Surgery

Debridement and or amputation of necrotic tissue are usually delayed. This has led to the adage “Frozen in January, amputate in July” [12]. Indications for surgical debridement are unreliable until 2–3 weeks postwarming. Debridement should be deferred until that point unless tissue is causing a life-threatening condition e. g. infection or gangrene [13].

It is difficult to predict at initial presentation what the final demarcation between viable and necrotic tissue will be. Therefor early surgery usually is contraindicated in frostbite, because the nonviable tissue requires time to demarcate. Older series show that debridement prior to 2–3 weeks postwarming significantly increases the amount of viable tissue removed and is harmful to the patient, resulting in an increased amputation rate, mortality, and morbidity.

After a period of watchful waiting commonly accepted indications for surgical debridement include clearly necrotic or nonfunctional tissue. The absence of accurate radiologic assessment of viability has meant that the appropriate level of amputation is not clear until the tissue declares itself. Some authors are now advocating a more aggressive approach with the advent of technetium scintigraphy and advancing role of magnetic resonance imaging [14–17]. Preliminary results suggest that improved imaging may lead to reduction in length of hospital stay and still allow maximum stump length preservation.

The functional outcome of any surgery needs to be considered and ideally, where major limb loss is foreseen, the early involvement of a multidisciplinary rehabilitation team will produce better long term functional results [18].

Sympathectomy

The role of sympathectomy has yielded mixed results. Sympathectomy performed within the first few hours of injury is said to increase oedema formation and leads to increased tissue destruction. However if performed 24–48h after injury it is thought to decrease tissue loss and to accelerate resolution of oedema. Sympathectomy can also serve as a useful treatment in the late sequelae of frostbite such as hyperhidrosis and pain due to vasospasm [19]. How-

ever, since a sympathectomy is irreversible, great caution should be exercised when considering its use in frostbite.

Vasodilators

Iloprost, a stable metabolite of prostacyclin, is a powerful vasodilator and has been used in the treatment of frostbite with some success [20]. It is used in arterial surgery to mimic the effect of a sympathectomy. Pentoxifyllin is considered to lower pathologically increased levels of fibrinogen yielding some promising results in human trials [21]. Both drugs may protect against damage of the vascular endothelium, improve tissue perfusion and therefore limit tissue damage caused by frostbite. The a-blocker buflomedil has been used to increase peripheral blood flow [22].

tPA

A small study assessing the effectiveness of tPA in reducing amputation rates in frostbite has recently been reported by Bruen et al. Among the six patients who received tPA within 24h of injury, six of 59 (10%) affected fingers or toes were amputated, compared with 97 of 234 (41%) among those who did not receive tPA. It is postulated that rapid clearance of the microvasculature improves tissue salvage [23].

Escharotomy and fasciotomy

Escharotomyandfasciotomyhavenoprovenprophylactic role in the management of frostbite. Ischemic injury in frostbite is most often caused by vascular compromise from thrombosis and not by compression from edematous tissue, making decompression unnecessary. Escharotomy or fasciotomy may be indicated in the early phase if compartment syndrome develops [24, 25].

Prognosis

A number of long-term squeal can occur after frostbite. These include: transient or permanent changes in sensation, electric shocks, increased sweating,