The neurological complications
of electrical injury: A nursing
case management perspective
By Valerie Coubrough and Paulette Warnell
Abstract
High-energy electrical injury, whether from lightning strike or
electrical shock, occurs primarily in the workplace.
Neurological dysfunction can be a devastating complication of
electrical injury. A review of the literature was undertaken to
develop a better understanding of the epidemiology,
mechanisms of injury and neuropathology associated with this
type of injury. The numerous challenges inherent in the
management of these complex cases were illustrated by three
case studies.
Introduction
A lightning storm is an awe-inspiring and sometimes terrorprovoking display of the power of nature. As a critical force
driving modern civilization, nothing surpasses electricity.
However, both lightning and generated electricity can be
extremely dangerous. The majority of serious electrical
injuries occur in the workplace (Cherrington, 1995; Cooper,
1995; Grube, Heimbach, Engrav, & Copass, 1990; Hammond
& Ward, 1988). Grube and colleagues refer to electricity as “a
particularly temperamental and unpredictable maimer of
young working males” (p. 256).
Neurological dysfunction is a dreaded complication of
electrical injury. Exposure to electrical current may result in
global or focal nervous system dysfunction. Symptoms may be
manifested immediately after injury or be delayed, and may
resolve over time or progress to reflect permanent neurological
impairment (Cherrington, 1995; Ratnayake, Emmanuel &
Walker, 1996). The presence of neurological sequelae places
tremendous stress on the injured person and the family, and
poses great challenges to acute care practitioners, the neuro
rehabilitation team, and the advanced practice nurse case
manager (APNCM).
The APNCM role in the serious injury program at the
Workplace Safety and Insurance Board (WSIB) provides a
unique opportunity to assist and support individuals and their
families throughout the health care continuum. This is
particularly true when severe electrical injury occurs. The
APNCM follows the injured worker from the regional burn
centre or trauma intensive care unit (ICU) to the rehabilitation
setting, and finally through reintegration into the home
community.
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This article is focused on individuals who experience
neurological dysfunction following electrical trauma in the
workplace. Epidemiological data and an overview of the physics
of electricity are presented. Mechanisms of injury are explored,
and compared/contrasted in lightning strike and electrical shock.
While the neuropathology of electrical injury is not fully
understood, current knowledge and understanding are discussed
in light of the most recent research findings from the literature.
The numerous challenges inherent in the management of these
complex cases are illustrated by three case presentations.
Epidemiology
Lightning strikes the earth approximately 100 times per
second (Blount, 1990). The true incidence and frequency of
injury or death from lightning is difficult to determine related
to inconsistent reporting practices (Cooper, 1995). It has been
estimated that lightning strikes kill 100 to 600 people in the
United States each year. Thousands more sustain serious
injuries, and many suffer permanent disability (Blount).
Lightning victims are generally involved in sports or
recreation activities or are engaged in outdoor employment
(Blount; Kleinschmidt-DeMasters, 1995; Patten, 1992). Men
are more likely to be struck by lightning than women at a ratio
of approximately 4:1, except when the electrical source is
conducted through the telephone system. In this case, a woman
is more likely to be the victim (Patten).
Accidental death by electrocution occurs with a yearly
frequency of approximately one per 200,000 population
Les complications neurologiques à la
suite d’une blessure par électrocution :
Une analyse des soins infirmiers
Résumé
Une blessure par électrocution à haute tension, causée par
la foudre ou une source électrique, se produit
principalement en milieu de travail. Des conséquences
neurologiques graves peuvent suivre ce genre de blessure.
Une recherche littéraire a permis de développer une
meilleure compréhension de l’épidémiologie, du
mécanisme de l’accident et de la neuropathologie reliés à
ce genre de blessure. Les nombreux défis rencontrés dans
le traitement de ces cas compliqués sont illustrés dans
l’étude de trois patients.
VOLUME 23 ❖ NUMBER 4 ❖ JUNE 2002
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(Danielson, Capelli-Schellpfeffer & Lee, 2000; Veneman, van
Dijk, Boereboom, Joore & Savelkoul, 1998). Electrical
injuries represent 3.5 to 6.5 per cent of admissions to burn
centres worldwide (Adler & Caviness, 1997; Breugem, Van
Hertum & Groenevelt, 1999; Cooper, 1995; Grube et al., 1990;
Hammond & Ward, 1988; Tredget, Shankowsky & Tilley,
1999). The Firefighters Burn Treatment Centre, University of
Alberta Hospital in Edmonton reported that 5.3 per cent of its
total admissions over a 10-year period were attributable to
electrical injury. Of these, 95.9 per cent were male and 4.1 per
cent female. The average age of electrical injury victims was
33.9 years. Almost 75 per cent of these individuals were
engaged in occupationally related activities at the time of
injury (Tredget et al.). These findings are consistent with data
from other centres that suggest that electrical injuries tend to
occur primarily in young male workers (Danielson et al.;
Hammond & Ward; Veneman et al.). At-risk occupations
include linepersons, electricians, overhead crane operators,
and construction workers (Cherrington, 1995). Young workers
newly entering the workforce are particularly vulnerable to
electrical injury (Veneman et al.).
The physics of electricity
Electrical injury occurs when a portion of the body completes
an electric circuit (Adler & Caviness, 1997). A number of
physical properties of electricity will have an impact on the
amount of tissue destruction that occurs following exposure to
electrical energy. These include the type of circuit, resistance,
duration of exposure, amperage, voltage, frequency, and the
anatomic pathway of the electrical energy through the body
(Blount, 1990; Cooper, 1995; Patel & Lo, 1993; Patten, 1992).
