CHAPTER II
General Considerations of Cold Injury
TYPES OF COLD INJURY
In addition to total freezing of the deep tissues, cold injuries include chilblains, trenchfoot, frostbite, and immersion foot. All of these injuries, irrespective of environmental and other modifying circumstances, are related by the common factor of cold. They are differentiated and can be classified chiefly according to the degree of cold which has given rise to the injury, the duration of exposure, and the environmental factors, chiefly wet, which intensify the effect of low temperatures.
The temperature level at which cold injury will occur is not absolute. The level is dependent upon the various factors which have just been listed. It is modified by such other factors as fatigue, malnutrition, and, perhaps, individual variations in resistance. The upper limit of temperature at which cold injury may occur has also not been established. During World War II, men shipwrecked in the Gulf Stream, in which the temperature was 60?-70? F. (15.6?-21.1? C.), presented immersion foot, with sensory changes and gangrene, after 8 days.1 Webster, Woolhouse, and Johnston,2 who reported some of these cases, were unwilling to accept cold as a causative agent, but their interpretation seems open to question in view of Lewis' demonstration (p. 235) that the skin begins to lose heat at 61? F. (16.1? C.) and that immersion in water hastens the loss. A variety of cold injury was observed in United States troops after the landing at Leyte in the Philippine Islands (p.211), and another variety, so-called shelterleg (p.9), was reported in persons who had spent the nights in damp, but not necessarily very cold, London subways during the bombings earl in the winter.
Cold is the agent which causes tissue damage. This is true whether it is the mild, continuous type of cold which causes chilblains; the severe, dry cold which causes frostbite; or the combination of cold and wet which causes trench-foot and immersion foot. Different degrees of cold may give rise to what appear to be significant pathologic differences,3 and the resulting clinical manifestations may also vary in severity, but basically the pathologic process
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1(1) White, J. C.: Vascular and Neurologic Lesions in Survivors of Shipwreck. I. Immersion Foot Syndrome Following Exposure to Cold. New England J. Med. 228:211-222, 18 Feb. 1943. (2) White, J. C., and Scoville, W. B.: Trench Foot and Immersion Foot. New England J. Med. 232:415-422, 12 Apr. 1954. (3) Webster, D. R., Woolhouse, F. M., and Johnston, J. L.: Immersion Foot. J. Bone & Joint Surg. 24:785-794, October 1942.
2 See footnote 1 (3).
3 Ariev, T. V.: Fundamental Outlines of Present Day Knowledge of Frostbite. Medgiz: Moscow, 1943. This is one of a series of 16 papers originally published in Russian from 1939 to 1944 and translated into English and published by Earl R. Hope, in Ottawa, Canada, in 1950 under the title "Frostbite."
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is essentially the same in all cold injuries. This observation, while it holds particularly for frostbite, trenchfoot, and immersion foot, which constitute the ground-type injuries of military importance, does not exclude the occurrence of immersion foot in tropical waters when the period of exposure is sufficiently long.4
The interrelationships of the various cold injuries can best be understood by defining them as entities and noting the etiologic factors which, in conjunction with cold, are responsible for their production.
Chilblains
Chilblain has been described as trenchfoot of the hand, though it may also occur on the lower extremity. The lesions are most frequently located on the dorsal surface of the phalanges, between, rather than over, the joints. Although any portion of the dorsal surface may be affected, the thumbs are relatively exempt. Any portion of the lower extremity may also be affected, though the anterior tibial surface of the leg, especially in women, is probably the most common location.5
Chilblains may disappear within a few days or may assume a chronic form and last for weeks and months. In the chronic form, the condition is also known as erythrocyanosis, Bazin's disease, lupus, pernio, and dermatitis hiemalis.
