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A COMPARISON OF LIGHTNING AND ELECTRICAL INJURIES DO YOU KNOW THE DIFFERENCE ?
LISA CAMPFENS MD, FRCP(C), FACEP
EPIDEMIOLOGY
LIGHTNING
ELECTRICAL
-150 - 250 fatalities per year
- more than 800 victims per year
- kills more people in the U.S.A. each year than any other natural disaster
- golfers, campers, hikers, joggers, construction workers, etc.
- 30% multiple victims
-2100 burn unit admissions per year
-more than 1000 fatalities per year
- most commonly occupational related
MYTHS ABOUT LIGHTNING





Lightning is always fatal
Lightning burns can turn victims into ‘crispy critters’
Lightning never strikes in same place twice
Victims remain ‘electrified’
Lightning injuries are like other high voltage injuries
DETERMINANTS OF ELECTRICAL INJURY
The exact pathophysiology is not well understood because of the large number of
variables that cannot be measured or controlled.

VOLTAGE

AMPERAGE
EFFECTS
Increased voltage leads to greater potential for tissue
destruction resulting in major amputations and tissue loss.
This is a measure of the amount of current or energy flowing
through an object.
Tingling
1 - 4 mA
Let-go Current 4 - 9 mA
Freeze to Circuit 10-20 mA
Resp Arrest 20-50 mA
V Fibrillation 50-100 mA
* very narrow range of safety between household current and that
which causes respiratory arrest or cardiac arrest.
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
RESISTANCE
LEAST
INTERMED
MOST

CIRCUIT
AC
DC
countershock to
 DURATION
 PATHWAY
VOLTAGE
AMPERAGE
RESISTANCE
CIRCUIT
DURATION
PATHWAY
Varies with the type of tissue. The higher the resistance of the tissue to
the flow of current, the potential for electrical energy to transform
to thermal energy.
nerves/ blood/ muscle GOOD CONDUCTORS
dry skin
tendon/ fat/ bone
HIGH RESISTANCE
Direction of flow of current
Much more dangerous because at 60cps (frequency of electrical
transmission in U.S.A.) produces tetany of muscle fibres.
This causes a single muscle spasm throwing the victim from the source
which results in only brief instantaneous exposure but increases the
likelihood of blunt trauma. Can also act as a massive
cause disturbances in cardiac rhythms.
Obviously increases the potential for injury.
Determines the tissues at risk, the type of injury seen and the degree of
conversion of electrical energy to heat.
Current often concentrates at entrance and exit sites but this may also
be only the ‘tip of the iceberg’.
Damage to internal tissues may be spotty, irregular, unpredictable, and
large distances away from entry (as nerves, blood, and muscles allow
for good conduction to more resistant and distant tissues).
LIGHTNING
VS
10-20 million V
~20,000 A
unclear
DC
brief instantaneous exposure
flashover phenomena
ELECTRICAL INJURY
110- 70,000 V
< 1000 A
unclear
AC or DC
prolonged tetany
internal
LIGHTNING PRODUCTION
In simplified terms, static charges are produced when a cold high pressure front
moves over a warm low pressure area. The moist warm air rises through the cold air causing
condensation. Friction between the moving air particles causes ionization. The end result is
the production of lightning and thunder.
What you visualize is the Leader Stroke which is the slow jagged path from cloud to
ground. As the leader stroke approaches the ground, an even stronger opposite charge is
induced and there is a massive amount of release of energy in the form of the Pilot Stroke.
Therefore, the majority of lightning discharge is actually in the upward direction.
Thunder is the result of the explosive expansion of air ionized and heated by the
stroke.
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LIGHTNING
MECHANISMS OF INJURY


DIRECT STRIKE
CONTACT

SIDE FLASH

STEP VOLTAGE

other, a
become part
responsible for the
BLUNT TRAUMA
Victim touches object in the path of current
eg. tree, tent pole, umbrella, golf club
‘splash’ or ‘flashover phenomena’
Current takes the path of least resistance and ‘splashes’ over
onto victim from other object because the air between the
object and the victim provides better conductance.
Lightning current will spread through the ground in a radial
pattern. If one foot is closer to the strike point than the
potential difference is created allowing the legs to
of the pathway. This is often the mechanism
death of livestock.
CLINICAL IMPACT
Nearly 70% will show sequelae, of which most are temporary in nature.