Type of current
Direct current (DC) usually causes a single muscle spasm,
often throwing the victim away from the source, resulting in
decreased exposure time but increasing the likelihood of
associated blunt trauma. Lightning is a source of direct
current. Some heavy industrial equipment utilizes DC, as do
electrical batteries, and electric buses and streetcars. However,
electrical power for most industrial and household applications
is generated and travels through power lines as alternating
current (AC). Alternating current is said to be much more
dangerous than direct current of the same magnitude, as
muscle tetany occurs that prevents the victim from letting go
of the current source, thus prolonging exposure time. In
general, the longer the duration of exposure to electrical
current, the greater the degree of tissue damage (Blount, 1990;
Cooper, 1995).
Resistance
Resistance, measured in ohms, is another critical factor in the
determination of the extent of electrical injury. Resistance is
the tendency of a substance to resist the flow of current. The
typical human body has a hand-to-hand resistance of
approximately 1,000 to 2,000 ohms (Bass, 1998). Resistance is
also specific for a given body tissue, with tendon, bone, fat,
and skin being more resistant to current flow than are blood
vessels and nerves (Blount, 1990; Breugem et al., 1999;
Cooper, 1995). The higher the resistance of a tissue to the flow
of current, the greater the potential for the conversion of
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electrical energy to thermal energy, as described by Joule’s
law, resulting in deep contact burns (Cooper; Danielson et al.,
2000). Moist skin or immersion of the body in water decreases
resistance to flow of current (Blount; Breugem et al.; Cooper).
Electrical current will always follow the path of least
resistance.
Amperage
Amperage (mA) is the measure of the amount of current that
flows through an object. There is a very narrow range of safety
with electric current from perception threshold (0.2 to 0.4 mA)
and let-go current (6 to 9 mA), the level at which a person
becomes unable to let go of the current source because of
tetanic contraction. In general, let-go amperage tends to be
higher for men than for women (Bass, 1998). Ventricular
fibrillation can occur at an amperage of 50 to 120 mA (Cooper,
1995).
Voltage
Voltage (V), on the other hand, can be defined as the electric
energy potential between two points. Electrical injuries are
traditionally divided into high and low voltage using 500 or
1,000 V as the usual dividing lines (Cooper, 1995). A helpful
analogy to understand the difference between amperage and
voltage is water running through a pipe, with the amperage
being the volume of water, and the voltage being the water
pressure. When contact with high voltage occurs, an arc
initially establishes the flow of electricity. An electric arc is
comprised of an extremely hot electrically conductive gas.
Approximately 10,000 to 20, 000 V are required to establish an
arc over a distance of one centimetre (Danielson et al., 2000).
Frequency
The frequency of the electrical current is as important as the
magnitude when evaluating electric shock injuries. Humans
are susceptible to frequencies as low as 50 to 60 hertz (Hz).
The frequency of the nerve signals controlling the heart is
approximately 60 Hz. Ventricular fibrillation occurs when
current at 60 Hz from an electric shock interferes with the
natural rhythm of the heart. Unfortunately, North American
power line frequencies are set to 60 Hz (Bass, 1998).
Lightning is transmitted at super high frequency (Danielson et
al., 2000). Lightning strike usually results in temporary
asystole. Sinus rhythm generally resumes when potential
redevelops, due to the heart’s inherent automaticity. More
dangerous with lightning strike injuries is respiratory centre
depression with apnea. Apnea may outlast cardiac arrest and
cause secondary ventricular fibrillation from hypoxia (Blount,
1990; Cooper, 1995; Stanley & Suss, 1985).
Current pathway
The pathway that the current takes determines the tissues at
risk, the types of injuries sustained, and the degree of
conversion of electrical energy to thermal energy, regardless of
the magnitude of the shock. For example, current passing
through the heart can cause cardiac arrhythmias and direct
myocardial damage; current passing through the brain can
result in coma, respiratory failure, seizures, and direct brain
injury; current passing through the spinal cord can result in
paralysis. Current passing close to the eyes can cause cataracts
(Blount, 1990; Cooper, 1995; Veneman et al., 1998). It has
VOLUME 23 ❖ NUMBER 4 ❖ JUNE 2002
15
been customary to refer to the terms “entry” and “exit” when
describing electrical wounds. Cooper, 1980, suggested that the
terms “source” and “ground” are more accurate, particularly
when referring to injuries caused by alternating current.
However, it is important to note that entrance and exit points
may not necessarily define the actual current pathway
(Primeau, Engelstatter & Bares, 1995).
Mechanisms of injury
Lightning can injure people in five ways: direct strike, splash
or side flash, ground current, blunt trauma, and occasionally it
can travel through telephone wires or water pipes (Blount,
1990; Cherrington, 1995; Cooper, 1995; Patten, 1992). Direct
strikes generally involve persons in the open or those in
contact with metal objects. Direct strikes result in the most
severe injuries. Lightning strikes near the head may enter
orifices such as the eyes, ears, or mouth (Cooper). Splash or
side flash occurs when lightning strikes an object like a tree,
tent pole or piece of machinery, and then jumps to a nearby
person of lower resistance. This is the most frequent
mechanism for lightning injuries (Blount). Ground current
occurs when lightning strikes the earth and then travels along
the surface of the ground and comes into contact with a person.
Ground current injuries are inversely proportional to the
distance from the strike. Most persons involved in multiplevictim strikes are injured by splash or ground current (Blount;
Patten). Blunt trauma occurs in approximately 32 per cent of
lightning victims, and results from the shock waves produced
by the expansion of rapidly cooling superheated air (Blount).
There are also five mechanisms of injury for generated
electrical power: direct contact, arc, flash, thermal, and blunt
trauma. It may initially be difficult to ascertain which
mechanism of injury was responsible for the burns when the
patient presents in the emergency department. Serious burns
may result when a person becomes part of the electrical arc,
where temperatures can exceed 2,500 degrees C, as it may
cause clothing to ignite. Electrical flash usually results in
superficial partial thickness burns. However, it is important to
distinguish between electrical flash burns and arc burns, which
may be superficial due to the limited heat capacity of gas and
the brief exposure time. Flash burns do not suggest the passage
of electrical current, but arc burns do (Danielson et al., 2000).