The disease is provoked by cold above freezing which is experienced intermittently over long periods of time. It is observed chiefly in climates characterized by moderate cold and a high degree of humidity. The subjects are usually young persons, whose hands are likely to be colder than normal, and sometimes deeply colored, all the year round. The majority give a history of daily exposure in a cold, moist atmosphere. As a result, the injury of the preceding day has not been compensated for before there is the insult of added exposure on the succeeding day, and one lesion thus tends to develop over another.
Skin which has previously been damaged in any way is peculiarly susceptible to chilblains. Lewis 6 has also demonstrated that the condition is prone to appear in persons whose skin is hypersusceptible to the stimulation of cold. If the histamine test is carried out under standard conditions, with the skin at its ordinary temperature, the reaction is abnormal. His explanation is that the predisposing cause of chilblains is a chronically defective circulation: "It is to the high vascular tone of the limb vessels, to the readiness with which the temperature of fingers or other parts falls to that of its surroundings, and to the long delay in the release of this spastic condition of the vessels after
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4 Ungley, C. C., and Blackwood, W.: Peripheral Vasoneuropathy After Chilling. "Immersion Foot and Immersion Hand." Lancet 2: 447-451, 17 Oct. 1942.
5 (1) Lewis, T.: Observations on Some Normal and Injurious Effects of Cold Upon the Skin and Underlying Tissues. II. Chilblains and Allied Conditions. Brit. M. J. 2: 837-839, 13 Dec. 1941. (2) Schaefer, C. L., and Sanders, C. E.: Pernio (Chilblains). J. Missouri M. A. 38:159-160, May 1941.
6 See footnote 5 (1).
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general vasodilatation sets in, that the chilblain subject seems to owe his predisposition to these lesions."
The typical chilblain first appears as a red, swollen, tender lesion, which is usually warm or hot to the touch and which is characterized by obvious vasodilatation and subcutaneous edema. The only symptom at this time is itching. When the lesion becomes chronic, the original state of vasodilatation is no longer apparent, but the swelling may increase and the tissues may become tenser. The color becomes a deep purple or reddish purple. Blister formation and ulceration may develop. In the chronic form, itching is replaced by tenderness and actual pain. Regardless of whether the condition is acute or chronic, indolence and slow healing are prominent and are to be explained by the defective circulation which underlies its development.
Shelterleg
Shelterleg is the term applied to the swollen lower extremities which physicians began to see in numbers soon after the initiation of the blitz of London in 1940.7 Knight,8 who first described the condition, referred to it as trenchfoot in civilians. Although all ages and both sexes were affected, shelterleg was most frequently observed in elderly, obese women. Contrary to expectations, however, neither varicose veins nor cardiac lesions were present in affected subjects any more frequently than they would be found in an average population of the same age.
Inquiry of these patients practically always revealed that they had been spending their nights in a sitting position, sometimes at home, more of ten in the subways. The platforms were crowded, no bunks had then been installed, 9 and people brought their own chairs, usually of the deck type, and slept upright in them. The subways were cold and damp, but the chief etiologic factor seemed to be dependency of the parts, plus pressure on the popliteal space from the crossbars of the chairs. In an occasional instance in which the condition was unilateral, it was found that the patient had spent the night with one leg crossed over the other. In other words, the responsible causes-cold, dampness, dependency, and interference with the circulation-were precisely the causes which were later responsible for the cold injuries observed in ground troops in Italy and western Europe. The lack of specific predisposing causes in most of the affected persons suggests that the capillary walls, even when the extremities are entirely sound, are incapable of maintaining their tone for an indefinite period against the influence of gravity without intervals of recumbency or of active movement.
When the nocturnal habits were changed, rapid relief occurred in all uncomplicated cases of shelterleg except for a small group of patients whose
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7 (1) Knight, B. W.: "Trench Foot" in Civilians (correspondence). Brit. M. J. 2:610-611, 2 Nov. 1940. (2) Shelter Legs (editorial). Lancet 2:722, 7 Dee, 1940. (3) The Shelter Problem (reports of societies). Brit. M. J. 2: 801-802. 7 Dec. 1940.
