Summary Frostbite is the extensive soft tissue damage associated with exposure to temperatures below freezing point. Diagnosis is made clinically with the appearance of a central whitish area with surrounding erythema and subsequent clear/cloudy blisters within 24 hours. Treatment involves prevention with prompt rewarming and potential surgical debridement depending on severity of soft tissue injury. Epidemiology Demographics males (M:F = 10:1) age 30-50 years Risk factors host factors alcohol abuse mental illness peripheral vascular disease peripheral neuropathy malnutrition chronic illness tobacco use race African descent more likely to sustain frostbite than Caucasians who have better cold induced vasodilatation smoking reduces nitric oxide (vasodilator) potentiates thrombosis by increasing fibrinogen levels and platelet activity environmental factors degree of cold temperature risk of frostbite is low at > -10°C risk of frostbite is high at < -25°C duration of exposure windchill tissues at -18°C freeze in 1h at windspeed of 10mph tissues at -18°C freeze in 10min at windspeed of 40mph altitude >17,000 feet contact with conductive materials (water, ice, metal) Etiology Pathophysiology with hypothermia (CBT <35°C) circulation shunted from periphery to maintain core body temperature (CBT) cardiac effects basal metabolic rate, HR and cardiac output drop myocardial irritability (abnormal EKG) neurological effects disorientation, coma shivering (anaerobic) until CBT drops below 30-32°C below 30-32°C, shivering stops and muscle rigidity ensures (like rigor mortis) resembles death (absent respirations, dilated pupils, muscle rigidity) must be rewarmed before pronounced dead (“no one is dead until warm and dead”) limbs (4 phases) phase I (cooling and freezing) vasoconstriction/vasospasm followed by transient arteriovenous shunting (hunting response) of cycles of vasodilatation/vasoconstriction every 10min those who do not have this response are more prone to cold injury with persistent cold, cycles cease and temperature in tissue drops to freezing point of tissue (<-2°C) intracellular ice crystals destroy cell membranes extracellular ice crystals causes sludging/stasis and intracellular dehydration (because of osmotic gradient) interstitial crystallization is exothermic, maintains latent heat to keep limb above freezing temperature when crystallization is complete, limb temperature falls to ambient temperature phase II (rewarming) reverses freezing process limb absorbs heat, intra/extracellular ice crystals melt intracellular swelling occurs endothelial cells of capillaries become permeable fluid extravasation leads to blisters/edema important to prevent re-freezing (freeze-thaw has severe effects on tissues) phase III (progressive tissue injury) inflammation, stasis/thrombosis, tissue necrosis diminished prostaglandin E2 (vasodilator, antiplatelet) elevated prostaglandin F2a and thromboxane B2 (vasoconstrictors, platelet-aggregating) phase IV (resolution) complete healing with no symptoms healing with sequelae early tissue necrosis/gangrene cell biology leads to movement of water from intracellular location to extracellular location cellular dehydration leads to cell death biochemistry sensory nerve dysfunction occurs at -10°C ice crystal formation occurs within the extracellular fluid at -2 to -15°C Associated conditions frostnip mildest cold exposure injury only affects superficial layers of skin (blanching, numbness) but no dermis damage reversible chilblain (pernio) occurs in cold, nonfreezing temperatures in dry conditions burning sensation, with pruritus, swelling, erythema may have blisters, ulceration resolves in 2 weeks may leave chronic vasculitis esp in young/middle-aged women trench foot (immersion foot) military personnel prolonged wet nonfreezing condition <10°C frostbite results in localized/extensive tissue necrosis may require amputation hypothermia when core body temperature is affected can be fatal Presentation Physical exam hypothermia (mild, 32-35°C; moderate, 28-32°C; severe, <28°C) tachycardia followed by bradycardia, decreased cardiac output, arrythymia (atrial and ventricular fibrillation) decreased respiratory rate CO2 retention leads to hypoxia/respiratory acidosis disorientation, comatose frostbite (similar to burns) traditional classification 1st degree – central whitish area with surrounding erythema 2nd degree – clear/cloudy blisters within 24h 3rd degree – hemorrhagic blisters / hard black eschars 4th degree – tissue necrosis newer classification superficial (1st and 2nd degree) has good prognosis deep (3rd and 4th degree) has poor prognosis blisters form 6-24 hours after rewarming superficial lesions present as clear blisters deeper lesions form hemorrhagic