Blunt trauma may occur in electrical shock in several ways.
First, the individual may be thrown clear of the electrical
energy source by intense muscular contraction, as is seen with
direct current. The victim may also fall from a height, or
sustain fractures or dislocations as a result of the violent
tetanic muscle contractions associated with alternating current
(Breugem et al., 1999; Cooper, 1995).
Pathophysiology
Multiple modes of tissue injury are likely involved in electrical
trauma. The most obvious are thermal burns. These result from
Joule heating, which occurs when electrical energy is
converted to thermal energy, and is dependent upon the
interaction of the multiple variables previously described.
Severe burns can occur with both lightning and generated
power, but are more often associated with the latter. The most
16
common sites of contact or entry are the hands and the skull.
The most common sites of ground or exit are the heels
(Cooper, 1995). Electrical burns are often much more
extensive than they initially appear. In high-energy injuries,
coagulation necrosis can extend to sites distant from the
observed skin injury (Cooper). Delayed limb amputations are
not uncommon (Danielson et al., 2000; Tredget et al., 1999).
The amputation rate following high-energy electrical injury is
reported in the range of 18 to 66 per cent (Danielson et al.;
Grube et al., 1990; Hammond & Ward, 1988; Tredget et al.,
1999), with somewhat lower rates being achieved in recent
years related to improved limb salvage techniques.
After a high-energy electrical injury, tissue damage often
extends beyond the burns, and can affect literally any body
system, including the nervous system. This appears to be
related to the passage of the current itself. In a report by
Grossman, Tempereau, Brones, Kulber, and Pembrook (1993),
the presence of neurological complications was compared
between two groups of patients with electrical burns. One
group experienced passage of current and the other
experienced electrical flash burns without passage of current.
They found that 75 per cent of the current exposure group
exhibited neurological signs and symptoms. None of the latter
group experienced neurological complications, although 22
per cent reported signs and symptoms consistent with posttraumatic stress disorder (PTSD). It would appear that
neurological sequelae occur when the brain, spinal cord, or
peripheral nerves lie within the current pathway (Grossman et
al., 1993; Kleinschmidt-DeMasters, 1995). Furthermore, the
neurological complications of electrical injury may be evident
immediately or be delayed, and can be transient or progressive
in nature, and may result in severe permanent impairment.
The primary cause(s) of the neuropathologic changes seen
after lightning and electric shock trauma is not fully
understood. However, several theories described in the
literature have been proposed to explain the various injuries
and clinical syndromes seen following electrical injury. The
most common are heat theory, vascular theory, cellular DNA
theory, and electroporation theory.
Heat theory
According to this theory, direct thermal damage within neural
tissues occurs when electrical energy is converted to thermal
energy. Electricity causes coagulation necrosis, whereby
permanent damage to neural tissue occurs, but generally does
not extend beyond the area of local tissue damage. This theory
explains the immediate nerve damage seen in a devastated
limb, but does not adequately explain delayed nerve loss
(Breugem et al., 1999; Cherrington, 1995; Parano, Uncini,
Incorpora, Pavone & Trifiletti, 1996). This theory also does
not explain why extensive nerve damage can occur in persons
with minimal thermal injury (Abramov et al., 1996; Lee,
Gaylor, Deepak & Israel, 1988).
Vascular theory
Proponents of the vascular theory contend that electrical
trauma damages blood vessel walls, setting the stage for slow
endothelial fibrosis, and intimal thrombosis with vascular
occlusion or ischemia of the microvascular circulation
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(Cherrington, 1995; Sirdofsky, Hawley & Manz, 1991). When
this occurs in the nervous system, damage to nutrient vessels
results in thrombosis, ischemia, and subsequent
demyelinization (Breugem et al., 1999). It has also been
suggested that delayed injury might be secondary to
vasospasm, with a mechanism similar to that seen with
subarachnoid hemorrhage (Stanley, 1986).
Cellular DNA theory
Farrell and Starr (1968) proposed an intriguing theory to explain
why almost any combination of neurological signs and
symptoms may follow electrical injury, and why a period of
time up to many months may intervene between the injury and
the development of neurological dysfunction. They noted that a
latent period of up to 36 months between exposure and
neurological disorder also occurs after irradiation of the nervous
system. It is believed that irradiation induces structural
alterations in biological macromolecules such as
deoxyribonucleic acid (DNA) and enzyme systems that may be
particularly lethal for cells undergoing division. They speculated
that exposure to electromagnetic fields could result in injury to
cellular DNA, leading to abnormal cell division and ultimate
cell death, similar to the delayed effects of ionizing radiation.
Electroporation theory
In this theory, electrical forces have damaging action on cells
whereby pores are formed in the lipid bilayer of cell
membranes, primarily in muscle and nerve cells. When these
pores are formed, significant amounts of sodium (Na+) ions
can follow the electrochemical potential, and flow into the
axon, upsetting the delicate electrochemical balance of the
cell. Eventually, the pores become larger and membrane
rupture and cell death occurs (Abramov et al., 1996; Breugem
et al., 1999; Cherrington, 1995; Danielson et al., 2000; Grube
et al., 1990; Lee, 1991; Parano et al., 1996). In an animal study
conducted by Abramov and colleagues, the electroporation
theory was supported. They also found that faster myelinated
axons were the most sensitive to electrical shock, and that the
number of damaged axons grew proportionally with the
magnitude of the applied electrical current.
For decades electrical trauma was believed to be simply a form
of thermal burn injury. Although thermal burn is one
component, there are other significant electric field effects,
which are dependant on frequency. At low field frequencies,
electrical forces act at the whole cell level. At radio
frequencies, biologic tissue damage occurs at the
macromolecular level. At microwave frequencies, energy
coupling affects smaller molecules such as water. At ionizing
radiation frequencies, the coupling is at the atomic level.