8 See footnote 7 (1).
9 See footnote 7 (2).
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deaths could be traced directly to these habits. Soon after Knight had described the condition, Simpson 10 called attention to a significant increase in the occurrence of fatal pulmonary emboli in London; there were 4 fatal cases in September and October 1939 and 24 for the same period in 1940. Twenty-one of these twenty-four fatalities had occurred in persons who were in the shelters or, more usually, who were just leaving them after a night, or a succession of nights, spent in them. The subjects were usually elderly, 18 of the 24 being over 60 years of age. Most of the patients were somewhat obese, and several had varicosities of the veins of the legs. In every instance, however, the precipitating circumstance seemed to be the long period spent in a deck chair or some similar chair, the front edge of which compressed the popliteal space and caused obstruction, with subsequent stasis, edema, and thrombosis, presumably in that order. Deaths from this cause, Simpson noted, were already decreasing at the time of his report, as the provision of bunks was increasing, and lie put the figures on record merely to emphasize the need for haste in providing the necessary equipment in the shelters. He also called attention to the mechanical factor, which is not ordinarily so clear cut, in the development of thrombosis and to the fact that the thrombi originated in the tibial veins and not in the large pelvic veins.
Shelterleg was no part of the war picture in the United States, since the circumstances which gave rise to the condition in England were never duplicated in this country. Dependency for long periods, however, without change of position, is responsible for the so-called traveler's legs sometimes observed in civilian practice after long trips in trains, automobiles, or airplanes. As a rule, the discomfort and edema are promptly relieved when movement is resumed, though it may be a matter of days before the edema disappears completely.
Immersion Foot
Immersion foot 11 is a form of tissue trauma which follows prolonged immersion of the feet in water not sufficiently cold to cause frostbite. It has been observed, as already mentioned, after exposure in subtropical waters. Ungley 12 described it as "peripheral vasoneuropathy after chilling." Clinically and pathologically, it is indistinguishable from trenchfoot, which would be expected, since it originates from essentially the same causes.
Immersion foot typically appears in shipwrecked persons who have been exposed to cold and wet for long periods of time. It is usually associated with ____________
10 Simpson, K. Shelter Deaths From Pulmonary Embolism. Lancet 2: 744, 14 Dec. 1940.
11 (1) See footnote 4, p. 8. (2) Brownrigg, G. M.: Frostbite in Shipwrecked Mariners. Am. J. Surg. 59:232-247, February 1943. (3) Ungley, C. C.: Immersion Foot and Immersion Hand (Peripheral Vasoneuropathy After Chilling). Bull. War Med. 4:61-65, October 1943. (4) Ungley, C. C.: Treatment of Immersion Foot by Dry Cooling. Lancet 1:681682, 29 May 1913. (5) Immersion Foot. Bull. IT. S. Army M. Dept. No. 70, pp. 26-33, November 1943. (6) White, J. C., and Warren, S.: Causes of Pain in Feet After Prolonged Immersion in Cold Water. War Med. 5:6-13, January 1944. (7) Blackwood, W.: Studies in the Pathology of Human "Immersion Foot." Brit. J. Surg. 31:329-350, April 1944. (8) Goldstone, B., and Corbett, H.: Aetiology of "Immersion Foot." Brit. M. Bull. 2:148-149, 1944. (9) Fausel, E. G., and Hemphill, J. A.: Study of the Late Symptoms of Cases of Immersion Foot. Surg., Gynec. & Obst. 81:500-503, November 1945. (10) Wayburn, E.: Immersion Hypothermia. Arch. Int. Med. 79:77-91, January 1947.
