Two thermal extremes — tissue freezing on one end, heat exhaustion and heat stroke on the other.
Also known as: frostbite, frostnip, heat exhaustion, heat stroke, hyperthermia, cold injury
Overview
Frostbite is freezing-induced tissue injury caused by extracellular ice crystal formation, microvascular thrombosis, and reperfusion injury. Heat-related illnesses span a continuum: heat cramps and heat exhaustion (volume/electrolyte depletion with intact thermoregulation), and heat stroke (core temperature >40°C/104°F with CNS dysfunction and multiorgan failure).
Epidemiology
Frostbite is most common in homeless persons, outdoor workers, alcohol intoxication, mountain athletes, military personnel, and patients with peripheral vascular disease. Heat illness is most common in athletes, military recruits, outdoor laborers, elderly with limited air conditioning, infants, and those on certain medications (anticholinergics, diuretics, antipsychotics). Climate change is increasing heat-illness incidence.
Try two board-style Frostbite and Heat-Related Illness questions
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Question 1DermatologyMedium
A 34-year-old man is brought to the emergency department after becoming stranded overnight on a mountain in subfreezing weather. His fingertips are cold, pale, and feel firm and wooden. With no risk of refreezing, the affected digits are rewarmed in circulating water at 38°C for 25 minutes. Over the next several hours the fingertips become erythematous and edematous, and clear and hemorrhagic blisters develop with progressive tissue darkening. Which of the following best explains the worsening of his digital injury after rewarming?
ACold- and stress-triggered triphasic arteriolar vasospasm of the digits
BExtracellular ice crystal formation drawing water out of the cells
CCold-induced cryoglobulin precipitation occluding digital capillaries
DCold-induced perivascular lymphocytic inflammation of the dermal vessels
EReperfusion injury with microvascular thrombosis and thromboxane release
Reveal answer & full explanation
Correct answer: E — Reperfusion injury with microvascular thrombosis and thromboxane release
ACold- and stress-triggered triphasic arteriolar vasospasm of the digits
BExtracellular ice crystal formation drawing water out of the cells
CCold-induced cryoglobulin precipitation occluding digital capillaries
DCold-induced perivascular lymphocytic inflammation of the dermal vessels
EReperfusion injury with microvascular thrombosis and thromboxane release✓
Why Reperfusion injury with microvascular thrombosis and thromboxane release is correct
In frostbite, freezing causes extracellular ice crystal formation and intracellular dehydration, directly damaging cell membranes and proteins.
The progressive injury seen AFTER rewarming is driven by microvascular thrombosis and reperfusion injury: restoring flow to damaged endothelium triggers release of thromboxanes and prostaglandins, causing vasoconstriction, platelet aggregation, and ongoing tissue loss.
This mechanism is the rationale for anti-prostaglandin therapy (ibuprofen for thromboxane inhibition) and, in severe early deep frostbite, thrombolysis or a prostacyclin analog to interrupt the thrombotic cascade.
Why the others are wrong
Cold- and stress-triggered triphasic arteriolar vasospasm of the digits - This describes Raynaud phenomenon (white to blue to red color change), a reversible vasospastic disorder, not true freeze injury with ice crystal formation and tissue necrosis.
Cold-induced cryoglobulin precipitation occluding digital capillaries - Cryoglobulinemia (linked to hepatitis C, connective tissue disease, or lymphoproliferative disorders) can cause cold-triggered purpura and digital ischemia, but cryoglobulins redissolve as tissue warms, so rewarming would not drive progressive injury; frozen, wooden digits after subfreezing exposure indicate frostbite.
Extracellular ice crystal formation drawing water out of the cells - This is the injury of the freezing phase itself; it ends once the tissue is thawed and cannot explain blistering and darkening that progress over hours after rewarming at 38°C, which reflect reperfusion injury and microvascular thrombosis.
Cold-induced perivascular lymphocytic inflammation of the dermal vessels - this describes the inflammatory reaction of pernio (chilblains), whose tender red to violaceous lesions also appear hours after cold exposure, but pernio follows damp, nonfreezing cold; frozen, wooden digits after subfreezing exposure indicate frostbite, and blistering with progressive darkening after rewarming reflects reperfusion injury and microvascular thrombosis.
Question 2DermatologyMedium
A 34-year-old man is brought to a remote mountain emergency department after becoming stranded for several hours during a snowstorm. He reports numbness and clumsiness of both hands. On examination, the fingers of both hands are cold, hard, and pale with a wooden texture; sensation is absent distally. He has been transported in a heated vehicle, and there is no possibility of further cold exposure on the way to definitive care. Vital signs are stable and his core temperature is 36.4°C (97.5°F). Which of the following is the most appropriate initial management?
BRapid rewarming in circulating water at 37 to 39°C✓
CRewarming by rubbing and massaging the fingers
DGradual passive rewarming at room air temperature
ERewarming with dry radiant heat from a space heater
Why Rapid rewarming in circulating water at 37 to 39°C is correct
Once refreezing is no longer a risk, rapid rewarming in circulating water at 37 to 39°C for 15 to 30 minutes until the tissue is pliable and erythematous is the cornerstone of frostbite care.