Electrical forces can alter and damage biologic tissues at all of
these levels in a totally non-heat-dependent fashion (Lee,
1997).
Clinical features
- lightning vs electrical injury
Skin
If skin burns occur as a result of lightning strike, superficial
and partial thickness burns are usually seen. Full thickness
burns are rare, affecting only about five per cent of lightning
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victims (Blount, 1990; Cooper, 1995). If deep burns are
evident, they usually only cover a small body surface area and
are more commonly seen at entrance and exit points or on the
skin under metal objects such as jewellery. Extensive tissue
destruction and limb amputation is relatively uncommon.
Dermal ferning or feathering is a unique feature of lightning
injury. This is not a true burn, but a non-blanching erythema
that disappears within a few days. It is formed when current
enters the skin and spreads out, eliciting an inflammatory
response. If dermal ferning is seen in a comatose patient,
lightning injury may be presumed (Blount). In contrast with
lightning strike, full thickness burns are common after
electrical shock. Early and aggressive surgical management
might include escharotomy, fasciotomy, carpal tunnel release,
skin grafting, and/or amputation of nonviable extremities
(Cooper; Hammond & Ward, 1988; Tredget at al., 1999).
Eyes/ears
Ocular damage is frequently seen following lightning injury
and may include optic nerve atrophy, retinal hemorrhage or
detachment, corneal abrasion, vitreous hemorrhage, and
cataracts. Cataracts are the single most common eye injury,
and may develop immediately or up to two years following the
lightning strike (Blount, 1990). Lightning victims should be
monitored for cataract development whenever injury has
occurred in the vicinity of the head (Cooper, 1995). Ocular
complications are also a feature of electrical shock. Hammond
and Ward (1988) reported an opthalomogical complication rate
of 10 per cent following electrical trauma. Cataract
development is probably more commonly seen after electrical
shock (Cooper).
Otologic injuries are also common (Blount, 1990; Grossman et
al., 1993). Tympanic membrane rupture accounts for half of
the otologic injuries resulting from lightning strike, and is
caused by the mechanical effects of the lightning shock wave.
Late sequelae include chronic otitis media and hearing loss.
Persons struck while talking on the telephone are particularly
susceptible to otologic damage (Blount). Tympanic membrane
rupture does not appear to be a feature of electrical shock.
However, Grossman and colleagues reported that 50 per cent
of the electric shock patients they studied showed persistent
auditory changes one year after injury.
Chest/abdomen
The heart is vulnerable to dysfunction after lightning injury. A
lightning strike causes a “short-circuiting” of the body’s
electrical systems (Blount, 1990). The heart may stop, but will
usually start beating within a few seconds due to its inherent
automaticity. More dangerous is the apnea that, if it occurs,
may lead to secondary ventricular fibrillation. EKG changes
and a variety of cardiac arrhythmias have been reported
following lightning and electrical trauma, but are usually
transient. Acute myocardial infarction is rare. Cardiac arrest
from ventricular fibrillation is a more common presenting
condition after electrical shock (Cooper, 1995).
Damage to other organs like the lungs, liver, pancreas, bladder,
intestines, and gallbladder has been reported, but is uncommon
following lightning strike (Blount, 1990; Cooper, 1995). As
the occurrence of deep burns is relatively infrequent,
VOLUME 23 ❖ NUMBER 4 ❖ JUNE 2002
17
myoglobinuria and renal failure are rare complications of
lightning strike (Blount; Cooper). By contrast, catastrophic
acute intra-abdominal injuries can occur as a consequence of
electric shock, and may include intestinal or pancreatic
necrosis (Buniak, Reedy, Caldarella, Bales, Buniak, &
Janicek, 1999; Cooper). Myoglobinuric renal failure is
common (Cooper). Delayed visceral damage can also occur. In
a report by Buniak and colleagues, 75 per cent of the electrical
injury victims they studied developed gastrointestinal tract
dysfunction weeks to months after injury that was still present
after 12 to 18 months. Fecal urgency and frequency were the
most commonly reported symptoms.
Psychological disorders
A wide variety of psychological disorders are associated with
both lightning and electrical shock trauma. These include
post-traumatic stress disorder (PTSD), conversion disorder,
major depression, anxiety disorders, phobias, and adjustment
disorder (Primeau et al., 1995). It is important in the
management of these individuals, to differentiate between
PTSD and persistent cognitive and/or neurobehavioural
dysfunction, as the treatment for each is very different
(Grossman et al, 1993). In addition, it is not uncommon for
affective disorder and cognitive impairment to be present in
the same individual, adding to the complexity of diagnosis
and treatment.
Nervous system
The central nervous system is quite sensitive to electrical
injury, whether by lightning or electric shock, probably
because neural tissue has the lowest resistance to current
flow (Blount, 1990). The neurological complications of
lightning and electrical injuries are similar, and can be
divided into three categories: 1) immediate and transient, 2)
immediate and prolonged or permanent, and 3) delayed and
progressive (Cherrington, 1995), and can include the brain,
spinal cord, autonomic nervous system, and peripheral
nerves (Blount, 1990; Cherrington, 1995; Cohen, 1995;
Cooper, 1995; Kleinschmidt-DeMasters, 1995; Yarnell &
Lammerise, 1995). Fortunately, the immediate, transient
neurological symptoms are reported with greater frequency
than the more serious and permanent neurologic sequelae
(Cherrington, 1995).
Immediate and transient
Keraunoparalysis is a curious, fleeting condition that is
thought to be unique to lightning strike (Blount, 1990;
Cherrington, 1995; Cooper, 1995). It is characterized by
cold, blue extremities with diminished pulses and
parasthesia that is more pronounced in the lower
extremities. This condition generally resolves within a few
hours, and is believed to be caused by vascular spasm and
sympathetic nervous system instability (Cherrington;
Cooper).