12 See footnote 11 (3).
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dependency and immobility of the lower extremities and with constriction of the limbs by clothing and shoes. Other factors which play more or less important roles are (1) body cooling, as the result of wind; (2) total immersion; (3) repeated immersion; and (4) inadequate clothing, seasickness, and starvation. In the reported cases, younger and older persons seemed to suffer more severely from immersion foot than persons between 17 and 40 years of age. It was also the experience of shipwrecked survivors during World War II that those who lost heart and gave up hope suffered more severely, and sometimes died more quickly, than their companions who were of better spirit. The incidence and severity of immersion foot, however, are more directly influenced by the duration of exposure and the temperature of the water than by any of the other factors listed, though Ungley 13 expressed the opinion that the only specific effect of immersion is to keep the parts cold.
Three stages of immersion foot are recognized:
1. A prehyperemic stage, lasting from a few hours to a few days. In this stage, the extremities are cold, numb, swollen, and discolored, and peripheral arteries may be transiently or persistently pulseless. If pulsations continue absent, gangrene will ensue.
2. A hyperemic stage, lasting from 6 to 10 weeks. In this stage, the symptoms and signs include tingling or pain, motor disturbances, temperature differentials of the skin, increased swelling, blister formation, ulceration, and sometimes gangrene.
3. A posthyperemic stage, lasting for weeks or months. In this stage, symptoms and signs are absent if the environment is reasonably warm, but there is often sensitivity to cold suggestive of the similar sensitivity observed in Raynaud's disease.
The immediate symptoms of immersion foot are numbness, moderate pain, tingling or itching, sometimes cramps in the calves of the legs, and a sensation, on walking, as if the feet were being pressed into cotton wool. Edema, which is the most prominent physical finding, may appear within a few hours or after several days. The skin, which is initially reddened, becomes successively pale, mottled, and finally blue or black.
Trenchfoot
Trenchfoot is a thermal injury sustained as the result of exposure to cold short of freezing in a damp or wet environment. Arbitrarily, it is said to occur in the temperature range between 32? and 50? F. (0? and 10? C.). Actually, as already noted (p.7), the maximum temperature has not been established. Recognized predisposing causes include immobility and dependency of the limbs, insufficient clothing, and constriction of the parts by shoes, socks, and other garments. Trenchfoot commonly occurs under combat conditions, when immobility is forced by enemy action and when circumstances make adequate foot care difficult or entirely impractical. The prevalence is
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13 See footnote 11 (4), p. 10.
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influenced by the weather, the type of combat action., the type of terrain, the supply of food and clothing, and individual and organizational training policies and procedures for the care of the feet.
Trenchfoot is characterized pathologically by circulatory, neurologic, and sudomotor changes, which are manifested by signs of local tissue damage and sterile inflammation. As some observers have pointed out, this type of cold injury is almost identical with gradual frostbite, which might be expected, since the primary etiologic factors are the same except for differences in the degree of cold.14
The term "trenchfoot" came into use in World War I for the obvious reason that the injury was prevalent when static trench warfare was the rule. Although this type of warfare was the exception during World War II, this type of cold injury was unfortunately very frequent at certain periods in certain theaters of operations, and the term was retained (p.187), partly for lack of a better one and partly because the implications of the nomenclature were so generally understood.
Frostbite
Frostbite is a tissue injury 15 which evolves actual freezing of the skin and subcutaneous tissues. It results from (1) prolonged exposure to freezing and subfreezing temperatures, as distinguished from trenchfoot, which is diagnosed (arbitrarily) when the temperature is above freezing, or (2) brief exposure to extremely low temperatures. The latter type of injury was observed in World War II chiefly in fliers, in the form of high-altitude frostbite.
Exposed portions of the body, such as the fingers, ears, nose, chin, cheeks, forehead, and feet, are most frequently frostbitten. Frostbite of the penis, from exposure during urination, is not infrequent in cold climates. Both the incidence and the severity of the condition depend upon the degree of cold, the duration of exposure, and the wind velocity. Contributory factors include circulatory stagnation caused by inactivity, constriction of the parts, general vasoconstriction, trauma, and nutritional deficiencies.
