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Electrical arcs have incredibly high temperatures and can cause
flash burns.
Electricity can ignite clothing or structures with secondary flame
burns.
INITIAL MONITORING
Based on ATLS guidelines (ABCDE)
Airway Maintenance: C-collar until c-spine cleared
Breathing and Ventilation—100% oxygen
Circulation and Cardiac status
Cardiac monitor
Two large-bore IV catheters
Assess peripheral perfusion
ECG
24-hour monitor if
Ectopy or dysrhythmia present
Loss of consciousness
Cardiac arrest
Abnormal rate or rhythm
Disability, Neurological Deficit, and Gross Deformity
Assess level of consciousness.
Note any neurological deficit.
Note any gross deformity.
Exposure and Environmental Control
Stop the burning process and remove clothes.
Avoid hypothermia.
Renal Function Analysis and Urine Myoglobin
FLUID RESUSCITATION
TBSA provides an inadequate estimation of burn severity
Unlike thermal injury, electrical injury often occurs deep to the
skin and is not visible. Thus, standard fluid resuscitation models
(Parkland formula) may underestimate fluid resuscitation needs.
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The Parkland formula can be used to provide a minimum
volume estimate. If no urine pigmentation is present, the
minimum acceptable urine output is 0.5 mL/kg/h.
Pigmented urine can be caused from myoglobin (secondary
to rhabdomyolysis) and/or free hemoglobin (from damaged
RBCs)
For myoglobinuria, the urine dipstick will be positive for
blood. However, microscopy will not demonstrate RBCs.
*The goal urine output for rhabdomyolysis and
myoglobinuria is 2 mL/kg/h or about 75-100 cc/h.
Insufficient volume resuscitation can predispose to
myoglobin-induced acute tubular necrosis.
In addition to adequate fluid resuscitation, myoglobin
excretion can be promoted using mannitol (12.5 g/h
osmotic diuresis) and/or urine alkalinization with 50
mEq/L of bicarbonate.
Follow urine myoglobin levels every 6 hours until a
downward trend is seen.
COMPARTMENT SYNDROME CAN
OCCUR AFTER HIGH-VOLTAGE
INJURY TO AN EXTREMITY
Current travels along bone, which has high resistance.
The bone serves as a conductor and “cooks” adjacent tissue
from deep to superficial.
*In the upper extremity, flexor digitorum profundus and
flexor pollicis longus will be most severely affected (closest
to bone).
Overaggressive fluid resuscitation can worsen tissue
edema, resulting in increased tissue pressures, and
exacerbating raised compartment pressures typically occurs
within 48 hours of injury.
Compartment Syndrome
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Clinical concern for raised compartment pressures
mandates an evaluation of compartment pressures or a trip
to the operating room.
The 6 “P” signs/symptoms include pain out of proportion,
paresthesia, pallor, paralysis, pulselessness, and
poikilothermia.
Raised compartment pressures can be used as an
adjunct to clinical diagnosis, or when the patient is unable
to participate in clinical examination
*Absolute pressure ≥30 mm Hg.
Pressure within 20 mm Hg of the diastolic blood
pressure is also diagnostic of compartment syndrome.
Compartment pressures can be measured using a Stryker
intracompartmental pressure monitor or an arterial line
pressure transducer.
Upper extremity compartment syndrome is managed with
surgical release of the volar and extensor compartments, the
mobile wad, carpal tunnel, Guyon canal, and nine compartments
of the hand.
Lower extremity compartment syndrome managed with
fasciotomies of the anterior, lateral, superficial posterior, and
deep posterior compartments.
CHEMICAL BURNS
GENERAL APPROACH TO CHEMICAL
BURNS
Protect yourself with personal protective equipment: always
consider that the chemicals are still present and must be
neutralized or temporized.
Clothing that is saturated with chemical should be removed. Any
powders that are present on the skin should be brushed off.
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With few exceptions (see below), all chemical burns should be
copiously irrigated with water. This dilutes but does not
neutralize the chemical and cools the burning area.
