Trench foot EDITORIAL

Transcription

1 Journal of Wilderness Medicine 4, (1993) EDITORIAL Trench foot Trench foot is the result of prolonged (many hours) cooling of the lower extremities to temperatures above freezing but below 60 F. Although trench foot is a significant cause of injury in military operations [1], it is rarely seen in civilian practice. Prolonged cooling of extremities produces direct injury to all the soft tissues, but primarily to peripheral nerves [2,3,4]. The injury is initially reversible, but becomes irreversible if cooling is sustained. Wet conditions increase the risk and accelerate the injury. In addition to environmental cooling, factors that reduce circulation to the extremities contribute to the injury. These factors include constrictive clothing and boots, prolonged immobility, hypothermia and cramped posture. When first seen, the injured part is pale, anesthetic, pulseless and immobile, but not frozen. The clinical hallmark of trench foot is the failure of these signs to change after warming. After several hours (occasionally h), a vigorous hyperemia develops associated with severe burning pain and reappearance of sensation proximally, but not distally. Edema, often sanguineous, and bullae develop as perfusion increases. Skin that remains poorly perfused after hyperemia appears, is likely to slough as the injury evolves. Persistance of pulselessness after 48 hours suggests severe deep injury and high likelihood of substantial tissue loss. The hyperemia appears to be due to a vasomotor paralysis with passive engorgement of cutaneous vessels, characterized by pallor on elevation and rubor on dependency. The hyperemic phase lasts a few days to many weeks, depending on the severity of the injury. In the second week after injury, sharp intermittent 'lightning' pains develop. The injury evolves slowly, as befits its neuropathic component. Improved sensitivity to light touch and pin prick in the area of persistent anesthesia within 4-5 weeks suggests reversible nerve injury and less likelihood of persistent symptoms. Persistence of anesthesia to touch beyond six weeks suggests neuronal degeneration. Injury of that degree requires much longer to resolve and has a greater likelihood of persistent disabling symptoms. Hyperhidrosis is a common, prominent late feature of trench foot and seems to precede the recovery of sensation both in time and location. A distinct advancing hyperhidrotic 'zone' can develop [5] which is presumed to mark the point to which regenerating sudomotor sympathetic nerves have advanced. The excessive sweating may be permanent and can predispose to blistering, skin maceration and dermatophyte infection. Two schemes of classification have been used, based on clinical series from World War II. These two systems correlate well and provide useful prognostic information. Both systems recognize four degrees of severity Chapman & Hall

2 Editorial 349 The Webster classification [6] is based on the appearance of the foot 2-3 days after injury. The Vngley classification [7] is based on the distribution of anesthesia seven days after injury. Minimal (Webster) or grade A (Ungley) This degree of trench foot manifests hyperemia and slight sensory change at 2-3 days. At seven days, neither objective finding nor anesthesia remains. Rapid reambulation is the rule, with only occasional cold sensitivity. Mild (Webster) or grade B (Ungley) Trench foot of this level manifests edema, hyperemia and definite sensory change at 2-3 days. At seven days, anesthesia is found only on the plantar surface of the foot and tips of the toes and lasts 4-9 weeks. This degree of injury is associated with 1-3 weeks of edema, 2-4 weeks of neuropathic pain and 3-7 weeks of hyperemia. Bullae and skin loss are not seen. Hyperhidrosis and cold sensitivity of the injured part occurs in about half the injuries, although not necessarily in the same individuals. Moderate (Webster) or grade C (Ungley) Trench foot of this nature manifests edema, hyperemia, bullae and mottling at 2-3 days. At seven days, complete anesthesia is found to some degree involving the dorsum of the foot. Edema persists for 2-3 weeks; pain and hyperemia last for up to 14 weeks. Both vibration and position sense and motor innervation of the intrinsic muscles of the foot are impaired. Sloughing of skin occurs, but loss of deep tissue does not occur. Hyperhidrosis and cold sensitivity occur in most cases. Persistent neuropathic symptoms and disability are common. Severe (Webster) or grade D (Ungley) This severe form of trench foot manifests acute edema, extravasation of blood and incipient gangrene at 2-3 days. At seven days, complete anesthesia is found in the entire foot, with paralysis of the intrinsic muscles. The injury often extends proximally to the foot. Edema in viable tissue lasts from three to seven weeks; hyperemia and pain last up to four months. Prolonged convalescence and permanent disability are the usual sequelae. Specific measures for preventing trench foot have been developed and proven effective [1]. Their efficacy depends on preventing prolonged chilling of the extremities. In World War I, the British eliminated trench foot as a significant medical problem by rigorous application of simple hygienic measures. They reduced the incidence of trench foot from cases in 1915 to a total of 443 cases in The same techniques were effective among British and American Forces in World War II. It is important to remember that these measures were effective without significant changes in equipment. These measures include:

