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Frostbite and Hypothermia. March 10 th , 2005 Tintinalli Chapters 191 and 192 George Filiadis. Epidemiology. Frostbite is the inability to physiologically compensate for cold that produces injury.

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Frostbite and Hypothermia

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Frostbite and Hypothermia

March 10th, 2005

Tintinalli Chapters 191 and 192

George Filiadis

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  • 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.

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  • 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

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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.

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  • 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.

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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.

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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.

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  • 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.

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  • 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

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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.

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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.

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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.

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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 full-thickness 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.

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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.

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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 field

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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 the ED

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Infection prophylaxis using topical bacitracin is as good as IV penicillin.

Tetanus immunization status should be assessed.


Early surgical intervention is not indicated in treatment of frostbite

Amputation if needed within 3 weeks

Treatment in ED

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  • 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.

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  • 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.

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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.

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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.

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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.

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Hypothalamic and CNS dysfunction



Dermal disease

Acute incapacitating illness

Iatrogenic (fluid resuscitation)


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  • 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.

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  • 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.

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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.

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  • 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 .

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  • 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.

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  • 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, cold-induced decrease in blood viscosity, and poor circulation may lead to intravascular thrombosis and subsequent embolic complications.

  • Pty are prone to DIC and coagulopathies.

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  • 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.

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  • 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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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  • 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.

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  • 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.

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  • 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

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  • D,A,A,T,C

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