Annals of Burns and Fire Disasters - vol. XVI - n. 1 - March 2003

FROSTBITE - EXCEPTIONAL CASES

Iliopoulou E., Lochaitis A.

Department of Plastic Reconstructive Surgery and Burns Unit, K.A.T. Kifissia General District Hospital, Athens, Greece

SUMMARY. Frostbite or cold injury is produced by prolonged exposure to subfreezing temperatures (below -6 øC) for at least 1 h. Localized cold injury is categorized by its pathogenesis as frostbite, and generalized injury is discussed as systemic hypothermia. Although Greece is a small country in the Mediterranean area with weather that rarely causes frostbite, in the last 12 years we have treated 11 such patients (two Greeks, one Pakistani, and eight Kurds). Two cases were the result of industrial accidents and the other nine were due to inappropriate use of sandals in very cold weather. The localization (hands in the Greeks and feet and digits in the others) and the different social and financial backgrounds suggest that it is difficult to recognize any social aetiology. Better prevention and the control of infection, together with effective nutritional and metabolic support, will minimize the extent of necrosis and future invalidity. Our conclusions are as follows: frostbite is closely related to social and financial status; it is not associated with death, although in the event of septicaemia or renal failure due to muscle necrosis or gas gangrene the prognosis may be poor, with inevitable transient or permanent invalidity; general therapy is related to hypothermia (with or without coma), shock treatment, septicaemia, and anticoagulant drugs; local therapy, starting after demarcation of necrosis, consists of partial or total amputation of fingers or limbs; and, above all, the most effective therapy is prevention.

Introduction

Frostbite was well known in the past, especially in relation to war casualties (Napoleon's campaigns in Russia, German soldiers in Siberia, Italian soldiers in Albania, Greek soldiers in the Korean war, etc.), cold water immersion, and accidents in the cold.1-4

In our day the term urban hypothermia describes the condition of city dwellers who present hypothermia, such as alcoholics, the homeless, the elderly, or persons with disabling medical problems.5

Progress in chemical technology causes industrial frostbite, as for example in accidents with liquid propane or freon and in anaesthesiology (nitrous oxide).6,7

The world's three highest mountain peaks have been climbed without cold injury, which highlights the fact that most cold injuries are preventable. Nevertheless, in mountaineering expeditions physicians are invited to participate not just because of their good company but also to provide proper treatment and prophylaxis against cold injury. The supplies in medical kits start with analgesics, antibiotics, and sterilized surgical instruments and finish with silver sulphadiazine cream for local treatment.8

All of these examples demonstrate that prevention is the best therapy for cold injury.

The change in temperature at freezing levels provokes the reaction of the hypothalamus. This mechanism starts from the thermal receptors of the skin's afferent pathways of

the spinal cord to the anterior hypothalamus-posterior hypothalamus, causing augmentation of heat production by muscle shivering (which also increases heat loss) and resultant metabolic thermogenesis (increase of catecholamines, thyroxin release, and rise of the basal metabolic rate).

Heat loss occurs through four mechanisms:

• radiation = loss to the environment via infrared radiation;
• convection = transfer to the environment by air or water in contact with the body and associated with air temperature and velocity;
• conduction = transfer to another object by direct contact (water or metal). In the presence of cold water, heat is transferred 32 times more than to the air;
• evaporation = the conversion of water to its gaseous phase at a cooling rate of 0.6 kcal/g.

Classification of cold injury

Cold injury presents many similarities to burn injury, such as extent, depth, and localization. It also provokes skin necrosis, together with severe metabolic changes.

The extent is usually limited, and is especially related to unprotected parts of body. Frostbite most commonly involves fingers, toes, the nose, cheeks, and ears1,3-5,9-11) and vary rarely the scrotum, penis, and gingiva.

The local physical deterioration of skin in frostbite can present various degrees of depth:

• first degree - erythema, local oedema in association with pain (involving nerve injury);
• second degree - vesicle formation, skin erythema, oedema (partial-thickness burn injury);
• third degree - local oedema with greyish-blue discoloration of the skin and development of gangrene after a few days (deep partial-thickness burn injury);
• fourth degree - deep cyanosis of the skin and development of gangrene after a few hours (full-thickness burn injury).

