneous activity indicative of myokymic discharges was observed at rest in the right deltoid, but also in the supraspinatus, trapezius, and paraspinal muscles, consisting of grouped motor potentials firing at 8-Hz continuously with 2 to 4 units within a burst. Distraction with physical (contralateral finger tapping) or mental activities (counting, singing) did not alter any of the above described activities. The same EMG patterns were reproduced in a stereotyped manner by repeating the flexion maneuver at the knee. No abnormal activity was seen in the left extremities.

Biological basis

	• Electrical injuries may occur from accidents during recreational activities or at work, household electric appliances, during medical procedures, and use of weapons such as Taser.
	• Injury involves energy transfer to an exposed individual in some combination of electrical, thermal, radiation, acoustic, and mechanical forms.
	•Late neurologic sequelae are difficult to explain, but several hypotheses have been proposed.

Etiology and pathogenesis

Etiology. Accidents at work are well known causes of electrical injury. Table 1 highlights nonoccupational causes of electrical injury.

Table 1. Common Causes of Nonoccupational Electrical Injuries and Fatalities

Setting	Source	Example
Households	Electrical appliances	Young children inserting metal objects into appliances
Medical	Iatrogenic	Electroconvulsive therapy
Weapon	Taser	Use by police to subdue suspected criminals
Recreational	Swimming pools	Electrocutions and electric shocks due to contact of electrical devices with water

Electrical weapons. Stun gun and the Taser, have been developed for use by law enforcement and security personnel to provide less lethal alternatives to conventional weapons. These devices deliver bursts of high-voltage, low-amperage direct current, either through a handheld device (stun gun) or through a hook and wire system fired using compressed gas (Taser). Electrical weapons are widely available and have been used for criminal purposes and torture. The authors of 2 systematic reviews concluded that prolonged observation and diagnostic testing are not necessary in patients who are otherwise asymptomatic and alert following such an exposure (33; 43).

However, in rare instances, various adverse outcomes related to the use of electrical weapons have been described in the literature over the years. Examples include cardiac arrhythmias resulting from fatal, blunt, or penetrating injuries, and neurologic sequelae such as seizures, altered mental status, and ischemic stroke (04). With 16 case reports in the literature, the use of Taser presents a small but real risk of death from fatal traumatic brain injury due to a fall, and old age represents an independent risk factor for such fatalities (24).

Electroconvulsive therapy (ECT). This is still used for the treatment of some psychiatric disorders and rarely may produce transient neurologic disturbances. There is a case report of a 50-year-old man who developed transient left hemiparesis (Todd paralysis) after electroconvulsive therapy for major depressive disorder, which completely resolved within 10 minutes without any permanent sequelae (26).

Maintenance electroconvulsive therapy is used for refractory psychiatric conditions. There is a report of 5 patients who developed temporal epileptiform abnormalities on EEG after receiving maintenance electroconvulsive therapy for at least 8 months, despite no history of epilepsy and no abnormality on neuroimaging (07). The EEG normalized in all patients after cessation of electroconvulsive therapy with no further clinical seizures. Therefore, maintenance electroconvulsive therapy may predispose to epilepsy with a seizure focus in the temporal lobe.

Pathogenesis. Fatal and nonfatal electrical injury incidents share 3 characteristics:

	(1) The unintentional exposure of the affected individual to electrical energy;
	(2) Compliance failure in at least 1 aspect of electrical design, installation, policies, procedures, practices, or personal protection; and
	(3) Energy transfer to an exposed individual in some combination of electrical, thermal, radiation, acoustic (pressure), mechanical, light, kinetic, or potential energy.

As electrical events unfold, physics, environmental factors, and individual traits can combine to result in nonuniform electrical exposures. Or the combination of electrical event, physics, environmental factors, and individual traits can result in nonuniform electrical exposures complicated by coincident energy exposures, including thermal, radiation, acoustic, and mechanical energy released from an industrial or commercial power source with the electrical event. Consequently, when an electrical injury survivor has been exposed to an electrical source, neurologic trauma evaluation may identify multifocal findings causally related to exposure to electrical and other forms of energy transfer.

