Patient professional reference
The severity of cold injury depends on the temperature, duration of exposure, environmental conditions, amount of protective clothing and the patient's general state of health. Exposure to cold can cause localised injury or generalised cooling of the entire body. See separate Hypothermia article.
Susceptibility to cold injury is increased by any factor that can increase heat loss or decrease heat production:
- Lower temperatures - especially windy conditions.
- Infancy, elderly age, malnutrition, exhaustion.
- Immobilisation - eg, fracture.
- Open wounds.
- Prolonged exposure.
- Peripheral arterial disease.
- Impaired cerebral function - for example, alcohol, other sedatives, psychiatric illnesses, hypoglycaemia.
- Smoking, diabetes and Raynaud's disease increase risk due to vasoconstriction.
- Peripheral neuropathy, autonomic neuropathy, head injury, spinal cord damage.
- Body parts previously frostbitten are at increased risk due to damaged microcirculation.
The initial response to the skin cooling is vasoconstriction. This is to help preserve core body temperature. This is followed by a cold-induced vasodilation which protects against cold injury at the cost of increased heat loss. This begins at about 10°C and the skin starts to lose sensation. With further cooling, blood viscosity increases and there is further vasoconstriction. At around −4°C, ice crystals will start to form in the extracellular space. During the freezing phase the body part will initially feel cold, then numb, with individuals describing clumsiness alongside anaesthesia.
Possible localised injuries caused by cold include the following clinical syndromes.
Frostnip is the mildest form of cold injury. There is initial pain, pallor and numbness of the affected area. It is completely reversible with re-warming - usually within 30 minutes - and does not result in any cellular damage, tissue loss or ongoing abnormality.
Frostbite involves freezing of the tissue with microvascular occlusion and subsequent tissue anoxia. Some of the tissue damage may result from reperfusion during re-warming. There is a four-tier classification in common use:
- First-degree: hyperaemia and oedema without skin necrosis.
- Second-degree: large clear vesicle formation in addition to hyperaemia and oedema with partial-thickness skin necrosis.
- Third-degree: full thickness with subcutaneous tissue necrosis, often with haemorrhagic vesicles.
- Fourth-degree: full thickness and subcutaneous tissue necrosis, also involving muscle and bone with gangrene.
A two-tier classification has also been described - superficial or deep frostbite. Superficial frostbite corresponds to first-degree and second-degree frostbite with no or minimal anticipated tissue loss. Deep frostbite corresponds with third-degree and fourth-degree injury where greater tissue loss will be anticipated.
The area is described as cold and numb, and there is often intense pain on thawing and re-perfusion. Signs will depend on the degree of injury and on the stage of thawing.
Non-freezing cold injury
Non-freezing cold injury is a clinical syndrome which occurs as a result of exposure to low temperature over a long time without freezing of tissue fluids. Prolonged pain and a sensory neuropathy may develop on re-warming. Increased sensitivity to cold persists in the long term. Potential complications include ulceration and tissue loss which can eventually lead to amputation.
Trench foot is a non-freezing injury of the hands or feet resulting from chronic exposure to wet conditions and temperatures just above freezing. The entire foot may appear black but deep tissue destruction may not be present. Progression to hyperaemia within 24-48 hours causes an intensely painful burning and dysaesthesia. Tissue damage causes oedema, blistering redness, bruising and ulceration. Complications include local infection, cellulitis, lymphangitis or gangrene. Proper attention to foot hygiene can prevent the occurrence of most such injuries.
Chilblains are also known as perniosis or pernio. They are localised inflammatory skin lesions on exposed extremities of the body which are precipitated by cold.
Chilblains can be classified as:
- Acute: they develop within 12-24 hours after exposure to cold and last for 1-2 weeks.
- Chronic: they occur with repeated exposure to cold, resulting in persistent lesions which can lead to subsequent scarring and atrophy.
Chilblains typically occur on the face, tibial surface, or dorsum of the hands or feet, areas poorly protected or chronically exposed to the environment. There are pruritic, red-purple skin lesions (papules, macules, plaques, or nodules). Continued exposure leads to ulcerative or haemorrhagic lesions which progress to scarring, fibrosis, or atrophy with itching replaced by tenderness and pain.
If there is a strong possibility that the affected tissue could re-freeze then it is safer to keep it frozen than for it to be actively thawed. There is significant damage to a limb that freezes again. However, most frostbite will thaw spontaneously and it should be allowed to do so - there should be no attempt to keep tissue deliberately below freezing temperatures. Early management of cold-injured patients includes:
- Treat hypothermia (measure core temperature) and trauma.
- Identify the type and extent of cold injury.
- Remove jewellery or material that could constrict the body part.
