Download Frostbite Gang Wang M.D.

Frostbite
LENG RUPU
Chapter Outline
History, Physiology, Pathophysiology, Clinical
presentation, Treatment, Sequelae, Prevention
HISTORY
Peripheral cold injuries are almost uniquely seen in
humans. Unlike cold-adapted animals, our peripheral
tissue temperatures can drop below freezing. The
highest homeostatic priority is to maintain the core
temperature. This is accomplished through
vasoconstriction and shunting, which prevents
adequate heat distribution to the extremities. As a
result, failure to achieve adequate protection from
the environment results in these preventable injuries.
Peripheral cold injuries include both freezing and
nonfreezing syndromes. These may occur
independently or in conjunction with systemic
hypothermia. Frostbite is the most common freezing
injury. Trench foot and immersion foot are
nonfreezing injuries resulting from exposure to wet
cold. Nonfreezing injury following exposure to dry
cold is termed chilblains (pernio).
one unique aspect of peripheral cold injury is the
pathogenesis of the freezing injury cascade.
Most civilian frostbite results from routine exposure
without consideration of risk factors. Increased
participation in outdoor recreational activities will
continue to produce exposure to unanticipated drastic
climactic changes. The unsheltered and the homeless
are no longer the most likely group at risk.
Military history is replete with accounts of the effects
of cold injury on combat troops. Trench foot was
particularly common among U. S. troops in the
Vietnam War.
soldiers would acutely thaw frozen extremities
directly over open fires. The subsequent refreeze
further increased tissue destruction.
Unfortunately, the resultant gangrene was
misattributed to this rapid thawing of frostbite and
trench foot injuries. Therefore gradual thawing, often
including friction massage with snow, remained the
standard treatment regimen until the 1950s. In addition
to dry radiant heat rewarming and massage, another
common rewarming modality was immersion thawing
in icy water.
PHYSIOLOGY
Human cold stress should produce adaptive behavioral
reactions in addition to complex endocrinologic and
cardiovascular physiologic responses. Peripheral
cooling of the blood activates the preoptic anterior
hypothalamus. This central thermostat orchestrates
temperature regulation. The dynamic process
encompasses catecholamine release, thyroid stimulation,
shivering thermogenesis, and peripheral
vasoconstriction. Consumption of stored fuels is
accelerated. The elevated metabolic rate eventually
fatigues with a chronic cold insult.
Acral skin structures (fingers, toes, ears, nose)
contain a plethora of arteriovenous anastomoses .
These facilitate shunting and subsequent drastic
reductions in blood flow to these areas. During a cold
stress peripheral vasoconstriction limits radiative heat
loss. This”life-versus-limb” mechanism reflects the
hemeostatic attempt to prevent systemic
hypothermia.
In contrast to heat exposure, humans do not appear to
display significant physiologic adaptation to the cold,
Exposing extremities to cold temperatures down to
15℃ results in maximal peripheral vasoconstriction
with minimal blood flow. Continued exposure to
progressively colder temperatures down to 10℃
produces the ``hunting response,'' which is termed
cold-induced vasodilatation (CIVD). These periods
of vasodilatation, recurring in 5-to-10-minute
cycles, interrupt vasoconstriction and serve to
protect the extremity. Eskimos, as well as Lapps and
others of Nordic extraction, are capable of stronger
CIVD responses than individuals from tropical regions.
PATHOPHYSIOLOGY
The pathologic phases that occur with local cold
injury often overlap and vary with the extent and
rapidity of the cold response (see box below).
Frostbite occurs when the tissue temperature
drops to below 0℃. There are two putative
mechanisms of tissue injury: architectural cellular
damage from ice-crystal formation and
microvascular thrombosis and stasis.
Freezing Injury Cascade
Prefreeze phase
1.
Superficial tissue”cooling”
2.
Increased viscosity of vascular contents
3.
Microvascular constriction
4.
Endothelial plasma leakage
Freeze-thaw phase
1.
Extracellular fluid ice-crystal formation*
2.
Water diapedesis across cell membrane
3.
Intracellular dehydration and hyperosmolality
4.
Cell-membrane denaturation/disruption
5.
Cell shrindage and collapse
Vascular stasis and progressive ischemia
1.
Vasospasticity and stasis coagulation
2.
Arteriovenous shunting
3.
