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Frostbite and Hypothermia

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    E pidemiology

    Frostbite is the inability to physiologicallycompensate for cold that produces injury.

    Duration of exposure, humidity, wind, altitude,clothing, medical conditions, behavior, andindividual variability are contributing factors.Inadequate clothing is the most preventable cause

    of cold related injuries with exposed head andneck 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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    E pidemiology

    Disease states as atherosclerosis, arteritis,hypovolemia, diabetes, vascular injury may

    predispose to cold-related injury.Dark-skinned people and those fromwarmer climates are more susceptible tofrostbite.Local cold-related injuries are classifiedinto nonfreezing and freezing injuries

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    N onfreezing coldinjuries:chilblains and trench foot

    Chilblains is characterized by mild butuncomfortably inflammatory lesions of the skin of

    bared body areas caused by intermittent exposureto damp, nonfreezing ambint temperatures.Hands, ears, lower legs, and feet are mostcommonly affected.

    Cutaneous manifestations which appear 12 h after exposure include localized edema, erythema,cyanosis, plaques , nodules , ulcerations, andvesicles.

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    ChilblainsPt 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 FootIt involves direct injury to soft tissue sustainedfrom prolonged cooling and is accelerated by wet

    conditionsPeripheral nerves are more sensitive to this formof injury.It develops over hours to days and is reversible

    initially.On physical exam, the foot is pale, mottled,anesthetic , pulseless, and immobile which doesnot change after rewarming.

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    Trench FootA 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 mayworsen.

    In severe cases, tissue sloughing and gangrenemay develop.Hyperhidrosis and cold sensitivity are commonlate features and may persist for months to years.

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    TreatmentTreatment of chilblains is supportive

    -affected skin should be rewarmed,gently bandaged, and elevated.-Some E uropean studies suggestnifedipine, pentoxifylline, or an oralanalogue of PG E 1, limaprost.-Topical corticosteroids or even oralcorticosteroids have been shown to beuseful.

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    TreatmentTreatment for trench foot includes

    -keeping warm, good boot fit-changing out wet socks several timesa day-dry, elevate feet

    -pentoxifylline or limaprost can be used

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    Freezing Cold injuries:Frostnipand 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 theextremities, 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 crystalformation in the extracellular space that leads toan intacellular dehydration and hyperosmolarity

    by pulling of fluids.

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    Freezing cold injuries:Frostnipand Frostbite

    As proteins get denatured , intracellular icecrystals form.

    Phase II is characterized by reperfusion injury asthe extremity gets rewarmed which leads toendothelium leakage, leakage of destructive

    prostaglandins and oxygen free radicals,vasoconstriction an arteriovenous shunting, andfinally necrosis and gangrene.

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    Freezing Cold Injuries:Frostnipand Frostbite

    Frostbite can be divided in three zones:zone of coagulation is the most severe, usually

    distal and irreversiblezone of hyperemia is the most superficial,typically proximal with the least cellular damageand recovers with no treatment.

    zone of stasis is characterized by severe, but possibly reversibly cell damage that can benefitfrom treatment.

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    Clinical featuresClassification 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 substantialedema over 3 to 4 h, and formation of clear

    blisters that desquamate to form black eschars andhas good prognosis.

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    Clinical FeaturesClassifications (continued) -third degree injury is characterized by damage that

    extends into the subdermal plexus and leads toformation of hemorrhagic blisters, skin necrosisand a blue-gray discoloration of skin, has poor

    prognosis -fourth degree injury is characterized by extensioninto subcutaneous tissues, muscle, bone, andtendon, there is little edema, nonblanchingcyanosis, bloody blebs, has extrememly poor

    prognosis.

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    Treatment in the fieldRemove wet andconstrictive clothing.

