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Aslam AF et al Hypothermia: evaluation, electrocardiographic manifestations, and management Am J Med 2006 Apr;119 (4):297 301 [PMID: 16564768] Di Lorenzo G et al Is there a role for antileukotrienes in urticaria Clin Exp Dermatol 2006 May;31(3):327 34 [PMID: 16681569] Kempainen RR et al The evaluation and management of accidental hypothermia Respir Care 2004 Feb;49(2):192 205 [PMID: 14744270] McCullough L et al Diagnosis and treatment of hypothermia Am Fam Physician 2004 Dec 15;70(12):2325 32 [PMID: 15617296] Smith LO Alpine climbing: injuries and illness Phys Med Rehabil Clin N Am 2006 Aug;17(3):633 44 [PMID: 16952756] Ulrich AS et al Hypothermia and localized cold injuries Emerg Med Clin North Am 2004 May;22(2):281 98 [PMID: 15163568]

thawing has occurred and the part has returned to normal temperature (usually in about 30 minutes), discontinue external heat Rewarming by exercise, rubbing, or friction is contraindicated in the early stage The patient is kept at bed rest with the affected parts elevated and uncovered at room temperature Casts, dressings, or bandages are not applied A combination of ibuprofen, 200 mg four times daily, and aloe vera has been used to prevent dermal ischemia Blisters should be left intact unless signs of infection supervene 2 Anti-infective measures Consider tetanus prophylaxis; frostbite increases susceptibility Protect skin blebs from physical contact Local infections may be treated with culturespecific antibiotics and local wound care Whirlpool therapy at 37 40 C twice daily for 15 20 minutes for a period of 3 or more weeks helps cleanse the skin and debrides superficial sloughing tissue Antibiotics may be required for deep infections but should not be administered empirically Fluid and electrolyte balance should be monitored

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The four disorders that comprise the spectrum of illness due to heat exposure are heat syncope, heat cramps, heat exhaustion, and heat stroke Heat disorders are caused by dehydration or electrolyte imbalance, or both

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Debridement and amputation should be considered if it is established that the tissues are necrotic Eschar formation without evidence of infection (even with black eschar formation) may be conservatively treated, since the underlying skin may sometimes heal spontaneously and the eschar can act as a biologic dressing

Recovery from frostbite depends on the tissue damage caused by the extent of initial injury, the reperfusion injury during rewarming, and the late sequelae (such as renal failure or postinjury infections), but there may be increased susceptibility to discomfort in the involved extremity upon reexposure to cold

Conduction (convection) the direct transfer of heat from the skin to the surrounding air occurs with diminishing efficiency as ambient temperature rises, especially above 372 C, the point at which heat transfer reverses direction At normal temperatures, evaporation accounts for approximately 20% of the body s heat loss, but at high temperatures it becomes the major mechanism for dissipation of heat; with vigorous exertion, sweat loss can be as much as 25 L/h This mechanism diminishes as humidity rises Health conditions that inhibit sweat production or evaporation and increase susceptibility to heat disorders include obesity, skin disorders (miliaria), reduced cutaneous blood flow, dehydration, malnutrition, hypotension, and reduced cardiac output Medications that impair sweating include anticholinergics, antihistamines, phenothiazines, tricyclic antidepressants, monoamine oxidase inhibitors, and diuretics; reduced cutaneous blood flow results from use of vasoconstrictors and -adrenergic blocking agents; and dehydration results from use of alcohol Illicit drugs eg, phencyclidine, LSD, amphetamines, and cocaine can cause increased muscle activity and thus generate increased body heat Drug withdrawal syndromes or prolonged seizures may have the same effect The risk of heat disorder increases with age, impaired cognition, concurrent illness, body mass index, reduced physical fitness, duration of exertion, and insufficient acclimatization

IMMERSION SYNDROME (IMMERSION FOOT OR TRENCH FOOT)

Immersion foot (or hand) is caused by prolonged immersion in cool or cold water or mud, usually less than 10 C The affected parts are first cold and anesthetic (prehyperemic stage) They become hot with intense burning and shooting pains during the hyperemic stage and pale or cyanotic with diminished pulsations during the vasospastic period (posthyperemic stage); blistering, swelling, redness, heat, ecchymoses, hemorrhage, necrosis, peripheral nerve injury, or gangrene and secondary complications such as lymphangitis, cellulitis, and thrombophlebitis can occur later Treatment is best instituted during the stage of reactive hyperemia Treatment consists of air drying, protecting the extremities from trauma and secondary infection, and gradual rewarming by exposure to air at room temperature (not ice or heat) without massaging or moistening the skin or immersing it in water Bed rest is required until all ulcers have healed

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