Frostbite may appear suddenly, as the result of direct exposure of unprotected parts during extremely cold or windy weather or as the result of contact of unprotected skin with cold metal during such weather. It may also develop gradually, and even insidiously, as the result of prolonged exposure of even protected parts. A local burning or stinging sensation or a twinge of pain followed by numbness usually supplies ample warning of what is occurring. The skin assumes a grayish or whitish, waxy appearance. Sometimes all the
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14 Greene, R.: Frostbite and Kindred Ills. Lancet 2:689-693, December 1941.
15 (1) See footnotes 3, p. 7, and 14. (2) Lewis, T.: Observations on Some Normal and Injurious Effects of Cold Upon the Skin and Underlying Tissues. III. Frost-Bite. Brit. M. J. 2:869-871, 20 Dec. 1941. (3) Frostbite. Bull. U. S. Army M. Dept. No. 71, pp. 24-27, December 1943. (4) Stucke. K.: Kaltesch?den and Erfrierungen im Felde [Cold Injuries and Frostbite on Active Service]. Bruns' Beitr. z. klin. Chir. 174:1-10, November 1942. Abstract Bull. War Med. 4:507, May 1944. (5) Richards, R. L.: Injury From Exposure to Low Temperature: Clinical Features, Prevention, Treatment. Brit. M. Bull. 2:141-142, 1944.
PLATE l.- Various types and stages of high-altitude frostbite.
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involved tissues are extremely hard and fixed. In other instances, the affected part is indicated by the presence of a small, superficial, plaquelike lesion.
The first pathologic response to frostbite is an acute inflammatory reaction, quite similar to that observed in burns. Thawing is invariably followed by a state of reactive hyperemia, the intensity of which depends upon (1) the degree and duration of the exposure and (2) the rate at which the temperature of the part is raised. As in burns, the triple response characteristically present in the affected area, which is explained by the release of histaminelike substances from injured tissue cells, consists of (1) local reddening, (2) the appearance of a blister or of a blister and a wheal, and (3) a flare.
The eventual tissue damage depends upon the degree and extent of the actual freezing which has occurred and to an equal or even greater degree upon the transudation of fluid, and sometimes of blood cells, into the tissue spaces during the period of reactive hyperemia. The transudation is the direct result of increased permeability of the damaged capillary endothelium, which leads to swelling of the tissues, edema, and gross blister formation. In severe cases, secondary thrombosis of arterioles and capillaries may produce regional anoxia and cyanosis, which may go on to gangrene. Whatever the pathologic manifestation, the basis of the process is the prolonged peripheral vasoconstriction induced by cold.
High-Altitude Frostbite
High-altitude frostbite (plate 1) is a type of cold injury sustained by aviators and other flying personnel when they are flying in altitudes in which extreme degrees of cold (-40? to -52? C.) are encountered and in which wind velocities may be in excess of 200 miles per hour. Among the contributing causes are freezing of the oxygen mask, insufficient clothing, inefficiency of electrically heated clothing, and inadequate supervision and discipline of flying personnel, which result in unnecessary exposure of the hands by removal of the gloves (p.131) and other failures to prevent exposure. This type of frostbite is most often observed on the hands, but it may occur on any exposed part of the body and after only a few seconds of exposure.
High-altitude frostbite was first described by Col. Loyal Davis, MC, Senior Consultant in Neurosurgery, Office of the Chief Surgeon, ETOUSA, and his associates,16 in 1943. Since then, there has been rather general acceptance of their thesis that this type of frostbite is essentially the same as other types of cold injury but that it differs from the ground type in clinical severity and in the rapidity with which pathologic changes occur. Cold, just as in the ground type, is the primary agent which produces the pathologic changes, but the extreme low temperatures introduce two secondary mechanisms; namely, (1) generalized anoxemia and (2) local anoxemia of the affected parts. The local anoxemia is caused by the reduction of the local blood flow as a result of acute
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16 Davis, L., Scarf, J. E., Rogers, N., and Dickinson, M.: High Altitude Frostbite. Preliminary Report. Surg., Gynec. & Obst. 77: 561-575, December 1943.