Controlled, rapid thaw limits the duration of the freeze and minimizes additional crystal-mediated injury; IV opioids are given for the deep aching pain that accompanies rewarming.
Why the others are wrong
Gradual passive rewarming at room air temperature - slow, spontaneous thawing prolongs the injury and yields worse tissue outcomes than rapid water-bath rewarming; it is acceptable only when rapid rewarming is unavailable, and this patient is in an emergency department with no risk of refreezing.
Rewarming with dry radiant heat from a space heater - dry or radiant heat warms unevenly and risks thermal burns of numb, insensate skin; rewarming must be done in temperature-controlled water.
Intra-arterial tissue plasminogen activator infusion - thrombolysis is reserved for deep frostbite within 24 hours to reduce amputation, but only after rapid rewarming and imaging-based viability assessment, so it is not the initial step.
Rewarming by rubbing and massaging the fingers - rubbing seems a natural way to restore warmth and circulation to numb, white fingers and is a common field practice, but friction adds mechanical trauma to tissue that is still frozen and worsens the injury; the hands should be immersed in circulating water at 37 to 39°C and otherwise handled gently.
Additional high-yield points
Never rub or massage frozen tissue; friction adds mechanical injury and is contraindicated.
Do not thaw in the field if refreezing is possible, because a freeze-thaw-refreeze cycle causes more damage than a delayed thaw.
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Frostbite: cold exposure, wind chill, wet clothing, alcohol or sedative use, smoking, prior frostbite, peripheral vascular disease, beta-blocker use, immobility, low body fat; in civilians, alcohol or drug intoxication (often with homelessness or psychiatric illness) is the most common and strongest predisposing factor because impaired judgment and immobility prolong unprotected exposure and cutaneous vasodilation increases heat loss
Heat illness: high ambient temperature and humidity, exertion, dehydration, lack of acclimatization, extremes of age, chronic illness, obesity, alcohol, drugs (anticholinergics, diuretics, antihistamines, beta-blockers, antipsychotics, stimulants like MDMA and cocaine), occlusive clothing
Pathophysiology
Frostbite: tissue cooling → intracellular dehydration as extracellular ice forms → membrane and protein damage → microvascular thrombosis on rewarming → reperfusion injury releasing thromboxanes and prostaglandins. Heat stroke: failure of heat dissipation → core temperature rise → endothelial injury, systemic inflammatory response, coagulopathy, rhabdomyolysis, hepatic and renal failure, and CNS dysfunction. Classic (non-exertional) heat stroke occurs during heat waves in vulnerable patients; exertional heat stroke occurs in young athletes/soldiers with high heat production.
Clinical presentation
Symptoms
Frostbite: numbness, clumsiness, deep aching pain on rewarming; tissues feel firm or wooden
Heat stroke: confusion, altered mental status, ataxia, seizures, coma; classic patients often have hot dry skin (anhidrosis); exertional patients may still be sweating
Signs / physical exam
Frostbite degrees: 1st — erythema, edema, no blisters; 2nd — clear blisters; 3rd — hemorrhagic blisters and full-thickness skin loss; 4th — involvement of muscle, bone, and tendon with mummification
Heat exhaustion: tachycardia, hypotension, normal or mildly elevated temperature (<40°C/104°F), diaphoresis, intact mentation
Heat stroke: core temperature >40°C/104°F, CNS dysfunction, possible hypotension, tachycardia, tachypnea, often diaphoretic in exertional and dry in classic forms
Classic findings
Cold, hard, pale 'wooden' digit that becomes hyperemic and blistered on rewarming (frostbite); confused or comatose patient with rectal temperature 41°C after a marathon (exertional heat stroke).
Differential diagnosis
Frostnip — Superficial cold injury with pallor and numbness but no ice crystal formation; fully reversible on rewarming with no tissue loss
Trench foot / immersion foot — Prolonged cold-wet (non-freezing) exposure; pale, cool, edematous foot with later hyperemia and pain
Chilblains (pernio) — Painful red-violaceous papules on fingers/toes/ears after cold-damp exposure; non-freezing; idiopathic or autoimmune
Raynaud phenomenon — Triphasic color change (white → blue → red) of digits with cold or stress; not freeze injury
Heat exhaustion — Core temp <40°C, fatigue, headache, nausea, tachycardia, sweating preserved, mentation intact; treat with rest, cooling, oral or IV fluids
Heat stroke — Core temp >40°C plus CNS dysfunction (confusion, ataxia, seizures, coma); medical emergency
Malignant hyperthermia / neuroleptic malignant syndrome / serotonin syndrome — Drug-triggered hyperthermia with rigidity (NMS, MH) or clonus/hyperreflexia (serotonin syndrome); specific antidotes (dantrolene for MH/NMS; cyproheptadine for serotonin syndrome)
Diagnostic workup
Diagnostic criteria
Frostbite: clinical diagnosis with degree determined post-rewarming. Heat stroke: core (rectal) temperature >40°C with central nervous system dysfunction in the appropriate setting.