CVS
Despite the ‘flashover phenomena’, internal leakage of current may occur
causing a massive DC countershock which depolarizes the entire myocardium
simultaneously.
ASYSTOLE>>V FIB
Although automaticity causes the heart to begin beating again, the respiratory
arrest may last long enough to cause a secondary arrest in the form of V Fib
or asystole which is now much more resistant to therapy.
If resuscitation is successful, delayed multiple dysrhythmias may be apparent.

RESP
Respiratory arrest is the result of a direct effect on the brain stem.
Blunt trauma- pulmonary contusion

CNS
LOC secondary to direct effect on brainstem,hypoxia, cerebal edema, blunt
trauma ( hemmhorage)
Seizures (blunt trauma, hypoxia)
Amnesia and confusion is universal and usually transient.
2/3 of severly injured: Lower extremity paralysis
1/3 of severly injured: Upper extremity paralysis
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This phenomena is usually due to vascular spasm resulting from sympathetic
instability. The extremities appear blue, cold, mottled, and pulseless.The
majority will recover completely over a few hours.

OPTH
vitreal

OTIC
>50% will develop cataracts. These can develop up to two years after the
injury. Other opthalmic injuries include corneal lesions, lens dislocation,
hemmhorage, retinal detachment, transient bilateral blindness, etc.
Dilated or unreactive pupils cannot be used as a criterion for brain death
in a lightning victim until all other functional lesions are ruled out.
facial
>50% sustain TM rupture (uni or bilateral). This may be a result of the shock
wave, direct burn, or a basilar skull fracture.
Other injuries include direct nerve damage with sensorineural loss and/or
palsies, and disruption of ossicles and mastoid.

EXTS
Blunt trauma- fractures/dislocations

ABD
Injury rare.

RENAL
Failure rare.

SKIN
Because of the ‘flashover phenomena’, deep burns occur in <5%.
Initially there may be no sign of injury and may take hours to display:
Linear
Punctate
Feathering
Thermal
Results secondary to steam production
(along ‘sweat’ lines).
Appear like multiple small cigarette burns.
PATHOGNOMONIC
These are not true burns and there is no damage to the skin.
They produce a ‘fern pattern’ and require no treatment.
These result if clothing is ignited or a victim is wearing metal
which then heats up.
PREHOSPITAL CARE





Always ensure own safety first. Remember lightning can strike in the same place twice.
Victims are not dangerous to providers.
Rules of triage are reversed - RESUSCITATE THE DEAD. In absence of respiratory or
cardiac arrest, victims unlikely to die of any other cause.
Recognition- have a high degree of suspicion and look for clues.
Concentrate on ABC’s.
ED MANAGEMENT
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PROVIDE ABC’S
- Prolonged CPR not indicated.
- Dilated pupils are not an absolute criteria for death.
- Ensure C-spine immobilization.
FLUID MANAGEMENT
- Massive fluid resuscitation rarely required.
- Shock may result from blunt trauma,cardiac or autonomic
dysfunction. Treat accordingly.
APPROPRIATE INVESTIGATIONS
- Blood work may include CBC, lytes, BUN, Cr, cardiac
enzymes,ABG’s
- Check urine for Myoglobin
- ECG, CXR, C-spine films, CT scan and other films as
indicated
MONITORING
- Cardiac monitor for potential dysrhythmias
- Insert foley catheter to monitor urine output
- NG tube as needed
TETANUS PROPHYLAXIS
Complications result from over-aggressive management. In contrast to electrical
injuries, massive fluid resuscitation, use of diuretics and alkalinization, fasciotomies,
amputations, and large tissue debridements, are rarely required.
DISPOSITION AND PROGNOSIS
Patients should be monitored in an ICU setting for 24 hours for potential cardiac
dysrhythmias. Consultation with Cardiology, Trauma service, ENT, and Opthalmolgy, will
depend on given injuries.
AWAKE/ALERT (+/- ear or eye injuries)
 expect full recovery
ALTERED MENTAL STATUS OR EXTREMITY INJURY
 expect neurologic sequelae
CARDIORESPIRATORY ARREST
 > 60% mortality
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ELECTRICAL ACCIDENTS
MECANISM OF INJURY


DIRECT CONTACT
ARCING CURRENT


RESCUER CONTACT
BLUNT TRAUMA
This can result from:
- being thrown from the source by intense contraction of
muscles.
- fall from height
- violent muscle spasms from prolonged tetany resulting in
fractures and/or dislocations.
- exit wounds resulting from AC current which tend to be
explosive in nature.
A current spark is formed between two objects of
different potential that are not in contact with each other.
This usually occurs between a highly charged source and a
ground. If victim becomes part of this arc, they sustain deep
thermal burns at point of contact or as a result of clothing being
ignited. Temperatures reach 2500o C.
CLINICAL IMPACT

BURNS
Seen in close to 100% of victims. There may be multiple entry and exit
sites. Entry wounds most commonly seen on hands and skull. Exit
wounds most common on heels. ‘Kissing burns’ are seen in flexor
creases as a result of arcing current.

