Transcript Frostbite and Hypothermia March 10 , 2005 Tintinalli Chapters 191 and 192

Frostbite and Hypothermia
March 10th, 2005
Tintinalli Chapters 191 and 192
George Filiadis
Epidemiology
• Frostbite is the inability to physiologically
compensate for cold that produces injury.
• Duration of exposure, humidity, wind, altitude,
clothing, medical conditions, behavior, and
individual variability are contributing factors.
• Inadequate clothing is the most preventable cause
of cold related injuries with exposed head and
neck accounting for 80% of heat loss.
• Alcoholic or drug-intoxicated persons acount for
the majority of frostbite cases in the US.
Epidemiology
• Disease states as atherosclerosis, arteritis,
hypovolemia, diabetes, vascular injury may
predispose to cold-related injury.
• Dark-skinned people and those from
warmer climates are more susceptible to
frostbite.
• Local cold-related injuries are classified
into nonfreezing and freezing injuries
Nonfreezing cold
injuries:chilblains and trench foot
• Chilblains is characterized by mild but
uncomfortably inflammatory lesions of the skin of
bared body areas caused by intermittent exposure
to damp, nonfreezing ambint temperatures.
• Hands, ears, lower legs, and feet are most
commonly affected.
• Cutaneous manifestations which appear 12 h after
exposure include localized edema, erythema,
cyanosis, plaques , nodules , ulcerations, and
vesicles.
Chilblains
• Pt may complain of pruritus and burning
paresthesias.
• Rewarming may result in formation of
tender blue nodules.
• More common in children and women ,
especially the ones with Raynaud
phenomenon.
Trench Foot
• It involves direct injury to soft tissue sustained
from prolonged cooling and is accelerated by wet
conditions
• Peripheral nerves are more sensitive to this form
of injury.
• It develops over hours to days and is reversible
initially.
• On physical exam, the foot is pale, mottled,
anesthetic , pulseless, and immobile which does
not change after rewarming.
Trench Foot
• A hyperemic phase begins within hours after
rewarming and is associated with severe burning
pain and reappearance of proximal sensation.
• Perfusion returns to the foot over 2 to 3days,
edema and bulla form, and the hyperemia may
worsen.
• In severe cases, tissue sloughing and gangrene
may develop.
• Hyperhidrosis and cold sensitivity are common
late features and may persist for months to years.
Treatment
• Treatment of chilblains is supportive
-affected skin should be rewarmed,
gently bandaged, and elevated.
-Some European studies suggest
nifedipine, pentoxifylline, or an oral
analogue of PGE1, limaprost.
-Topical corticosteroids or even oral
corticosteroids have been shown to be
useful.
Treatment
• Treatment for trench foot includes
-keeping warm, good boot fit
-changing out wet socks several times
a day
-dry, elevate feet
pentoxifylline or limaprost can be used
Freezing Cold injuries:Frostnip
and frostbite
• At 10 0Cof skin temperature cutaneous blood flow
becomes negligible, with occurrence of 5-10 min
cycles of vasodilation and vasoconstriction.
• As cooled blood is carried back from the
extremities, the core temperature falls.
• The body attempts to maintain thermal integrity
by shutting down flow to the coldest extremities.
• This begins the phase I of frostbite with ice crystal
formation in the extracellular space that leads to
an intacellular dehydration and hyperosmolarity
by pulling of fluids.
Freezing cold injuries:Frostnip
and Frostbite
• As proteins get denatured , intracellular ice
crystals form.
• Phase II is characterized by reperfusion injury as
the extremity gets rewarmed which leads to
endothelium leakage, leakage of destructive
prostaglandins and oxygen free radicals,
vasoconstriction an arteriovenous shunting, and
finally necrosis and gangrene.
Freezing Cold Injuries:Frostnip
and Frostbite
• Frostbite can be divided in three zones:
• zone of coagulation is the most severe, usually
distal and irreversible
• zone of hyperemia is the most superficial,
typically proximal with the least cellular damage
and recovers with no treatment.
• zone of stasis is characterized by severe, but
possibly reversibly cell damage that can benefit
from treatment.
Clinical features
• Classification of frostbite
-first degree is characterized by partial skin
freezing, erythema, mild edema, lack of blisters,
and occasional skin desquamation, has excellent
prognosis.
-second degree is characterized by fullthickness skin freezing, formation of substantial
edema over 3 to 4 h, and formation of clear
blisters that desquamate to form black eschars and
has good prognosis.
Clinical Features
• Classifications (continued)
third degree injury is characterized by damage that
extends into the subdermal plexus and leads to
formation of hemorrhagic blisters, skin necrosis
and a blue-gray discoloration of skin, has poor
prognosis
fourth degree injury is characterized by extension
into subcutaneous tissues, muscle, bone, and
tendon, there is little edema, nonblanching
cyanosis, bloody blebs, has extrememly poor
prognosis.