According to the law of conservation of energy, represented in the equation below, energy cannot be created or destroyed, merely transformed from 1 variety to another:

Delta E-universe = 0

In relation to failures in electrical power systems, this physical law suggests that the electrical energy input to an electrical fault can be expected to equal the sum of the energy output or energy released from the fault in its various physical forms. Conceptually, this can be represented as follows:

Energy input (joules) = Energy output (joules), or

Electrical power in (watts) = Electrical power out (watts) + Plasma formation (watts) + Heat flow (watts) + Light power (watts) (including optical infrared UV and associated heat) + Mechanical work (watts) (including acoustic waves and shock waves)*

*(The output terms in the above equation can be linked to their hazard potential or ability to harm nearby individuals. Note electrical power, plasma, heat, and light, including visible and invisible light, all can contribute to tissue damage directly and via temperature extremes.)

Note conversion rules:

1 joule per second is equal to 1 watt: 1 J/s = 1 W
1 joule is equal to 0.239 calorie: 1 J = 0.239 cal
1 calorie is equal to 4.184 joules: 1 cal = 4.184 J

In commercial and industrial power supplies, although the energy input may be 50- to 60-Hz alternating current or direct current, ie, a specific form of electromagnetic energy (referred to as extremely low frequency, or ELF), the energy output may span the electromagnetic spectrum to include electrical energy and other energy forms.

The electromagnetic spectrum can be considered as a continuum, with different forms of energy characterized by their frequency and wavelength. The percentage distribution of the physical forms of energy in the output consequent to an electric arc is variable, described by physics and influenced by environmental considerations.

Environmental considerations include:

Geography Altitude Humidity Geology Meteorological factors (such as ambient pressure, temperature, winds)

Table 2. Effects of Electrical Current on the Body for Source Currents of Less than 600 Volts

Source current	Human response
1 mA	Perception of faint tingling
5 mA	Perception of slight shock, which may be disturbing but not painful. At this exposure, most people can “let go” or voluntary relax a forceful hand grip. An involuntary startle response may result to this level of exposure, may cause loss of balance during work, contact with nearby equipment, or other secondary injury.
6 to 12 mA (female); 9 to 30 mA (male)	Painful shock associated with loss of muscular control. Within this range of current it may not be possible for the victim to voluntarily release a forceful grip or relax contracted muscles.
50 to 150 mA	Perception of extremely painful shock, respiratory paralysis, and severe muscle contractions. Asymmetry in flexor and extensor muscle contractions can result in unpredictable spasmodic movement. Death is possible.
1000 to 4300 mA (1 to 4.3 A)	Ventricular fibrillation due to interference from extra-physiologic electrical source with cardiac conduction; muscle contraction; neural damage. Death is likely.
10,000 mA (10 A)	Cardiac arrest and severe burns occur. Death is probable.
15,000 mA (15 A)	Lowest over current at which a typical electrical circuit protector (fuse, breaker) will operate.
Adapted from the National Institute of Occupational Safety and Health and US Department of Labor, based on a presentation by Lee (25).

Heat refers to the form of energy transfer that results when there is a temperature difference. Heat energy is measured in calories, where 1 cal equals 4.184 joules (J). With temperatures rising in and around electric current, burn hazard is present from ohmic heating due to electrical power flow; ignition and combustion of nearby materials, notably worn clothing and adjacent equipment; and sprayed or blown hot or melting installation elements moved by the mechanical forces if an electric arc accompanies the electric shock exposure. Additionally, radiation is another major source of heat.

The injuries that accompany high temperature exposures at the body surface are commonly referred to as skin burns. High temperature exposures that occur volumetrically, or that distribute within the body’s tissues, are also called burns. The term burn generally refers to a physicochemical change in the human tissue. Neurologic tissue damage from deep tissue burns usually manifests during triage assessment.

Electroporation, a process by which an electrical field induces formation of pores through the cell membrane allowing free passage of ions and fluid, has been identified as a primary cause of neurologic injury following electrical exposure (06). Other mechanisms of injury may also play a role, such as the breakdown of the cytoskeleton due to excessive intracellular calcium.