3 350 Editorial (1) Assure the best possible fit of the boots with heavy socks; (2) keep the body as warm as possible; avoid chilling; (3) remove boots and socks at least twice a day; three times is better. Wash, dry, massage and move the feet to restore circulation and feeling. Allow enough time to complete this task. After warming the feet, put on clean, dry socks or if dry socks are not available, remove as much water from the socks as possible before putting them on; (4) do not sleep wearing wet footgear. Remove wet boots and socks for sleep. Protect the feet with as much dry cover as possible to keep them warm; (5) dry wet socks by keeping them in the sleeping bag during sleep or placing them inside the field jacket against the trunk or across the shoulders; (6) in fixed positions, use rocks, boards or brush to keep the feet out of water and mud; (7) keep the feet and legs moving to stimulate warming circulation. If keeping low in a fixed position, keep the feet elevated to avoid swelling; (8) watch carefully for numbness or tingling. These are early symptoms of trench foot. If these develop, immediately take measures to warm the feet; (9) keep the clothing and footgear loose enough to permit easy circulation. Despite the success of these simple measures in 1916, 1943 and 1944, outbreaks of trench foot continue to occur [8,9,10]. Drs Tek and Mackey [11] report an 11 % cumulative incidence of trench foot in a 358 man US Marine infantry battalion during a 1988 cold weather amphibious training exercise. Their intent in performing the review was to document the occurrence of trench foot in a contemporary military operation and to assess race and smoking as contributory risk factors. From data in the battalion's medical records, they calculated the cumulative incidence of trench foot during the exercise in the entire battalion and in subgroups based on race, smoking status and company. They also calculated the mean number of days of non-weight-bearing disability for the entire group of injured Marines and the two subgroups based on race and smoking. The cumulative incidence of trench foot during this single training exercise was alarmingly high. More than one in ten Marines was hospitalized for care of a serious cold-induced injury. Some may look at the number of days of non-weight-bearing disability reported for the injured Marines (2.26 days) and question my use of the term 'serious' to describe these injuries. Almost all of the injuries had a Webster Grade of minimal. After all, how bad can an injury be that produces less disability than an average ankle sprain? Even Tek and MacKey describe the injuries to be of 'low severity'. I will defend my view of the seriousness of these injuries by considering the evolution and residual effects of environmental cold injury. Both the individual severity and the total number of injuries depend on the duration and intensity of exposure to cold [1]. The appearance of a cold injury is a warning that both a greater number of injuries and more severe injuries will occur as exposure continues. Considering this, how much worse would this battalion's experience have been if these same Marines had been exposed in combat with constraints on supply and evacuation? I consider the injuries serious not so much for their clinical presentation, but for the potential for disaster that they represented. The high incidence of injury shows a significant failure of attention to effective prevention.

