Once a condition reserved for the armed forces and explorers, frostbite presenting itself more frequently at emergency departments. Vagrancy and homelessness are increasingly common and are often predisposing factors to the development of frostbite in urban areas. More commonly, the presentation is associated with unexperienced and unprepared thrill-seekers partaking in extreme winter sports such as glacier climbing, mountaineering and off-piste skiing. Manufacturing with coolants and nitrous oxide also puts users at risk. Recently there has been significant research into management techniques and emphasis has shifted from surgical to medical techniques to treat frostbite.
Development of frostbite
Frostbite is caused by prolonged exposure to cold temperatures, typically below -0.55ºc. Higher temperatures with prolonged exposure can lead to a similar pathological process, non-freezing cold injuries (NFCI), previously known as trench foot. It is usually a disease of the extremities, however the nose, lips, ears and other exposed areas are commonly affected.
The oldest recorded case is that of a mummy found deep in the mountainous Andes.
The physiological process involved in the development of frostbite is similar to that of burns. The extremities contain arteriovenous malformations which are designed to shunt blood to preserve body temperature at the expense of local tissue perfusion. Once temperatures go below 15ºc there is vasoconstriction with 5-10 minute bursts of vasodilation a few times per hour. At 10ºc, tissue losses its sensation and below 0ºc there is almost no cutaneous blood flow allowing tissue to freeze. Ice crystals form, damaging tissues and causing dehydration due to electrolyte shifts. Intravascular stasis causes thrombus formation, microvascular occlusion and tissue ischaemia. Reperfusion leads to a large-scale inflammatory response, hypoxia and cell death.
Studies have shown African Americans to be at greater risk of developing frostbite and a linear relationship with increasing age. Although some research has shown a greater prevalence in males, the study groups are often military personnel and thus have selection bias.
Frostbite risk is increased by the following factors:
- Wind chill
- Increased length of exposure
- Raynauds disease
- Repeated cold water immersion
- Alcohol consumption & altitude can indirectly influence frostbite development due to increased risk-taking behaviour.
Acute mountain sickness can lead to altered mental state and some sufferers have been reported to remove their clothing, refuse to sleep in shelters and be unable to perform simple acts of self care. By nature, these people will be in high risk situations and at greater risk of developing thermal injuries.
How to treat frostbite
Frostbite falls into an awkward category of conditions whereby those who know how to treat it do not possess the skills in which to do so and those who do possess the skills are unaware of the management. Vascular surgeons, who normally take responsibility for these patients may be unaware of the recent advances in research. The mainstay of treatment is now medical. Surgery is reserved for 3-6 weeks after the injury, once finite necrotic boundaries are well-demarcated.
There are many classification systems for frostbite. The two we refer to here are the Hota & Singh 4 grade classification and Cauchy et al. 4 grade, 3 descriptor classification.
Hota & Singh:
- Grade 1- A numb central white area with oedema and redness without necrosis.
- Grade 2-Blister formation with surrounding oedema and redness. Blisters may be clear or cloudy.
- Grade 3- Haemorrhagic blisters with some necrosis of skin
- Grade 4- Complete necrosis with possible self amputation.
Cauchy et al. base their 4 grade classification on the initial extent of the injury after rewarming, bone scanning at day 2 and blisters at day 2. From these three descriptors they predict prognosis.
- No lesion after rewarming and absence of blisters on day 2.
- Distal phalanx lesion after rewarming, Hypofixation of radiotracer uotake on bone scan and clear blisters at day 2.
- Proximal phalanx involvement after rewarming, Absence of radiotracer uptake on bone scan and haemorrhagic blisters at day 2.
- Carpal/Tarsal involvment after rewarming, absence of radiotracer uptake, haemorrhagic blisters over carpal/tarsal at day 2.
In both systems grade 3 and 4 usually result in amputation of part or all of the digit. Grade 4 can also progress to systemic sepsis.
It is sometimes safer to continue on a frozen extremity until medical care can be provided than risk a limb or digit refreezing. Once you have completely ruled out any potential of re-freezing you can commence treatment in the field.
- Seek warm shelter
- Remove wet clothing and replace with dry alternatives
- Remove any jewellery
- Take photographs of the affected areas
- Place the frozen area under a companions armpit or in their groin to warm
- If possible, give warm fluids
- Give analgesia – rewarming can be extremely painful!
A multi-disciplinary approach is most appropriate; to adequately treat frostbite requires intensive care, multiple interventional radiological procedures and potential surgery. There has been significant progress since WWII when surgeons would perform sympathectomies. Other treatments have included sympathetic blocks and radical amputations. Following research into how to treat frostbite, early intense medical treatment means much of the affected area can be salvaged.
First 24 hours
- Treat hypothermia first with warmed intravenous fluids and bear-huggers.
- IV fluids to rehydrate especially if the sufferer is from altitude.
- Rewarming – place the affected area in a warm bath with chlorhexadine or iodine at 38ºc. Do this for an hour or until a purple colour appears.
- Encourage movement and exercises.
- Provide good analgesia – the process will often require opioids.
- De-roof any clear or cloudy blisters.
- Aloe Vera gel for its anti-thromboxane effect.
- Ibuprofen – use 12mg/kg in 2 daily doses. This will provide analgesia and is also a potent anti-prostaglandin.
- Aspirin 300mg daily for its anti-platelet function.
- Cover the area with loose dressings
- Consider antibiotic coverage if there is any evidence of cellulitis or in urban cases.
- Medical treatments include: Vasodilators, TPA (Tissue plasminogen activator) & Iloprost (prostacyclin analogue)
Use Intravenous vasodilators to counteract the vasospasm and TPA to thrombolyse any emboli, allowing tissue perfusion. TPA is not without its risks; do not use if there is any concurrent trauma, recent surgery or haemophilia. You must monitor patients closely on an intensive care unit due to the bleeding risk.
Iloprost, although not yet available for use in the USA, iloprost is widely used to treat frostbite. It is a prostacyclin analogue, causing vasodilation and reducing platelet aggregation. Gradually increase the dose until a patient develops intolerable side effects (headache and hypotension). At this point reduce the dose slightly and continue treatment for 6 hours/day for 6-8 days. Patients receiving iloprost do not require intensive care and there is less radiographic monitoring than with TPA.
Iloprost dose: 0.5ng/kg/min, increase in 0.5ng increments to a maximum 2ng/kg/min.
Technetium-99 Scan – Bone scintigraphy is a modality used in the Cauchy et al. classification. It has good accuracy when predicting level of amputation if performed two days post injury.
Angiography is used frequently in conjunction with TPA and repeated at 12 hour intervals. This modality requires significant radiation doses and involves renal-toxic contrast materials.
Magnetic resonance angiography is a newer technique which is yet to have sufficient evidence to support its use, however it may well have better predictive value than previous modalities.
There is currently insufficient evidence to routinely recommend any alternative therapies to treat frostbite. Existing evidence thus far is fairly inconclusive. Masters et al. published a recent case study in the journal of burn care and research documenting the use of hyperbaric oxygen therapy to treat frostbite. A 24 year old with significant damage to his upper extremities received 20 hyperbaric oxygen therapies in conjunction with TPA treatment. On initial presentation both hands were stiff and white and after rewarming there was little improvement. 6 weeks later, he required amputations at the level of the distal inter-phalangeal joint of the 1st digit and proximal inter-phalangeal joint of the 2nd and 3rd digits of his right hand.
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