Docstoc

ENVIRONMENTAL EMERGENCIES

Document Sample
ENVIRONMENTAL EMERGENCIES Powered By Docstoc
					ENVIRONMENTAL EMERGENCIES
ELECTRICAL AND LIGHTNING INJURIES
Critical Care Clinics - Volume 15, Issue 2 (April 1999)

Subin Jain MD
Venkata Bandi MD


Address reprint requests to
Venkata Bandi, MD
Department of Pulmonary and Critical Care Medicine
Ben Taub General Hospital
1504 Taub Loop
Houston, TX 77030
Department of Pulmonary and Critical Care Medicine, Ben Taub General Hospital,
Baylor College of Medicine, Houston, Texas

Electricity and lightning account for a large number of deaths per year worldwide.
According to data from the Centers for Disease Control and Prevention (CDC), 100 out
of more than 500 fatalities caused by electricity are due to lightning and at least two to
three times as many nonfatal injuries are reported every year in the United States.
Lightning is the third most common cause of deaths from natural causes. The
pathophysiology and management of electrical and lightning injuries are unique.
Physicians who may encounter such patients in their practice should be knowledgeable in
their management. This article reviews the current knowledge about this topic and details
a schema for management.




EPIDEMIOLOGY

Deaths caused by electricity are almost always accidental and largely preventable. Work-
related accidents and children account for most cases. In children, a bimodal distribution
is seen, with low-voltage injuries in children less than 6 years of age and high-voltage
injury in older children and adolescents. [9] [14] [15] The majority of high-voltage
accidents in adults are occupationally related and occur mostly in construction and
electrical workers. [16] [91] [102] It is estimated that 3% to 4% of all admissions to burn
units are from burns caused by electrical injuries. [31] [41] Lightning-related casualties
are commonest in May through September when thunderstorm activity is the highest.
Victims are predominantly males of age 15 to 44 engaged in outdoor recreational
activities. [67] [101] From 1980 through 1995, Florida and Texas had the greatest
number of deaths attributable to lightning but New Mexico, Arizona, Arkansas, and
Mississippi had the highest rate per million population per year. [71] It is generally
believed that casualties caused by lightning are underestimated. A study by Lopez et al
[66] showed that Storm Data, a monthly publication of the National Oceanic and
Atmospheric
320
Administration (NOAA), underestimated lightning deaths by 28% and lightning injuries
requiring hospitalization by 42%.



PATHOPHYSIOLOGY

Electricity causes injury by several different mechanisms: (1) direct effect of electric
current on body tissues, (2) conversion of electrical energy to thermal energy and
subsequent superficial and deep burns, (3) blunt injury caused by severe muscle
contractions or fall. [16] [31] [47] [91] The primary determinant of electrical injury is the
amount of current flowing through body tissues. [36] [86] Kouwenhoven [61] described
six variables that affect the extent of electrical injury: voltage (V), resistance (R),
amperage (I), type of current, current pathway, and duration of contact.

Voltage is the electric pressure that causes current to flow. With 1000 V as the cutoff,
injuries have been arbitrarily classified into high voltage and low voltage. [50] Voltage in
high-tension transmission lines exceeds 100,000 V. The voltage in distribution lines is
reduced to 7000 to 8000 V and further stepped down to 110 V (North America) or 220 V
(Europe) before delivery to homes. [104] In lightning strike, the electric pressure
generated between clouds and earth commonly exceeds 107 V.

Current is the flow of electrons per second and is measured in amperes (A). It is of two
types, alternating current or AC and direct current or DC. Injuries caused by electricity
are almost entirely attributable to AC, whereas lightning is DC. AC is three times more
dangerous than DC of the same voltage. [50] [92] DC causes a single muscle contraction
and throws the victim away from the source and thus reduces time of contact. Lightning
generates peak DC of 20,000 to 40,000 A for a span of 1 to 3 microseconds and a
continuing current of hundreds of amperes occurs for tens of milliseconds after. [62] The
physical effects of such massive amounts of current flowing through or around the human
body in an incredibly short period are unique. AC on the other hand causes repetitive
muscle stimulation or tetany at a frequency of 50 to 60 Hz with current flows as low as 8
to 22 mA. [28] Most often contact with the source is through the hand and since flexors
of the arm are stronger than extensors, the victim tends to grip the source and thus
prolong the contact. The amount of AC needed to cause injury increases in proportion to
its frequency, and at 10 kHz, a 20-mA current may not even be perceived. [44] An AC of
20 to 30 mA can cause paralysis of respiratory muscles and at 50 to 150 mA can cause
ventricular fibrillation. [17] [104]

Resistance depends on area of contact, pressure applied, magnitude and duration of
current flow, and presence of moisture. [36] The most important resistor to the flow of
current is skin. Dry skin over palms and soles has a resistance of approximately 100,000
ohms and drops to as low as 2500 ohms when moist. Immersion in water further drops
skin resistance to 1500 ohms. [50] The extremely short duration of contact and the wet
skin prevent skin breakdown in lightning injuries. Instead the current travels on the skin
surface and discharges to the ground in a phenomenon known as flashover. [39]
However, if the victim is well grounded, e.g., wearing metal cleats, it will travel through
the body causing more injury. [77] Resistance of bone, fat, and tendons exceeds that of
dry skin, whereas muscle, blood vessels, and nervous tissue exhibit much lower
resistance. [50] It has been suggested that in high-tension electrical injuries the internal
milieu acts as a single uniform resistance and the cross-sectional area of the part of body
involved is more important than resistance of individual tissues. [5] [47] [69] [87]
Extensive damage is seen in tissues with a smaller cross-sectional area as the
321
current density is higher. [47] [91] [97] This may explain why serious injuries to
extremities are often seen but major injury to the trunk is rare. [5] [16] [31] [43]

Current pathway in the body plays a crucial role in determining injury to vital organs,
including the central nervous system, respiratory system, heart, and pregnant uterus in
women. [19] [32] [37] [60] [91] A vertical pathway, parallel to the body's axis, is more
dangerous with a higher incidence of respiratory arrest, ventricular fibrillation, fetal
deaths, and central nervous system (CNS) complications than hand-to-hand pathway. A
current pathway entirely below the symphysis pubis is unlikely to cause any life-
threatening injury.