A different classification system regards the environmental conditions in which the injury occurs. The five categories, in order of increasing severity, are as follows:

• Chilblains. These are caused by prolonged contact with high humidity associated with low temperature, without freezing. The result is discomfort in the areas exposed, without skin discoloration, resolving spontaneously without loss of tissue.
• Immersion foot (trench foot). This occurs after exposure of wet feet for a few hours to low temperature (0-10 øC) without actual freezing. This condition was typical in soldiers standing for hours in the trenches during World War I. The symptoms are tingling discomfort and numbness, in association with skin erythema with or without skin loss.
• Frostbite. This is caused by exposure to temperatures below 0 øC for a number of hours. The deterioration of the skin reaches various depths (partial- to full-thickness injury) and gangrene rapidly occurs. Tingling, pain, numbness, and a certain amount of tissue loss occur. The skin is waxy-white, the limbs are immobile, sensation is absent, and prognosis is bad. This condition was typical during the war in Korea.
• High-altitude frostbite. This is seen after exposure to very low temperatures in association with a low atmospheric oxygen concentration and high wind velocities, i.e. conditions to which aviators and mountaineers are exposed. Such conditions accelerate heat loss. Extensive tissue loss and numbness, in association with waxy-white hard and stiff skin, gangrene, and autoamputation, occur after a short exposure of only a few minutes; the face and hands are frequently involved. Such cases were commonly seen in World War II.
• Hypothermia. This is related not to the duration of contact with low temperature but to organic reactions in any ambient temperature below that of the body core. When the core (oesophageal and rectal) temperature drops below 32 øC, this can lead to the clinical appearance of death.
• Three phases of progressive hypothermia are clinically recognized:⁵
• With a rectal temperature between 32 and 37 øC, there is shivering, the patient complains of the cold, but blood pressure is normal. The patient is conscious.
• With a rectal temperature between 24 and 32 øC, the patient presents shivering, muscle rigidity, dilated pupils, ventricular fibrillation, decreased breathing rate, and low blood pressure.
• With a rectal temperature of less than 24 øC, the patient is comatose and flaccid, presenting apnoea and spontaneous ventricular fibrillation. The body temperature drops, accompanied by progressive decrease of the pulse and pressure, collapse, and loss of consciousness. Victims present the clinical appearance of a deceased person even if they have myocardial electric activity (ECG J waves).

Predisposing factors

Various factors (metabolism, central nervous system, skin disorders, and drug use) can be involved:

• Metabolic factors. These include hypothyroidism, hypoglycaemia, renal failure, and malnutrition.
• Central nervous system. In certain conditions (spinal cord transection, head injury, cerebrovascular disease, hypothalamus lesion, Alzheimer's disease, and Wernicke's disease), skin disorders and previous cold injury will provide a field for frostbite, and tissue damage appears more rapidly than in normal tissue (burn injury, erythroderma).
• Age (the elderly and neonates). The elderly are more prone to become hypothermic because of the impairment of their ability to perceive cooler temperatures (regardless of whether they wear additional clothing) and their reduced capacity to produce heat (reduced muscle mass), correlated with certain pathologies (cardiovascular, respiratory, diabetes mellitus, low peripheral flow). Neonates are prone because of their large surface-to-body-mass ratio.
• Insufficient conservation of body heat (improper use of underwear and excessively tight clothes can provoke constriction and reduce the extent of heat-retaining air insulation).
• High humidity (wet socks, wet boots). Water has a good heat conductibility and the body loses heat easily. The same thing occurs with metal objects in direct contact with the bare skin.
• Alcohol or drugs. Drugs such as ethanol, phenothiazine, general anaesthetics, barbiturates, benzodiazepines, opiates, and reserpines lead to a reduced capacity of judgement and the self-protection instinct and to fatigue and apathy.
• Infection (peritonitis, meningitis, bacteraemia).
• Immobility (movement provides better vascular circulation and heat production).
• Race and climate (dark-skinned persons are more susceptible to cold injury).

Pathophysiology

The principal mechanism of cold injury develops at the level of the cell wall and passes to the progressive formation of extracellular ice crystals without disruption of the cell membrane (when the freezing process is slow) or of intracellular ice crystals with disruption of the cell membrane (when freezing is rapid).

