Cold Injuries
Cold-induced skin injuries cover a wide range of conditions caused by low environmental temperatures acting on the skin and soft tissues. By mechanism, they fall into two main groups: freezing cold injuries (frostbite) and non-freezing cold injuries (chilblains/pernio and trench foot).
The damage results from two processes working together: intense constriction of the microcirculation, which starves tissue of blood, and direct physical and chemical injury to cells as ice crystals form.
- Vasoconstriction and the hunting reaction:
- Once skin temperature drops below 15 °C, sympathetic reflexes clamp down the peripheral vessels as far as possible to protect core body temperature.
- To stop tissue from dying straight away, the body switches on cycles of alternating vasodilation and vasoconstriction (the Lewis hunting reaction): the vessels open briefly, then close again. With prolonged cold exposure, however, this protective response breaks down completely.
- Ice crystal formation and cell damage:
- Extracellular crystallization: Water in the interstitial space freezes first. This raises extracellular osmotic pressure and draws water out of the cells, causing severe cellular dehydration and protein damage.
- Intracellular crystallization: When temperature falls very quickly, ice crystals form inside the cells themselves, tearing the cell membrane and organelles (mitochondria, lysosomes) and causing irreversible cell death.
- Reperfusion injury:
- As the tissue is rewarmed and blood flow returns, a surge of reactive oxygen species (ROS), thromboxane A2 and prostaglandin F2-alpha is released. Platelets clump, microvascular clots form, and a secondary wave of inflammation and necrosis follows.
- Histopathology:
- Acute: Extensive epidermal necrosis, fluid leakage forming subepidermal bullae, collapsed dermal microvessels and fibrin thrombi within vessel lumens.
- Chronic (pernio/chilblains): A dense lymphocytic infiltrate around superficial and deep dermal vessels, papillary dermal edema and thickening of the vessel walls.
Emergency care for cold injury, frostbite in particular, depends on precise controlled rewarming. Rubbing the skin, applying snow or rewarming incorrectly can all add permanent tissue loss, because the ice crystals mechanically shred the tissue.
Clinical Grading of Cold Injuries
Cold injuries are divided into two broad groups depending on whether the tissue actually freezes.
Freezing Injury (Frostbite – Four Degrees)
- First degree (frostnip, superficial): The skin turns pale and temporarily numb. After rewarming it becomes red and swollen with mild stinging pain. No blisters form, and it recovers fully within a few days.
- Second degree (epidermis and superficial dermis): The skin is firm, red and clearly swollen. Within 12–24 hours, large blisters filled with clear or pale yellow fluid appear, with intense burning pain. Once the crust peels away, it leaves thin, sensitive skin.
- Third degree (full-thickness skin and subcutis): The skin turns deep purple or ash gray, and blood-filled (hemorrhagic) blisters develop. There is deep, throbbing pain or complete loss of sensation, and the area progresses to a hard, dry black eschar.
- Fourth degree (through the skin into tendon, muscle and bone): The tissue is wood-hard, black and dry (dry gangrene). Over several weeks the line between living and dead tissue becomes clear, and the affected part may separate on its own (autoamputation).
Non-Freezing Cold Injuries
- Chilblains (pernio): Common in cold, damp climates (0–10 °C). Red-purple papules or plaques appear on the fingers, toes, ears and nose, with swelling, intense itching and burning pain.
- Trench foot (immersion foot): Caused by feet staying in cold, wet conditions (0–15 °C) for days on end. Prolonged vessel spasm damages the peripheral nerves and soft tissue: the foot is first pale, cold and numb, then becomes swollen and necrotic.
- Cold panniculitis: Seen mostly in children and women, for example firm red plaques on a toddler's cheeks after eating ice cream or holding ice, or on the thighs of people who ride horses in winter.
How the Main Types of Cold Skin Injury Compare
| Chilblains (Pernio) | Frostbite | Trench Foot |
|---|---|---|
| Cold, damp conditions (0–10 °C), above freezing | Severe cold (below 0 °C), contact with ice or snow | Prolonged immersion in cold water or wet conditions (0–15 °C) |
| Tissue does not freeze | Tissue freezes | Tissue does not freeze |
| Usually no blisters (occasionally small blisters or ulcers) | Blisters with CLEAR fluid or BLUE-BLACK (hemorrhagic) contents | No blisters (or only superficial ones) |
| No deep tissue necrosis | Superficial or deep necrosis | Wet necrosis from chronic ischemia |
| Intense itching, burning pain on warming | Burning, pins and needles, or complete numbness | Numbness, chronic nerve pain |
Diagnosis, Emergency Rewarming and Treatment at Haute-Derma
At Haute-Derma, patients with cold injuries are managed according to our emergency controlled-rewarming and microcirculatory vasodilator protocol (Haute-Derma Cold Injury Protocol):
Rapid Controlled Rewarming to International Standards
- Never do the following: do NOT rub the tissue with snow or your hands; do NOT warm it over a flame or with a dry heater (numb skin is easily burned on top of the cold injury); and do NOT start rewarming if there is any chance it will freeze again (refreezing causes far more severe necrosis).
- Warm-water immersion: The injured area is immersed in a bath held at 37–39 °C (ideally 38 °C) containing a mild antiseptic (povidone-iodine).
- Immersion time: 15–60 minutes, until the skin turns warm and pinkish-red and is completely soft.
Limiting Reperfusion Injury and Controlling Pain
- Ibuprofen: 400–800 mg every 8 hours. Beyond pain relief, ibuprofen plays a key biological role: it blocks the arachidonic acid pathway, preventing the formation of thromboxane A2 and prostaglandin F2-alpha, which drive vasoconstriction and secondary vessel occlusion.
- Blister care:
- Clear-fluid blisters (second degree): The blister roof is left intact as a natural sterile dressing.
- Hemorrhagic blisters (third degree): The fluid is gently aspirated while the roof is preserved, and an antibiotic or bismuth tribromophenate dressing is applied.
Microcirculatory Vasodilators and Thrombolysis
- Nifedipine (for chronic chilblains/pernio): Extended-release nifedipine 20–60 mg/day relaxes the smooth muscle of small vessels, noticeably reduces pain and itching, and helps chilblain lesions heal quickly.
- Prostacyclin infusion (iloprost): Indicated for deep (third- to fourth-degree) frostbite within the first 48 hours. Intravenous iloprost at 0.5–2 ng/kg/min for 6 hours a day reopens the blocked microcirculation and significantly lowers the rate of amputation.
- Thrombolytics (tPA – alteplase): Given by peripheral intra-arterial infusion for third- to fourth-degree frostbite that threatens the limb, within the first 24 hours.
Rehabilitation and Conservative Surgery
- Low-level light therapy (LLLT, 630 nm): Boosts mitochondrial ATP production and speeds up regeneration of the epidermis.
- Delayed debridement: The boundary of cold-induced necrosis takes 4–8 weeks to declare itself ("Frostbite in January, amputate in July"). Early amputation is avoided unless complications such as gas gangrene or serious systemic infection develop.