Thermal energy (E) generated by passage of electric current is determined by the formula
E= I2 RT where T is the duration of contact. Heat is measured in joule (J). It can be seen
that prolonged contact with the source of electricity, as occurs commonly with AC,
causes greater heat and more injury. In lightning strikes, the duration of contact is
measured in milliseconds and, consequently, serious burns are infrequently seen. If the
area of contact is large the thermal energy is dissipated over a larger area and burns will
be less serious. [47] [91] The most common heat injury in both electrical and lightning
injuries is arc burns and splash burns. [97] Electric arc has a temperature in excess of
3000°C and occurs owing to poor contact between tissue and source. [11] [81] It is seen
on the volar surface of the forearm, the elbow, and the axilla and is usually associated
with an entry wound of the palm with electrical injuries. [16] [49] [50] In lightning
injuries the head or neck is usually the point of contact. The high temperature can cause
severe burns or ignition of clothing or of surrounding combustible materials, causing
flame burns. If the current spreads over a larger area a partial-thickness splash burn
results. On the other hand if a major portion of current flows through the victim, deep
electrothermal burns may result.

Several variables determine the nature and extent of injuries caused by electricity. A
salient feature is the presence of extensive deep injuries with only minimal superficial
evidence. This has led to the comparison of electrical injuries to crush injury. [6] As in
crush injury, myoglobinuria is seen in serious electrical injuries. Besides burn injuries to
skin and deeper tissues, electricity can injure the heart, the central nervous system, and
the viscera. The extent of injuries from lightning depends on how the victim is struck. A
direct strike results in maximum damage and most often involves an open space with the
victim in contact with a metal object. [39] Splash or side flash occurs when the current
jumps to the victim from another object or person presumably because that pathway
offers lower resistance. [39] If lightning strikes the ground near the victim, a potential
difference may exist between the victim's legs; this difference causes the current to enter
the body through one leg and exit through the other. This is referred to as stride potential
or step voltage. [25] Besides blunt injury caused by a fall or a severe muscle contraction,
lightning can cause blunt trauma in a unique fashion. The peak temperature in the
lightning stroke channel rises within milliseconds to 30,000 K, which is five times hotter
than the surface of the sun. [62] This generates a cylindrical shock wave of as much as 20
atm owing to the heating of air in the channel and results in mechanical trauma to any
organ in its path as it decays. [65]


MECHANISM OF INJURIES
Burns

Electricity can result in partial-thickness skin burns, full-thickness burns, or more
extensive burns with injury to deeper tissue of the body. The patient
322
has a true high-tension injury when the burn extends deeper than skin and subcutaneous
fat. More superficial injuries are often caused by flash burns or splash burns and cause
only local erythema or partial-thickness burns. [6] [69] In a study of 217 accidental
deaths caused by electrical injuries, visible electric burns were found in 57% of low-
voltage deaths and in 96% of high-voltage victims. [104] It has been estimated that 20 to
35 mA/mm2 for 20 seconds raises skin temperature to 50°C, causing first-degree burns
with swelling and blistering of skin [97] ; 75 mA/mm2 for the same time causes charring
and perforation of skin by raising the temperature to 90°C. [17] Contact with the source
of current occurs most often with hands. [16] [84] The estimation of surface burns so as
to guide therapy (rule of 9's) may lead to fatal mistakes as minor superficial burns may
hide massive coagulation necrosis of muscle and other deep tissues. [11] [15] [31] [69]
As mentioned above, most of the damage is concentrated in the extremities. [43] [98]
Bony structures are more resistant to electricity and retain heat longer than muscle.
Therefore, a central core of necrotic muscle with relative sparing of superficial muscle is
sometimes seen. [48] In children who bite or suck on an electrical cord, the current arcs
through the lips causing burns to the oral structures. [8] [38] An eschar may form,
covering the labial artery, and serious bleeding occurs when it falls off or is dislodged.
[91]

Cooper [23] described an 89% incidence of burns with lightning injury, but only 5% had
deep burns. The short duration and flashover effect prevents deep burns in most cases.
The cutaneous manifestations in one series included feathering pattern, erythema with
blistering, flash burns, contact burns (from metal), linear charring, and, most common of
all, punctate full-thickness skin loss. [3] Punctate full-thickness skin loss is a
characteristic feature with depressed central area of necrosis surrounded by congestion.
The feathering pattern, also called Lichtenberg figures, is not a true burn. Various
theories such as electron shower, travel of current along lines of moisture or superficial
vasculature, and even fractals have been hypothesized to explain their occurrence. [83]
They typically disappear within 24 hours even in the postmortem state, and along with
the punctate full-thickness burns, are pathognomonic of lightning injury. [10] [101]
Vascular

