Frostbite

FROSTBITE

CLINICAL ASPECTS

Frostbite is a local injury due to the direct action of cold below 0°C for a non specific period of time. Frostbite injuries are usually classified in three (or four) degrees of severity according to their clinical aspect and evolution

First degree is characterized by pallor or transitory cyanosis followed by erythema during rewarming, numbed sensitivity, and complete healing within a few weeks. Superficial second degree is defined by the development of clear blisters in about 12 hours; the evolution is the same; the sensitivity problems can last longer. Deep second degree is characterized by a complete anesthesia, some haemorragic blisters and an important swelling higher up. When these deep frostbite injuries result in necrosis, then amputation, this is classified as third degree.

Several conditions promote the development of frostbite: the external temperature, the wind (higher convective loss), the humidity (conduction), an impairment of blood circulation (tight clothes and shoes, displaced fractures), the hydration state of the patient, hypoxia, high altitude hypoxia, and the quality of equipment. All people are not equal in the face of frostbite; the most classical risk factors are vasospastic disorders, autoimmune diseases, nicotine addiction and above all prior frostbite.

Clinical diagnosis is obvious, it is generally made by the patient himself, very rapidly for the fingers, more slowly for the toes.

At Chamonix hospital, we receive about 80 cases a year. 75% of cases are superficial frostbite. For deep frostbite, the aim of the traitment is to prevent amputation (8% of cases) but also neuro vascular and trophic sequels. In our series, frostbitten feet represent 57% of cases (especially the big toe) and 46% of patients have frostbitten hands (but usually keeping the thumb). Finally, frostbite of the face is not rare (17%), especially for the nose and ears

PATHOPHYSIOLOGY

Primary phase: cooling and frost effects

When it is exposed to cold, the organism responds by a peripheral vasoconstriction. This vasoconstriction causes a decrease of the capillar perfusion gradient and the development of local stagnation phenomenoms, hyperviscosity, hypoxia and acidosis.

Frost concerns the extracellular space first. In this area, the growing of ice cristals causes an increase of osmolarity, and then an intracellular dehydration by passive diffusion of water through the membrane. The cause of cellular death depends on the rapidity of development of the lesions. Often due to the mechanical aggression of extracellular crystals, it can be caused by the ultimate effects of the dehydration mechanism.

Second phase: thawing and progressive necrosis

During rewarming, arteriolar vasoconstriction is replaced by a reactional hyperhemia which facilitates the movement of liquids to the interstitium, and causes an increase in the blood viscosity followed by a slowing down of the microcirculatory flow. The desquamation of endothelial cells and the alteration of the basal membrane provoke an activation and adhesion of leucocytes. The activation of the acid arachidonic cascade in platelets causes the release of thromboxane A2. This reperfusion injury ends in a total interruption of the microcirculation within a few hours.

Late phase: permanent lesions

This is the richest phase in clinical demonstrations due to the progressive vascular necrosis (oedema, blisters, necrosis), it begins 48 hours after the rewarming. The lesions are then irreversible and if the treatment is begun only at this stage, the results are disappointing.

PROGNOSIS

The early prognosis is difficult to establish clinically. Three to four days are usually necessary to know if it is superficial or deep frostbite and, in this case, it is necessary to be patient until the appearance of the cut line of demarcation, more than 30 days after, to locate the level of amputation. This waiting for the verdict is intolerable for the patient; fortunately the bone scintiscanning with Technetium 99 makes it possible to shorten this delay. The examination should not be done too early because it can be falsely reassuring if the lesions of progressive necrosis have not have time to settle. In all of our series of 80 cases where the scintiscanning showed a normal fixing of the tracer at the late phase (osseous), there was no amputation. On the contrary, if the late phase showed a clear hypofixation, the patient had to have an amputation.

THERAPEUTIC APPROACHES

The treatment is based on pathophysiology: it is necessary to rewarm, to fight against vascular spasms, hyperviscosity, thrombosis and to prevent inflamation and infection.

The more effective treatment is immediate thawing in warm water (38°). This treatment may be done in the mountain hut. After that, refreezing must be absolutely avoided. The oedema which appears generally prevents the patient from putting his shoes back on.

For the first and superficial second degree frostbite, we associate aspirin (250 mg/day); buflomedil (Fonzylane®, LAFON), of which the dosage increases according to the severity (up to 800 mg/day); and a non steroid anti-inflammatory drug.

For more severe cases, we use iloprost (Ilomédine® SCHERING) (up to 50 µg/day) for 5 to 7 days and sometimes rTPA (30 to 50 mg) at the time of admission. Anticoagulation is maintained by a low molecular weight heparin. Aspirin is always mandatory. An appropriate blood volume is essential, as well as the respect of asepsis rules. Frostbitten parts are kept in a upward position as long as the oedema persists (one week). Whirlpool antiseptic baths are repeated twice a day. They clean the wounds, kill the bacteria and promote soft excising. As soon as the oedema has disappeared, the patient must actively do excercise in the bath to prevent tendinous retractions. Blisters are respected, except if they are constrictive or infected; in this case, antibiotics are prescribed.

Scintiscanning is done in the first 48 hours, it can be repeated a week later to estimate the effectiveness of the treatment.

Surgery is started after the first week, with blister and superficial necrosis removal. A good nutritious and psychological state must be maintained.

Amputation is delayed for as long as possible, in order to allow time for dry necrosis to settle, and to respect the natural delimitation.

SEQUELS

Sensitivity problems (pain, hypo or hyperesthesia), hyperhydrosis, finger ankylosis in flexion, skin and integument trophic troubles are regularly noted; they can persist for a long time. In the longer term (several years), osteoporosis and early arthrosis appear, caused by cartilage injuries. In amputated patients, plastic surgery often allows a good functional recovery.

CONCLUSION

Prevention remains essential. Rewarming by warm water is a therapeutic emergency. Afterwards there is the intervention of the inhibitors of the arachidonic acid cascade, the micro-circulation vasodilators and the antithrombotic drugs. Healing is always slow, amputations are rare, but the functional and trophic after effects can be disabling.

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