From a clinician’s viewpoint, knowledge of the electrical event’s voltage conditions alone is of limited helpfulness because the extent of survivor’s electrical injury is a function of the power frequency energy transfer due to a combination of the current density in the tissue and the contact duration. Similarly, from a medical perspective, the heat, radiation, and pressure damage to the body are predicated on the efficiency of the electromechanical and electrochemical coupling between the hazardous source, event space, and the body. This information is not usually available to the medical team.

Regardless of the means of transmission, electricity enters a victim at an “entrance” point, travels a certain path, and leaves via an “exit” point. Entrance points can come in direct or indirect contact with the source of electricity and may or may not suffer burns when the electrical current meets the resistance of the skin.

The most common entrance points are the hands and the head. Exit points allow the electricity an avenue to leave the body in search of a grounding source. Although the exit point is determined by the path of the electrical current, some of the most common exit points are feet, legs, or hands. The exit of the current from the body may be a violent event leading to an excessive amount of damage. In cases of AC contact, the terms entrance and exit points may be mute because the electrical current is continuously flowing into and out of the individual through the same point.

The path of the electrical current through the body is determined by the path of least resistance as the current searches for a grounding source (ie, the earth). Different tissues in the body have different levels of resistance and electrical current follows those tissues with the least resistance preferentially. Because nerves and blood vessels have low levels of resistance compared to bones and fat, the current tends to travel along nerves and blood vessels when it overcomes the resistance of the skin. This may be 1 reason for the high rates of neurologic, psychiatric, and neuropsychological sequelae associated with electrical injuries. If, however, the current is dense enough, it will flow through whatever is in its path on route to the ground (eg, muscle, tendons, bones). Common pathways through the body are hand-to-hand, hand-to-foot, or head-to-foot. Different pathways have been hypothesized to have different patterns of sequelae associated with them. For example, hand-to-hand pathways are associated with a greater risk of mortality, presumably because vital organs (eg, heart) are likely to fall in that path. It is reasonable to assume that pathways from head-to-anywhere would be associated with higher levels of neuropsychological impairments because the brain falls in the path. Unfortunately, the effects of pathways on sequelae have not been studied extensively.

It has been noted that AC is 3 times as dangerous to the body as DC; there are 2 primary reasons for this. First, AC can cause tetanic spasms in muscles leading to repetitive contractions of those muscles. For example, if an individual’s hand comes into contact with AC via an exposed electrical wire, the muscles in the hand may contract and the individual is unable to let go of the wire (ie, “no let-go” response), leading to increased duration of electrical contact. Second, the cardiac and respiratory systems appear to be especially sensitive to AC and damage to those systems can lead to severe sequelae or death.

After a severe electrical contact injury, a survivor’s injured muscles can swell massively due to cell membrane damage, leading to a rise in local extracellular pressures identified clinically in tissues as a “compartment syndrome.” In a compartment syndrome, the blood supply to affected muscle is compromised and oxygen supply diminished. With hypoxia, further metabolic compromise and tissue destruction may result.

Other significant features of severe electrical exposure include disturbances in cardiac conduction, with possible refractory cardiac arrhythmias.

The pathophysiology of electrically induced neurologic sequelae is not fully understood. Direct damage to the nervous system, as well as delayed indirect effects such as denervation hypersensitivity, ephaptic transmission, oxidative reactions, and aberrant neuronal sprouting are other hypotheses that have been proffered.

A sequence of cellular events may be triggered by electrical insults in genetically predisposed individuals. A variety of cellular DNA damage and excitotoxicity mechanisms may contribute to ongoing and progressive damage following an initial trigger, such as electrical trauma. Morphological changes in the central nervous system are diverse following electrical injury and include neuronal chromatolysis, neuronophagia, and neuron loss. Infiltration of macrophages and neutrophils via the blood-brain barrier is seen, and microglial activation is a prominent and early event in central nervous system damage (21).

Various hypotheses have been reviewed to help explain the poorly understood phenomenon of delayed neurologic injury following lightning or electrical injury (36). In cases where there is delayed neurologic damage with a vascular origin, it is possible that free radicals resulting from oxidative stress may gradually damage spinal vascular endothelial cells, cutting off blood supply, and ending in death of spinal neurons. When the delayed condition is demyelination without vascular damage, it is possible that the free radicals from oxidative stress are formed directly from the lipids found in abundance in myelin cells. The electroporation hypothesis, the formation of additional pores in neurons, may best explain immediate or progressive changes in structure and function after lightning or electrical injury. However, there are differences in the pathophysiology of tissue injury from exposure to electric current and lightning. Studies on lightning are speculative, and sometimes they are extrapolated from research on electrical injuries as information on this topic is limited due to small numbers in human case series and difficulties in producing animal models (10).