    E levate and wrap in drysterile gauze the involvedextremities.Rapid rewarming if rapidaccess to hospital40 0 to 42 0 C clean water should be used

    There is controversy withregards to debridement of clear blisters on the fieldPain management shouldstart with N SAIDS tocounteract the arachidonicacid cascade, in additionto opioidsSmoking should bediscouraged

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    Treatment in theE

    DInjured extremity should be placed in circulatingwater at a temperature of 400 to 42 0 C for approximately 10-30 minuntil the distal extremity is

    pliable and erythematousPain should be treatedwith parenteral antibioticsClear blisters should bedebrided or aspirated

    Hemorrhagic blistersshould not be debridedAlo vera cream should beapplied to the blistersRole of antibiotics isunclear.Staph aureus, Staph epi,

    beta-hemolytic Strep,Pseudomonas, andE nterococus are important

    pathogens.

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    Treatment inE

    DInfection prophylaxisusing topical

    bacitracin is as goodas IV penicillin.Tetanus immunizationstatus should beassessed.Ibuprofen

    E arly surgicalintervention is not

    indicated in treatmentof frostbiteAmputation if neededwithin 3 weeks

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    DispositionAdmit all but the most isolated andsuperficial frostbite cases.Homeless or elderly should never bedischarged into subfreezing temperatures.If hospital is not equipped to treat thedegree of severity, transfer pt after theinitial rewarming.

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    Hypothermia

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    E pidemiology

    Hypothermia is defined as temperature of less than 35 0C (95 0F).

    An average of 700 people die fromhypothermia in the United States annually.Half of those who die are older than 65

    years of age.E xtremes of age and those with alteredsensorium are susceptible to hypothemia.

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    Temperature homeostasisHeat loss can occur either by conduction,convection, radiation , or evaporation.

    Conduction is the transfer of heat by direct contactdown a temperature gradient, e.g. from warm bodyto the cold environment.Convection is the transfer of heat by the actualmovement of the heated material, e.g. winddisrupting the layer of warm air surrounding the

    body.

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    Temperature homeostasisRadiation is the loss of heat from noninsulated body areas.E vaporation causes heat loss by evaporation of water contained in exhaled water-saturated air Opposing mechanisms to heat loss is conservationand gain which are controlled by thehypothalamus.

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    Temperature homeostasisHeat is conserved by peripheral vasoconstrictionand importantly, by behavioral responses (dressing

    up or coming inside).Heat gain is effected by shivering and bynonshivering thermogenesis which consists of increase in the metabolic rate brought out byincreased output from the thyroid and adrenalglands.

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    Etiology

    Accidental(enviromental)

    MetabolicHypothalamic andC N S dysfunction

    Drug-induced

    SepsisDermal diseaseAcute incapacitatingillnessIatrogenic (fluid

    resuscitation)

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    Etiology

    Accidental hypothermia is divided into immersionand nonimmersion cold exposure.

    Metabolic causes include hypothyroidism,hypoadrenalism, hypoglycemic, andhypopituitarism.Hypothalamic and C N S dysfunction include head

    trauma, tumor , stroke, Wernicke diseaseDrug-induced hypothermia is usually due toethanol that causes vasodilation, insulin and other hypoglycemic agents.

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    Etiology

    Sepsis may alter the hypothalamic temperature set point.

    Dermal disease like burns or exfoliative dermatitismay prevent cutaneous vasoconstriction andincrease trascutaneous water loss.Hypothermia may be also induced by fluidresuscitation with either room-temperature fluid or cold blood.

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    Pathophysiology and ClinicalFeatures

    Mild hypothermia consists of temperature between320C 35 0C,where the patient tries to retain and

    generate heat (responsive stage)When temp falls below 32 0C, there is a progressive slowdown of the bodily functions andmetabolism (adynamic stage).

    Shivering ceases when when body temperaturefalls below 30 0 C.In the initial responsive stage, cardiac output ,heart rate, and blood pressure rise but start todecline as temperature declines.

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    PathophysiologyAt temperatures below 30 0C, the risk of dysrhythmias increases.

