Electrical and Lightning Brain Injuries

CHAPTER 8

SHRAVAN PARIKH

JOSEPH FINK

MAIA FEIGON

NEIL PLISKIN

OVERVIEW

Electricity pervades modern society; it is often taken for granted, in terms of the utility, power, and ease with which it provides consumers innumerable benefits. Although electrical power is virtually ubiquitous in everyday life, injuries associated with accidental contact are relatively rare in the general population. However, electric shock is a common type of trauma in the workplace, where significant electrical injuries (EIs) disproportionately affect younger men (Martinez & Nguyen, 2000). Similarly, EI caused by lightning strikes is a relatively uncommon weather event that causes even fewer fatalities. However, the impact of electricity-related injuries and the significant amount of short- and long-term medical, social, and personal consequences deserve unique consideration.

EIs are sometimes poorly understood by neuropsychologists, as well as by physicians, clinicians, and allied health professionals. Because of the relatively low incidence rate of EI, neuropsychologists may have little or no experience with injury dynamics and issues when they first encounter a patient with such an injury. Moreover, EIs are often compared to traumatic brain injuries. However, neuropsychological sequelae of EI do not typically follow the symptom and recovery path as seen in cases of traumatic brain injury (TBI; Barrash, Kealey, & Janus, 1996; Heilbronner, 1994). In particular, perceived neuropsychological changes following a mild TBI typically resolve within 8 months to 1 year postinjury, whereas the neuropsychological sequelae found in EI may emerge after some time has elapsed and last much longer.

EI survivors may see numerous clinicians from various disciplines and specialties depending on the nature of their injuries and complaints, but it is often difficult for patients to obtain a comprehensive and integrated assessment that takes into account the physical, cognitive, and emotional changes that can occur after EI, especially when brain involvement is not evident on neuroimaging or standard neurological exam. The role of neuropsychological assessment can be particularly crucial for situations in which overt physiologic manifestations of injury are minimal or lacking, in order to help guide clinical care and medical–legal decisions.

In this chapter, we review the epidemiology of electrical and lightning injuries and consider some of both the known and poorly understood aspects of the pathophysiology of these injuries. We review the patterns of symptom presentation, diagnostic considerations, treatment, and prognosis. Finally, we conclude with two case studies that highlight the intricate details of assessing and treating individuals who have experienced a trauma due to electrical and lightning injuries.

HISTORY

EI from sources other than lightning is a relatively new phenomenon in the history of humankind. With the advent of the light bulb and industrialized electricity, the incidence of EI increased significantly in the 19th and 20th centuries. The first recorded death caused by electrical current from an artificial source was reported in 1879 when a carpenter in Lyons, France came in contact with a 250-V alternating current (AC) generator. In the United States, the first reported fatality occurred in 1881 when an intoxicated man passed out on a similar type of generator in front of a crowd in Buffalo, New York (Price & Cooper, 2013).

Lightning-related injury has presumably always been a rare part of humankind’s experience. From a historical perspective, the incidence of lightning-related fatalities in the United States decreased from an average of 94 over the period from 1891 to 1894, to only 26 in 2014 (Holle, López, & Navarro, 2005; National Weather Service, 2015). Despite this, the sheer amount of lightning strikes per day, the propensity to cause significant injury or death when an individual is struck, and the magnitude of the economic, social, and personal costs deserve in-depth exploration in order to better assist health professionals in understanding the unique injury characteristics.

PATHOPHYSIOLOGY

The exact pathophysiologic mechanisms of electrical and lightning injury are not well understood because of the numerous variables that cannot be measured or controlled when an electrical current passes through tissue. However, the nature and severity of these injuries is thought to depend on the following factors (Kouwenhoven, 1949):

Direct current (DC) versus alternating current (AC)

Duration of exposure

Voltage and amperage

Body resistance

Pathway of current

Type of Current

High-voltage DC contact tends to cause a single muscle spasm, often throwing the victim from the source, resulting in shorter duration of exposure compared with AC exposures. However, the likelihood of secondary blunt trauma due to falls, blast trauma, and trauma from flying debris is increased. Generally, the longer the duration of contact with a high-voltage current, the greater the electrothermal heating and tissue damage. However, even brief contact with a DC source can still result in cardiac arrhythmias, depending on the phase of the cardiac cycle affected (Price & Cooper, 2013; Wesner & Hickie, 2013).

The electric current involved in lightning strikes is also via DC. The amount of DC delivered by a lightning strike is far greater than that produced by typical AC domestic electricity sources. The duration of exposure, however, is generally much shorter, lasting approximately 10 to 100 ms. This current causes the release of a significant amount of heat, raising temperatures of the lightning-strike channel to approximately 30,000 K (Ritenour, Morton, McManus, Barillo, & Cancio, 2008).

