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Chapter 12. Electrical Injuries
usually know the exact amount of current that was being used
during the injury. Most of the further treatments and complications discussed in this chapter relate to high-voltage injuries. These injuries are often devastating.
271
Lightning Strikes
In the United States, lightning kills more people than any
other weather phenomenon with the most deaths occurring
in Texas and Florida [19–21]. Although lightning strikes are
millions of volts of electricity, injury severity varies greatly
depending on distance from strike (closer the more severe) or
if a nearby object has become incandescent causing a flash or
flame burn, in addition to an electrical injury. The pathognomonic sign of lightning strikes is a Lichtenburg figure or
keraunographic markings which are a dendritic, arborescent,
or fernlike erythematous cutaneous branching pattern due to
the extravasation of blood in the subcutaneous tissue. It will
often fade within an hour of injury [22, 23]. Isolated burns to
the tips of the toes can also be characteristic of a lightning
injury [24]. When a lightning strike causes a cardiac or respiratory arrest, CPR is effective if initiated early, however, 10%
will still die [25, 26]. Patients can still successfully be resuscitated even if the person appears dead or there is a delay in
starting resuscitation. Glasgow Coma Scale or pupillary exam
will be unreliable and is a poor predictor of outcome [27–29].
Patients will often develop ophthalmic injuries ranging from
cataracts and uveitis to vitreous hemorrhage, retinal detachment, and optic neuropathy [28, 30, 31]. An ophthalmology
consultation should be obtained when the patient arrives and
follow-up should be arranged to monitor for any long-term
complications. The ears also need to be examined because
injuries are common with the most frequent being ruptured
tympanic membranes [32]. Long term, it can cause sensorineural hearing loss and increase the risk of vertigo [33].
Neurologic complications are common with patients often
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M. Guerrero et al.
presenting unconscious or with seizures. Paralysis and paresthesias may develop over the next several days after the
injury. Keraunoparalysis, a complete tetraplegia and a loss of
sensory awareness of the limbs and trunk, can occur but is
usually transient [34]. It is important to have physical and
occupational therapy involved early. If patients present with
altered level of consciousness, intracranial pathology such as
subdural hematoma, epidural hematoma, or intraparenchymal hemorrhages must be ruled out with a CT scan [21].
Lightning strike patients with neurologic injuries tend to
recover better than other traumatic brain injuries, and a study
of 10 patients over a 12.3year period demonstrated no longterm neurologic or psychologic deficits [35]. However, 30%
of lightning strike patients have been found to suffer from
posttraumatic stress disorder [36].
Acute Management
Management of electric injuries should always start with the
basics of Advanced Trauma Life Support (ATLS) and focus
on airway, breathing, and circulation. Many of these patients
may have a fall from height as injuries often occur on a ladder
or working on power lines and should undergo a full trauma
work-up to identify any concomitant injuries. There are
unique challenges that present in injuries due to electric current that are not seen in other trauma patients or those who
were thermally injured. These include:
1. Who needs electrocardiographic monitoring and for how
long.
2. How to proceed with uid resuscitation in patients with
deep tissue injury or myoglobinuria.
3. Who is at risk for compartment syndrome and may need
emergent surgical intervention.
4. Who is at high risk of respiratory failure secondary to
pulmonary parenchymal injury.
Chapter 12. Electrical Injuries
273
Electrocardiographic Monitoring
Cardiac abnormalities can occur after low or high-voltage
injury and are the most frequent cause of death [10, 37]. For
this reason, it is imperative to obtain an EKG during the initial evaluation. The most common abnormality is non-specific
ST changes, and sinus bradycardia or tachycardia is often
seen [15, 38]. Atrial fibrillation is the most common dysrhythmia [38, 39], but ventricular fibrillation is the most common
cause of on scene death [40]. EKG changes are usually present shortly after injury and a recent paper studying 490 lowvoltage electrical injury patients demonstrated that there
were no late onset malignant arrythmias. All arrythmias or
abnormalities had been present on admission EKG [15].
A direct myocardial injury similar to a traumatic contusion
may also occur in these patients but they do not have the
same hemodynamic compromise as most myocardial infarctions. Many etiologies have been proposed, such as direct
electrical current to the heart, coronary spasm and thrombus,
and inadequate perfusion secondary to hypotension, however none has been definitely proven. There has been conflicting data using cardiac markers in electrical injury but no
biomarker has proven to be consistently accurate. For
instance, CK and CK-MB both can be elevated secondary to
severe muscle injury [15, 41–46].