According to Cooper (1980), 75 per cent of lightning
victims lose consciousness, with 86 per cent demonstrating
transient disorientation and confusion. Some will
experience a single seizure. Thirty per cent experience
temporary paralysis of the lower extremities. Transient
neurological symptoms like these likely develop as a result
18
of the “short-circuiting” phenomenon, and occur with
similar frequency in electrical shock (Cherrington, 1995).
Autonomic nervous system dysfunction, including cardiac
dysrhythmias and hypertension, occurs early, is usually
transient, and is more common following lightning strike
(Cohen, 1995).
Immediate and prolonged or permanent
Prolonged coma or chronic vegetative state may occur as a
result of hypoxic encephalopathy secondary to cardiac arrest
following lightning strike or electric shock. Unfortunately,
these individuals have a very poor prognosis (Cooper, 1995;
Cherrington, 1995; Yarnell & Lammerise, 1995).
A number of neuropathological changes have been reported
following lightning strike, including petechial hemorrhages
and subarachnoid bleeding, fissuring of the cortical layers,
and dilatation of the subarachnoid space surrounding
cerebral blood vessels (Stanley & Suss, 1985). Several other
cerebral lesions have also been identified by magnetic
resonance imaging (MRI) and include infarction, hematoma,
and edema (Cherrington, 1995). In the case of intracranial
hematomas, it may be impossible to determine whether the
hematoma formation was the result of the lightning or
electrical trauma or secondary to a fall (Cherrington; Cooper,
1995). A seizure disorder may develop related to anoxic or
traumatic brain damage (Cooper, 1995). In many cases,
nervous system damage can be very subtle, so much so that
lesions may not be able to be identified on CT or MRI scans
(Arevalo, Lorente, & Balseiro-Gomez, 1999; Breugem et al.,
1999).
Cerebellar dysfunction has also been established as a
consequence of lightning injury. Cherrington (1995)
reported that an MRI performed one week after lightning
strike demonstrated marked cerebellar atrophy in a patient
whose initial MRI was normal. There are no detailed case
reports of cerebellar lesions following electrical injury in the
literature (Cherrington). Cerebral venous thrombosis has
been reported in association with electrical injury (Patel &
Lo, 1993).
Prolonged and/or permanent cognitive and neurobehavioural
dysfunction has also been demonstrated from a variety of
lesions in both lightning and electrical shock victims (Cooper,
1995; Primeau et al., 1995; Yarnell & Lammerise, 1995). The
most common neuropsychological complication after
electrical injury is memory loss. Confusion/disorientation,
concentration and learning problems, compromised
intellectual functions, and, rarely, aphasia, have also been
reported (Cooper, 1995; Cherrington, 1995; Lee, 1997).
Lightning and electrical shock victims may sustain spinal cord
injury from fractures of the cervical, thoracic or lumbar spine.
Patients who demonstrate immediate spinal cord findings in
the absence of traumatic cord injury develop symptoms of
weakness and parasthesia that may go unnoticed until
ambulation is attempted. Lower extremity findings are more
common than upper extremity findings. These patients have a
good prognosis for an eventual complete or partial recovery
(Cooper, 1995).
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It is common for electrical injury survivors to present with
symptoms of transient or persistent peripheral nerve damage,
despite normal neurophysiological studies. Whether the nerve
dysfunction is temporary or permanent appears to be related to
the length of time and the magnitude of exposure (Lee, 1997).
Immediate presentation of persistent upper extremity dystonia
syndrome with reflex sympathetic dystrophy (RSD) has also
been reported in the literature, and is more commonly seen in
association with electric shock (Adler & Caviness, 1997;
Cohen, 1995).
Delayed neurological syndromes
The lightning and electrical trauma literature contains many
case reports of delayed neurological syndromes occurring a few
days to several years after injury. These include motor neuron
disease (Arevalo et al., 1999; Breugem et al., 1999; Ratnayake
et al., 1996; Sirdofsky et al., 1991), dystonia (Adler & Caviness,
1997; Ondo, 1997), and peripheral neuropathies (Parano et al.,
1996; Vasquez, Shusterman & Hansbrough, 1999).
Spinal cord damage is by far the most common of the delayed
neurological syndromes associated with electrical injury, and
is thought to occur when the path of the current is either hand
to hand or hand to foot (Farrell & Starr, 1968). The spinal cord
syndromes generally fall into one of three clinical pictures:
ascending paralysis, amyotrophic lateral sclerosis, or
transverse myelitis (Breugem et al., 1999; Cherrington, 1995;
Cooper, 1995; Farrell & Starr; Sirdofsky et al., 1991).
Although complete and partial recoveries have been reported,
the majority of patients with delayed spinal cord symptoms are
left with a permanent and sometimes progressive disability
(Cherrington).
Peripheral nerves have the least resistance to current flow,
and are the most conductive of all living tissue (Parano et al.,
1996). It is not surprising that they are vulnerable to
electrical damage. Delayed peripheral neuropathies occur in
approximately 20 per cent of patients injured by electrical
current (Grube et al., 1990). The median, ulnar, and radial
nerves are most often affected (Lee, 1997). Furthermore,
delayed reflex sympathetic dystrophy (RSD) can develop as
a result of peripheral nerve damage. This occurs more
frequently with electrical shock (Cohen, 1995).
Unfortunately, peripheral nerve damage is common, and
recovery is usually poor for all types of electrical injuries
(Cooper, 1995).
Case presentations
The following is a summary of the circumstances, injuries,
treatments and outcomes related to three males who sustained
electrical injuries while working in Ontario.
Case one
History
Mr. R. was 52 years of age at the time of his accident. While
working as a remote control operator with locomotives, he was
struck by lightning. At the time of the accident, it was raining
and he was working outside with a partner. He was wearing a
remote control device around his neck that he used to
communicate with his partner. While talking to his partner, he
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was struck by lightning. It entered at the base of his neck and
upper left quadrant of his chest and exited through his right leg
and groin.