Vascular endothelial cell damage/prostanoid release
4.
Interstitial leakage/tissue hypertension
5.
Necrosis/demarcation/mummification/slough
*Extremely rapid cooling produces more initial intracellular than extacellular ice crystallization.
Nerve and muscle tissues are more susceptible to
cold injury than connective tissue. For example,
nonviable hands and feet can be moved after thawing
if the tendons are intact.
Edema progresses for 48 to 72 hours after tissue
has been thawed. Leukocyte infiltration, thrombosis,
and early necrosis become apparent as this edema
resolves. The dry gangrene carapace of frostbite is
superficial in comparison to arteriosclerotic induced
full-thickness gangrene. Final demarcation between
viable and nonviable tissue often requires more than
60 to 90 days. Hence the surgical aphorism,
``Frostbite in January, amputate in July”.
Predisposing Factors
Physiologic
Genetic
Core Temperature
Prior cold injury
±Acclimatization
Dehydration
Overexertion
Trauma:multisystem/extremity
Dermatologic diseases
Physical conditioning
Diaphoresis/hyperhidrosis
Hypoxia
Cardiovascular
Hypotension
Atherosclerosis
Arteritis
Raynaud’s syndrome
CIVD
Anemia
Sickle cell disease
Diabetes
Hypovolemia; shock
Vasoconstrictors/vasodilators
Psychologic
Mental status
Fear/panic
Attitude
Peer pressure
Fatigue
Intense concentration on tasks
Hunger; malnutrition
Intoxicants
Environmental
Ambient temperature
Humidity
Duration of exposure
Wind chill factor
Altitude±associated conditions
Orantity of exposed surface area
Heat loss: conductive, evaporative
Mechanical
Constricting/wet clothing
Tight boots
Vapor barrier/alveolite liners
Inadequate insulation
Immobility/cramped positioning
CLINICAL PRESENTATION
Symptoms
The symptoms of frostbite usually reflect the severity
of the exposure. All patients will have some initial
sensory deficiency in light touch, pain, or
temperature. The most common presenting symptom
is numbness, present in over 75% of patients.
Anesthesia is produced by intense vasoconstrictive
ischemia and neuropraxia.
Patients often complain of clumsiness and report a
``chunk of wood'' sensation in the extremity.
``Frostnip'' is a superficial cold insult manifested by
transient numbness and tingling that resolves after
rewarming. This does not represent true frostbite
because there is no tissue destruction.
Chilblains (pernio) is a mild form of dry-cold
injury often following repetitive exposure. These
``cold sores'' usually affect facial areas and the
dorsum of the hands and feet. Persistent vasospasm
and vasculitis result in pruritus, erythema, and mild
edema. Plaques, blue nodules, and ulcerations can
develop. Trench foot (immersion foot) is produced
by prolonged exposure to wet cold at temperatures
above freezing. Initially the feet often appear
cyanotic, cold, and edematous. There is often
numbness and leg cramping. After warming, the skin
remains erythematous, dry, and very painful to touch.
Vesiculation proceeds to ulceration and liquefaction
gangrene in severe cases.
Signs
Classically, the initial presentation of frostbite is
deceptively benign. Frozen tissues will often appear
mottled or violaceouswhite, waxy, or pale yellow.
Favorable presenting signs include normal sensation,
warmth and color. Soft, pliable subcutaneoustiss..
suggests a superficial injury. A residual violaceous
hue after rewarming is ominous. Lack of edema
formation may also suggest significant tissue damage.
Postthaw edema usually develops in less than 3 hours.
In severe cases, frostbitten skin forms an early black,
dry eschar until mummification and apparent
demarcation.
Classification
Historically, frostbite has been classified into degrees
of injury similar to burns. Anesthesia and erythema are
characteristic of first-degree frostbite. Superficial
vesiculation surrounded by edema and erythema is
considered second degree. Third-degree frostbite
produces deeper hemorrhagic vesicles . Fourth-degree
injuries extend into subcuticular osseous and muscle
tissues.
Classification by degrees is often prognostically
incorrect and thus therapeutically misleading. Mills
suggests two simple classifications. Superficial or
mild frostbite does not entail tissue loss, whereas
deep or severe does
TREATMENT
Prehospital
The ultimate goal of prehospital treatment is
preservation of life. Since accidental hypothermia
and frostbite often coexist, prevention of further
systemic heat loss is the highest priority.
