Core Skills, News & Features — 17 June 2013 at 5:16 pm


Chris Imray / Consultant Vascular Surgeon, Coventry and Warwickshire NHS Trust
Andy Grieve / Deputy Senior Medical Officer, RAF Valley, Anglesey
Charles Handford / RAMC, Medical Student, University of Birmingham
Ben Cooper / Charge Nurse, A&E, Northern General Hospital, Sheffield
Sean Hudson / General Practitioner, Maryport

Prevalence and pathophysiology of frostbite

The prevalence of frostbite amongst the civilian population has risen in part because of an increase in the numbers of homeless, but also because of greater ease of air travel, participation in winter sports, and ascents to high altitude.

The feet and the hands account for 90% of frostbite injuries reported. Frostbite also affects the face, particularly the nose, chin, earlobes, cheeks and lips, the buttocks/perineum from sitting on metal seats and the penis in joggers.

The pathophysiological processes have been studied extensively using both human and animal models. Local cold injury produces a succession of changes which are commonly divided into:

  1. Prefreeze phase
  2. Freeze–thaw phase
  3. Vascular stasis phase
  4. Progressive or late ischaemic phase

Skin sensation is lost around 10-15°C. With further cooling, vascular contents become more viscous, there is microvascular constriction and transendothelial leakage of plasma. As skin cools further (0°C), freezing occurs and frostbite develops. Low ambient temperatures, wind and moisture accelerate this rate.

Unless freezing is very rapid, ice crystals form first in the extracellular fluid spaces. Extracellular osmotic pressure increases, drawing free water across the cell membrane. This causes intracellular dehydration and hyperosmolality.

As freezing continues, there are extra- and intracellular electrolyte and pH changes, dehydration, and destruction of enzymes. Cell volume reduction and possibly direct damage from ice growth occur. Cell membranes are damaged, microvascular function is compromised and endothelial cells are injured, with the endothelium separating from the arterial wall lamina.

Depending on the method of rewarming, hyperaemia, ischaemia, cyanosis, or total circulatory failure develops. Blebs or blisters may appear secondary to vasodilatation, oedema, and stasis coagulation. Platelet and erythrocyte aggregates clog and distort the vessels in viable tissue. Associated injury may cause increased compartment pressures.

As is seen in burns, reperfusion injury occurs. This may involve oxygen-free radicals, neutrophil activation, and other inflammatory changes.

Prostaglandin F2a (PGF2a) and thromboxane A2 (TXA2) cause platelet aggregation and thrombosis which results in ischaemia and elevated concentrations of PGF2a and TXA2 are found  in frostbite blister fluid. These eicosanoid derivatives have been heavily implicated as mediators of progressive dermal ischaemia in burns, frostbite and ischaemia/ reperfusion injuries.

Depending on the degree of microvascular damage, one of two processes occurs: either vascular recovery with dissolution of clots, or vascular collapse which results in thrombosis, ischaemia, necrosis and gangrene.

Clinical Presentation

Symptoms / Patients initially describe a cold numbness with accompanying sensory loss.  The extremity feels cold to touch and it feels clumsy, “like a block of wood”.  Thawing and reperfusion is often intensely painful. Residual tingling sensation starting after one week has been described and may be due to an ischaemic neuritis.

Signs / Initial appearances are often deceptively benign. However with thawing, frozen tissue may appear mottled blue, yellowish-white or waxy. Following rapid rewarming, there is an initial hyperaemia even in severe cases.

Classification / Frostbite injury has been classified as either mild/superficial (no tissue loss) or severe/deep (with loss of tissue), and this classification is based upon final outcome. Cauchy of Chamonix proposed a predictive classification system that is based on the topography of the lesion(s) and early technetium-99 bone scanning. Using these techniques it is now possible to predict the likely outcome as early as two days.


Treatment of frostbite can be divided into three phases: field care, immediate hospital care, and post thaw care. Rapid evacuation, usually by helicopter, from mountain to hospital eliminates the first phase.

Field Care / If there is a possibility of developing frostbite the subject should move out of the wind and seek shelter. A combination of warm drinks, removal of boots (consider problems with replacement if swelling occurs), and replacement of wet gloves and socks with dry ones,  warming of the  cold extremity by placing in companion’s armpit or groin for 10 minutes only, finally putting the boots back on should help.

Aspirin (150-300mg) or ibuprofen (400mg) may improve the circulation. Do not rub the affected part, or apply direct heat. If sensation returns, one can continue to walk. If there is no return of sensation, go to the nearest warm shelter (hut or base camp) and seek medical treatment. If at high altitude, give oxygen, fluids and descend.

Field Rewarming / Field rewarming should only be undertaken if there is minimal risk of refreezing since refrozen tissue almost always dies. The decision to thaw the frostbitten tissue in the field commits the provider to a complex course of action involving pain control adequate warming and hydration in a hostile environment and subsequent protection of frostbitten tissue from further injury during evacuation. Frostbitten extremities cannot be used for ambulation once rewarmed.