Because of the crush-injury pattern of electrical burns, compartment syndrome occurs in
extremities, thereby compromising circulation. [72] Cyanosis of distal uninjured skin,
impaired capillary filling in the nail beds, progressive neurologic changes, and brawny
edema with extreme tightness of muscle compartments on palpation are urgent
indications for fasciotomy. [31] Electric current directly damages blood vessels. In larger
arteries, rapid flow dissipates the heat, but delayed thrombosis may be seen because of
medial necrosis, leading to delayed aneurysm formation and rupture of vessel with
secondary hemorrhage. [31] [72] The high temperature produces coagulation necrosis
and occlusion of small vessels, and nutrient branches supplying muscle are particularly
susceptible. [15] [48] On arteriography this is revealed as arterial pruning proximal to
occlusion and indicates a skip area of irreversible muscle injury. This may give the
impression of progressive muscle necrosis, but in reality, the damage occurs at time of
electrical injury. [47] [48] Coagulation necrosis and deep injury to vessels and muscle
have only rarely been described with lightning injuries. [22] [40] [106] However,
lightning may gain access to internal organs through cranial orifices such as eyes, ears,
and mouth, resulting in considerable damage. [2] Cranial burns and leg burns are poor
prognostic factors with 38% and 30% mortality, respectively, in a series by Cooper. [23]
323
Cardiac

Patients in whom the electric current takes a vertical pathway are at high risk for cardiac
injury. [19] [52] Arrhythmias are frequently seen and result from passage of current
through the heart or damage to conducting pathways. [16] [29] [60] Damage to
myocardium is uncommon and occurs because of heat injury, as seen with skeletal
muscle, or by coronary spasm, causing myocardial ischemia or infarction. [56] [63] [105]
James et al [51] have postulated that in immediately fatal electrocution, electric current
itself causes a brief but very powerful positive inotropic stimulus that results in typical
finding of patchy contraction band necrosis on necropsy.
Arrhythmias

DC current and high-tension AC current are more likely to cause ventricular asystole,
whereas low-tension AC produces ventricular fibrillation. [68] [86] [92] Therefore,
ventricular fibrillation must be considered if a household electrical injury results in
cardiac arrest. The commonest ECG abnormalities, however, are sinus tachycardia, and
nonspecific ST-T wave changes that resolve spontaneously. [43] [59] [92] [102] Other
nonfatal arrhythmias seen are atrial and ventricular ectopy, atrial fibrillation, first- and
second-degree heart block, bundle branch block, and QT interval prolongation. [16] [29]
[31] [92] Sinus and atrioventricular nodes are especially vulnerable to AC current, and if
affected, can result in long-term sequelae. [24] [51] Chronic arrythmogenic foci can arise
in the heart owing to patchy necrosis at time of electrical injury and subsequent fibrosis.
[53] The effect of lightning on the heart has been described as cosmic cardioversion and
results in ventricular standstill. [7] Automaticity results in spontaneous return to sinus
rhythm, but often, the accompanying respiratory arrest persists. [82] [93] [94] This causes
a secondary deterioration of the rhythm to ventricular fibrillation and asystole, which is
more resistant to therapy than the first cardiac arrest. [22] [25] Some reports have
described ventricular fibrillation as the initial event in cardiac arrest from lightning
injury. [57] [101] In patients who do not suffer immediate arrest, the ECG abnormalities
seen are most often nonspecific ST-T changes and interval delays that resolve
uneventfully. [40] [65] [77] If initial electrocardiographic changes are not seen, it is
unlikely that significant arrhythmias will occur later. [25] [80]
Myocardial Damage

Myocardial damage in electrical injury may be difficult to determine clinically because
typical symptoms and ECG changes are not seen. [19] [70] Because the damage is rarely
transmural, ST-T elevation may not occur. [7] The role of creatinine kinase MB fraction
(CK-MB) in helping to make a diagnosis has also been questioned. [8] [70] A study by
Chandra et al [19] has suggested that vertical pathway and greater body surface burns
increase the likelihood of the presence of myocardial damage. Coagulation necrosis may
result in myocardial rupture in exceptional cases. [56] Coronary artery spasm can cause
myocardial infarction, but this is probably responsible for only a small proportion of
cases. [55] [63] [105] Massive release of adrenomedullary catecholamines and
cardiogenic hypertensive chemoreflex may play a role in compounding the cardiac injury.
[51] It has been speculated that the proximity of the right coronary artery to the chest wall
in its initial course makes it especially vulnerable, producing damage to the sinus and the
atrioventricular nodes as well as inferior-wall infarction. [18] [19] [51] [55] [70] [85] In
lightning-related deaths, a review of 45 autopsies by Wetli [101] concluded that
myocardial
324
infarction occurs rarely, if at all, and all four victims who had cardiac injury in his series
showed evidence of myocardial contusion not infarction. CK-MB levels were thought to
be unhelpful in determining injury. Lichtenberg et al [65] showed echocardiographic
evidence of cardiac injury in three out of four patients who suffered a direct strike. They
too believe the mechanism to be myocardial contusion that occurs from the shock wave
generated by the lightning strike, as described above.