Neutralization of a chemical burn is generally contraindicated
because neutralization may generate heat and cause further
burn injury.
Water irrigation is contraindicated or ineffective in several
scenarios
Contraindicated with elemental sodium, potassium, and
lithium as this will precipitate an explosion.
Dry lime should be brushed off, not irrigated.
*Phenol is water insoluble and should be wiped from
the skin with 30% polyethylene glycol–soaked
sponges.
TYPES OF CHEMICAL BURNS (TABLE
10-1)
Table 10-1 Chemical Burns
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Alkali mechanism of injury is via liquefaction necrosis and
protein denaturation
Oven, toilet and drain cleaners, fertilizer, wet cement.
Alkali injury will extend deeper into tissues until the source
is removed or diluted.
Acids damage tissue via coagulation necrosis and protein
precipitation
Acid injury is typically self-limited and confined to the region
of exposure.
Acids are commonly found in household cleaners and rust
removers.
Organic compounds cause damage via multiple mechanisms
Phenol and petroleum
Cutaneous damage due to fat solvent action (cell
membrane solvent action)
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Systematic absorption with toxic effects on the liver and
kidneys
When in doubt about the type of burn, check the label on the
can or bottle. Your local poison control office may be a helpful
resource.
SPECIFIC TYPES OF CHEMICAL
BURNS
Hydrofluoric acid (HF) is a potent and corrosive acid
commonly used as a rust remover, in glass etching, and to clean
semiconductors
HF is a weak acid but the fluoride ion is toxic.
HF can cause severe pain and local necrosis.
Acid exposure is treated with copious water irrigation.
*Fluoride ion can be neutralized with topical calcium
gel (1 amp calcium gluconate in 100 g lubricating jelly).
If symptoms persist, can consider intra-arterial calcium
infusion (10 mL calcium gluconate diluted in 80 mL of
saline, infused over 4 hours) and/or subeschar injection of
dilute (10%) calcium gluconate solution.
*Fluoride ion can bind free serum calcium. Make sure
to check the serum calcium and replace with IV calcium
as needed.
Phenol is commonly used in disinfectants and chemical
solvents
Phenol is an acidic alcohol with poor water solubility.
Phenol causes protein disruption and denaturation that
results in coagulation necrosis.
Phenol is associated with cardiac arrhythmia and liver
toxicity: cardiac and liver function should be monitored.
Phenol is cleared by the kidneys.
Phenol causes demyelination and has a local anesthetic
effect. Thus, pain is not a reliable indicator of injury.
*Treatment of phenol exposure includes copious water
irrigation and cleansing with 30% polyethylene glycol
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or ethyl alcohol.
EKG is required.
Tar is used in the paving and roofing industry as a durable,
waterproof coating
Tar can be heated to 260 °C (~500 °F) prior to application.
In addition to thermal injury, tar solidifies as it cools and will
become enmeshed with hair and skin.
Tar should be cooled with copious water irrigation to stop
the burning process.
Tar removers promote micelle formation to break the tarskin bond.
A sterile surfactant mixture (De-Solv-it or Shur-Clens)
allows tar to be wiped away in real time.
Wet dressings using polysorbate (Tween 80) or
neomycin cream for 6 hours prior to tar removal can
also be effective.
White phosphorus is used in the manufacture of military
explosives, fireworks, and methamphetamine
White phosphorous explosions will deposit chemical
particles on the skin.
These particles will smoke when exposed to air.
Obvious particles should be brushed off. The skin should be
irrigated with a 1%-3% copper sulfate solution.
Copper sulfate stains the particles black for identification.
Copper sulfate will also prevent ignition when particles are
submerged in water.
After copper sulfate irrigation, the exposed area should be
placed in a water bath and the white phosphorous should
be removed.
Anhydrous ammonia is an alkali used in fertilizer
Skin exposure is treated with irrigation and local wound
care.
Anhydrous ammonia exposure is associated with rapid
airway edema, pulmonary edema, and pneumonia:
consider early intubation for airway protection.
