Overview
Definition
Frostbite is injury to tissue resulting from cold exposure at temperatures below 0°C (32°F). Frostbite exists on the severe end of a spectrum, with frostnip and pernio at the milder end.
Epidemiology
- Poor population statistics (no formal reporting)
- Vulnerable populations:
- Homeless
- Military personnel
- Children
- Elderly
- Risk factors:
- Low ambient temperature
- High-velocity wind
- Exposure to water or snow
- Clothing that is wet, constrictive, or inadequately insulating
- Impaired judgment (ethyl alcohol, drugs, fear/panic)
- History of peripheral vascular disease or Raynaud’s phenomenon
- Commonly affected areas: poorly vascularized periphery
- Fingers
- Toes
- Nose
- Ears
- Penis
Clinical classification
| Phase | Symptoms | Signs |
|---|---|---|
| Early | Cold, pain, paresthesia | Deceptively few: discoloration, waxy/stiff tissue texture |
| Middle | Numbness, complete sensory loss, loss of dexterity | Formation of blisters or bullae, desquamation |
| Late | Throbbing pain that may persist for months or weeks | Tissue loss, demarcation, dry gangrene |
Pathophysiology
Frostbite injury results from:
- Immediate cold-induced cell death
- Tissue cools below subfreezing → extra and intracellular ice crystals form
- Fluid and electrolyte fluxes → lysis of cell membranes with subsequent cell death
- Inflammatory process mediated by thromboxane A2, prostaglandin F2-alpha, bradykinins, and histamine
- Leads to tissue ischemia and necrosis
- Worsened in setting of thawing followed by refreezing
- Tissue ischemia
- Decreased temperatures increase blood viscosity → microthrombi
- Vasodilation and stasis result in tissue hypoperfusion and ischemia.
- Reperfusion-related localized inflammatory processes
- Caused by return of blood flow to ischemic areas
- Activated endothelial cells release activated oxygen species, initiating inflammatory response.
- WBCs flood to perfused area, releasing inflammatory mediators.
- Leads to cell death
4 phases:
- Pre-freeze:
- Tissue cooling
- Vasoconstriction
- Ischemia
- Endothelial leakage
- Freeze-thaw:
- Ice crystal formation
- Cellular dehydration and death
- Vascular stasis: microvascular thrombus formation
- Late progressive ischemia:
- Hypoperfusion
- Inflammation
- Tissue necrosis
Diagnosis
The diagnosis of frostbite is clinical and should be distinguished from less severe forms of cold injury (frostnip).
- Frostnip:
- No ice formation, no tissue loss
- Cannot clinically distinguish between frostnip and frostbite initially
- Passive rewarming
- If no tissue loss, frostnip
- Frostbite (severe form of injuries that may present in any of following stages):
- Stage 1: involves superficial areas of skin and presents with hyperemia, itching
- Stage 2: characterized by blisters, desquamation, edema
- Stage 3: ulceration and involvement of skin and subcutaneous tissue
- Stage 4: deeper injury of connective tissues, muscle, and bone necrosis leading to gangrenous limbs
Initial presentation of frostbite on day 2
Image: “Grade IV frostbite requiring bilateral below knee amputations: a case report” by Ramdass MJ. License: CC BY 3.0
Frostbite in a 12-year-old girl who presented to the emergency department after waiting at a bus stop in winter
Image: “Urban blisters” by Chang N, Nunn R, Milner SM, Price LA. License: CC BY 2.0
Appearance of grade IV frostbite with completely mummified feet 3 weeks post-injury
Image: “Grade IV frostbite requiring bilateral below knee amputations: a case report” by Ramdass MJ. License: CC BY 3.0
Management
Prehospital
- Remove any wet clothing.
- Bring patient to a warm environment.
- Do not put pressure on frostbitten extremities (e.g., rubbing frostbitten extremities or walking on feet affected by frostbite).
- Do not rewarm if there is a chance that freezing will recur.
Rewarming
- Rewarm in warm water (37–39°C (98.6°–102.2°F)) bath.
- Provide parenteral analgesia during rewarming.
- Thawing completed when tissue is red or purple and soft to the touch
Wound care
- Application of bulky dressing
- Elevation to reduce edema
- Daily hydrotherapy to improve range of motion
- Aspirin and nonsteroidal anti-inflammatory drugs (NSAIDs) to help reduce inflammation
- Tetanus-reported complication; prophylaxis recommended
Thrombolysis
- Used in severe, limb-threatening cases, presenting within 24 hours
- Options include intravenous or intra-arterial tissue plasminogen activator (tPA), or intravenous or intra-arterial heparin or enoxaparin.
Surgical management
- Initial assessment might overestimate real extent of tissue injury.
- No surgical treatment until demarcation occurs
- “Frostbite in January, amputation in July”
Clinical Relevance
- Raynaud’s phenomenon: exaggerated vascular response to cold temperatures or emotional stress causing sharply demarcated color changes of digits. Blood vessels constrict, which leads to digits turning blue. Digits return to normal color 10–20 minutes after cold is removed.
- Hypothermia: drop in core body temperature ＜ 35°C (95°F). Classified into mild, moderate, and severe forms. Management involves rewarming of patient by external or internal methods, depending on severity.
References
- Petrone P, Kuncir EJ, Asensio JA. (2003). Surgical management and strategies in the treatment of hypothermia and cold injury. Emerg Med Clin North Am.
- Murphy JV, Banwell PE, Roberts AH, McGrouther DA.(2000). Frostbite: pathogenesis and treatment. J Trauma.
- Long WB 3rd, Edlich RF, Winters KL, Britt LD. (2005). Cold injuries. J Long Term Eff Med Implants.
- Imray CH, Oakley EH. (2005). Cold still kills: cold-related illnesses in military practice freezing and non-freezing cold injury. J R Army Med Corps. doi: 10.1136/jramc-151-04-02.
- Rintamäki H. Predisposing factors and prevention of frostbite. (2000). Int J Circumpolar Health. PMID: 10998828.