Field rewarming of frozen tissue is rarely practical.
If possible, remove constricting or wet clothing.
Gently insulate and immobilize the affected areas.
Friction massage is not efficacious, and will increase
tissue loss. Frozen parts should be kept away from
dry heat sources in the transport vehicle to prevent
a gradual partial thaw.
Emerpency Department
Prethaw: obtain pertinent history regarding the
ambient temperature, wind velocity, and duration of
exposure. Determine the type of apparel and the
circumstances surrounding rescue. Document
preexistent cardiovascular or neurologic diseases that
could affect tissue loss. After stabilizing the core
temperature and addressing associated conditions,
prepare to initiate rapid thawing.
Thaw: Frozen or partially thawed tissue should be
rapidly and actively rewarmed by immersion in
gently circulating water. Carefully maintain the
temperature at 40 to 43℃ by thermometer measurement.
They are invariably hypothermic and at risk for
significant fluid and electrolyte fluxes during
rewarming. The acute thawing of large amounts of
distal musculature extinguishes peripheral
vasoconstriction. This results in the sudden return of
cold, hyperkalemic, acidotic blood to the central
circulation. This ``core temperature after-drop'' is
dysrhythmogenic. In the most severe cases,
extracorporeal rewarming should be considered to
manage these massive metabolic and electrolyte
derangements .
Emergency Department Rewarming Protocol
Prethaw
•Protectpart
•Stabilize core temperature
•Address medical/surgical conditions
•Hydration
•Nofriction massage
Thaw
•Rapid rewarming in 38℃-41℃ circulating water until distal flush
(thermometer monitoring)
•Requires 10-30 min with active motion of part without friction massage
•Parenteral analgesia
Postthaw
•Clear vesicles –aspirate (if intact) vs. debride
•Hemorrhagic vesicles – aspirate
•Apply topical aloe vera (Dermaide) q6h
•Ibuprofen 400 mg q12h
•Tetanus prophylaxis
•Streptococcal prophylaxis for 48-72hr
•Elevation
SEQUELAE
Sequelae
Neuropathic
Pain
Phantom
Causalgia
“Tabes” burning
Chronic
Sensation
Hypesthesia
Dysesthesia
Paresthesia
Anesthesia
Thermal sensitivity
Heat
Cold
Autonomic dysfunction
Hyperhidrosis
Raynaud’s
Musculoskeletal
Atrophy
Compartment syndrome
Rhabdomyolysis
Tenosynovitis
Stricture
Epiphyseal fusion
Osteoarthritis
Osteolytic lesions
Necrosis
Amputation
Dermatologic
Edema
Lymphedema
Chronic/recurrent ulcers
Epidermoid/squamous carcinoma
Hair/nail deformities
Miscellaneous
Core temperature afterdrop
Acute tubular necrosis
Electrolyte fluxes
Psychic stress
Gangrene
Sepsis
Electrical Injures
EPIDEMIOLOGY
The first report of electrical injury from man-made
sources occurred in 1746 after the development of the
capacitor.
The first recorded death due to electrical current
from a man-made source was reported in 1879, when
a carpenter in Lyons, France, inadvertently contacted
a 250- volt AC dynamo. The first U. S. fatality
occured in 1881, when a local inebriate, Samuel W.
Smith, passed out on a generator in front of a crowd
in Buffalo, New York.
The apparent painlessness of his death impressed the
crowd, and electrocution began to be thought of as a
``humane'' mode of execution. In 1890 William
Kemmeler became the first man to be put to death in
New York State's electric chair.
Electrical burns account for 4% to 6.5% of all
admissions to burn units
PATHOPHYSIOLOGY
The exact pathophysiology of electrical injury is not
well understood because of the large number of
variables that cannot be measured or controlled when
an electrical current passes through tissue. Most of the
injury appears to be thermal, and most histologic
studies reveal coagulation necrosis consistent with
thermal injury. A magnetic field exists wherever an
electric current passes, there may be magnetic effects.
Factors Determining Electrical Injury
Type of circuit
Resistance of tissues
Amperage
Voltage
Current pathway
Duration
Environmental factors
Type of Circuit
The type of circuit, alternating current (AC) vs.