Methamphetamine
Tachycardia (greater than expected with a similar size burn)
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Hyperthermia
Agitated
Paranoid
INJURY TO EYES
Prolonged irrigation with Morgan lenses.
Eyelids may need to be forced open due to edema or spasm.
Utilize topical ophthalmic analgesic.
Consult an ophthalmologist.
Electrical injuries can cause late cataracts, therefore, good to
get a baseline.
Can cause increase in intra-ocular pressures.
Can get corneal abrasions if corneas not protected and/or
lubricated.
FROSTBITE
PATHOPHYSIOLOGY
Heat loss can occur via four distinct mechanisms
Evaporation: direct absorption of body heat by water
(sweat)
Conduction: direct loss of heat via contact with colder object
Convection: heat loss via movement of current/airflow
Radiation: direct loss of body heat to air
Patients at highest risk for frostbite have decreased awareness
of cold, loss of instinct to seek shelter, loss of shivering reflex,
and/or cutaneous vasodilation. An easy way to remember these
risk factors is the “I’s” of frostbite (from Mohr, 2009).
Intoxicated (alcohol or other drugs)
Incompetent (patients with mental illness or dementia)
Infirm (elderly patients ± falls)
Insensate (extremity neuropathy)
Inducted (increased risk in wartime)
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Inexperienced (those new to cold climates)
Indigent (homeless)
SPECTRUM OF COLD INJURY (TABLE
10-2)
Table 10-2 The Spectrum of Cold Injury
The spectrum of cold injury relates to:
How rapidly the body part is cooled.
Presence or absence of ice crystals in the tissue.
Rapid freezing causes intracellular ice crystallization,
leading to architectural damage and cell death.
Slow freezing causes extracellular ice crystallization,
leading to intracellular dehydration from osmotic fluid
shift out of cells.
Frostnip is a mild, reversible cold injury with skin pallor,
pain, and local numbness.
Pernio or chilblains is a more severe cold injury from repeat
exposures to near-freezing temperatures. This presents as
violaceous nodules and plaques with local pain and pruritus
on repeat cold exposure.
Flash freezing occurs when tissue is rapidly cooled,
resulting in ice crystal formation. An example of this would
be licking a metal pole in winter.
PATHOPHYSIOLOGY AND STAGING
Frostbite occurs in response to slow rate of cooling with ice
crystal formation in tissue.
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Ice crystal formation occurs when tissue temperature reaches
28 °F.
Concentrated solutes draw fluid out of cells and ice crystals
subsequently cause cell membrane puncture.
Intravascular ice crystals cause direct vascular damage and
indirect vascular sludging.
With rewarming, tissue thaws from blood vessels outward.
Freeze-induced endothelial damage allows capillary leak that
allows extravasation of polymorphonuclear leukocytes and mast
cells. This results in inflammation, edema, and microvascular
stasis and occlusion.
Blisters will form at 6-24 hours when extravasated fluid collects
beneath detached epidermal sheet. If dermal vascular plexus is
disrupted, hemorrhagic blisters will be present.
Stages of Frostbite
First degree: hyperemia, intact sensation, no blisters on
rewarming, no tissue loss expected
Second degree with blisters containing clear or milky fluid,
local edema, no tissue loss expected
Third degree with hemorrhagic blisters, edematous tissue,
shooting or throbbing pain, and likely tissue loss
Fourth degree with mottled or cyanotic skin, hemorrhagic
blisters, and frozen deeper structures. Mummification
occurs over several weeks.
TREATMENTS AND OUTCOMES
General treatment considerations
Do not rewarm if any chance of refreezing exists.
Multiple freeze-thaw cycles causes multiplicative, not
additive, damage to the affected tissues.
Intact blisters should be left alone. Débride ruptured
blisters and apply bacitracin ointment or silvadene.
Beware of the afterdrop phenomenon during rewarming
Afterdrop occurs when central rewarming results in
peripheral vasodilation.
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