As documented in his reports, Mr. R. was thrown a distance
from where he was hit. His clothing was blown off and his
remote device was liquefied onto the left side of his chest. Mr.
R. was unresponsive at the scene. He was resuscitated,
intubated, and taken to the emergency department of the local
hospital. The duration of time that he was unconscious is
difficult to ascertain. One report indicated that upon arrival at
the hospital Mr. R. was unresponsive and required aggressive
fluid resuscitation, while another indicated that Mr. R was
conscious upon arrival at the emergency department, agitated,
and required sedation.
Mr. R. was transferred to the burn trauma unit where he was
heavily sedated over the first week. A gradual withdrawal of
the sedating medication was undertaken and he was alert and
responsive by the middle of the second week. He remained in
the acute care setting for approximately one and a half months.
He was then transferred to a neurological rehabilitation unit.
He remained there as an inpatient for three months. He was
then discharged home, but continued to attend a day hospital
rehabilitation program, five days per week, three hours per
day, for three months. Following discharge from the day
hospital program, an in-home rehabilitation program was
instituted. At the time of each of these transitions, Mr. R. and
his family experienced a great deal of distress, and required
ongoing support and education from the team. The major
concern was that he would never recover his previous abilities
and would not be able to return to work or his previous
lifestyle.
Health issues
Mr. R.’s injuries included superficial burns to his arms, torso,
right groin, left leg and left toes. These healed well and
quickly.
Mr. R. also sustained a significant electrical injury to his brain
(a dense left cerebral lesion was identified), brachial plexus,
and spinal cord. The presenting issues as a result of these
injuries were problems with mobility, balance, weakness and
stiffness in his left leg, decreased fine motor skills, partial right
facial droop with dysarthria, absent reflexes in his left arm,
including weakness and conduction abnormalities consistent
with lower motor neuron deficit, pelvic weakness and pain,
reduced tolerance to hot environments, and numbness,
decreased circulation and loss of sensation in his hands.
Mild cognitive impairments related to calculation and
concentration, as well as lability of mood were also identified
as issues. He occasionally presented as being very sad and
crying, or being very angry. Mr. R. also experienced some
anxiety and nightmares related to the injury and electrical
storms.
Mr. R. exhibited language difficulties including the use of nonword substitutions (neologisms), misperceptions of words
presented, loss of fluency in retrieving language-based
information, inefficiency with sequencing, and impairment of
attention and information processing.
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19
Mr. R. related a strong belief that he survived for a reason. He
looked for a purpose for his survival and believed that he had
a responsibility to ensure that others were aware of the dangers
of lightning strikes. Mr. R. gained great comfort in relating his
story to others. He was very pleased when his story was
printed in a local newspaper.
Mr. R. continues to be involved in a community-based
rehabilitation program and continues to struggle on a day-today basis with the neurological sequelae related to his
electrical injury.
Case two
History
Mr. A. was 32 years old at the time of his accident. Mr. A. was
shocked with approximately 110,000 volts when a crane
attached to a wrecking ball that he was guiding manually came
in contact with some high tension wires. He had entry sites on
his left hand and arm and exit sites on both feet.
He had burns to the feet, the left forearm and a devitalized
right third toe that was eventually amputated. He was
unconscious at the time that emergency staff arrived. There
was one report that indicated that he was comatose for 10
days. He was hospitalized for approximately three months in
acute care. In addition to the burns, it was noted that he was
depressed. The depression included passive suicidal
ideation.
Mr. A. lived at home with his wife and son. He was born in
Portugal and spoke English with difficulty. He was referred to
an occupational recovery program and was admitted seven
months after discharge from acute care. He received
physiotherapy upon discharge. An outpatient chronic pain
program was also accessed. Unfortunately, positive outcomes
were not obtained.
Mr. A. is presently cared for by his family. Rehabilitative
attempts have not lessened the neurological dysfunction to
date. Counselling continues for family members in order
to assist them in coping with their change in
circumstances.
Health issues
Mr. A.’s MRI scan identified a number of lesions in the
subcortical regions and in the right midbrain area. Possible
brain stem involvement was also noted. In terms of prognosis,
the brain damage was permanent and it was predicted his
neurological function might deteriorate over time.
Pain was of major concern to Mr. A. He experienced pain
along his entire spine, as well as severe headaches. Noises
of everyday living, light, odours and voice tones increased
his discomfort. He described the pain as head-to-toe
pressure at times, and very acute at other times. He was
never pain-free.
Balance was an increasing problem. He fell on numerous
occasions, although he used a cane to ambulate. Mr. A. also
experienced edema in both his feet and neck, weakness in his
hands, photosensitivity, nausea and vomiting, and
constipation.
20
Memory loss, confusion, anxiety, irritability and depression
were of major concern to Mr. A. and his family. He
demonstrated fear of electricity and occasionally experienced
nightmares related to this. Post-traumatic stress disorder was
of concern. These ongoing symptoms have greatly interfered
with relationships.
Case three
History
Mr. P. was 31 years of age when the spout of the cement
truck that he was driving came in contact with live hydro
wires. The high voltage (5,000 volts for three minutes) was
conducted to his body, entering through his right hand and
exiting through his left elbow, left knee and proximal part of
tibia, proximal aspect of the right tibia and both great toes.
He reported that he was “clinically dead” for four minutes.
Full thickness burns were experienced at all entry and exit
points.
Mr. P. also experienced renal failure at the time of the accident.
Since the accident he has experienced problems with his
bowels, specifically loose stools and urgency.
Mr. P.’s initial hospitalization lasted approximately eight
weeks. During this time, wound healing, including
debridement and skin grafting, was the focus. Following his
discharge from hospital, Mr. P. participated in intensive
physiotherapy and occupational therapy. He was also involved
in a vocational rehabilitation program.