When water is transformed to ice, the osmolality in the extracellular space increases and leads to passive diffusion of water from the intracellular space.12 Microvascular insults also play an important role in the pathogenesis, due to local vascular constriction, thrombosis, and occlusion (which can be reversible), spreading to larger vessels with ischaemia and necrosis when the contact with low temperatures continues for several hours. Subsequent reconstructive surgery must be planned. In first- and second-degree frostbite, recovery is normally successful. Hypothermia also induces clot disease owing to three mechanisms:

• enzymatic reactions;
• enhancement of plasma fibrinolytic activity
• adverse effect on platelet morphology and sequestration, which probably justify the use of antithrombotic drugs and extracorporeal bypass.
• Metabolic changes related to cold injury are:
• plasma protein alteration (due to increased capillary permeability), involving albumin, fibrinogen, and globulin, an increase in blood viscosity, and alteration of the sodium-potassium pump, especially after cell disruption, possibly resulting in elevated potassium levels;
• elevated serum lipid concentrations due to mobilization of serum triglycerides, inhibition of lipid storage in fat depots, and release of phospholipids from disrupted cell membranes;
• impaired coagulation and disseminated i.v. coagulation (haemolysis of circulating erythrocytes, similar to the burn injury mechanism).

Treatment

A.In the field (pre-hospital care)

First aid in the field consists in the control of cardiac and respiratory functions and the transport of the patient away from the freezing environment, removal of clothing, and slow warming of the limbs. When patients are hypothermic they can be rewarmed using a plastic bag or a sleeping bag. If hypothermia is severe it is preferable to wait until hospitalization because the warming and rewarming of the limbs can provoke permanent tissue damage. Studies of the late phase of freezing have demonstrated the presence of stasis coagulation, arachidonic acid, metabolites, and thromboxane A2. Topical Aloe vera cream has been described as a potent inhibitor of thromboxane A2 synthesis and is widely used in the treatment of frostbite, improving tissue survival in association with aspirin, indomethacin, and ibuprofen.13

B. In the emergency department (hospital care)

Continuous monitoring of vital signs, with a complete blood count and full examination, must be performed. The fact that standard clinical thermometers do not record temperatures below 34 øC can be a problem in the assessment of the type of hypothermia. The diagnosis in relation to freezing conditions will lead to differentiated therapy. The thawing process must be properly conducted:

• rapidly, by immersion in heated water (40-42 øC), when the limb is frozen, hard, and inflexible and the skin is waxy; rewarming is painful and the patient will need morphine. Care must be taken not to increase the temperature because this could cause burn injury. After 30 min the skin becomes soft and erythematous, and vesicles will form, depending on the depth. If they do not appear, gangrene will develop;
• slowly, by massage, warm gloves, and cloths (32-37 øC), when the limbs are erythematous, soft, and sensitive.

Rewarming techniques are divided into:

• passive (no added heat), using environmental items such as blankets, plastic bags, clothes, etc.;
• active (heat added) - this can be either external, using heating pads, immersion in warm water, and environmental heaters, or internal, using i.v. heated solutions (40 øC), haemodialysis, gastric-colon lavage, peritoneal lavage, inhalation of heated oxygen, and extracorporeal blood rewarming.

The general assessment of cold injury is related to the development of hypothermia, collapse, and the sludge obstructive process. A tetanus toxin booster is given as soon as possible in association with antibiotics, low molecular weight heparin, and low molecular dextran. Nicotine is prohibited because of its vasoconstrictive properties. The extremities involved are elevated in order to minimize oedema, and kinesiotherapy is quickly initiated, especially in the hands.

Local treatment depends on the localization and depth of the injury because in the first days it is impossible to determine tissue viability. Daily cleaning and whirlpool treatment for gentle "physiological debridement" must be performed for some weeks. Complementary examinations that facilitate early prognosis (bone scintigraphy Technetium 99) can be used to prevent early amputation.⁹

Surgical treatment is normally performed after the final demarcation between viable and nonviable tissue and the stabilization of necrosis, unless the dry eschar is constrictive or the necrosis beneath the eschar is very productive, making surgical decompressing incisions imperative. Careful debridement is performed early in order to prevent damage to underlying tissues. Dry gangrene developing at the level of the upper or lower limbs will require amputation, and future reconstructive surgery must be planned. As already said, in first- and second-degree frostbite recovery is normally successful.