Epidemiology

	• The incidence of electrical injuries for work-related injuries in the United States are noted.
	• Risk factors for electrical injuries have been identified.
	• Limited information is available on neurologic sequelae of electrical injuries.

Approximately 1000 deaths per year occur in the United States as a result of electrical injuries. Of these, approximately 400 are due to high-voltage electrical injuries, and according to health analyses of the U.S. Department of Labor, lightning causes 50 to 300 deaths.

In the latest statistical data on work-related electrical incidents shown on the website of U.S. Bureau of Labor Statistics, Census of Fatal Occupational Injuries and Survey of Occupational Injuries and Illnesses cover the years 2011 to 2015 and can be accessed at the following website:www.bls.gov. Electrical power-line installers and repairers were included in the list of 10 civilian occupations with high fatal-work-injury rates. Their rates of fatal work injuries per 100,000 full-time equivalent workers were 19.5% in 2011, 23.9% in 2012, 21.5% in 2013, 19.2% in 2014, and 20.5% in 2015. Telecommunications line installers and repairers had published rates of 7.9% in 2013 and 10.0% in 2014. In comparison, the rates for all workers in 2011 to 2015 ranged from 3.3% to 3.5%. During the same period, the rates of nonfatal occupational injuries (per 10,000 full-time equivalent workers) for electrical power-line installers and repairers were considerably higher than the rates for all occupations. In addition, the nonfatal rates for telecommunications line installers and repairers were higher than both the rates for all occupations and the rates for electrical power-line installers and repairers.

Predisposing factors for fatal outcome of electrical injuries at the workplace include the following:

• Lack of protective equipment • Lack of cover • Lack of grounding • Induced voltage • Failure to follow safety procedures

In an epidemiological study, risk of electric injury was assessed to develop an electric shock job-exposure-matrix (JEM) by using occupational accident registries across Europe (20). Of 116 job codes, occupations with high potential for electric injury exposure were electrical and electronic equipment mechanics and fitters, building frame workers and finishers, machinery mechanics and fitters, metal moulders and welders, assemblers, mining and construction laborers, metal-products machine operators, ships’ decks crews, and power production and related plant operators. Agreement between the electrical injury and magnetic field JEM was 67.2%. This JEM might contribute to disentangling risks from electric injury from those of extremely low frequency magnetic field exposure.

A retrospective cohort study on the risk of neurologic diseases among people in Denmark who had survived an electric accident in 1968 to 2008, which included 3133 persons, suggested an association between a single electric shock and increased risks for peripheral nerve diseases, migraines, vertigo, and epilepsy (19).

Prevention

	• Electrical injuries are mostly preventable.
	• Several strategies for prevention of electrical injuries aim to reduce the amount of possible energy transfer during an unintentional electrical exposure.
	• These measures do not necessarily effectively eliminate the heat hazard from an unintentional electric arc.

Based on human physical and biological characteristics, it is known that a fatal electrical event transfers a greater amount of energy to its victim than a nonfatal event. This knowledge about the fatal risk of energy transfer underlies the use of consumer product and industrial equipment designs (for example, grounded plugs, required doors, specified space clearances, venting systems on equipment to discharge combustion products, “umbilical corded” controls, infrared monitoring ports for doors-closed heat monitoring) and barrier protection (such as leather gloves, flash suits, safety glasses, face shields, long sticks, extended handles, and flame-resistant clothing).

By reducing the amount of possible energy transfer during an unintentional electrical exposure, strategies including equipment design and barrier protection can increase the likelihood of survival after an electrical incident.

These strategies include:

• Engineering design limiting available fault energies. • Control systems relying on electronic, electrical, and mechanical devices. • Installations built to channel, contain, or deflect the effects of electric arcs. • Information and communication systems and practices to identify and warn of electric fault possibility or occurrence.