In 1992, he was readmitted to hospital for amputation of three
fingers and tendon lengthening on his right hand. Grafting of
the right median nerve to the digital nerves of the thumb and
index finger was also done. He again went through extensive
physiotherapy.
In June of 1993, he underwent tendon lengthening and transfer
on his right hand as well as grafting to his palm. Physiotherapy
was again undertaken.
He was assessed psychologically in the fall of 1993. A
diagnosis of adjustment disorder was made and he participated
in psychotherapy regularly for about two years.
Health isues
Mr. P. has visible scarring at all entry and exit sites. Three
fingers of his right hand have been amputated and he has had
extensive nerve damage in both his right and left hand. He now
has carpal tunnel syndrome from overuse of his left hand. Mr.
P. also experiences pain and numbness in his right hand and
forearm.
Mobility is a problem related to the joint impairment in his left
knee resulting from the skin grafting and subsequent scarring.
The grafting and scarring on his great toes have also placed a
limitation on his mobility. Any amount of walking will cause
the graft sites to fissure and bleed, resulting in increased pain.
Pain in his left leg has also been a problem following the nerve
grafting.
Mr. P. was very motivated to return to his pre-accident
lifestyle. However, the residual physical issues undermined his
attempts to accomplish this. In 1993, he demonstrated
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decreased self-esteem and self-confidence. He experienced
labile mood, insomnia and periods of depression. This further
diminished his feelings of self-worth and his relationships with
family and others.
After numerous attempts at vocational rehabilitation,
and despite his high level of motivation, Mr. P. was not
able to return to work. He and his family continue to
struggle on a day-to-day basis with their change in
circumstances.
Treatment
As noted in the above case studies, the complications of
electrical injury are varied and complex. All aspects of the
individual’s life are affected. The physical issues related to
burns, mobility, loss of function and pain are just one
dimension of the trauma. The early identification and
treatment of the psychological and relationship issues must
occur if optimum recovery and quality of life are to be
achieved.
Frequently, in our role as advanced practice nurse case
managers, we find that the long-term neurological issues
are not recognized or addressed. Issues with pain,
deteriorating functional ability, problems with memory and
mood, problems with bowel and bladder, are not always
recognized as being related to the electrical injury. “The
complexities of the rehabilitation of electrical shock
survivors are very often under-appreciated by the medical
community” (Danielson et al., 2000, pp. 232-233). Without
a coordinated, holistic approach to treatment by a
knowledgeable team of professionals, the trauma can be
prolonged and intensified.
The treatment plan must address the physical, psychological
and spiritual issues that arise following neurological trauma.
The preferred treatment team would consist of nurses,
physicians, social workers, physiotherapists, occupational
therapists, recreational therapists, speech language
pathologists and rehabilitation support workers. The team
should also ensure that the individual has access to a spiritual
support of his/her choosing.
Table One: Health issues
The advanced practice nurse case manager plays an integral
role in ensuring that a coordinated, integrated approach to
treatment that involves the client/family as expert, occurs
across the continuum of health care. The role of the
APNCM includes, but is not limited to, the provision of
dynamic, holistic health assessments, consultation with
health
care
providers,
recommendations
for
service/treatment/equipment, reviews of the service
provided to ensure it is research-based best practice,
advocacy, environmental assessments, health education,
and supportive counselling.
Prevention
This paper has focused on the complications that occur
following electrical injury. As advanced practice nurse case
managers, prevention of these injuries is our goal.
Education of the public is critical if this goal is to be
achieved.
The majority of lightning strike injuries can be prevented if
the appropriate precautions are taken. Individuals should
immediately stop work/play outdoors when thunder or
lightning is present in the area and take shelter indoors or in
a vehicle. The lightning does not need to be directly overhead
for a strike to occur. If unable to take immediate shelter,
discard metal objects (cell phones, tools, umbrellas, golf
clubs, etc.), take shelter in deep woods (not an isolated tree
or tent), lie in a low-lying area and make your body as small
as possible. If you are at home, avoid using the phone or
taking a bath/shower during an electrical storm (Blount,
1990; Patten, 1992).
Electrical injuries in the workplace can also be prevented
through the provision of a comprehensive safety-focused
orientation and training program for all staff, development of
and strict adherence to electrical safety procedures and
protocols, as well as properly-installed, grounded, and
maintained electrical equipment (Patten, 1992).
In order to maximize the potential for the prevention of
electrical injuries, a coordinated multimedia multi-sector
approach to prevention is necessary.
Physical
Psychological
Relationship
Spiritual
Balance
Weakness
Stiffness
Fine motor
Pain
Sensory impairment
Edema
Nausea/vomiting
Bowel problems
Headaches
Progressive symptoms
Burns
Organ failure
Cognitive impairment
Memory loss
Labile mood
Anxiety
Nightmares
Decreased selfesteem/confidence
Depression
Insomnia
Social isolation
Anger management
Communication issues
Abuse
Searching for meaning
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VOLUME 23 ❖ NUMBER 4 ❖ JUNE 2002
21
Summary
Electrical injuries are variable and complex in nature. Severe
nervous system dysfunction can be a tragic consequence of
lightning strikes and electrical shocks. The permanent
disability experienced by the survivors of electrical trauma is
disproportionate to the number of injuries that occur.
Electrical injury carries significant costs for victims, their
families and their employers. Further research with regard to
the biophysical mechanisms of electrical injury will hopefully
aid in the identification of more effective therapies.
References
Abramov, G.S., Bier, M., Capelli-Schellpfeffer, M., & Lee,
R.C. (1996). Alterations in sensory nerve functioning following
electrical shock. Burns, 22(8), 602-606.
Adler, C.H., & Caviness, J.N. (1997). Dystonia secondary
to electrical injury: Surface electromyographic evaluation and
implications for the organicity of the condition. Journal of the
Neurological Sciences, 148, 187-192.