Because hypothermia induces clot disease, the use of anti-clot drugs and extracorporeal bypass is justified. A study conducted in Austria related to the use of iloprost (with regard to profibrinolytic and vasodilator activity) reports some benefits for frostbite treatment, but the five cases described are insufficient proof.¹²

Possible sequels of frostbite include cold sensitivity, hyperhydrosis, intrinsic muscle atrophy, skin colour change, arthritis, hyperaesthesia, chronic pain, and - very rarely - squamous cell carcinoma and pineal calcification. The diagnosis is based on a past history of cold injury, radiographs (abnormality of phalanges, irregularities of the articular surfaces), severe growth disturbances, and degenerative local skin changes,¹⁴ especially evident in children. The direct effect on the chondrocytes, bone growth (Wolkman's ischaemia), and prolonged tissue swelling may be the reason for this damage.

Despite the effectiveness of the classical management of cold injury (rewarming techniques), there are numerous new considerations and controversies about these techniques, their timing, and how to perform them. The "after drop" phenomenon (reported after the use of external rewarming in animals), which is a paradoxical decrease in core temperature after initiation of shell rewarming, has engendered many doubts about proper timing and the manner and rate of rewarming. It is not clear how we can achieve a high survival rate using

the new methodology when the references relate to different types of cold injury and different weather conditions, and when different clinical trials are used for a wide variety of populations (age, race, pre-morbid condition).

Materials and methods

In the last 12 years we have treated 11 patients suffering from frostbite (two Greeks, one Pakistani, and eight Kurds), all male, with ages ranging between 20 and 40 yr. Professionally, one patient was a nurse, two were labourers, one was a technician, five were teachers, and two were farmers.

The causes of frostbite were as follows: three work accidents (contact with freon, an oxygen tube, and ice in an industrial transport freezer truck for vegetables and fruit) and eight cases of improper use of sandals in the crossing of Greek mountain borders by Kurdish political refugees in winter time.

The localization was the upper limb (right palm) in the Greeks) and the lower limb in the non-Greeks (both feet in all cases). The depth was partial-superficial in the hands and deep- and full-thickness in the lower limbs. To be precise, in two cases the damage involved cuneiform bones (lateral, intermediate, and mediate), while in four patients the cuboid bone was also affected, with partial amputation of multiple fingers in association with partial necrosis of the metatarsophalangeal joints with open bone surface, inflammation, and infection.

In two cases (Greeks) hospital admission was immediate (i.e. in less than 1 h), in one case (Pakistani) after seven days, and in eight cases after three weeks (political immigrants passing through Greece to reach the rest of Europe).

Treatment was conservative in the hand localization, and surgical in plantar and finger necrosis. Treatment consisted of antibiotics and tetanus prophylaxis in the Greeks, and analgesia and a full clinical examination, including radiology, were performed in three of our cases. No systemic infection occurred. Amputation of all the fingers was the rule in the Kurds, while the left toe and two fingers and the first right metatarsophalangeal joint were amputated in the Pakistani. The operations were performed step by step in the dressing room in the Pakistani, starting on day 10 after the accident, in the presence of clear demarcation and stabilization of necrosis. The eight Kurds were treated in our hospital as out-patients twice a week for two weeks.

The evolution of frostbite in the palm was very good, and the patients were dismissed on day 4; they stayed away from work for 10 days and no permanent infirmity was reported. In the Pakistani, the partial amputation of the left toe and the amputation of two fingers and the first metatarsophalangeal joint resulted in permanent infirmity and problems in the patient's financial and social status (he lost his job). This patient was hospitalized free of charge for three weeks (in Greece all foreigners receive treatment free of charge on first admission if the cause is accidental).

Discussion

Accidental hypothermia is exceptional in Greece, and in 12 years we encountered only 11 cases. The frequency of this type of thermal injury is much lower here than in other countries (e.g. France, Finland, and Canada) that have high peaks⁹ or cold climates.^15,16 Over a period of 12 years in the prairies in Saskatchewan, 125 patients presented lower extremity frostbite (47%), which is similar to our cases (72% foot localization).