Direct current (DC), will help to determine the
severity of the injury. High-voltage DC tends to
cause a single muscle spasm, often throwing the
victim from the source. This results in a shorter
duration of exposure but increases the likelihood of
traumatic blunt injury. It is well-known that contact
with a DC source can result in disturbances in
cardiac rhythm, depending on the phase of the
cardiac cycle affected, a phenomenon that is utilized
in the common defibrillator.
AC tends to be three times more dangerous than
direct current of the same voltage.
The hand is frequently the site of entry as it grasps
a tool that comes into contact with an electric source.
Because the flexors of the hand and forearm are
much stronger than the extensors, contraction of the
flexors at the wrist, elbow, and shoulder occur,
causing the hand holding onto the current source to
pull the source even closer to the body. At currents
above the let-go threshold (6 to 9 mA) this can result
in the victim's being unable to voluntarily release the
current source, prolonging the duration of exposure
to the electrical current.
Resistance
The Row of electrical energy through a substance is
described by Ohm‘s law:
R = V/I
Resistence(R) of a tissue , electrical energy(I) to
thermal energy(P) at any given current as described
by Joule's Law:
P=I2×R
Duration
In general the longer the duration of contact, the
greater the degree of tissue destruction.
Current
Current, expressed in amperes, is a measure of the
amount of energy that flows through an object.
Voltage
Voltage is a measure of potential difference
between two points and is determined by the
electrical source.
Effects of Amperage Levels in Milli-ampheres(mA)
Tingling sensation
1-4
Let-go current
Children
4
Women
7
Men
9
Freezing to circuit
10-20
Respiratory arrest from thoracic muscle tetany 20-50
Ventricular fibrillation
50-100
Pathway
The pathway that a current takes determines the
tissues at risk, the type of injury seen, and the degree
of conversion of electrical energy to heat. Current
passing through the heart or thorax can cause cardiac
dysrhythmias and direct myocardial damage. Current
passing through the brain can result in respiratory
arrest, seizures, and paralysis. Current passing close to
the eyes can cause cataracts. It has been suggested that
current flowing through the left side of the body may
be more dangerous than through the right side or one
isolated to an extremity.
As the cross-sectional diameter of the tissue a given
current passes through increases the less heat is
generated, and less damage occurs as the energy is
``diluted‘’ by the tissue.
Because the current is often concentrated at the
entrance and exit sites, the greatest degree of damage
is often observed there, although deep destruction of
the tissues in between may often occur, leading some
to describe the surface damage as only ``the tip of
the iceberg.
MECHANISMS OF INJURY
The mechanisms of electrical injury are listed in the
box below. Obviously the victim who becomes part of
an electrical circuit, particularly if it is of high voltage,
may suffer significant injury. Nonconductive thermal
injury can occur by several mechanisms.
The most destructive indirect injury occurs when a
victim becomes part of an electrical arc. it can
cause very deep thermal burns . Sometimes the arc
may cause clothing to ignite, resulting in secondary
thermal burns. The electrical flash burn. a third
mechanism of nonconductive injury, usually results in
only superficial partial thickness.
Traumatic injury is frequently seen in patients
sustaining electrical injury because they may be
thrown clear of the source by intense contraction of
their muscles or by falling from a height.
The histologic changes seen in muscle injury are
coagulation necrosis with shortening of the sarcomere.
Vascular damage is greatest in the media, possibly
because of the diffusion of heat away from the intima
by the flow of blood, but can lead to delayed
hemorrhage when the vessel eventually breaks down.
Intimal damage may result in either immediate or
delayed thrombosis and vascular occlusion
Damage to neural tissue may occur from many
mechanisms. It may show an immediate drop in
conductivity as it undergoes coagulation necrosis similar
to that observed in muscle tissue. In addition, it may
suffer indirect damage as its vascular supply or myelin
sheath is injured.
The brain is frequently injured, focal petechial
hemorrhages in the brainstem, widespread chromatolysis,
and cerebral edema.
Immediate death in electrical injury may be from
asystole, ventricullar fibrillation, or respiratory
paralysis, depending on the voltage and pathway.