blisters which may be painless Imaging MRI T2-weighted images shows enhanced signal in necrotic muscles because of disrupted cell membranes and increased extracellular fluid Serial bone scans (99mTc) can be used to evaluate the severity of the soft-tissue damage 1st scan at 2 days after initial injury absence of uptake has poor prognosis but may not indicate necrosis 2nd scan at 5 days after initial injury normal blood/bone pool = treat expectantly diminished blood/bone pool = observation, with potential early debridement absent blood/bone pool = early debridement or amputation Treatment for Hypothermia protect patient from further exposure to freezing temperature rewarming only after confirmation that the patient can be maintained in a constant warm environment (avoid freeze-thaw cycles) external-surface rewarming (for mild hyperthermia) passive dry clothes and warm room active disadvantage is too-rapid vasodilatation leads to metabolic waste rushing to core, leading to paradoxical drop in core temperature (“afterdrop”) that can worsen arrythmia heat lamps, radiant heaters, heating blanket, immersion in warm water with cardiac monitoring internal-core rewarming (for moderate and severe hypothermia) warmed oxygen, warm IV fluid body cavity lavage (invasive) cardiac bypass requires systemic heparinization continuous arteriovenous rewarming blood from femoral arterial catheter into fluid heat exchanger returns to body through subclavian venous catheter achieves 1°C every 15min avoid alcohol/sedatives dulls shivering response and further lowers CBT Treatment for Frostbite Nonoperative prevention footwear thermal insulation is the most important factor for protection against cold-induced injury protect limb from mechanical trauma e.g. walking, rubbing pad/splint, wrap with blanket for transportation initial resuscitation with warm IV fluids, tetanus prophylaxis, NSAIDS, silver sulfadiazine ointment or topical antibiotics to open wounds, rapid rewarming indications superficial frostbite water bath 40-42°C with mild antibacterial agent x 30min successful when skin becomes pliable and red-purple avoid repetitive freeze-thaw cycles IV analgesia / conscious sedation wound care with topical aloe vera, extremity elevation and splinting IV antibiotics if secondarily infected rehabilitation whirlpool hydrotherapy PT and OT for preserve joint motion adjunctive (low molecular weight dextran, anticoagulants, tissue plasminogen activator) intravenous tPA within 24h reduces rate of digital amputations indications no blood flow on bone scan 2nd or 3rd degree (NOT superficial frostbite) contraindications general contraindications alcoholic patients (risk of bleeding from concomitant head injuries) active internal bleeding intracranial hemorrhage/surgery within past 3 months concurrent trauma major surgery within previous 14 days known aneurysm or vascular malformation known bleeding diathesis pregnancy labile hypertension cold-related contraindications > 24 hours of cold exposure warm ischemia times >6h multiple freeze-thaw cycles hyperbaric oxygen (anecdotal evidence) Operative immediate surgical escharotomy circumferentially constrictive lesion of digit fasciotomy for compartment syndrome debride clear blisters and apply aloe vera reduces high levels of prostaglandin F2 and thromboxane B2 drain/aspirate hemorrhagic blisters (represents deep injury) but leave intact prevents dessication of underlying dermis late debridement/amputation for necrosis “frostbite in January, amputate in July” after demarcation occurs at 1-3months surgical sympathectomy reduces duration of pain and time to demarcation of tissue does not reduce extent of necrosis Complications Adults persistent pain (50%) intolerable in 15% cold intolerance vasospastic disease (Raynauds phenomenon, cold sensitivity, persistent color changes, hyperhidrosis) treatment calcium channel blockers, vasodilators, beta blockers, surgical sympathetectomy indications late, persistent vasospastic disease neuropathy (cold/heat hypersensitivity, hypesthesia, paresthesia) decreased motor/sensory NCV treatment decompression e.g. carpal tunnel release musculoskeletal (osteopenia) subchondral bone loss (frostbite arthropathy), joint contractures esp in DIPJ > PIPJ of hands and feet treatment joint arthroplasty, resection arthroplasty Children premature growth plate closure 1-2 years after exposure secondary to chondrocytic injury joint laxity, angular deformities, short digits, excess skin, degenerative joint changes seen after age 10 in patients with prior frost bite injuries treatment physeal arrest, osteotomy, arthrodesis Prognosis Severity is increased with alcohol consumption/intoxication contact of skin with metal or ice elevated wind chill factor