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vascular spasm. The basic morphologic change, according to these observers, is damage by cold to the endothelium of the terminal capillary loops. In mild injuries, the change is limited to a pathologic permeability of the capillary walls. In more serious injuries, thrombus formation occurs at the arteriolar-capillary junction. In the few pathologic specimens available for study, both arteries and arterioles showed a remarkable thickening of the intima (fig. 1), the vessels resembling those seen in endarteritis obliterans. The veins were not involved.
FIGURE 1.- Photomicrograph of cross section of small artery 2 cm. proximal to line of demarcation of gangrene in finger amputated because of severe high-altitude frostbite, dry type. Note marked thickening of intima and absence of central thrombus and of evidences of recanalization. The endothelium is intact.
In the mild type of high-altitude frostbite, the fingers, after a brief period of exposure, become painfully cold, numb, stiff, waxy white, hard, brittle, and completely insensitive to touch. They cannot be flexed or extended voluntarily, and often they cannot be moved passively. Surface temperatures of the affected fingers may be 7.2? to 10.8? F. (4? to 6? C.) lower than those of the corresponding fingers on the unaffected hand. Even early in the injury, capillary microscopy shows no blood at all in the terminal capillaries on the dorsum of the fingers about the nail beds (fig. 2). This phenomenon, according to Davis and his associates, can be explained in two ways. It may be the result of an initial intense vasomotor spasm of the terminal portions of the arterioles, or, in some instances, it may be the result of a secondary thrombus at the point at which the arteriole, with its muscular wall, joins the thin-walled capillary.
Recovery from even mild high-altitude frostbite may be quite slow (fig.3) . Several hours are likely to elapse before the tips of the fingers begin to soften. If, however, the extremities and body can be brought back to normal body temperature there will be no blister formation, gangrene, or evident residuals, though the fingers may ache and throb for several hours and paresthesia may persist for days or weeks.
If the exposure to cold has been prolonged, tissue damage is severe and often permanent, and clinical manifestations are also severe. Two types of lesions, a wet type and a dry type, have been observed.
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FIGURE 2.- Drawing of microscopic appearance of capillary bed at base of nail in normal finger and in frostbitten finger. Note hairpin appearance of parallel capillary loops in normal finger and their absence in affected finger. The thrombosed stumps of the arterioles are characteristic of the frostbitten finger.
FIGURE 3. -Persistent blanching of fingers due to vasoconstriction 7 hours after exposure to high-altitude temperature of -40? C. (-40? F.).
The wet lesion (figs. 4, 5, 6, 7, 8, 9) takes the form of multiple small cutaneous blisters, which appear almost at the same time upon many areas of the skin of the affected part. They increase rapidly in size and eventually coalesce to form one or more huge blisters, which may involve the entire dorsum of a finger or even the whole hand. Though these blisters sometimes resemble the simple vesicles of second-degree burns, more often the pathologically excessive fluid is held fast within the tissues composing the superficial layers of the skin.
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FIGURE 4.- Wet type of moderately severe high-altitude frostbite. A. Typical blister formation. The index finger shows a single vesicle which has completely collapsed after incision. The middle finger shows a blister which has failed to collapse after liberal incision, because of the excess fluid held within the tissues. Neither blister is hemorrhagic. B. Fingers shown in view A 1 month later. Blisters have dried, and desquamation has occurred. Note loss of nail and absence of normal skin markings, as well as the delicate, tight, shiny, new epithelium. These fingers remained sensitive to cold for many months.
On aspiration, a small amount of fluid is obtained, if any at all, but fluid which is sometimes clear and sometimes contains red blood cells will ooze slowly for several hours from the puncture hole. Hemorrhage most often takes place beneath the nails, which are likely to be lost. Superficial layers of skin are eventually dissected away from the deeper layers by extravasated fluid and are cast off, frequently in the form of a complete cast of the part (fig.8). Most of the germinal layer comes away with the cast (fig.9), and epithelial regeneration is therefore possible only from the remnants of germinal epithelium left in the ducts of the sweat glands. The newly regenerated skin varies in color from dusky pink to dusky blue. It is thin, smooth, shiny, and tightly drawn. Cold tolerance is greatly reduced (chart 1), and anesthesia or hypesthesia to pain and touch, with loss of sweating, may continue for months (fig.10).