Hypothermia and concomitant injuries should be evaluated and systemic hypothermia should be corrected to a core temperature of 34°C. Patients are often dehydrated; moreover, hypothermia causes cold diuresis due to suppression of antidiuretic hormone, so intravenous fluids are often advisable.

Post-Thaw Care / Blisters containing clear or milky fluid should be debrided and covered in aloe vera, a potent antiprostglandin agent 6 hourly. The limb(s) should be splinted, elevated to reduce reperfusion oedema, and wrapped in a loose, protective dressing. Padding should be put between the patients’ toes.

Haemorrhagic blisters should be left intact to prevent desiccation of the underlying tissue. If they restrict movement they can be drained with their roofs left on.

Tetanus toxoid and opiate analgesia should be given if indicated. Ibuprofen (400mg orally, every 12 hours) provides systemic antiprostaglandin activity that limits the cascade of inflammatory damage. Antibiotics should be prescribed if there is evidence of infection.

Thrombolytic Therapy / There is emerging evidence that treatment of severe frostbite injuries with intra-arterial thrombolytic agent (tPA) or synthetic prostacyclin analogue (Iloprost) improves outcome. Patients to consider for thrombolysis/Iloprost are those presenting within 24 hours of original exposure with apparently severe injuries where digit / limb loss is predicted.

A review of absolute and relative contraindications of t-PA should be undertaken. The treatment should occur in a facility with vascular surgery and HDU/ITU monitoring capabilities.

Early Surgery / Fasciotomy should be performed if a compartment syndrome develops, but amputation should be delayed for up to three months, and certainly until the level of demarcation is clear. However systemic infection resistant to intravenous antibiotics warrants early surgical debridement/amputation.

Nursing Care / Goals include keeping the patient comfortable, pain free, well nourished and adequately hydrated. Twice daily antibacterial whirlpool baths encourages the blister eschars to separate from underlying healthy tissue. Early mobilisation with help of physiotherapists is beneficial but further trauma must be avoided.

Amputation / Failure to delay surgery remains a major cause of avoidable morbidity. Better long term functional results are achieved with the early involvement of a multidisciplinary rehabilitation team. Early mobilisation of patients with partial foot amputations on weight bearing custom made orthoses has shown promising results.

Telemedicine / A recent development in accessing expert advice, which has been driven both by the patient’s themselves and also those clinicians with a more limited experience of frostbite, is the use of the internet. A virtual opinion can be sought from anywhere in the world. The UK based service can be accessed via the Diploma in Mountain Medicine or the British Mountaineering Council websites.


Although still potentially a disastrous injury associated with a high morbidity, frostbite can now be treated more effectively to ensure tissue loss is minimised and functional outcome maximised. With adequate preventative measures the risk of frostbite injury can be reduced.

With the rising prevalence of frostbite, future research remains important. However, a number of factors mean that progress is likely to be slow. Injuries tend to be variable and unpredictable, presentation is often significantly delayed and often to a wide range of different centres, there is no good animal model for basic research, and apart from the  military there is little likelihood of achieving significant funding for research programmes.

Research over the past 15 years has led to a new understanding of the pathophysiology of cold injury. Understanding of the role of inflammatory mediators, such as PGF2 and TXA2, has led to new active medical regimens such as the use of ibuprofen and aloe vera. Improved imaging assessment using MRA, and technetium scintigraphy, coupled with further research into the use of adjunctive therapies such as the use of thrombolytic agents and vasodilators further advancement in the treatment of frostbite.

However, prevention, early warming, early medical treatment and delayed surgery are likely to remain the mainstays of treatment for the foreseeable future.


  1. Wilderness Medical Society practice guidelines for the prevention and treatment of frostbite. McIntosh SE, Hamonko M, Freer L, Grissom CK, Auerbach PS, Rodway GW, Cochran A, Giesbrecht G, McDevitt M, Imray CH, Johnson E, Dow J, Hackett PH; Wilderness Medical Society. Wilderness Environ Med. 2011 Jun;22(2):156-66
  2. Cauchy E, Chetaille E, Marchand V, Marsigny B. Retrospective study of 70 cases of severe frostbite lesions: a proposed new classification scheme. Wilderness Environ Med 2001;12:248-55
  3. Cauchy E, Cheguillaume B, Chetaille E. A controlled trial of a prostacyclin and rt-PA in the treatment of severe frostbite. N Engl J Med. 2011 Jan 13;364(2):189-90
  4. A clinical review of the management of frostbite. Grieve AW, Davis P, Dhillon S, Richards P, Hillebrandt D, Imray CH. J R Army Med Corps. 2011 Mar;157(1):73-8
  5. Managing frostbite. Hallam MJ, Cubison T, Dheansa B, Imray C. BMJ. 2010 Nov 19;341:c5864. doi: 10.1136/bmj.c5864
  7. Cold damage to the extremities: frostbite and non-freezing cold injuries. Imray C, Grieve A, Dhillon S; Caudwell Xtreme Everest Research Group.Postgrad Med J. 2009 Sep;85(1007):481-8.

27.05.14 Note from editor / If you enjoyed reading this article, the authors have recently published a more in-depth review of frostbite management, giving advice on novel therapies. It can be accessed online for free, just follow this link.