Treatment in the field
• Remove wet and
constrictive clothing.
• Elevate and wrap in dry
sterile gauze the involved
extremities.
• Rapid rewarming if rapid
access to hospital
• 400 to 420 C clean water
should be used
• There is controversy with
regards to debridement of
clear blisters on the field
• Pain management should
start with NSAIDS to
counteract the arachidonic
acid cascade, in addition
to opioids
• Smoking should be
discouraged
Treatment in the ED
• Injured extremity should
be placed in circulating
water at a temperature of
400 to 420 C for
approximately 10-30 min
until the distal extremity is
pliable and erythematous
• Pain should be treated
with parenteral antibiotics
• Clear blisters should be
debrided or aspirated
• Hemorrhagic blisters
should not be debrided
• Alo vera cream should be
applied to the blisters
• Role of antibiotics is
unclear.
• Staph aureus, Staph epi,
beta-hemolytic Strep,
Pseudomonas, and
Enterococus are important
pathogens.
Treatment in ED
• Infection prophylaxis
using topical
bacitracin is as good
as IV penicillin.
• Tetanus immunization
status should be
assessed.
• Ibuprofen
• Early surgical
intervention is not
indicated in treatment
of frostbite
• Amputation if needed
within 3 weeks
Disposition
• Admit all but the most isolated and
superficial frostbite cases.
• Homeless or elderly should never be
discharged into subfreezing temperatures.
• If hospital is not equipped to treat the
degree of severity, transfer pt after the initial
rewarming.
Hypothermia
Epidemiology
• Hypothermia is defined as temperature of
less than 350C (950F).
• An average of 700 people die from
hypothermia in the United States annually.
• Half of those who die are older than 65
years of age.
• Extremes of age and those with altered
sensorium are susceptible to hypothemia.
Temperature homeostasis
• Heat loss can occur either by conduction,
convection, radiation , or evaporation.
• Conduction is the transfer of heat by direct contact
down a temperature gradient, e.g. from warm body
to the cold environment.
• Convection is the transfer of heat by the actual
movement of the heated material, e.g. wind
disrupting the layer of warm air surrounding the
body.
Temperature homeostasis
• Radiation is the loss of heat from noninsulated
body areas.
• Evaporation causes heat loss by evaporation of
water contained in exhaled water-saturated air
• Opposing mechanisms to heat loss is conservation
and gain which are controlled by the
hypothalamus.
Temperature homeostasis
• Heat is conserved by peripheral vasoconstriction
and importantly, by behavioral responses (dressing
up or coming inside).
• Heat gain is effected by shivering and by
nonshivering thermogenesis which consists of
increase in the metabolic rate brought out by
increased output from the thyroid and adrenal
glands.
Etiology
• “Accidental”(envirom
ental)
• Metabolic
• Hypothalamic and
CNS dysfunction
• Drug-induced
• Sepsis
• Dermal disease
• Acute incapacitating
illness
• Iatrogenic (fluid
resuscitation)
Etiology
• Accidental hypothermia is divided into immersion
and nonimmersion cold exposure.
• Metabolic causes include hypothyroidism,
hypoadrenalism, hypoglycemic, and
hypopituitarism.
• Hypothalamic and CNS dysfunction include head
trauma, tumor , stroke, Wernicke disease
• Drug-induced hypothermia is usually due to
ethanol that causes vasodilation, insulin and other
hypoglycemic agents.
Etiology
• Sepsis may alter the hypothalamic temperature set
point.
• Dermal disease like burns or exfoliative dermatitis
may prevent cutaneous vasoconstriction and
increase trascutaneous water loss.
• Hypothermia may be also induced by fluid
resuscitation with either room-temperature fluid or
cold blood.
Pathophysiology and Clinical
Features
• Mild hypothermia consists of temperature between
320C 350C,where the patient tries to retain and
generate heat (responsive stage)
• When temp falls below 320C, there is a
progressive slowdown of the bodily functions and
metabolism (adynamic stage).
• Shivering ceases when when body temperature
falls below 300 C.
• In the initial responsive stage, cardiac output ,
heart rate, and blood pressure rise but start to
decline as temperature declines.
Pathophysiology
• At temperatures below 300C, the risk of
dysrhythmias increases.
• The typical progression is from sinus bradycardia
to atrial fibrillation with slow ventricular response,
to ventricular response, and ultimately to asystole.
• The Osborn (J) wave, a slow, positive deflection at
the end of the QRS complex is characteristic
though not pathognomonic of hypothermia.
• ECG changes in hypothermia include T-wave
inversions, PR, QRS, QT prolongation, muscle
tremor artifact .
Pathophysiology
• Pulmonary manifestations include mild tachypnea
initially with progressive decrease in the
respiratory drive and tidal volume, depression of
cough and gag reflexes making aspiration
pneumonia a common complication.