These strategies do not necessarily effectively eliminate the heat hazard from an unintentional electric arc. Consequently, additional protection strategies to reduce occupational exposure are needed. Result of a retrospective study of electrical burn patients admitted to the burn centers in South China indicates that more attention should be paid to prevention of electrical burns in male adults, with a particular focus on industrial workers, incidents in the spring and summer, and high-voltage injuries (16).

An incident was reported that occurred while using a nerve stimulator for assessing the neuromuscular block when it delivered a significant electric shock to the anesthetist resulting in arm pain (03). An investigation of this incident showed the charging cable plug provided by the manufacturer had 2 parts that were separated by traction, and the anesthetist touched the end that remained attached to the back of the nerve stimulator. To prevent this from happening again, the manufacturer was asked to provide a 1-piece plug for the nerve stimulator.

Differential diagnosis

Confusing conditions

History of circumstances surrounding electrical injury are important. Neurologic complications of electrical injuries should be differentiated from those due to lightning, particularly in a patient who is not conscious, and history or circumstances of injury are not available.

Lightning. In survivors of lightning, the most common immediate findings are amnesia, loss of consciousness, tympanic membrane rupture, and other neurologic or musculoskeletal injuries. The most common long-term and disabling injuries are neurologic in nature: brain injury like post-concussive syndrome and chronic pain (10). Patients hit by lightning may present special clinical manifestations; keraunoparalysis is a temporary paralysis specific to lightning injuries that is characterized by blue, mottled, and pulseless extremities (lower more commonly than upper). These findings are felt to be secondary to vascular spasm and often resolve within hours but can be permanent (13). They also may present with pupils that are fixed, dilated, or asymmetric due to autonomic dysfunction. Complications of lightning strikes can include hypoxic encephalopathy, intracerebral hemorrhage, cerebral infarction, and spinal fractures.

Differentiation from other neurologic conditions resembling complications of electrical injury. The differential diagnosis of the neurologic complications of electrical injuries may include those related to anoxia/hypoxia, cardiac arrest, convulsions, explosion/blast effects, falls, or mechanical trauma from the affected individual being caught by machinery or moving equipment.

Detection of malingering. The rate of malingering is as high as 40% in compensation seeking workers in general and 25% in electrical injury in particular (28). Many electrical injury patients report neurocognitive impairment or movement disorders. It would be helpful to have indicators that the body had actually absorbed a sufficient amount of electrical energy to produce injury. Entry and exit wounds are a certain indication that the body has conducted a significant amount of electrical current. Although entry and exit wounds are an indication that the body has absorbed sufficient electricity to cause injury, their presence does not necessarily indicate that the electrical exposure has caused nervous system injury. At the same time, the absence of entry and exit wounds does not necessarily mean that electrical injury has not occurred. Therefore, other indicators of acute CNS dysfunction such as those used to grade transient brain injury severity (eg, Glasgow Coma Scale score, length of coma and/or posttraumatic amnesia, structural damage to the nervous system) may also be helpful. Criteria that represent a systematic, comprehensive, integrated, research-based approach to the diagnosis of malingering (40). Bianchini and colleagues support the application of the Slick and colleagues criteria for the diagnosis of Malingered Neurocognitive Dysfunction (05).

Diagnostic workup

• Diagnostic tools that are reported to be useful for detection of neurologic sequelae of electrical injury include biomarkers of muscle damage, imaging studies, and electrophysiology studies.

In general, the diagnostic approach to the neurologic consequences of an electrical injury patient is consistent with the neurologic evaluation of a multi-trauma injury patient. A high degree of clinical suspicion for neurologic involvement is warranted, especially when no information about the electrical events may be available, and there are no external wounds to indicate localization of exposure. Table 3 summarizes the diagnostic evaluation for an electrical injury patient.