AC, which is the standard form of electrical transmission, may be more dangerous than non–lightning-associated DC of the same voltage (Koumbourlis, 2002). EI from AC can cause repetitive muscle contraction, or tetany, wherein the muscle fibers are stimulated between 40 and 110 times per second by the AC cycles (Price & Cooper, 2013). The hand is the most common contact point, such as with a tool, appliance, or machinery, which results in contact with an AC electrical source. The upper extremity flexors are much stronger than the extensors, often causing the hand grasping the current source to both grip and pull the source even closer to the body. Currents greater than the “let-go threshold” (6–9 mA) can prevent the victim from releasing the current source, resulting in the “no let-go” phenomena, which extends the duration of exposure to the electrical current (Price & Cooper, 2013).

Voltage

Voltage is a measure of the difference in electrical potential between two points and is determined by the electrical source. In the scientific literature, EIs are typically divided into low (<1,000 V) or high voltage (>1,000 V). Although both can cause significant morbidity and mortality, high voltage tends to have a greater potential for tissue damage and major amputation (Bryan, Andrews, Hurley, & Taber, 2009a; Price & Cooper, 2013).

Current, expressed in amperes, is a measure of the amount of energy that flows through an object. The heat generated, as defined by Joule’s law, is proportional to the amperage squared. Amperage depends on the source voltage and the resistance of the conductor. Although the voltage of the source is often known, the resistance varies according to the affected tissues and may change markedly during the exposure, making predictions of actual amperage difficult for any given EI (Price & Cooper, 2013).

Resistance

Resistance is the tendency of a material to resist the flow of electrical current. It varies for a given tissue, depending on its moisture content, temperature, and other physical properties. The higher the resistance of a tissue to the flow of current, the greater the potential for transformation of electrical energy to thermal energy. The least amount of resistance involves nerves, blood, mucous membranes, and muscle. Dry skin represents an intermediate amount of resistance, and bone, fat, and tendon yield the most resistance (Bryan et al., 2009a).

Path of Current Flow

Electric current enters a victim at contact points on the body (i.e., usually an extremity). In the case of DC, electricity enters at an “entrance” point and, after traveling along a pathway through the body, leaves through an “exit” point (Bryan et al., 2009a). In the case of AC current, which repeatedly alternates its directional flow, there are technically only contact points, none of which is solely an entrance or an exit point because of the bidirectional current flow. Contact wounds are only an indication that the body has conducted a significant amount of electrical energy to cause injury. However, the mere presence or absence of contact wounds is not sufficient to accurately predict the severity of EI. A close examination of the direct and indirect effects of the electric shock is necessary to determine the severity of the injury, course, and prognosis (Koumbourlis, 2002; Price & Cooper, 2013).

When lightning strikes an individual, the primary current arc typically travels outside the body, a phenomenon known as “flashover” (Ritenour et al., 2008). The immense current generates large magnetic fields perpendicular to the body’s surface, which in turn transiently create secondary electrical currents within the body itself.

When lightning hits the ground, current spreads out from the ground contact point such that if a victim is standing nearby with feet apart, the potential difference between the feet may be in the range of 1,500 V (Pfortmueller et al., 2012). Thus, lightning injuries are more severe when a person’s feet are apart in line with the ground contact point than when they are close together. When lightning directly strikes a victim’s upper body, a very large potential difference between the upper and lower body is created, resulting in a brief but large current flow. Although the duration is generally not sufficient to cause Joule heating, as in high-voltage nonlightning injuries, it is sufficient to damage muscle and nerve cells (Ritenour et al., 2008).

ETIOLOGY

The causes of electrical and lightning-related injury are varied; however, research suggests that young men working in the construction or utility industry are at higher risk (American Burn Association, 2015). Subsequent injuries, such as electrical or thermal burns, deep-tissue and organ damage, brain injury, and secondary systemic disorders require prompt, comprehensive, and multidisciplinary care. The primary cause of death in these cases is typically cardiac or respiratory arrest (Price & Cooper, 2013). The following areas have been identified as high risk, in which EI is often the primary mechanism for injury and fatality (Electrical Safety Authority, 2012):

Powerline contact

Electrical/construction workers

Misuse of electrical products and unapproved or counterfeit products

Electrical infrastructure fires in buildings

In cases of lightning-related injury, the risk of being struck is contingent on regional, seasonal, and temporal factors. The following is a list of mechanisms that can occur in lightning-related injury (Ritenour et al., 2008):

Direct strike: Most of the current flows through the body.

Contact voltage: Occurs when lightning strikes an object that the victim is touching.

Ground current: Ground current passes from the strike point through the ground and into the victim.

Side flash: Splashing of current from a nearby object or person onto the victim.

Upward streamer: Passage of lightning from the victim upwards.

Blast injury: Sudden expansive explosion of the air around the lightning channel causing blunt trauma.