Therefore the question becomes, how to identify who
needs cardiac monitoring. There are 5 indications for admission for cardiac monitoring:
1. Loss of consciousness at time of injury.
2. EKG abnormality or concern for ischemia.
3. Dysrhythmia either prior to or after ED admission.
4. Pre-hospital CPR.
5. Any patient with a standard indication for cardiac
monitoring.
Asymptomatic patients with no cardiac risk factors and a
normal EKG do not need inpatient monitoring. For those
that need to stay for observation, the optimal length of moni-
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toring is unknown, although most publications have used
24–48h [47–49]. In our institution, we monitor at risk patients
for approximately 24h. If they have a low-voltage injury with
no criteria for monitoring and no other indication for admission, they will be discharged home from the emergency
department. Most high-voltage injuries will be admitted for
observation, however, if they are going to have dysrhythmias,
they tend to occur early in the hospital course [45]. Currently,
we are looking into targeted temperature management for
patients who present to the emergency department in a coma
after cardiac arrest due to electrical injuries. Other than the
mechanism of cardiac arrest, these patients fulfill the requirements put forth by the International Liaison Committee on
Resuscitation, and we are hopeful that targeted temperature
management will prove to be neurologically protective as it
has in other populations [50].
Fluid Resuscitation andRhabdomyolysis
Per consensus protocol, resuscitation for an electrical injury
with a cutaneous burn greater than or equal to 20% total
body surface area would be 4mL/kg/% burn with the first
half of the resuscitation volume given over the first 8h. This
is twice the recommended amount for cutaneous burns alone
as electrical injuries often have extensive internal injuries
which are underestimated. However, when large cutaneous
burns are not associated with the electrical injury, there is no
accepted formula to determine the starting fluid rate, although
high-voltage injuries can require almost double the amount
of fluid as a low-voltage injury [51].
In our institution, one of the first steps in evaluating an
electrical injury is to look for pigmented urine. Visible myoglobinuria is a sign of rhabdomyolysis and ongoing ischemia
which needs to be cleared promptly to avoid tubular
obstruction and acute renal failure [52, 53]. This is achieved
by starting the patient on 1.5–2 times the maintenance fluid
rate of lactated Ringer’s with a Foley catheter in place to
Chapter 12. Electrical Injuries
maintain urine output at 100 mL/h. or twice the standard
urine output in a burn patient. Aggressive resuscitation continues until the urine appears clear. Some burn centers have
adopted the use of osmotic diuretics (mannitol) and alkalinization of the urine to help protect renal function during rhabdomyolysis, however, there is no level I evidence to support
these measures [54]. If myoglobinuria has failed to improve
after a few hours of aggressive resuscitation, it is a sign of
ongoing muscle ischemia and the patient should be reexamined for a missed compartment syndrome or may
require debridement of necrotic tissue. If there is no visible
myoglobinuria, then the patient is started on a normal maintenance fluid rate and titrated to a goal urine output of
30–50mL/h.
275
Compartment Syndrome
Electrical injuries and their sequalae place patients at risk for
compartment syndrome. However, not all electrical injuries
carry the same risk and patients with high-voltage electrical
injuries are at highest risk for developing deep tissue damage
and compartment syndrome.
Electrical injury results in an immediate inflammatory
response, however, tense compartments and muscle necrosis
may develop during the first 48 h after injury. Damaged
muscle and edema within the investing fascia of the extremity
may increase pressure to the point at which muscle blood
flow is compromised. Venous blood flow obstruction is com-
promised first followed by arteriolar collapse [55, 56]. The
actual absence of pulses is one of the last signs of compartment syndrome. A high index of suspicion is paramount for
this early diagnosis, and adjunct tests such as serial CK’s and
compartment pressures are most often not needed. Treating
compartment syndrome in electrical burn patients has
changed in recent years. In the past, a very aggressive early
approach of debridement and exploration was recommended,
however, this approach led to amputation rates in the
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35–40% range [57]. Newer indications for operation are evidence based and highlighted in the ABA guidelines.
Indications include: (1) progressive neurologic dysfunction,
(2) vascular compromise, (3) increased compartment pressure, and (4) systemic clinical deterioration from suspected
ongoing myonecrosis. Patients not meeting these indications
may be debrided on the third to fifth postinjury day [10].
If a patient develops compartment syndrome, four
compartment fasciotomies of the lower leg are the standard
of care. For forearm fasciotomies, the surgeon must
decompress the flexor (volar) compartment, the mobile wad
(brachioradialis, extensor carpi radialis longus, and extensor
carpi radialis brevis), and the extensor (dorsal) compartment.