Table 3. Investigation of Central Nervous System, Muscle, and Peripheral Nerve Injury resulting from Electrical Injury

Diagnostic	Description
Laboratory studies	Serum biomarkers of muscle damage (eg, creatine kinase), serum myoglobin if urinalysis reveals myoglobinuria.
Radiology studies	X-rays, CT scans, MRI, MRA, ultrasound, and nuclear medicine examination can evaluate nervous system structural damage and confirm fractures, local tissue edema, focal areas of inflammation, ischemia, thrombosis, or hemorrhage.
Electrophysiology studies	Electrophysiology studies are guided by the patient’s history and physical examination. Muscle weakness, easy fatigue, loss of endurance, paralysis, pain, rigidity, or tremor are indications for electromyography and peripheral nerve conduction studies (sensory and motor). Further evaluation may be needed with peripheral nerve refractory period spectroscopy and MRS. Symptoms of peripheral neuropathy should be investigated even when there are minimal cutaneous burns. Transcranial magnetic stimulation can diagnose electrical burn-induced myelopathy even though MRI reveals no abnormal signal changes in myelopathy patients. Neurophysiologic evaluation may also be indicated by additional complaints. For example, history of loss of consciousness or seizures, CNS complaints such as headache, impaired memory, attentional problems, personality changes, or cognitive changes suggests EEG and EKG. A history of temporary or persistent loss of hearing, ringing in the ears, or change in memory to verbal communication are indications for auditory evoked potentials. A change in visual acuity or visual disturbance is an indication for visual evoked potentials Cardiac rhythm disturbances, syncope, chest pain, and easy fatigue are indications for an EKG.

Management

	• In the emergency phase, after initial resuscitation, triage and planning is done for diagnostic procedures and further treatment.
	• Hospital admission is warranted following exposure to an electrical source of more than 200 V potential, burns involving greater than 15% of body area, and history of cardiopulmonary resuscitation.
	• Neuropsychiatric sequelae of patients with electrical injuries should be taken care of as a routine part of multidisciplinary care.

In the emergency or first response period, American Burn Association Advanced Burn Life Support guidelines outline triage, initial resuscitation, and emergency transport protocols. On admission to emergency medical services, physical examination, laboratory studies, and diagnostic radiology evaluation are prioritized, depending on the patient’s clinical course. Cardiac monitoring should be initiated in all patients that have experienced anything greater than a minor low-voltage burn.

Neurologic evaluation of the CNS and auditory, visual, and peripheral sensorimotor function can be managed simultaneously with stabilization of cardiorespiratory status and wounds in a manner consistent with best practices.

Electrical injuries are traditionally divided into low-voltage electric power injuries (less than 1000 V) and high-voltage (more than 1000 V). In contrast with other types of trauma, high-voltage injuries present some rather unique problems that require a high index of suspicion and awareness of all possible manifestations. Electrical injury should be viewed and managed as a multisystem injury because there is virtually no organ that is protected against it (12). When there is evidence or suspicion of exposure and electromechanical contact with an electrical source of more than 200 V potential and capable of more than 200 mA, hospital admission is warranted even in the absence of physical findings.

Additional indications for hospital admission are: history of cardiopulmonary resuscitation or cardiac findings, including refractory cardiac arrhythmias; history of loss of consciousness or disorientation; history of fall from a height; associated thermal injury to greater than 15% of the body surface area, or including burn to the hands, feet, face, or groin; suspicion of smoke/vapor inhalation or respiratory distress; spine fractures; serum electrolyte derangements; and compartment syndromes.

Burn care teams must also address the impending neuropsychiatric sequelae of patients with electrical injuries as a routine part of multidisciplinary care. Although the rehabilitation and resuscitation phases of burn care may partly determine neuropsychiatric outcomes, these outcomes may in turn determine reconstructive success. For example, posttraumatic stress disorder results in more anxiety before, during, and after painful medical procedures. Patients with electrical injuries may benefit from earlier, more focused, and intensive psychiatric support. Although useful guidelines and models exist to systematically address the complex physical morbidities of electrical burn patients, newer models and strategies are needed to prevent and treat neuropsychiatric sequelae (09).

Special considerations

Pregnancy

Limited information is available regarding pregnancy-to-term delivery following electrical shock exposure. Effects of electrical injuries during pregnancy range from transient unpleasant sensation with no effect on the fetus to sudden maternal and fetal death. Reported adverse effects include abnormalities of the fetal heart, damage to the fetal central nervous system, and fetal growth retardation (41).

Anesthesia

Considerations regarding anesthesia are related to trauma severity and level of neurologic impairment.