EPIDEMIOLOGY

Electrical and lightning injuries are relatively uncommon; however, their impact on victims and families is often significant. The prototypic electrical accident victim is a young man shocked while working in the electrical or construction trade, bringing significant risks for death and morbidity. Epidemiological rates of lightning-related EIs are less reliable and difficult to discern because state and federal agencies do not require they be reported (Ritenour et al., 2008). However, some studies have suggested that lightning-related injuries disproportionately affect young adult men, with low rates of fatal injuries (Jensenius, 2015; Price & Cooper, 2013; Ritenour et al., 2008).

Information on rates of burn admissions related to EI in the United States between 2005 and 2014 showed an overwhelming decline of incidents and complicating injuries sustained per year (American Burn Association, 2015). Over this period, burns related to EIs represented only 3.6% of all burn admissions that were reported. The majority of these cases was work related (60.8%) and occurred within an industry setting (38.9%). The highest rates of EIs occurred at several age peaks, including in the 20- to 29.9-year-old age group (13%) and among the 60-and-over age group (13.5%; American Burn Association, 2015).

Between 1992 and 2010, fatal EIs in the United States have declined significantly by more than 50% on an annual basis (Electrical Safety Foundation International, 2011). The dramatic reduction of EIs, especially within an industrial setting, has been attributed to better training, electrical safety standards, and even a slowdown in economic activity (Electrical Safety Foundation International, 2011). Victims who came in contact with overhead power lines comprised the largest fatal-accident category, representing 44% of all electrical fatalities between 1992 and 2010. From 2003 to 2010, the construction industry experienced the highest rates of fatal EIs (52%) compared with other industries such as professional and business services; trade, transportation, and utilities; natural resources and mining; and manufacturing. Nonfatal EIs have shown similar declining trends as well. In 2010, nonfatal EIs were down by more than 60% when compared with rates in 1992. Victims who came in contact with electric current from a machine, tool, appliance, or light fixture represented the largest group (Electrical Safety Foundation International, 2011).

From 2006 to 2014, 287 people were struck and killed by lightning in the United States (Jensenius, 2015). Men accounted for 81% of all fatalities, and more than 90% of these deaths were related to fishing and sports accidents. Ages of the victims predominantly ranged from 10 to 60 years, with somewhat fewer in the 30- to 39-year-old age group. In general, the summer months (June–August) represent a peak in lightning activity across the country. For instance, over 70% of lightning fatalities recorded between 2006 and 2014 were during the summer months (Jensenius, 2015). Some estimates on the global prevalence of lightning-related fatalities are estimated to be around 24,000 per year, while nonfatal lightning-related injuries are estimated to be approximately 240,000 per year (Holle, 2008).

CLINICAL PRESENTATION

Symptom presentation in victims of electrical and lightning injury can include a variety of physical, neurological, cognitive, and emotional changes that manifest in the acute, postacute (1 month to 5 years postinjury), and long-term phase (5 or more years postinjury). The severity of injuries can range widely from minimal (e.g., minor burns, transient confusion) to very severe (e.g., paraplegia, permanent memory loss, death; Duff & McCaffery, 2001; Fink, Rog, Bush, & Pliskin, 2010; Silversides, 1964).

Although immediate effects of EI can be quite obvious like burns and cardiac abnormalities, frequent and often clinically significant central and peripheral nervous system dysfunction is sometimes less evident in the immediate aftermath of electrical shock. Additionally, the degree of neuropsychological impairment and emotional disturbance can persist for months and years, unlike cases of uncomplicated mild TBI, in which symptoms typically dissipate in the weeks or months following the injury (Aase, Fink, Lee, Kelley, & Pliskin, 2014; Barrash et al., 1996; Hahn-Ketter et al., 2015; Pliskin et al., 1994; Wesner & Hickie, 2013).

Physical

Clinical manifestations of dermal and subcutaneous burns are among the most common acute symptoms in EI, and often lead to pain, scarring, fibrosis, and joint stiffness (Price & Cooper, 2013). Low-voltage EI burns tend to create small, well-defined burns at the sites of skin contact (Czuczman & Zane, 2009). In high-voltage injuries, the burns are typically more significant and may appear as painless, depressed, yellow-gray, charred craters with central necrosis (Czuczman & Zane, 2009; Price & Cooper, 2013). Although high-voltage injuries may spare the skin surface, they can cause significant damage to underlying soft tissues and bones. In cases of lightning-related EI, the prevalence of significant burns or soft tissue destruction is rather low due to the brief duration of the actual strike itself. However, four main types of superficial burns are typically seen: linear, puncture, feathering, and thermal (Price & Cooper, 2013; Ritenour et al., 2008).