Mechanisms of Injury
Direct contact
Arc
Flash
Thermal
Blunt trauma
CLINICAL FINDINGS
Prehospital Considerations
When first reaching the scene, paramedic personnel
should secure the area so that no other injuries can
occur to bystanders or rescuers. It is essential that the
power source be turned off Although many approaches
to this have been touted, Use of electrical gloves by
emergency medical service (EMS) groups has been
condemned,
A downed high-tension line may jump as it repowers
periodically (similar to a water hose that jumps when
turned off and on) and may land anywhere in its radius,
causing more injuries. Therefore the rescue vehicle
should park at least one entire span away from the line.
The victim of an electrical incident should be
approached like any other trauma patient because the
person may have suffered injury as a result of violent
muscle contraction or a fall, in addition to having
severe burns that are often more extensive than they
initially appear. Attention should be paid to the
airway, breathing, and circulation. High-flow
oxygen and intubation should be provided if
necessary. Cardiac monitoring is essential. If the
victim has experienced cardiac arrest, standard
advanced life support protocols should be instituted.
Emergency Department Assessment
History.
Specific injuries:
Cardiovascular System. Cardiac arrest, either
from asystole or ventricular fibrillation, is a common
presenting condition in electrical accidents.
Skin. Skin injury are burns. The most common
sites of entry for the current include the hands and
the skull. The most common areas of exit are the
heels. painless, depressed, yellow-grey, punctate
areas with central necrosis.
Extremities. Muscle necrosis Massive release of
myoglobin from the damaged muscle may lead to
myoglobinuric renal failure.
Vascular damage Damage to the vessel wall at the
time of injury can result in delayed thrombosis and
hemorrhage, especially in the small arteries to the
muscle. Progressive loss of muscle because of vascular
ischemia downstream from damaged vessels may lead
to the need for repeated deep debridements.
`kissing burn," occurs at the flexor creases.
Nervous System. Loss of consciousness is common
and usually transient, Patients may exhibit confusion
flat affect, and difficulty with short-term memory and
concentration. A seizure may occur after electrical
injury . Peripheral nerve damage in extremities
sustaining injury is common, and recovery is usually
poor.
Other Viscera.
Skeletal System.
Eyes. Cataracts develop in approximately 6% of
cases
Mouth. Mouth burns secondary to sucking on
household electrical extension cords are the most
common electrical injury seen in children under 4
years of age.
Complications
Primary Complications and Causes of
Death in order of Occurrence
Cardiopulmonary arrest
Overwhelming injuries
Cardiac arrhythmias
Hypoxia and electrolytes
Intracranial injuries
Myoglobinuric renal failure
Abdominal injuries
Sepsis
Tetanus
Iatrogenic
Suicide
TREATMENT
Resuscitation. Once the accident scene is controlled.
a quick initial assessment of the patient is indicated,
with attention to the airway, breathing, and circulation.
Cardiac monitoring is helpful and cardiopulmonary
resuscitation (CPR) should be initiated, if indicated,
with institution of advanced life support.
Cardiac monitoring is more controversial and is
probably only necessary for the severely injured
patient and for those who have the indications listed
in the Box below.
Indication for Electrocardiographic Monitoring
Cardiac arrest
Documented loss of consiousness
Abnormal ECG
Dysrhythmia observed in prehospital or emergency
department setting
History of cardiac disease
Presence of significant risk factors for cardiac disease
Concommitant injury severe enough to warrant addmission
Suspicion of conductive injury
Hypoxia
Chest pain
Rhabdomyolysis. Patients with heme pigment in the
urine should be treated as though they have
myoglobinuria.
Burn Wound Care.
Extremity Injuries. The current trend with regard to
damaged extremities favors early and aggressive
surgical management, including early decompressive
escharotomy, fasciotomy, carpal tunnel release, or
even amputation of an obviously nonviable extremity.
Extremities should be splinted in functional position to
minimize edema and contracture formation.
DISPOSITION
All patients with significant electrical burns should
be stabilized and transferred to a regional burn center
if possible.
Electrical injury during pregnancy from low voltage
sources has been reported to result in stillbirth.
Obstetric consultation should probably be obtained in
all pregnant patients reporting electrical injury,
Treatment of pediatric patients with oral burns is
more controversial. In general, these patients need
surgical and dental consultation for planning of
debridement, oral splinting and occasionally,
reconstructive surgery.
Lightning Injuries
EPlDEMlOLOGY
As would be expected, lightning incidents are most
common where there are more thunderstorms,
They also occur more frequently during the times
that people tend to be outdoors, in the afternoon and
early evening, and during the thunderstorm season,
May to September.