The dry type of high-altitude frostbite (figs. 11, 12, 13, 14, 15, 16), which usually follows more severe exposure to cold, at first resembles the wet type. Thawing is a slow process, however, and instead of blister formation the affected parts become extremely tense, the skin has the appearance of dull ground glass and becomes progressively drier, and the deeper tissues assume a progressively darker shade of dusky gray. All the tissues eventually shrivel and mummify, the changes being most marked at the distal portions of the extremities. After 2 or 3 weeks, a line of demarcation is clearly evident, and spontaneous natural amputation will take place unless surgical intervention terminates the process.
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FIGURE 7.-Wet type of severe high-altitude frostbite, with hemorrhagic blister formation, 24 hours after injury.
FIGURE 8.-Wet type of severe high-altitude frostbite. Cast desquamation of tips of fingers followed severe blistering.
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FIGURE 9.- Photomicrograph of section of skin from blister in wet type of moderately se ere high-altitude frostbite. Note separation of epidermis from dermis and, in particular, loss of basal germinal layer with epidermis.
THE SPECTRUM OF COLD INJURY
Injuries caused by cold may be roughly grouped according to their primary causes. In frostbite and freezing of the tissues, cold is the sole agent. In immersion foot, cold and wet both play roles, with wetness occupying the predominant role. In trenchfoot, cold and wet play approximately equal parts.
It is possible to postulate a range or spectrum of cold injury, beginning with mild chilblains and ending with severe frostbite at low temperatures and death from freezing of the deep tissues. While the place of the various injuries in the spectrum is determined by the degree of cold, the effect of cold may be greatly intensified by contributing factors, such as wet in trenchfoot and immersion foot, and anoxemia in high-altitude frostbite.
Precise data gathered by long observation and study have made possible the quantitative evaluation of disease. A range from inapparent disease on the one hand through fulminating disease on the other can be easily demonstrated in relation to deaths. Data collected in World War II and from other sources do not support a similar gradient of cold trauma, though th explanation may well be the shortcomings of the available data rather thean any defect in the principle itself. The variety of contributing factors also helps to explain why it is difficult to formulate a gradient of cold trauma. Epidemiologically, the establishment of such a gradient would be highly desirable. Future experience must supply the data required and overcome other difficulties. Meantime, it is possible to postulate the probably behavior of cold trauma (chart 2).
Many factors come into play in a cold-trauma gradient. Each component constitutes a gradient to itself, and each is influenced by multiple properties of the agent, the host, and the environment. The development and interpretation.
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CHART 1 - Graph showing cold tolerance of normal right hand and frostbitten left hand.
of the gradient of cold injury are influenced by the degree of cold, the degree of wetness, individual susceptibility, the duration of exposure, the use of protective measures and equipment, and other modifying factors.
If the relationships illustrated in the gradient which has been postulated (chart 2) are correct, the total area of cold trauma is divided, through not equally, into four principal components. Severity or degree of injury varies in each component; it is least for chilblains and greatest for freezing of deep tissues, thus forming an ascending gradient of severity from left to right. Trenchfoot
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FIGURE 10.-Persistent hypesthesia in high-altitude frostbite, sustained at temperature of 40? C. (-40? F.). Solid lines represent limits of hypesthesia and dotted lines limits of hypalgesia 7 hours after exposure. There was complete loss of pain and touch over the distal phalanges of the index and little fingers.