- Rapidly re-warm in water heated and maintained between 37-39°C until the area becomes soft and pliable. This could take 30 minutes. Allow passive thawing if rapid re-warming is not possible. Add chlorhexidine or povidone iodine to the water used for re-warming where available.
- Give ibuprofen and other pain medication - opiates may be needed as re-warming can be painful.
- Air dry the area - do not rub it at all.
- Apply topical aloe vera cream or gel if available.
- Protect from re-freezing and any direct trauma. Use large, dry, bulky dressings and elevate the body part if possible.
- Ensure the patient is rehydrated. Give warm fluids where possible.
- Avoid walking on a thawed lower limb (it may be acceptable if only the distal toes are affected).
Treatment in hospital (or some kind of field clinic) follows the same principles as the early management in the field. There are some additional measures that can be implemented and more definitive surgical care may be necessary. Additional areas to consider:
- Tetanus prophylaxis if indicated.
- Debridement - this may involve selective drainage of clear blisters. Haemorrhagic blisters should be left intact.
- Systemic hydration with intravenous fluid.
- Systemic antibiotics: reserved for identified infections. Prophylactic antibiotics may be considered for severe injury. Tobacco, nicotine and other vasoconstrictive agents must be withheld. Weight-bearing is prohibited until oedema is resolved.
- An experienced surgeon should be involved to assess for interventions. As well as clinical examination, angiography and technetium 99m bone scan can be used to assess surgical margins.
- Thrombolytic therapy can be considered. Most used is tissue plasminogen activator (tPA). This may be appropriate for deep frostbite where there is potentially significant morbidity. It should be used in the first 24 hours after thawing the affected tissue. Angiography can be used for pre-thrombolytic intervention and subsequent monitoring. Thrombolytic therapy should only be undertaken where intensive-care facilities exist.
- The vasodilator effect of the prostacyclin analogue iloprost has also been found to be effective, although this is not available in the UK for intravenous administration.
After initial therapy there are some interventions that can be considered and may reduce long-term sequelae:
- Hydrotherapy. There is no evidence that it improves outcomes but it may improve circulation and help with debridement.
- Hospitalisation will usually be necessary to manage deep frostbite but individual factors would otherwise determine whether the cold injury could be managed on an outpatient basis.
- Surgical treatment, including amputation. Estimation of depth and extent of tissue damage is not usually accurate until demarcation is evident. This can take 1-3 months, although investigations may help with assessment.
- A multidisciplinary approach will help achieve better long-term functionality - eg, protective footwear and orthotics in cases of deep frostbite to the lower limb.
- Sympathectomy is not usually recommended, as there is not enough evidence to support its use and it is irreversible.
- Hyperbaric oxygen therapy is not recommended due to insufficient evidence of any benefit.
Management of other cold injuries
Non-freezing cold injury
Gradual re-warming is the first stage of treatment. Affected extremities should not be rubbed. Analgesia may be required. Pain may be relieved by tricyclic antidepressant treatment. In later stages, the involvement of a specialised foot service may be helpful for consideration of insoles and advice about footwear. A pain specialist may be needed to advise about pain relief.
Most idiopathic chilblains resolve spontaneously without treatment. Careful protection from further exposure should be advised. Nifedipine may be helpful for prevention or treatment if symptoms are severe or recurrent.
When combined with hypothermia or wound-related sepsis, localised cold injuries may lead to death. Complications are more common in those with arterial or systemic disease.
- Secondary wound infection.
- Fluid sequestration in damaged tissues and diuresis may cause volume depletion.
- Hyperglycaemia, acidosis.
- Possible long-term sequelae of cold injury include:
The prognosis depends on the severity and duration of the cold environment and the presence of any risk factors.
Further reading and references
Excess winter deaths and morbidity and the health risks associated with cold homes; NICE Guideline (March 2015)
Ingram BJ, Raymond TJ; Recognition and treatment of freezing and nonfreezing cold injuries. Curr Sports Med Rep. 2013 Mar-Apr12(2):125-30. doi: 10.1249/JSR.0b013e3182877454.
Climatic illness and injury in the armed forces: Force protection and initial medical treatment; Ministry of Defence May 2016
Chilblains; DermNet NZ
Zafren K; Frostbite: prevention and initial management. High Alt Med Biol. 2013 Mar14(1):9-12. doi: 10.1089/ham.2012.1114.
McIntosh SE, Hamonko M, Freer L, et al; Wilderness Medical Society practice guidelines for the prevention and treatment of frostbite. Wilderness Environ Med. 2011 Jun22(2):156-66. doi: 10.1016/j.wem.2011.03.003.
Chilblains; NICE CKS, August 2013 (UK access only)
Handford C, Buxton P, Russell K, et al; Frostbite: a practical approach to hospital management. Extrem Physiol Med. 2014 Apr 223:7. doi: 10.1186/2046-7648-3-7. eCollection 2014.
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