When severe flash and flame burns are present, the patient is expected to develop severe hemodynamic, autonomic, cardiopulmonary, renal, metabolic, and neuroendocrine responses that may have devastating effects on long-term recovery (Koumbourlis, 2002). In the case of electrical arc events, injuries may include perforated eardrums; blast effects affecting lung, abdomen, and/or head, plus acceleration–deceleration head injury; and blunt head trauma from falling or being hit by explosion shrapnel (Capelli-Schellpfeffer, Miller, & Humilier, 1999; Fink et al., 2010).

The skeletal system may have fractures or joint dislocations either from severe tetanic muscle contractions or from injury due to falls. Fractures are more common in the long bones of the upper limb and in vertebrae and increase the risk of spinal cord injury (Bryan et al., 2009b). In cases of lightning injury, skull fractures and cervical spine injury from either direct strikes or associated trauma are often seen (Pfortmueller et al., 2012). In high-voltage EI, direct electrothermal energy leading to coagulation and necrosis is the main cause of muscle injury (Czuczman & Zane, 2009).

Ocular injuries (e.g., cataracts, keratitis) and auditory sequelae (e.g., hearing loss, tinnitus, vertigo) are also common. Cardiac complications (e.g., sinus tachycardia, supraventricular tachycardia, atrial fibrillation, cardiac arrest) may occur, particularly when AC and/or high voltages are involved (Price & Cooper, 2013; Spies & Trohman, 2006).

In the postacute and long-term phases, common physical complaints include pain, fatigue, reduced range of motion, joint stiffness, headache, motor weakness, coordination problems, blurred vision, dizziness, insomnia, contracture, and paresthesia (Daniel, Haban, Hutcherson, Bolter, & Long, 1985; Hooshmand, Radfar, & Beckner, 1989; Ramati et al., 2009; Theman, Singerman, Gomez, & Fish, 2008; Wesner & Hickie, 2013).

Neurological

Although central and peripheral nervous system injury are common clinical sequelae of EI, there are no specific histologic or clinical findings that are considered pathognomonic for victims of EI. However, loss of consciousness, confusion, and cognitive impairment tend to be common among victims (Wesner & Hickie, 2013). Victims of EI have been reported to experience isolated seizures following shortly after the accident, as well as recurring seizures that may last for years after injury (Bryan et al., 2009b; Daniel et al., 1985; Hooshmand et al., 1989; Wesner & Hickie, 2013). Acute dysfunction of peripheral motor and sensory nerves is also relatively common and may cause a variety of motor and sensory deficits. This is largely in part due to the process of electroporation, which results in the formation of pores in the lipid bilayers that form cell membranes and eventually lead to rapid and diffuse necrosis (Bryan et al., 2009b).

Keraunoparalysis is a transient type of neurological paralysis that is considered to be a pathognomonic sign of lightning-related EI (Czuczman & Zane, 2009; Pfortmueller et al., 2012; Ritenour et al., 2008). Immediate and persistent neurologic syndromes associated with lightning injury include hypoxic encephalopathy and intracranial hemorrhage, usually occurring in the basal ganglia and brain stem. Delayed neurologic sequelae may include motor neuron disease and movement disorders, traumatic falls resulting in spinal cord injury, and epidural and subdural hematomas (Czuczman & Zane, 2009; Pfortmueller et al., 2012; Ritenour et al., 2008).

Cognitive and Emotional Disturbances

A large body of research suggests that a variety of cognitive deficits are frequently observed, including impairments of attention, processing speed, and memory, as well as disruptions in emotional well-being that could adversely affect cognition (Aase et al., 2014; Grigorovich, Gomez, Leach, & Fish, 2013; Pliskin et al., 2006; Wesner & Hickie, 2013). Despite the heterogeneity of neuropsychological symptom presentation, a controlled investigation concerning neuropsychological symptom constellation in EI victims highlights specific impairments. In particular, cognitive deficits in attention/concentration, mental processing speed, and motor skills were more pronounced when compared with demographically and occupationally matched samples (Pliskin et al., 2006). Furthermore, these symptoms were not directly related to the severity of the physical injury as measured by surgery and hospitalization statistics, voltage exposure, litigation, or return-to-work status (Pliskin et al., 2006).

Emotional disturbance and problems with emotion regulation are very common symptoms reported by patients following EI. Although the victims of EI are sometimes mistakenly compared with patients who have experienced uncomplicated mild TBI, symptoms observed in EI may, in contrast, persist and in some cases, worsen over time (Bianchini, Love, Greve, & Adams, 2005; Chico, Capelli-Schellpfeffer, Kelly, & Lee, 1999; Hahn-Ketter et al., 2015; Pliskin et al., 2006). The following symptoms are commonly reported and may contribute to poorer cognitive ability and affect return-to-work status (Hahn-Ketter et al., 2015). Additionally, the significance of these emotional and cognitive symptoms may be more evident postacute injury and long-term (Aase et al., 2014; Pliskin et al., 2006; Ramati et al., 2009):

Depression