CNS
25 -100%
IMMEDIATE
LOC, seizures, amnesia, confusion, parasthesias, and paralysis. Spinal c
cord injury results from fractured vertabrae, ligamentous injury with
instability, and spinal artery spasm with thrombosis.
INTERMEDIATE
Pain, headache, paralysis, and autonomic disturbances.
DELAYED
These injuries may become apparent days to years after the initial insult
and carry a very poor prognosis. It may include aphasia, ataxia,
hemiplegia, seizures, Parkinson’s Disease, ascending paralysis,
mononeuritis, ALS, transverse myelitis, and disseminated spinal
degeneration.
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
CVS
10 - 40%
100 mA can cause V Fib or asystole. Multiple dysrhythmias may be
seen. ST elevation is usually transient. AMI is rare despite elevated
CK-MB fractions resulting from massive tissue damage. These levels
must be interpreted with caution and require more detailed
investigations to rule out permanent myocardial damage.

RESP
50 mA can cause respiratory arrest usually secondary to a direct effect on the
brainstem.

EXTS
You cannot predict the amount of underlying tissue damage from the amount
of cutaneous involvement. Massive muscle necrosis, venous thrombosis,
vascular ischemia, and tissue edema leads to secondary compartment
syndromes requiring fasciotomies, amputations, and wide tissue debridement.
Fractures and dislocations result from blunt trauma.

RENAL
20%
Rhabdomiolysis with the release of Myoglobin cause Acute Renal Failure.

GI
25%
Complications include stress ulcers, mesenteric thrombosis, gallbladder
necrosis.

OPTHAL Cataracts may develop up to 2 years after but unlike with lightning, only seen
in 6%.

MOUTH This is the most common electrical injury seen in children < 4 years old. They
will chew and suck on household extension cords and sustain injuries to the
mouth as a result of ‘local arc burns’ ( current arcs through saliva).
Temperatures reach 2500o C.
The concern is that there is a 10% risk of delayed bleeding 4-5 days later from
the Labial artery when the eschar separates. Splinting is also required to
minimize cosmetic deformities.
PRE-HOSPITAL CARE



‘Protect the rescuers’ - the only time extrication is safe is when the power is shut off.
Downed high-tension wires may repower or continue to pour current into the ground.
Approach the victim as a Trauma Patient:
-ABC’s
-C-spine immobilization
-cardiac monitoring
-two large-bore IV’s- these patients require tremendous fluid resuscitation.
Combined ACLS / ATLS protocols.
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ED MANAGEMENT
PROVIDE ABC’S
- cardiac monitoring
- maintain C-spine immobilization.
FLUID MANAGEMENT
- aggressive fluid resuscitation: treat for shock, burns, and
potential ARF.
- rule of ‘9’s doesn’t apply- aim for UO of 1-1.5 ml/kg/hr.
- treatment of an electrical burn more like a crush injury than a
thermal burn because of large amount of tissue damage under
the skin.
APPROPRIATE INVESTIGATIONS
- Blood work should include CBC, lytes, BUN, Cr, cardiac
enzymes, ABG’s
- urinalysis for Myoglobin
- ECG, CXR, +/- CT scan
- other films as needed
MONITORING
- cardiac monitor
- CVP/ Swan Ganz catheter
- foley catheter / NG tube
TETANUS PROPHYLAXIS
ANTIBIOTICS
- Will depend on individual Burn Centre.
COMPLICATIONS
Complications include cardiopulmonary arrest, overwhelming injuries,
hypoxia,intracranial injuries, myoglobinuric renal failure, and multiple organ failure.
SEPSIS is the most common cause of death after initial resuscitation.
DISPOSITION
Significant electrical burns must be transferred to a Regional Burn Centre.
Asymptomatic patients suffering low voltage injuries with minimal cutaneous injury, normal
ECG, and normal urinalysis may be observed for 6 hours and then discharged.
Pediatric oral burns and pregnant patients in their 2nd or 3rd trimester should be
admitted for observation.
PROGNOSIS
MORTALITY
With high V ~10%
Early- cardiorespiratory arrest
Late- ARF, sepsis