Nervous System

Neurologic involvement includes cerebral injury, spinal-cord lesions, peripheral nervous
system involvement, and neuropsychological sequelae. [26] [41] [43] [52] Loss of
consciousness, confusion, and poor recall immediately after high-voltage injury is
common. [41] [43] [52] [90] Nearly half of all patients who have high-voltage injury
have loss of consciousness at the scene, but full recovery is the general rule unless there
is associated anoxia. [15] [41] Associated fall may result in intracranial hemorrhage or
vertebral fractures, leading to central nervous system damage. [74] Cranial-nerve deficits
and seizures may occur acutely. [16] [52] Spinal-cord injuries that manifest immediately
have a better prognosis than those that present later, although partial recovery may occur.
[64] [99] Levine et al [64] described three kinds of injury: amyotrophic lateral sclerosis,
ascending paralysis, and transverse myelitis with recovery occurring in only 2 of 40
patients. Upper-motor neuron-type of motor deficit is seen most often, with lower
extremities being affected more commonly. [22] [64] [99] Paraplegia, quadriplegia,
impotence, and bladder dysfunction have all been described. [11] [89] [99] Peripheral-
nerve injuries and motor neuropathies occur owing to demyelinization, vacuolization,
gliosis, and perivascular hemorrhage. [31] [98] Permanent damage generally does not
extend beyond the area of local tissue damage, except when nerve entrapment occurs
owing to scar formation. [98] The median and ulnar nerves are most frequently affected.
[16] [31] [34] [41]

The most serious central nervous system complication of lightning injury is respiratory
arrest caused by depression of the respiratory center. This can result in secondary cardiac
arrest and death in a potentially salvageable victim. Common neurologic sequelae include
loss of consciousness, confusion, paresis, and transient paralysis (keraunoparalysis). [23]
[26] [96] Autonomic instability with hypertension, peripheral vasospasm, and transient
paralysis are thought to occur owing to massive catecholamine release. [42] Extremities
may be pulseless, cyanotic, and weak. [20] These resolve over a few hours, but residual
effects such as neuritis, paraplegia, and amnesia can occur. [13] [25] Ten Duis [96] has
described reflex sympathetic dystrophy as the most common autonomic disorder
occurring after electrical injury. A series by Janus and Barrash [52] showed that cognitive
impairment is common after serious electric injury with the most frequent areas of deficit
being attention and memory, especially verbal memory. Depression, anxiety, and
sometimes posttraumatic stress disorder may be seen years after injury. [52] [79]
Viscera

Damage to the abdominal viscera occurs rarely. [75] High-tension injury to the
gallbladder, pancreas, and small and large intestine has been described in case reports.
Rarely, injuries may occur from low voltages. [95] [103] Curling's ulcers or stress
ulceration of the gastric mucosa and adynamic ileus are the commonest gastrointestinal
complications and are seen more often in patients who have
325
injuries from electricity than in patients who have burns caused by other causes. [16] [95]
Ileus may be the only manifestation of more serious underlying gastrointestinal
pathology, and if it persists for more than a few days, investigation by laparotomy should
be considered. [103] Lung injury as a result of artificial electricity has been reported in a
single case by Hartford and Ziffren. [43] Lightning can cause damage to viscera and lung
by blunt trauma from the shock wave generated. [73]

Ophthalmologic

Cataracts are the most common injury to the eye and are seen most often from lightning
injury but only rarely with electrical contact to the head. [1] [23] [37] [54] They may
occur months to years after the injury and respond well to surgery. Complications such as
corneal ulceration, iridocyclitis, hyphema, and vitreous hemorrhage are also commonly
seen with lightning. [94] Autonomic disturbance may cause mydriasis, anisocoria,
Horner's syndrome, failure of accommodation, and loss of red reflex. [54] This is
noteworthy because patients may present with dilated, nonreactive pupils as a result. [4]
[40]
Otologic

Rupture of the tympanic membrane occurs in more than 50% of patients who have
lightning injury. [3] [23] [101] This causes a conductive hearing loss that is often
accompanied by a sensorineural hearing loss at high frequencies. [12] [100] Injury to the
facial nerve, otorrhea, tinnitus, vertigo, and nystagmus are other complications that occur
less frequently. [12] [76]
Musculoskeletal

Forceful tetanic contractions can cause fractures and tendon rupture, but falls resulting
from the electric shock are the most important cause of injury to the musculoskeletal
system. [16] Injury to the musculoskeletal system, occurring as a result of electrothermal
burns, has been described above.


MANAGEMENT
Resuscitation and Triage

The rescuers must first and foremost create a safe environment in which to carry out
emergency care. In the case of electricity, this may mean disconnecting the power supply
before rescue is attempted. The patient who is alive immediately after a lightning strike
or electrical accident will probably survive. Immediate attention must therefore be
directed toward resuscitation of patients in respiratory or cardiac arrest. Keeping in mind
the airway, breathing, and circulation (ABC), the airway is secured, breathing is
established, and circulation is restored with advanced cardiac life support (ACLS)
protocol as required. Electricity results in ventricular fibrillation and requires
defibrillation in addition to respiratory support. Lightning causes asystole, and a sinus
rhythm is oftentimes reestablished spontaneously; however, if respiratory support is not
provided, a
326
secondary cardiac arrest caused by ventricular fibrillation can occur. Fixed, dilated pupils
can occur after lightning injury owing to autonomic effects and are not a reason to stop
resuscitation. [4] [42] Aggressive cardiopulmonary resuscitation is especially important
in victims of lightning injury. [82] In serious electrical injury, aggressive fluid
resuscitation must be started in the field. Normal saline or Ringer's lactate through a large
bore intravenous line is appropriate. Fluid resuscitation is not needed in lightning injury.
Once the decision to move the patient is made, precautions similar to any trauma victim
are used. This includes immobilization of the cervical spine and any other obvious
dislocation or fracture.