• Hypothermia causes a leftward shift of the
oxyhemoglobin dissociation curve, impairing
oxygen release to tissues.
• CNS manifestations include depression of
consciousness, lethargy, coma, dilated and
unreactive pupils.
Pathophysiology
• Hypothermia impairs renal concentrating abilities
and induces cold diuresis leading to significant
volume losses.
• The immobile hypothermic pt is prone to
rhabdomyolysis.
• The combination of hemoconcentration, coldinduced decrease in blood viscosity, and poor
circulation may lead to intravascular thrombosis
and subsequent embolic complications.
• Pty are prone to DIC and coagulopathies.
Pathophysiology
• Endocrine function is fairly well preserved.
• Pancreatitis may occur in hypothermia.
• Hepatic function is depressed by cold and
drugs metabolized, conjugated or detoxified
by the liver may accumulate rapidly to toxic
levels.
Treatment
• Pt should be handled carefully and gently because
manipulation can precipitate ventricular
fibrillation.
• Oxygen and IVF should be warmed.
• Most dysrhythmias require no therapy and revert
spontaneously with rewarming.
• Hypothermic heart is resistant to atropine, pacing
and countershock.
• In case of V-fib, defibrillate three times, if
unsuccesful do CPR and rapid rewarming, resume
defibrillation when temp reaches 300C.
Drug therapy
• Thiamine 50 mg IV should be given because many
of the hypothermic pt are thiamine-depleted
alcoholics.
• If accu-check shows low sugar give 50-100cc of
50% glucose.
• Administration of antibiotics, steroids , and
thyroid hormone must be individualized.
• Empirical antibiotic therapy is appropriate when a
noninfectious cause of hypothermia cannot be
identified.
Drug therapy
• Hydrocortisone should be given to patients
with history of adrenal insufficiency and
myxedema coma.
• Thyroid hormone replacement is indicated
only in pt with known history of
hypothyroidism, a thyroidectomy scar, or
clinical evidence of myxedema coma.
Rewarming techniques
• Passive rewarming includes removal from cold
environment and insulation.
• Active external rewarming includes warm water
immersion , heating blankets, set at 400C, radiant
heat, forced air.
• Disadvantages of the external include that is
innefective with poor peripheral circulation,
causes topical vasodilation leading to rewarming
shock, can increase lactic acid thus leads to
increase in metabolic demands.
Rewarming techniques
• Active core rewarming includes inhalation
rewarming, heated IV fluids, GI tract lavage,
bladder lavage, peritoneal lavage, pleural lavage,
extracorporeal rewarming, mediastinal rewarming
via thoracotomy.
• Its advanages include that is less irritant to the
myocardium, peripheral vasodilation is avoided
thus there is less chance of shock and acidosis
while its disadvantages include the fact that is
invasive.
Rewarming techniques
• Inhalation rewarming is the administration of
warmed , humidified air or oxygen by face mask
or endotracheal tube.
• IV fluids should be warmed to 400C before
administration.
• GI or bladder lavage with warmed sterile saline is
simple though you have to protect the airway in
obtunded patients.
• Peritoneal lavage allows rapid rewarming using
potassium-free dialysis solution.
Rewarming techniques
• Pleural lavage using thoracostomy on the
left side due to the proximity of the heart.
• Extracorporeal rewarming is technically
challenging and surgical intervention
• Warm mediastinal irrigation through open
thoracotomy has been used successfully
though it’s very invasive, should be
considered only in arrested patients.
Approach to rewarming
• Most important consideration is the pt’s
cardiovascular status.
• Secondary consideration is given to the
body temperature.
• There are no firm guidelines when to start
rapid rewarming or start with passive
rewarming other than the pt’s
cardiovascular status.
Prognosis
• If hypothermia was uncomplicated, prognosis is
good.
• You should look for the underlying diseases
because they weigh more on the outcome than the
initial temperature.
• Patients with hypothermia after asphyxia (e.g.near
drowning) have poor prognosis.
• Resuscitative efforts should continue until core
temp is 300to 32 0C.
Questions
• Which of the following diseases doesn’t contribute
to a frostbite injury: a)diabetes,b)arteritis
c)atherosclerosis, d)sepsis
• Which of the following regarding frostbite injuries
is true: a)dark-skinned people are more susceptible
to frost bite, b)Homeless are the majority of the
patients, c)duration of exposure, medical
problems, wind don’t contribute to the severity of
the frost bite, d)head and neck account only for
10%of heat loss.
Questions
• If you were unfortunate enough to sustain a
frostbite injury what stage would you prefer it to
be at; a)stage of hyperemia, b)stage of
coagulation, c)stage of stasis
• Nobody is warm until they are warm and dead T/F
• Which of the following EKG changes are not seen
with hypothermia :a)T wave inversion b)Osborn
wave c)QRS narrowing d)tremor artifact
Answers
• D,A,A,T,C