The extensor compartment is simpler and requires a straight
longitudinal incision over the dorsal surface of the forearm
[40].
Debridement of clearly nonviable muscle is recommended
at initial operation. A conservative approach is taken with
tissue of questionable viability. Amputation at initial operation is done mostly for mummified or contracted nonviable
extremities. After the initial operation, a second look at
24–48 h with debridement or amputation is usually performed. Skin coverage of the ensuing wound is temporarily
achieved with a biological dressings such as allograft or xenograft [40]. Wounds with associated skin and muscle loss often
require skin grafting; however, closure can sometimes be
facilitated with negative pressure wound therapy (NPWT).
Wound Care
High-voltage injuries require a thorough evaluation to rule
out urgent surgical intervention. If urgent surgical intervention is not required, initial wound care and observation are
suitable. Low-voltage injuries affecting small areas that do
not meet criteria for cardiac monitoring and have adequate
pain control can be discharged home. For those injuries
requiring local wound care, mafenide acetate cream works
Chapter 12. Electrical Injuries
well for contact point with deep tissue injury. Mafenide acetate has great eschar penetration and broad antimicrobial
coverage. Other topical antibiotics can be used alternatively
or for more superficial injuries. These include silver sulfadiazine, bacitracin, and silver containing dressings [58].
Surgical excision of electrical burns is delayed for 48–72h
if patient does not require an urgent fasciotomy or debridement. This allows for revaluation of tissue with questionable
viability which should be retained and reassessed every day.
If necrotic tissue is present at revaluation, it should be
removed. This pattern is repeated until all nonviable tissue is
ultimately removed [59]. Some authors believe that a conservative course of tissue removal and wound closure using
either or both skin grafts and flaps allow for the best functional outcome [60]. NPWT assisted closure devices can also
help with these wounds. They can safely be placed over questionable tissue and later be removed for assessment every
third to fifth day. If the hand is involved the consultation of a
plastic surgeon with burn reconstruction experience can
result in improved functionality of the extremity [40]. Daily
physical therapy and functional splinting are vital to decrease
contractures and round out the complete care of the patient.
277
Complications
Early complications of electrical injuries can be similar to
other burn and ICU patients, including septic, cardiac, pulmonary, and renal complications. They have unique ocular and
neurologic complications that can develop. Ocular issues can
affect all aspects of the eye with cataracts being the most
frequent ocular manifestation [61, 62]. Between 5 and 20% of
patients will develop some degree of ocular changes; therefore, all electrical burn patients should have follow-up with
an ophthalmologist [63]. Injuries can appear as early as
3weeks or as delayed as 11years with 77% of patients who
develop cataracts eventually requiring surgery [64].
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Neurologic complications are extremely variable and may
present early directly after the injury or not manifest for
years. Approximately 82% of patients will have some kind of
neurologic complication. Defects include paresis, paralysis,
Guillain–Barre Syndrome, amyotrophic lateral sclerosis, and
transverse myelitis [65] with the most common reported
symptoms being numbness (42%), weakness (32%), memory
problems (32%), paresthesias (24%), and chronic pain (24%)
[66]. Grube etal. found that 67% of high-voltage electrical
injuries develop immediate central or peripheral neuropathies. It was also noted that there was no delayed onset of
central neuropathies but one-third of peripheral neuropathies were persistent [12]. Neurologic complications are not
limited to high-voltage injuries. Low-voltage injuries had
similar neuropsychological symptoms, limited return to work
(only 30% return), or delayed return to work [67, 68]. Early
lesions are more likely to resolve than late lesions. Weakness
is the most common clinical finding with function more
affected than sensation, and spasticity is more common than
flaccidity. It is important to get a complete baseline neurologic exam in these patients so they can be followed long
term for complications. Patients also experience a range of
psychological symptoms including anxiety (50%), nightmares
(45%), insomnia (37%), and flashbacks (37%) [66]. Studies
focused on neuropsychological testing have discovered that
PTSD is a significant problem in this population leading to
difficultly with cognition and decreased ability to return to
work [69]. It has also been noted that there was a correlation
with the no-let-go phenomenon seen in low-voltage injuries
and higher rates of depression and PTSD [70]. Electrical burn
patients who undergo long bone amputations have an 80%
chance to develop heterotopic ossification at the cut ends of
the amputation site with 28% requiring surgical revision. This
does not occur in small bone amputations or in disarticulations [71]. While electrical burns only make up a fraction of
burns seen in the hospital, they require tremendous resources
both in terms of the acute and chronic care of these patients
and the complications associated with electrical injury.
Chapter 12. Electrical Injuries
279
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