After successful resuscitation, an attempt is made to obtain a brief history. The nature of
electrical contact, voltage, duration of contact, and any resulting fall have obvious
implications. The speed with which resuscitation was commenced and duration of arrest,
if any, affects prognosis. The patient's personal history, especially cardiac risk factors, is
also important. Each patient must receive a complete physical examination, including a
detailed neurologic assessment and a thorough examination of the skin for any entry and
exit wounds or other burns. After the clinician has assessed the seriousness of injury, the
patient can be appropriately triaged. The low-voltage electrical injury victim with an
intact neurologic examination and no skin burns probably does not need much more than
reassurance and counseling regarding electrical hazards. [8] [27] [35] [38] The majority
of lightning victims who survive suffer little injury because of the flashover effect and
can similarly be discharged from the emergency room if the initial examination is
unrevealing.
Subsequent Care

After the initial stabilization, the most immediate risk is from cardiac arrhythmias. The
majority of rhythm and conduction disturbances, however, run a benign course. [27] [35]
Even in high-voltage injuries and patients who have burns, prolonged cardiac monitoring
is required only if there is (1) history of arrest or loss of consciousness, (2) cardiac
arrhythmia in the field or in the emergency room, (3) abnormal ECG on admission, and
(4) admission is considered appropriate owing to burn size or age of patient. [80] Jensen
et al [53] described case reports of delayed cardiac arrhythmias, and in cases in which the
electric current passes through the thorax, 24 hours of cardiac monitoring may be
appropriate. A small number of patients who have high-tension electrical injury may
suffer from myocardial damage. CK-MB elevation, lactate dehydrogenase (LDH)
isoenzymes, and ECG changes are unreliable clues. [8] [19] [58] [70] The role of newer
cardiac troponins in assessing myocardial injury has not been defined. Echocardiography
may show focal wall motion abnormalities and a technetium pyrophosphate scan of the
heart has also been used. [18] Hemodynamic support and antiarrhythmics are used as
indicated. Reperfusion therapy, including thrombolytics or percutaneous transluminal
coronary angioplasty, has no role in management except if there is angiographically
proved occlusion of coronary vessel. [18] A judicious use of fluids is necessary to
prevent pulmonary edema in patients who have myocardial damage.

Loss of consciousness is common in high-tension electrical injury and lightning victims.
Prolonged unconsciousness should prompt the clinician to perform imaging studies of the
head to exclude intracranial damage caused by falls or direct injury by electric current.
EEGs are generally believed to be unhelpful except when seizures occur. [52]
Radiographs of cervical spine are required for excluding fracture or dislocation before
neck immobilization can be discontinued.
327
Lightning victims often have keraunoparalysis with paraplegia or quadriplegia that
resolves over a short period. This may be accompanied with autonomic instability that
manifests as hypertension or cold, pulseless, and cyanotic extremities but that also
resolves in a few hours. [42] Patients who have prolonged paresis or paralysis of
extremities may have spinal-cord injury. Spine radiographs exclude vertebral fractures as
a cause of spinal cord injury.

Fluid resuscitation should be instituted as soon as possible in victims of high-voltage
injury. [16] [102] As with crush injury, the risk of rhabdomyolysis is high. The goal
should be to maintain a urine output of 70 to 100 mL/h until urine is cleared of pigment
after which urine output is kept at 50 mL/h. [5] [69] Alkaline diuresis with intravenous
sodium bicarbonate may improve clearance of myoglobin. Osmotic diuresis with
mannitol can be tried in patients who have increased pigment. [11] If compartment
syndrome has been excluded, early amputation may be necessary when there is persistent
myoglobinuria. [11] Hemodialysis is instituted if the patient is in acute renal failure.
Normal saline and Ringer's lactate are appropriate choices for initial fluid resuscitation.
[30] The fluid requirement is approximately 1.7 times the calculated fluid requirement for
the percentage of body surface area burnt by standard formulas. [69] Because of large
fluid shifts, close monitoring of electrolytes is also necessary with replacement as needed.

All patients who have serious burn injuries should receive tetanus prophylaxis. The role
of antibiotic prophylaxis is controversial, and some authors recommend penicillin to
prevent clostridial myositis. [31] Skin burns are cleaned, and after initial debridement,
open wounds are covered with topical antibiotics such as silver sulfadiazine and mafenide
acetate and dry dressings are placed on them. [16] Mafenide can better penetrate eschar
and is preferred except in large burns for which a generous amount of antibiotic may be
needed, and mafenide may cause metabolic acidosis by inhibition of carbonic anhydrase.
Homografting with serial debridement is done over several days until the wound is clear
of all necrotic tissue, and then a split-thickness autograft is applied. [11] With burns of
the oral commissure in children, parents must remain vigilant of profuse bleeding that can
occur once the labial artery is exposed by removal of eschar. Conservative management
with delay of any reconstruction by at least 6 to 9 months provides the best cosmetic
results. [45] [78] Referral to an oral and maxillofacial surgeon may be appropriate for
follow-up of other late complications. [88] The characteristic punctate burns seen in
lightning require only dressing with topical antibiotics and heal by themselves, often
without scarring. [16] It is uncommon to see severe burns in lightning injury. [25] [33]

