Frostbite: Pathophysiology, Classification, and Emergency Management

Frostbite is freezing injury to tissues from cold exposure. It is not a "burn" but causes similar tissue destruction via ice crystal formation, vascular damage, and inflammatory cascade.

Pathophysiology

1. Ice crystal formation: Extracellular first (osmotic shift → cellular dehydration); intracellular in rapid freezing.
2. Vascular injury: Endothelial damage → thrombosis, stasis, ischemia-reperfusion injury on rewarming.
3. Inflammation: Prostaglandins, thromboxane A₂, cytokines → vasoconstriction, increased permeability.

Classification

Degree	Depth	Appearance	Prognosis
1st (Frostnip)	Epidermis	Pale, numb, waxy; reversible on rewarming	Full recovery
2nd	Dermis	Clear blisters (24-48h); erythema, edema	Usually heals; possible sensitivity
3rd	Subcutaneous	Hemorrhagic blisters; blue-gray, hard	Tissue loss likely
4th	Muscle/tendon/bone	Black, mummified; no capillary refill	Amputation often needed

Prehospital / ED Management

1. Remove from cold. Prevent refreezing (worse than delayed thaw).
2. Rapid rewarming: 37-39°C (98.6-102°F) water bath 15-30 min until pliable/red. No dry heat, rubbing, snow.
3. Pain control: NSAIDs, opioids (rewarming is painful).
4. Elevate, splint, protect blisters.
5. Tetanus, ibuprofen 400 mg q12h (anti-thromboxane), consider iloprost/TPA (severe, specialized centers).
6. No early debridement: Demarcation takes 1-3 months. "Frozen in January, amputate in July."

Prevention

• Layered clothing (wicking base, insulating mid, wind/waterproof shell).
• Protect extremities: insulated gloves, socks, face mask.
• Stay dry (moisture ↑ heat loss 25×).
• Nutrition/hydration; avoid alcohol, nicotine, fatigue.
• Buddy system for early detection.

Frostbite is a surgical disease — definitive tissue viability assessment requires time. Early aggressive rewarming and anti-inflammatory therapy salvage tissue.