Lightning incidents were once most frequently
reported among farmers.
With the population shift to the cities, where
lightning strikes are less frequent, those most
commonly reported in lightning incidents are campers,
joggers and other athletes, and construction workers.
LIGHTNING PRODUCTION
Lightning is produced from the static charges that
occur as a cold high-pressure front moves over a
warm, moist, low-pressure area. The warm, moist air
rises through the cold air, allowing the moisture to
condense into a cloud. The friction of moving air
particles within the cloud causes ionization and
complicated energy changes .
In most cases the lightning begins as a leader stroke
from a cloud and takes a slow, jagged, irregular path
downward the oppositely charged earth below the
storm cloud.
A pilot stroke rising from ground upward cloud
cause the column of ionized air to flicker and
brighten momentarily as massive amounts of energy
are discharged. Although the majority of the
lightning discharge occurs in an upward direction,
lightning is perceived as a downward stroke because
of the irregular, weak, slower leader stroke.
MYTHS AND MISTREATMENTS
From ancient times lightning has played a prominent
part in the religions and folklore of many cultures,
giving rise to many superstitions and myths.
Unfortunately many of these myths persist today,
including some in the medical literature. They include:
1. Lightning is always fatal.
2. Lightning burns can turn victims into “crispy critters”.
3. Lightning never strikes in the same place twice.
4. Victims of lightning strikes remain electrified.
5. The bodies of victims of lightning strikes can remain in
“suspended animation”.
6. Lightning injuries are like other high-voltage injuries.
Because of the general lack of experience of most
urban physicians with lightning injuries, a great deal
of confusion exists between lightning injuries and
other high-voltage electrical injuries. Usually much
less energy is imparted to the lightning victim than to
the victim of regular high-voltage exposure, and
consequently far less injury occurs. Although the
body's electrical systems may be short-circuited by
lightning, resulting in cardiac arrest, tinnitus,
temporary blindness, and paralysis, injuries typical of
man-made high-voltage electricity such as burns,
myoglobinuria, and deep-muscle damage are rare.
PATHOPHYSIOLOGY OF
LIGHTNING INJURY
Mechanisms of Lightning Injury
Direct strike
Contact
Side flash, "splash"
Ground current or step voltage
Blunt trauma
A direct strike is self-evident. Injury from contact
occurs when the person is touching an object that is
part of the pathway of lightning current. Side flash or
splash occurs as lightning jumps from its pathway to a
nearby person.
Step voltage occurs as a result of lightning current
spreading radially through the ground. A person who
has one foot closer than the other to the strike point
will have a potential difference between his or her feet
so that a current may be induced through the legs and
body. This is a frequent killer of large livestock such as
cattle and horses because of the distance between their
hindlegs and forelegs.
Blunt injury can occur from two mechanisms. (1) the
person may be thrown a considerable distance by the
opisthotonic contraction caused by current passing
through the body or (2) from the explosive/implosive
force caused as the lightning pathway is instantaneously
superheated and then rapidly cooled after the passage of
the lightning is over. The heating is seldom long enough
to cause severe burns but does cause rapid expansion of
air followed by rapid implosion of the cooled air as it
rushes back into the void.
Factors Governing Electrical Injuries
Type of circuit(AC or DC)
Duration
Voltage
Amperage
Resistance of tissues
Pathway
Not only is there an absolute energy difference, but
the duration of lightning is so incredibly short that
the energy seldom has time to break down the skin
and cause any significant internal current flow or
tissue damage. Thus the pathway is also different. As
with metal conductors, the vast majority of the
current travels around the outside of the conductor,
``flashing over'' the outside of the victim.
Although a small amount of current may leak
internally, causing short-circuiting of electrical
systems such as the heart, respiratory centers, and
autonomic nervous system or causing spasm of
arteries and muscles, lightning seldom causes any
significant burns or tissue destruction. Thus burns and
myoglobinuric renal failure play a small part in the
injury pattern, whereas cardiac and respiratory arrest,
vascular spasm, and autonomic instability play a much
greater role.
PREHOSPlTAL
CONSIDERATIONS
The prehospital personnel must remember that
lightning can strike the same place twice and guard
themselves against also becoming victims.