Patients who sustain more extensive burns should be considered for transfer to a
specialized burn unit. Intense swelling of extremities requires early exploration and
fasciotomy to prevent more extensive damage caused by compartment syndrome. [11]
[69] [91] [102] Frequent, periodic assessments of peripheral circulation and neurologic
checks can identify a compromised extremity. [15] [31] The fasciotomy incision must
extend through the skin, subcutaneous tissue, and investing fascia of all muscle
compartments. [5] [11] It may be very difficult initially to tell viable from unviable
tissue, and repeat exploration and debridement are often required. [6] [102] Despite the
best efforts of physicians, amputations are necessary in a proportion of patients. [15] [31]
[34] [102] In such cases, the level of injury must be accurately determined. Delaying the
amputation by a few days stabilizes the patient for general anesthesia and also helps
better define the level of amputation. [11] [16] Arteriography has been used to better
define the level of amputation; however, it only reveals blockage in larger vessels and
does not always identify injury to nutrient vessels that correspond to areas of skip
necrosis. [5] [48]
328
Other methods such as technetium muscle scans, xenon-133 washout, and frozen-section
microscopy have also met with only limited success. [15] [21] [46] [81]
In patients who have persistent adynamic ileus beyond a few days, an abdominal CT
scan, peritoneal lavage, or exploratory laparotomy may be needed to confirm the
diagnosis of injury to abdominal organs. [103] Because of the multiplicity of lesions
usually seen in cases with abdominal injuries, a second-look operation at 2 to 5 days after
the initial repair is advocated. [11] Gastrointestinal prophylaxis with acid suppressants
should be provided to all patients who have serious injury.

Once the patient is stabilized, a careful otologic examination and audiogram may reveal
hearing loss. Repair is deferred for several months, as the tympanic membrane may heal
spontaneously. The delay also permits vascularization of damaged tissue and improves
the success of tympanoplasty or tympanotomy. [12] It is useful to document an
ophthalmologic examination in patients who have contact near the head, in case cataracts
develop later on. Spinal-cord injury and peripheral-nerve injury may manifest only after a
few days. Early institution of physical therapy helps minimize functional loss. [64]
Counseling may be needed in patients who suffer psychiatric or behavioral sequelae.


SUMMARY

Electricity and lightning can cause injury in a variety of ways, some of which may remain
hidden from the unsuspecting physician until it is too late. Prompt and, if necessary,
prolonged resuscitation are of proven benefit. Particular attention must be paid to the
patient who suffers high-voltage injury, and deep electrothermal burns or damage to vital
organs should be excluded. Uncommonly late sequelae are seen, and such patients require
appropriate care.
References

1. Adams AL, Klein M: Electrical cataract: Notes on case and review of the literature. Br
J Ophthalmol 29:169, 1945

2. Andrew C: Structural changes after lightning strike, with special emphasis on special
senses orifices as portals of entry. Semin Neurol 15:296, 1995

3. Arden GP, Harrison SH, Lister J, et al: Lightning accident at Ascot. BMJ 1:1450, 1956

4. Art JL: The pupillary responses after being struck by lightning. JAMA 254:3312, 1985

5. Arturson G, Hedlund A: Primary treatment of 50 patients with high-tension electrical
injuries. I. Fluid resuscitation. Scan J Plast Reconstr Surg Hand Surg 18:111, 1984

6. Artz CP: Electrical injury simulates crush injury. Surg Gynecol Obstet 125:1316, 1967

7. Auerbach PS: Lightning strike. Top Emerg Med 2:129, 1980
8. Bailey B, Gaudreault P, Thivierge RL, et al: Cardiac monitoring of children with
household electrical injuries. Ann Emerg Med 25:612, 1995

9. Baker MD, Chiavello C: Household electrical injuries in children: Epidemiology and
identification of avoidable hazards. AJDC 143:59, 1989

10. Bartholome CW, Jacoby WD, Ramchand SC: Cutaneous manifestations of lightning
injury. Arch Dermatol 111:1466, 1975

11. Baxter CR: Present concepts in the management of major electrical injury. Surg Clin
North Am 50:1401, 1970

12. Bergstrom L, Neblett LW, Sando I, et al: The lightning damaged ear. Arch
Otolaryngol Head Neck Surg 100:117, 1974

13. Blount BW: Lightning injuries. Am Fam Physician 42:405, 1990

14. Brokenshire B, Cairns FJ, Koelmeyer TD, et al: Deaths from electricity. N Z Med J
97:139, 1984

15. Burke JF, Quinby WC, Bondoc C: Patterns of high tension electrical injury in
children and adolescents and their management. Am J Surg 133:492, 1977
329


16. Butler ED, Gant TD: Electrical injuries, with special reference to the upper
extremities: A review of 182 cases. Am J Surg 134:95, 1977

17. Cabanes J: Physiological effects of electric currents on living organisms, more
particularly humans. In Bridges JE, Ford CL, Sherman IA, Valnberg M (eds): Electrical
Shock Safety Criteria: Proceedings of the First International Symposium on Electrical
Shock Safety Criteria. Tarrytown, New York, Pergamon Press, 1985, p 7

18. Carleton SC: Cardiac problems associated with electrical injury. Cardiol Clin 13:263,
1995

19. Chandra NC, Siu CO, Munster AM: Clinical predictors of myocardial damage after
high voltage electrical injury. Crit Care Med 18:293, 1990

20. Cherington M, Yarnell PR, London SF: Neurologic complications of lightning
injuries. West J Med 162:413, 1995

21. Clayton JM, Hayes AC, Hammel J, et al: Xenon-133 determination of muscle blood
flow in electrical injury. J Trauma 17:293, 1977
22. Cooper MA: Emergent care of lightning and electrical injuries. Semin Neurol 15:268,
1995

23. Cooper MA: Lightning injuries: Prognostic signs for death. Ann Emerg Med 9:134,
1980

24. Cotoi S, Dragulescu SI: Idiopathic persistent atrial fibrillation precipitated by
electrocution in a 40-year old man. G Ital Cardiol 4:80, 1974