FIGURE 11.- Dry type of mild high-altitude frostbite. A. Early stage. Blistering has not occurred but note ground-glass appearance of skin of fingertips. The deeper underlying tissues were under great tension and were quite painful. Gangrene of the affected parts followed. B. Hand shown in view A 5 months later, showing loss of nails and tissue of fingertips.
and immersion foot occupy the largest area and chilblains the smallest in terms of defect or more severe injury. This is the precise proportionate relationship of these cold inuries in terms of their military importance. Few, if any, deaths are caused by chilblains, and the disability they cause is not great. Though deep freezing of the tissues is accompanied by a high case fatality rate and by some disability in the survivors, its importance, in terms of numbers of cases, is far less than that of trenchfoot and immersion foot, as shown by the
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FIGURE 12.- Dry type of severe high-altitude frostbite. A. Early state (1 hour after injury). B. Hand shown in view A 3 days later. Note almost total absence of blistering. C. Hand shown in view B 3 weeks later, showing far-advanced dry gangrene.
comparable areas in the schema. Trenchfoot and immersion foot are responsible for few deaths but for much temporary and permanent disability. Frostbite, while it carries a high case fatality rate than either trenchfoot or immersion foot, is proportionately less important in terms of temporary and permanent disability or defect and over-all military cost.
It should be emphasized that these assumptions hold only for mility operations conducted in winter in a temperate climate, such as that of western Europe. They would be greatly altered for operations conducted in the intense and sustained cold of the Arctic.
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FIGURE 13.- Dry type of severe high-altitude frostbite. A. Photograph 10 hours after injury. The hand has been dressed with sulfanilamide powder. B. Hand shown in view A 5 weeks later, showing spontaneous amputation of tissues as result of dry gangrene.
The specific causative agent in cold injury is cold, 17 but evaluation of the World War II experience makes it clear that wet, because it speeds loss of body heat, is closely related. The influence of wetness, however, is entirely synergistic. It cannot of itself cause cold injury. Factors related to the soldier himself and to his environment also play a part in the ttal causation of cold injury. Recognized human factors include the status of individual training, the individual nutritional status, fatigue, previous experience with cold injury, and inherent constitutional and psychosocial qualities, in addition to the mechanical factcors of posture and dependency. Elements of the physical environment which enter the picture are the weather (that is, temperature, precipitation, and wind), the altitude, the terrain, and thawing. Socioeconomic influences include clothing supply and equipment, foot discipline, command leadership and attitude, training and experience as applied to the unit, and ration of personnel.
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17 See footnote 3, p. 7.
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CHART 2.- Gradient of cold injury (schematic)
All of these factors enter into the total causation of cold injury. Effective prevention and control, however, can be established only by evaluating the weight of each factor by studying each of them in individual units. The control of mass injury or disease depends upon methods and measures directed at causes. Analyses of cause and effect provide the only means for developing a concerted plan for meeting the problem in any future war.
The simple, sound epidemiologic methods used in the field in World War II to identify the several components in the total causation of cold injury demonstrate that only a few of these components are amenable to practical control and preventive practices. Thus, the type of combat action, terrain, and weather are universal causes which influence the incidence of cold trauma wherever it occurs but which are not amenable to control. On the other hand, as field studies during World War II clearly demonstrated, the level of the clothing supply, individual and unit discipline, rotation policies and practices, and the training and experience of troops, all of which exert a variable influence upon the incidence of cold injury, are all subject to control within the limits of the tactical situation. Further study and research should be directed to the intangible causative factors, which are not susceptible to precise measurement, to determine whether the base of practical control of cold injury can be broadened.
NOTE.- For statistical purposes, trenchfoot and frostbite are not always separated in Army reports. Clinically, as already indicated, they are often indistinguishable. Practically, it would have been better if no attempt had been made to differentiate them (p.303). Generally speaking, whatever is said about one in the following pages may be regarded as equally applicable to the other unless specific exception is made. Similarly, whatever is said about cold injuries of the feet may be regarded as equally applicable to cold injuries of the hands, which, as a practical consideration, are affected in only a very small proportion of the injuries of this type.