In the hands, the localization of the injury was the result of the non-use of protective gloves and improper use of sandals in trucks for fruit and vegetable freezing. The use of woollen gloves with neoprene was successful in experimental animals, but to decrease the possibility of labour accidents in workers the glove has to be worn only up to the mid-arm or elbow, since the liquid can flow into the glove during exposure.⁶

As we have already pointed out, the world's highest mountain peaks have been climbed without cold injury, underlining the preventability of most cold injuries - prevention is always better than cure. Nevertheless, our patients, except those involved in work accidents, were the victims of environmental cold weather in winter. Their age range was from 20 to 40 yr, i.e. they were young men, healthy, with no history of psychiatric disease and no problem of alcohol or drug consumption. In the list of pre-morbid conditions we found only starvation with low protein levels in close correlation with trench foot casualties and high altitude frostbite. The real cause of cold injury in the majority of our cases (72.7%) was political and financial instability and not military or winter sports activities.^8,9,15,16

In two patients the hand localization with superficial partial-thickness lesions was small and did not provoke infirmity or disability, compared to the nine patients with foot and plantar localization and deep partial-thickness to full-thickness injuries. After several days in freezing conditions, high humidity resulted in the autoamputation of fingers and in open wounds with exposed metatarsal bones, inflammation, and extensive skin necrosis. The social and financial status of the non-Greeks was very low and offered very uncertain prospects.

Conclusions

Frostbite is produced by prolonged exposure to subfreezing temperatures (below 6 øC) for at least 1 h. There are various predisposing factors and conditions (age, race, insufficient conservation of body heat, alcohol and drug use, psychiatric disease, skin disorders), but we believe in particular that:

• frostbite is closely related to social and financial status;
• even if frostbite is not related to death (except in cases of septicaemia or renal failure due to muscle necrosis or gas gangrene), prognosis can be poor, with inevitable transient or permanent invalidity;
• general therapy should be directed at hypothermia (with or without coma), shock treatment, septicaemia, and anticoagulant drugs;
• local therapy, starting after definite demarcation of necrosis, consists of partial or total amputation of the fingers or limbs;
• and, above all, the most effective therapy is prevention (protective gloves, socks, military shoes).

RESUME. La gelure, ou la l‚sion par froid, est caus‚e par l'exposition prolong‚e … une temp‚rature au-dessous de -6 øC pour au moins 1 h. La l‚sion localis‚e due au froid est cat‚goris‚e par sa pathogenŠse comme gelure, tandis que la l‚sion g‚n‚ralis‚e est d‚finie comme hypothermie syst‚mique. Bien que la GrŠce soit un petit pays m‚diterran‚en avec un climat qui rarement provoque la gelure, les Auteurs ont trait‚ 11 de ces patients dans ces derniers 12 ans (deux Grecs, un Pakistanais et huit Kurdes). Deux cas ont ‚t‚ caus‚s par des accidents industriels et les autres par l'emploi inappropri‚ de sandales par temps trŠs froid. La localisation (les mains dans les patients grecs et les pieds et les doigts dans les autres) et les divers ‚l‚ments socio‚conomiques font penser qu'il serait difficile d'‚tablir une ‚tiologie sociale. Une pr‚vention meilleure et le contr“le de l'infection, unis … un soutien nutritionnel et m‚tabolique efficace, peuvent minimiser l'importance de la n‚crose et l'invalidit‚ future. Les Auteurs tirent les conclusions suivantes: la gelure est ‚troitement li‚e … la condition sociale et ‚conomique; elle n'est pas associ‚e … la mort, mˆme si en cas septic‚mie ou d'insuffisance r‚nale due … la n‚crose musculaire ou … la gangrŠne gazeuse le pronostique peut ˆtre m‚diocre, avec une invalidit‚ transitoire in‚vitable et possiblement permanente; la th‚rapie g‚n‚rale est li‚e … l'hypothermie (avec ou sans coma), au traitement du choc, … la septic‚mie et aux m‚dications anticoagulantes; la th‚rapie locale, qui doit commencer aprŠs la d‚marcation de la n‚crose, consiste en l'amputation partiale ou totale des doigts ou des membres; et, surtout, la th‚rapie la plus efficace est la pr‚vention.

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