25. Craig SR: When lightning strikes: Pathophysiology and treatment of lightning
injuries. Postgrad Med 79:109, 1986

26. Critchley M: Neurological effects of lightning and of electricity. Lancet 1:68, 1934

27. Cunningham PA: The need for cardiac monitoring after electrical injury. Med J Aust
154:765, 1991

28. Dalziel CF: The threshold of perception currents. Trans Am Inst Electrical
Engineering 73:990, 1954

29. Das KM: Electrocardiographic changes following electric shock. Indian J Pediatr
41:192, 1974

30. Demling RH: Fluid resuscitation after major burns. JAMA 250:1438, 1983

31. DiVincenti FC, Moncrief JA, Pruitt BA: Electrical injuries: A review of 65 cases. J
Trauma 9:497, 1969

32. Einarson A, Bailey B, Inocencion G, et al: Accidental electric shock in pregnancy; a
prospective cohort study. Am J Obstet Gynecol 176:678, 1997

33. Epperly TD, Stewart JR: The physical effects of lightning injury. J Fam Pract 29:267,
1989

34. Esses SI, Peters WJ: Electrical burns: Pathophysiology and complications. Can J Surg
24:11, 1981

35. Fatovich DM, Lee KY: Household electric shocks: Who should be monitored? Med J
Aust 155:301, 1991

36. Fish R: Electric shock, Part I: Physics and pathophysiology. J Emerg Med 11:309,
1993

37. Fraunfelder FT, Hanna C: Electric cataracts: I. Sequential changes, unusual and
prognostic findings. Arch Ophthalmol 87:179, 1972
38. Garcia CT, Smith GA, Cohen DM, et al: Electrical injuries in a pediatric emergency
department. Ann Emerg Med 26:604, 1995

39. Golde RH, Lee WR: Death by lightning. Proc Inst Electrical Eng 123:1163, 1976

40. Graber J, Ummenhofer W, Herion H: Lightning accident with eight victims: Case
report and brief review of the literature. J Trauma 40:288, 1996

41. Grube BJ, Heimbach DM, Engrav LH, et al: Neurologic consequences of electrical
burns. J Trauma 30:254, 1990

42. Hanson GC, McIlwraith GR: Lightning injury: Two case histories and a review of
management. BMJ 4:271, 1973

43. Hartford CE, Ziffren SE: Electrical injury. J Trauma 11:331, 1971

44. Hawkes GR, Warm JS: The sensory range of electrical stimulation of the skin. Am J
Psychol 73:485, 1960

45. Hirschfeld JJ, Assael LA: Conservative management of electrical burns to the lips of
children. J Oral Maxillofac Surg 42:197, 1984

46. Hunt J, Lewis S, Parkey R, et al: The use of technetium-stannous pyrophosphate
scintigraphy to identify muscle damage in acute electrical burns. J Trauma 19:409, 1979
330


47. Hunt JL, Mason AD, Masterson TS, et al: The pathophysiology of acute electric
injury. J Trauma 16:335, 1976

48. Hunt JL, McManus WF, Haney WP, et al: Vascular lesions in acute electric injuries. J
Trauma 14:461, 1974

49. Hunt JL, Sato RM, Baxter CR: Acute electric burns. Arch Surg 115:434, 1980

50. Jaffe RH: Electropathology: A review of pathologic changes produced by electric
currents. Arch Pathol Lab Med 5:835, 1928

51. James TN, Riddick L, Embry JH: Cardiac abnormalities demonstrated post-mortem in
four cases of accidental electrocution and their potential significance relative to non-fatal
electrical injuries of the heart. Am Heart J 120:143, 1990

52. Janus TJ, Barrash J: Neurologic and neurobehavioral effects of electric and lightning
injuries. J Burn Care Rehabil 17:409, 1996
53. Jensen PJ, Thomsen PEB, Bagger JP, et al: Electrical injury causing ventricular
arrythmias. Br Heart J 57:279, 1987

54. Johnson EV, Kline LB, Skalka HW: Electrical cataracts: A case report and review of
the literature. Ophthalmic Surg Lasers 18:283, 1987

55. Kinney TJ: Myocardial infarction following electrical injury. Ann Emerg Med
11:622, 1982

56. Kirchner JT, Larson DL, Tyson KRT: Cardiac rupture following electrical injury. J
Trauma 17:389, 1977

57. Kleiner JP, Wilkin JH: Cardiac effects of lightning stroke. JAMA 240:2757, 1978

58. Kleinot S, Klachko DM, Keeley KJ: The cardiac effects of lightning injury. S Afr
Med J 40:1141, 1966

59. Kobernick M: Electrical injuries: Pathophysiology and emergency management. Ann
Emerg Med 11:633, 1982

60. Kouwenhoven WB, Hooker DR, Langworthy OR: The current flowing through the
heart under conditions of electric shock. Am J Physiol 100:344, 1932

61. Kouwenhoven WB: Effects of electricity in the human body. Electrical Engineering
68:199, 1949

62. Krider PE, Uman MA: Cloud to ground lightning: Mechanisms of damage and
methods of protection. Semin Neurol 15:227, 1995

63. Ku CS, Lin SL, Hsu TL, et al: Myocardial damage associated with electrical injury.
Am Heart J 118:621, 1989

64. Levine NS, Atkins A, McKell DW, et al: Spinal cord injury following electrical
accidents: Case reports. J Trauma 15:459, 1975