The major cause of death in lightning injuries is
cardiorespiratory arrest. victims are unlikely to die of
any other cause. Thus triage of lightning victims
should concentrate on those who appear to be in
cardiorespiratory arrest. Lightning acts as a massive
DC countershock, sending the heart into asystole.
Although automaticity may lead to the heart
restarting, the respiratory arrest often lasts longer
than the cardiac pause and may lead to a secondary
cardiac arrest with ventricular fibrillation from
hypoxia.
CLINICAL FINDINGS
Patients may present with little evidence of injury
or, alternately, cardiopulmonary arrest. After initial
resuscitation, additional, rarely life-threatening,
conditions may be identified.
Head and Neck. including skull fractures, Over
50% of victims have at least 1 tympanic membrane
ruptured. Although most recover without serious
sequelae, disruption of the ossicles and mastoid may
occur, as well as cerebrospinal fluid otorrhea,
hemotympanum, and permanent deafness.
Cataracts may occur. Other injuries to the eyes may
occur.Cervical spine injury may be caused by a fall or
being thrown.
Cardiopulmonary. Pulmonary contusion and
hemorrhage have been reported. Cardiac damage or
arrest caused by either the electrical shock or induced
vascular spasm may occur. Numerous dysrhythmias
have been reported in the absence of cardiac arrest.
Nonspecific ST-T wave-segment changes may occur,
and serum levels of cardiac enzymes are sometimes
elevated. Hypertension is often present initially but
usually resolves in an hour or two so that treatment is
not usually
Abdominal. Blunt abdominal injuries have been
reported but are rare. None of the other intraabdominal
catastrophies associated with electrical injury (e.g. gallbladder necrosis, mesenteric thrombosis) have been
reported with lightning injury.
Extremities. On initial presentation, two-thirds of the
seriously injured patients have keraunoparalysis with
lower and sometimes upper extremities that are blue,
mottled, cold, and pulseless because of vascular spasm
and sympathetic nervous system instability. Generally
this clears within a few hours, although some patients
may be left with permanent paresis or paresthesias.
Skin. The skin may show no signs of injury initially.
Deep burns occur in less than 5% of the reported
injuries. As mentioned previously, burns are usually
superficial, if present at all. They consist of four types
(see box below and Fig. 1).
Lightning Burns
Linear
Punctate
Feathering
Thermal
COMPLICATIONS
Complications of lightning injury fall into two areas.
(1) those which could be reasonably predicted from the
presenting signs and which can be treated routinely (i.
e. ,hearing loss from tympanic membrane rupture,
paresthesias and paresis from neurologic damage) and
(2) those complications which are iatrogenically
caused by over-aggressive management.
Lightning injuries tend to cause few external or internal
burns, rarely myoglobulinuria, and little tissue loss,
although there may certainly be permanent functional
impairment. As a result, treatment of lightning victims
seldom requires massive fluid resuscitation, fasciotomies
for compartment syndromes, mannitol and furosemide
diuretics, alkalinization of the urine, amputations, or
large repeated debridements. In fact, most lightning
victims, particularly those with head injuries, should
probably have their fluids restricted to decrease the
likelihood of cerebral edema.
DIFFERENTIAL DIAGNOSIS
Differential Diagnosis
Cardiac dysrhythmias
Myocardial infarction
Cerebrovascular accident
Subarachnoid hemorrhage
Seizures
Closed-head injury
Spinal cord trauma
Tick-bite paralysis
Heavy-metal poisoning
TREATMENT
Initial care must be given to the ABCs (airway,
breathing, and circulation), with primary attention
going to those in cardiac arrest or near arrest.
All victims should be transported to a hospital and
receive an ECG, cardiac isoenzyme level study,
urinalysis for myoglobin, CBC, and other tests and xray studies as appropriate for their injuries. Most
should be monitored for 24 hours and receive
standard antidysrhythmia medications if they develop
any signs of cardiac irritability.
The vast majority of lightning victims will behave as
though they have had electroconvulsive psychiatric
therapy and will be confused and have an anterograde
amnesia covering several days after the incident. If
any neurologic deterioration occurs, CT or MRI
scanning is indicated to rule out intracranial
hemorrhage.
Long-term sequelae include insomnia and other
sleep disturbances, anxiety attacks, decrease in fine
mental functions, fear of storms, and paresthesias and
paresis of affected extremities.
Arctic Bear