    The typical progression is from sinus bradycardiato 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 characteristicthough not pathognomonic of hypothermia.E CG changes in hypothermia include T-waveinversions, PR, QRS, QT prolongation, muscletremor artifact .

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    PathophysiologyPulmonary manifestations include mild tachypneainitially 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 theoxyhemoglobin dissociation curve, impairingoxygen release to tissues.C N S manifestations include depression of consciousness, lethargy, coma, dilated andunreactive pupils.

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    PathophysiologyHypothermia impairs renal concentrating abilitiesand induces cold diuresis leading to significant

    volume losses.The immobile hypothermic pt is prone torhabdomyolysis.The combination of hemoconcentration, cold-

    induced decrease in blood viscosity, and poor circulation may lead to intravascular thrombosisand subsequent embolic complications.Pty are prone to DIC and coagulopathies.

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    PathophysiologyE ndocrine function is fairly well preserved.Pancreatitis may occur in hypothermia.Hepatic function is depressed by cold anddrugs metabolized, conjugated or detoxified

    by the liver may accumulate rapidly to toxiclevels.

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    TreatmentPt should be handled carefully and gently becausemanipulation can precipitate ventricular

    fibrillation.Oxygen and IVF should be warmed.Most dysrhythmias require no therapy and revertspontaneously with rewarming.

    Hypothermic heart is resistant to atropine, pacingand countershock.In case of V-fib, defibrillate three times, if unsuccesful do CPR and rapid rewarming, resume

    defibrillation when temp reaches 300

    C.

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    Drug therapyThiamine 50 mg IV should be given because manyof 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.E mpirical antibiotic therapy is appropriate when anoninfectious cause of hypothermia cannot beidentified.

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    Drug therapyHydrocortisone should be given to patientswith history of adrenal insufficiency andmyxedema coma.Thyroid hormone replacement is indicatedonly in pt with known history of

    hypothyroidism, a thyroidectomy scar, or clinical evidence of myxedema coma.

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    Rewarming techniquesPassive rewarming includes removal from coldenvironment and insulation.

    Active external rewarming includes warm water immersion , heating blankets, set at 40 0C, radiantheat, forced air.Disadvantages of the external include that is

    innefective with poor peripheral circulation,causes topical vasodilation leading to rewarmingshock, can increase lactic acid thus leads toincrease in metabolic demands.

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    Rewarming techniquesActive core rewarming includes inhalationrewarming, heated IV fluids, GI tract lavage,

    bladder lavage, peritoneal lavage, pleural lavage,extracorporeal rewarming, mediastinal rewarmingvia thoracotomy.Its advanages include that is less irritant to themyocardium, peripheral vasodilation is avoidedthus there is less chance of shock and acidosiswhile its disadvantages include the fact that isinvasive.

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    Rewarming techniquesInhalation rewarming is the administration of warmed , humidified air or oxygen by face mask

    or endotracheal tube.IV fluids should be warmed to 40 0C beforeadministration.GI or bladder lavage with warmed sterile saline is

    simple though you have to protect the airway inobtunded patients.Peritoneal lavage allows rapid rewarming using potassium-free dialysis solution.

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    Approach to rewarmingMost important consideration is the ptscardiovascular status.

    Secondary consideration is given to the body temperature.There are no firm guidelines when to startrapid rewarming or start with passiverewarming other than the ptscardiovascular status.

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    PrognosisIf hypothermia was uncomplicated, prognosis isgood.

    You should look for the underlying diseases because they weigh more on the outcome than theinitial temperature.Patients with hypothermia after asphyxia (e.g.near

    drowning) have poor prognosis.Resuscitative efforts should continue until coretemp is 30 0to 32 0C.

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    QuestionsIf you were unfortunate enough to sustain afrostbite injury what stage would you prefer it to

    be at; a)stage of hyperemia, b)stage of coagulation, c)stage of stasisN obody is warm until they are warm and dead T/FWhich of the following EK G changes are not seenwith hypothermia :a)T wave inversion b)Osbornwave c)QRS narrowing d)tremor artifact

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