65. Lichtenberg R, Dries D, Ward K, et al: Cardiovascular effects of lightning strikes. J
Am Coll Cardiol 21:531, 1993

66. Lopez RE, Holle RL, Heithamp TA, et al: The under-reporting of lightning injuries
and death in Colorado. Bull Am Meteor Soc 74:2171, 1993

67. Lopez RE, Holle RL: Demographics of lightning casualties. Semin Neurol 15:286,
1995

68. Lown B, Neuman J, Amarasingham R, et al: Comparison of alternating current with
direct current electroshock across the closed chest. Am J Cardiol 10:223, 1962
69. Luce EA, Gottlieb SE: "True" high-tension electrical injuries. Ann Plast Surg 12:321,
1984

70. McBride JW, Labrosse KR, McCoy HG, et al: Is serum creatine kinase-MB in
electrically injured patients predictive of myocardial injury. JAMA 255:764, 1986

71. MMWR: Lightning-Associated Deaths--United States, 1980-1995. MMWR 47:391,
1998

72. Moncrief JA, Pruitt BA: Electric injury. Postgrad Med 48:189, 1970

73. Moulson AM: Blast injury of the lungs due to lightning. BMJ 289:1270, 1984

74. Myers GJ, Colgan MT, VanDyke DH: Lightning strike disaster among children.
JAMA 238:1045, 1977

75. Newsome TW, Curreri PW: Visceral injuries: An unusual complication of an electric
burn. Arch Surg 105:494, 1972

76. Ogren FP, Edmunds AL: Neuro-otologic findings in the lightning-injured patient.
Semin Neurol 15:256, 1995

77. Peters WJ: Lightning injury. CMAJ 128:148, 1983
331


78. Pitts W, Pickrell K, Quinn G, et al: Electrical burns of the lip and mouth in infants
and children. Plast Reconstr Surg 44:471, 1969

79. Primeau M, Engelstatter GH, Bares KK: Behavioral consequences of lightning and
electrical injury. Semin Neurol 15:279, 1995

80. Purdue GF, Hunt JL: Electrocardiographic monitoring after electrical injury:
Necessity or luxury. J Trauma 26:166, 1986

81. Quinby WC, Burke JF, Trelstad RL, et al: The use of microscopy as a guide to
primary excision of high tension electrical burns. J Trauma 18:423, 1978

82. Ravitch MM, Lane R, Safar P, et al: Lightning stroke: Report of a case with recovery
after cardiac massage and prolonged artificial respiration. N Engl J Med 264:36, 1961

83. Resnik BI, Wetli CV: Lichtenberg figures. Am J Forensic Med Pathol 17:99, 1996

84. Robinson DW, Masters FW, Forrest WJ: Electrical burns: A review and analysis of
33 cases. Surgery 57:385, 1965
85. Robinson NM, Chamberlain DA: Electrical injury to the heart may cause long term
damage to conducting tissue: A hypothesis and review of the literature. Int J Cardiol
53:273, 1996

86. Sances A, Larson SJ, Myklebust J, et al: Electrical injuries. Surg Gynecol Obstet
149:97, 1979

87. Sances A, Myklebust JB, Larson SJ, et al: Experimental electrical injury studies. J
Trauma 21:589, 1989

88. Savara BS, Takeuchi Y: A longitudinal study of electrical burns on growth of the oro-
facial structures. ASDC J Dent Child 44:367, 1977

89. Sharma M, Smith A: Paraplegia as a result of lightning injury. BMJ 2:1464, 1978

90. Silversides J: The neurological sequelae of electrical injury. CMAJ 91:195, 1964

91. Skoog T: Electrical injuries. J Trauma 10:816, 1970

92. Solem L, Fischer RP, Strate RG: The natural history of electrical injury. J Trauma
17:487, 1977

93. Strasser EJ, Davis RM, Mechey MJ: Lightning injuries. J Trauma 17:315, 1977

94. Taussig HB: "Death" from lightning--and the possibility of living again. Ann Intern
Med 68:1345, 1968

95. Taylor PH, Pugsley LQ, Vogel EH: The intriguing electrical burn: A review of thirty-
one electrical burn cases. J Trauma 2:309, 1962

96. ten Duis HJ, Klasen HJ: Keraunoparalysis, a `specific' lightning injury. Burns 12:54,
1985

97. ten Duis HJ: Acute electrical burns. Semin Neurol 15:381, 1995

98. Ugland OM: Electrical burns--a clinical and experimental study with special
reference to peripheral nerve injury. Scand J Plast Reconstr Surg Hand Surg 2:1, 1967

99. Varghese G, Mani MM, Redford JB: Spinal cord injuries following electrical
accidents. Paraplegia 24:159, 1986

100. Weiss KS: Otologic lightning bolts. Am J Otolaryngol 1:334, 1980

101. Wetli CV: Keraunopathology: An analysis of 45 fatalities. Am J of Forensic Med
Pathol 17:89, 1996
102. Wilkinson C, Wood M: High voltage electrical injury. Am J Surg 136:693, 1978

103. Williams DB, Karl RC: Intestinal injury associated with low-voltage electrocution. J
Trauma 21:246, 1981

104. Wright RK, Davis JH: The investigation of electrical deaths: A report of 220
fatalities. J Forensic Sci 25:514, 1980

105. Xenopoulos N, Movahed A, Hudson P, et al: Myocardial injury in electrocution. Am
Heart J 122:1481, 1991

106. Yost JW, Holmes FF: Myoglobinuria following lightning stroke. JAMA 228:1147,
1974