Arevalo, J.M., Lorente, J.A., & Balseiro-Gomez, J. (1999).
Spinal cord injury after electrical trauma treated in a burn unit.
Burns, 25, 449-452.
Bass, J. (1998). The physical effects of electricity
[Online]. Available: www.bassengineering.com/Effect.html. Bass
Associates Inc.
Blount, B.W. (1990). Lightning injuries. American Family
Physician 42(2), 405-415
Breugem, C.C., Van Hertum, W., & Groenevelt, F. (1999).
High voltage electrical injury leading to a delayed onset
tetraplegia with recovery. Annals New York Academy of
Sciences, 888(4), 131-136.
Buniak, B., Reedy, D.W., Caldarella, F.A., Bales, C.R.,
Buniak, L., & Janicek, D. (1999). Alteration in gastrointestinal
and neurological function after electrical injury: A review of four
cases. The American Journal of Gastroenterology, 94(6), 15321536.
Cherrington, M. (1995). Central nervous system
complications of lightning and electrical injuries. Seminars in
Neurology, 15(3), 233-239.
Cohen, J.A. (1995). Autonomic nervous system disorders
and reflex sympathetic dystrophy in lightning and electrical
injuries. Seminars in Neurology, 15(4), 387-390.
Cooper, M.A. (1980). Lightning injuries: Prognostic Signs
for death. Annals of Emergency Medicine, 9(3), 134-138.
Cooper, M.A. (1995). Emergent care of lightning and
electrical injuries. Seminars in Neurology, 15(3), 268-278.
Danielson, J.R., Capelli-Schellpfeffer, M., & Lee, R.C.
(2000). Upper extremity electrical injuries. Hand Clinics, 16(2),
225-234.
Farrell, D.F., & Starr, A. (1968). Delayed neurological
sequelae of electrical injuries. Neurology, 18, 601-606.
Grossman, A.R., Tempereau, C.E., Brones, M.F., Kulber,
H.S., & Pembrook, L.J. (1993). Neurological consequences of
electrical burns. Journal of Burn Care and Rehabilitation,
14(2), 169-175.
Grube, B.J., Heimbach, D.M., Engrav, L.H., & Copass,
M.K. (1990). Neurological consequences of electrical burns. The
Journal of Trauma, 30(3), 254-258.
Hammond, J.S., & Ward, C.G. (1988). High-voltage
electrical injuries: Management and outcome of 60 cases.
Southern Medical Journal, 81(11), 1351-1352.
22
A holistic, coordinated approach to care is required if optimum
health and recovery is to be achieved. The advanced practice
nurse case manager has a major role to play in ensuring that
this occurs. However, prevention must remain the key focus if
the elimination of electrical injuries in the workplace is to be
realized.
About the authors
Valerie Coubrough, RN, MSN, and Paulette Warnell, RN, MN,
CNN(c) are Advanced Practice Nurse Case Managers with the
Workplace Safety and Insurance Board in Toronto, Ontario.
Kleinschmidt-DeMasters, B.K. (1995). Neuropathology of
lightning-strike injuries. Seminars in Neurology, 15(4), 323-328.
Lee, R.C., Gaylor, D.C., Deepak, B., & Israel, D.A. (1988).
Role of cell membrane rupture in the pathogenesis of electrical
trauma. Journal of Surgical Research, 44, 709-718.
Lee, R.C. (1991). Physical mechanisms of tissue injury in
electrical trauma. IEEE Transactions on Education, 34(3), 223229.
Lee, R.C. (1997). Injury by electrical forces:
Pathophysiology, manifestations, and therapy. Current Problems
in Surgery, 34(9), 684-764.
Ondo, W. (1997). Lingual dystonia following electrical
injury. Movement Disorders, 12(2), 253.
Parano, E., Uncini, A., Incorpora, G., Pavone, V., &
Trifiletti, R.R. (1996). Delayed bilateral median nerve injury due
to low-tension electrical current. Neuropediatrics, 27, 105-107.
Patel, A., & Lo, R. (1993). Electrical injury with cerebral
venous thrombosis: Case report and review of the literature.
Stroke, 24(6), 903-905.
Patten, B.M. (1992). Lightning and electrical injuries. The
Neurology of Trauma, 10(4), 1047-1058.
Primeau, M.P., Engelstatter, G.H., & Bares, K.K. (1995).
Behavioral consequences of lightning and electrical injury.
Seminars in Neurology, 15(3), 240-252.
Ratnayake, B., Emmanuel, E.R., & Walker, C.C. (1996).
Neurological sequelae following a high voltage electrical burn.
Burns, 22(7), 574-577.
Sirdofsky, M.D., Hawley, R.J., & Manz, H. (1991).
Progressive motor neuron disease associated with electrical injury.
Muscle & Nerve, 14(10), 977-980.
Stanley, L.D. (1986). Comment. Neurological Surgery,
19, 204.
Stanley, L.D., & Suss, R.A. (1985). Intracerebral
hematoma secondary to lightning strike: Case report and review
of the literature. Neurosurgery, 16(5), 686-688.
Tredget, E.E., Shankowsky, H.A., & Tilley, W.A. (1999).
Electrical injuries in Canadian burn care. Annals New York
Academy of Sciences, 888(4), 75-87.
Vasquez, J.C., Shusterman, E.M., & Hansbrough. (1999).
Bilateral facial nerve paralysis after high voltage electrical injury.
Journal of Burn Care and Rehabilitation, 20, 307-308.
Veneman, T.F., van Dijk, G.W., Boereboom, F., Joore, H.,
& Savelkoul, T.J.F. (1998). Prediction of outcome after
resuscitation in a case of electrocution. Intensive Care Medicine,
24, 255-257.
Yarnell,
P.R.,
&
Lammerise,
D.P.
(1995).
Neurorehabilitation of lightning and electrical injuries. Seminars
in Neurology, 15(4), 391-396.
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