Labs
Frostbite: CBC, BMP, CK (rhabdomyolysis from severe injury), coagulation studies
Heat stroke: CBC, BMP, LFTs, CK, coagulation (DIC), troponin, lactate, ABG, urinalysis (myoglobinuria), pregnancy test in women
Toxicology screen if drug-induced hyperthermia possible
Cultures and sepsis workup as indicated
Imaging
Frostbite: angiography or technetium-99m perfusion scintigraphy soon after rewarming helps select deep frostbite for thrombolysis (tPA within 24 hours); Tc-99m scintigraphy or MR angiography at about 2-3 days predicts tissue viability and amputation level
Heat stroke: CT or MRI of brain if focal neurologic findings or refractory altered mental status; imaging to evaluate end-organ damage as indicated
Diagnostic algorithm
Condition
Core Temp
Mental Status
Skin/Tissue
Treatment Priority
Frostnip
Normal
Intact
Pale, numb digits; fully reversible
Rewarm gradually; no tissue loss
Frostbite (superficial 1°-2°)
Often normal core
Intact
Erythema, clear blisters
Rapid rewarm 37-39°C, ibuprofen, tetanus
Frostbite (deep 3°-4°)
Often normal core
Intact
Hemorrhagic blisters; mummification
As above + consider tPA/iloprost; delayed amputation
Heat cramps
Normal
Intact
Sweating
Rest, fluids, electrolytes
Heat exhaustion
<40°C
Intact (may be fatigued)
Sweating, pale, tachycardia
Cool environment, rest, fluids
Heat stroke (classic or exertional)
>40°C
Altered (confusion, seizure, coma)
May be hot/dry (classic) or sweating (exertional)
Rapid cooling (cold-water immersion); ABC; treat organ dysfunction
Thermal injury spectrum — cold injury and heat illness side by side.
Treatment
First-line
Frostbite, prehospital: remove wet clothing, gently insulate; do NOT rub or use dry heat; do NOT rewarm if there is any chance of refreezing en route
Frostbite, hospital: rapid rewarming in circulating water at 37-39°C (98.6-102.2°F) for 15-30 minutes until tissues are pliable and erythematous
Topical aloe vera to blistered tissue; debride clear blisters and leave hemorrhagic blisters intact
For deep frostbite presenting within 24 hours: consider IV tPA or intra-arterial thrombolysis at centers with experience (Bruen et al., Arch Surg 2007; reduces amputation rates in carefully selected patients)
IV iloprost (prostacyclin analog; FDA-approved in 2024 for severe frostbite in adults to reduce the risk of digit amputation) for deep frostbite, including when tPA is contraindicated (Cauchy et al., NEJM 2011)
Surgical decisions for amputation delayed until tissues fully demarcate ('frostbite in January, amputate in July')
Heat exhaustion: move to cool environment, remove clothing, oral or IV isotonic fluids, rest; resolves within 30-60 min
Heat stroke: rapid cooling is the single most important intervention — every minute counts; cold-water immersion is most effective (target core <39°C within 30 min); alternative cooling (evaporative cooling with fans plus tepid water mist, ice packs to neck/axilla/groin) when immersion impractical
Heat stroke: stop cooling at 38.5-39°C to avoid overshoot hypothermia
Heat stroke: ABCs, IV crystalloid for hypotension (use cautiously — avoid pulmonary edema in elderly), benzodiazepines for shivering or agitation, treat seizures
Avoid antipyretics (acetaminophen, NSAIDs) — ineffective in heat stroke (hypothalamic set point is not elevated) and may worsen hepatic/renal injury
Complications
Frostbite: tissue necrosis with amputation, chronic neuropathic pain, cold sensitivity, hyperhidrosis, joint contractures, growth plate injury in children, secondary infection
Heat stroke: multiorgan failure, rhabdomyolysis-induced AKI, DIC, hepatic failure, ARDS, permanent neurologic deficits, death (mortality 20-65% in classic heat stroke without rapid cooling)
Long-term temperature dysregulation and persistent cognitive deficits after severe heat stroke
PANCE pearls
Do not rewarm frostbite if there is any chance of refreezing — repeated freeze-thaw cycles cause much worse damage.
Rapid rewarming in 37-39°C water (not hot water, not dry heat, not rubbing) is the cornerstone of frostbite treatment.
Drain clear blisters but leave hemorrhagic blisters intact (they cover deeper, more devitalized tissue).
Defer amputation decisions until tissue clearly demarcates — often weeks to months ('amputate in July').
Heat stroke = core temp >40°C + CNS dysfunction. Antipyretics do not work; cool the patient as fast as possible.
Cold-water immersion is the most rapid and most effective cooling modality in exertional heat stroke and substantially reduces mortality.
Acclimatization over 1-2 weeks dramatically reduces heat-illness risk in athletes, soldiers, and laborers.
References
Wilderness Medical Society — McIntosh SE et al. Wilderness Medical Society clinical practice guidelines for the prevention and treatment of frostbite: 2024 update (Wilderness Environ Med 2024;35(2):183-197)
Cauchy NEJM 2011 — Cauchy E et al. A controlled trial of a prostacyclin and rt-PA in the treatment of severe frostbite (NEJM 2011)
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