4 Editorial 351 Second, career-limiting cold intolerance is a frequent consequence of cold injury, even when the injury appears minor. If cold intolerance is sufficient to prevent a soldier from deploying to the field, he faces a substantial likelihood of separation from the service. In these Marines, Tek and MacKey were unable to learn their long-term outcome. However, if experience is any guide, it's reasonable to conclude that some of them have been medically discharged because of their injuries. What beyond evidence of a failure of injury prevention do these data suggest? A principal goal of Tek and MacKey was to determine whether race and smoking are risk factors for trench foot. In their statistical analysis of the data, they were unable to show differences between any of the subgroups at the p < 0.05 level. As they point out in the conclusion of their paper, it is important that the analysis not stop at that point. The absence of 'statistical' significance should not be taken to mean that there are not important issues raised by the data. For example, Hotel Company had 4% of its Marines admitted for care of trench foot; the next best record (Fox Company) had a cumulative incidence almost three times higher (11%). The difference is striking and strongly suggests that the leadership of Hotel Company managed to reduce the rate of injury. As Tek and MacKey report, the 'p' value of the difference between Hotel and the other three companies was 0.08 and so, did not meet the usual criterion of 'significance'. However, this statistic means that there is about one chance in 12 that the difference found in the study is 'real' and not due to chance. Dismissing the difference as 'insignificant', risks a failure to recognize that there may well have been practices in Hotel Company that reduced the incidence of trench foot. In this sort of investigation, where the point is not so much to refute a specific hypothesis but more to identify potential risk factors for a focused investigation, it may be an error to use a criterion so restrictive that valuable potential associations are not seen. The difference in trench foot incidence between smokers and nonsmokers can be approached with the same perspective as the differences between the companies. The,cumulative incidence of trench foot among smokers was about twice that found in nonsmokers (14% vs 8%). Its,,2 statistic indicated 'p= 0.09', i.e., only 1 chance in 11 that the difference is due to chance. Although smokers represented only 43% of the battalion, they suffered 58% of the trench foot hospitalizations. There are a variety of ways by which smoking (or any other form oftobacco use) could account for a greater risk of trench foot. For example, tobacco use is associated with higher rates of vascular disease [12], leaner body composition [13] and lower extremity injury [14]. From the data of this study, race appears to have no relationship to the incidence of trench foot. The association with freezing injury is fairly well established from data carefully collected in the Korean War [10]. The mechanism of the apparent greater susceptibility of black soldiers to freezing injury is not known. Some experiments have shown that melanocytes are more sensitive to injury from freezing cold than are nonpigmented skin cells [15]. If this is true and important in the pathogenesis of freezing injury, then it may explain a racial difference in susceptibility to freezing and nonfreezing injury. Tek and Mackey have shown elegantly the value of medical record review as a powerful means of discovering important injury risk factors. Their paper is an important reminder that trench foot is still of tremendous concern in military training and operations.

5 352 Editorial Department of Defense disclaimer The opinions expressed in this editorial are the personal views of the author. They should not be construed as representing official policy of the Department of the Army or the Department of Defense. ROBERT E. BURR, FACP, FACEP Massachusetts, USA References 1. Whayne, T.F. and Debakey, M.E. Cold Injury, Ground Type, in World War ll. Washington, D.C: Office of the Surgeon General, Department of the Army, Denny-Brown, D. et al. Pathology of injury to nerve induced by cold. J Neuropath Exp Neural 1945; 40, Stray, K. Experimental investigations of the reactions of the skin to cold. Skrifter Norske Videnskaps-Iacad i Oslo. 1. Mat-Naturv Klasse 1943; No Kennet, RP., and Gilliatt, RW. Nerve conduction studies in experimental nonfreezing cold injury. II: Generalized nerve cooling by limb immersion. Muscle Nerve 1991; 14, Guttmann, L. Topographic studies of the disturbances of sweat secretion after complete lesions of the peripheral nerves. J Neural Psychiatry 1940; 3, Webster, D.R et al. Immersion foot. J Bone Joint Surg 1942; 24, Ungley, c.c. The immersion foot syndrome. In Andrus, W.O., ed. Advances in Surgery. Vol. 1. New York: Interscience Publishers, 1949: Barat, A.K. et al. Cold injuries in Kashmir, December Ann R Call Surg Eng/1978; 60, Marsh, A.R A short but distant war - the Falklands campaign. J R Soc Med 1983; 76, Orr, K.D. and Fainer, D. Cold injuries in Korea in the winter of Medicine (Baltimore) 1952; 31, Tek, D. and Mackey, S. Non-freezing cold injury in a Marine infantry battalion. J Wilderness Med 1993; 4, Lepantalo, M. and Lassila, R Smoking and peripheral arterial disease. Clinical review. Eur J Surg 1991; 157, Klesges, RC. et al. Smoking status: effects on the dietary intake, physical activity, and body fat of adult men. Arner J Clin Nutr 1990; 51, Reynolds, K.R et al. Association of smoking and training injuries in light infantry soldiers (Abstract 154). Med Sci Sport Exer 1992; 42, S Post, P.W. et al. Cold injury and the evolution of 'white' skin. Laboratory experiments demonstrate that pigmentation influences the degree of cold injury to the skin. Hum Bioi 1975; 47,65-80.