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Podology

Materials about such pathological processes as “trench foot” and “wet foot” were provided to the editors by <a href="https://www.facebook.com/tetyana.svyatenko">Tatyana Svyatenko</a> , professor at the Dnieper Medical University, Doctor of Medical Sciences, member of the EAGV. “Thanks to Victoria Kozlovskaya, our colleague from the United States, we found and began to translate from English a textbook on military dermatology, Textbook of Military Medicine,” said Tatyana Svyatenko. CLINICAL REVIEW Damage to the extremities from prolonged immersion in water or exposure to different temperature ranges may be called “wet foot syndrome.” Such lesions, associated with constant exposure to cold temperatures and humidity, are divided into “trench” and “wet” lesions. The review describes each condition to reduce confusion in nomenclature and aid in diagnosis and treatment. Defeat in cool and cold climates All of the wet foot syndromes described below are characterized by ongoing pain for several weeks. This condition can affect a large number of soldiers in units at the same time due to the general influence of an unfavorable environment. Let&#39;s look at two syndromes caused by cold, wet conditions. Trench feet Trench foot refers to lesions resulting from prolonged exposure to wet conditions without getting wet in cold weather. The term originates from the First World War, when many warriors were concentrated in the trenches in cold, wet weather for long periods of time. The condition was recognized as a cause of significant loss of life during the Greek campaigns, Napoleonic and Crimean wars. However, these lessons seem lost in the newest armies. In Europe during the Second World War, eleven thousand cases of trench foot were recorded in November 1944 and more than six thousand cases in the US Third Army alone. Trench foot is almost identical in presentation with a gradual onset of frostbite, but there is no established maximum temperature at which this condition can develop. Ice crystals do not form in tissues at temperatures above 0 degrees Celsius, but from 0 to 15 o C, clinical signs of trench foot appear when exposed to negative circumstances for 48 hours or longer. Other additional factors include nutritional deficiencies, trauma (chafing or walking on the affected leg), wind, inappropriate clothing type and integrity, stagnation of circulation, tissue oxygen deprivation caused by bandaging, lack of movement, hemorrhage or shock, and inappropriate technique. . Clinically, trench foot is insidious, at first soldiers feel nothing but a sensation of cold to numbness. Paresthesia and pain may be seen with forceful exercise. With constant exposure there is complete anesthesia to touch, pain and temperatures: a sensation that is described as “walking on a piece of wood”. The leg appears pale and swollen and may show signs of vesiculobulous lesions. The degree of edema during the ischemic or hyperhyperemic stage depends on whether the leg is periodically heated during the negative effect (manifested by a decrease in edema). The foot may appear mottled or purple, indicating impending gangrene, however this permanent appearance is usually minimal with proper care. The hyperemic or inflammatory stage appears several hours after removing shoes and warming the limb. Sensations return proximally and distally, initially as rapidly progressing tingling to intense heat, throbbing pain. Soldiers have a hard time tolerating heat and are more comfortable when the extremity is cooled. Hyperesthesia replaces anesthesia, except in the most distant areas, which may remain insensitive for weeks or months. The leg quickly swells and becomes warm, dry, erythrematous, and pulsating. In milder cases, this stage reaches its peak within 24 hours. Severe cases can progress over 48 to 96 hours and produce areas of blistering and poor circulation that are more likely to become gangrenous. Hemorrhage and ecchymosis may occur. Milder cases of trench foot subside slowly, over 1 to 4 weeks, and are often accompanied by severe peeling in the affected areas. More complex cases progress to the posthyperemic stage. Although patients with trench foot are susceptible to sepsis, uncomplicated overflow of these injuries does not have systematic manifestations. Posthyperemic or postinflammatory stages are unbent. The initially hot, dry leg becomes cold, wet, mottled, or completely blue with no pulse. Acute pain during the hyperemic stage changes to deep pain, which is usually felt remotely and is often associated with joint pain. Hyperesthesia and paraesthesia disappear quickly, although sensory loss may persist for months or years. Late changes may include skin atrophy, osteoporosis, muscle atrophy and deformity (especially the bell-bottom type). Histologically, trench foot is a manifestation of microvascular damage. Petersson and Hugar state that prolonged exposure to cold causes an increase in blood viscosity, precipitation of red blood cells in the vessels. In combination with vasoconstriction and loss of serum proteins due to damaged endothelium, it can cause thrombosis, ischemia and cell damage. Thrombosed vessels of the dermis and subcutaneous tissue with reflex vasodilation, rupture of capillaries and increased vascular permeability contribute to edema, vesiculation and ecchymosis of the hyperemic stage. Work by Smith et al., in which the trench foot condition was replicated in rabbits, also showed fibrin deposition on vascular walls and muscle bundles, edema and neutrophilic infiltration of skin and muscle collagen, swelling of nerve axons, and vacuolization of muscle fibers. endothelium. Smith and others observed various lesions of lymphatic tissue. Tissue biopsy in the posthyperemic stage showed atrophy and thinning of the dermis, fibrosis and collagen deposition around nerve endings and blood vessels, and replacement of muscle bundles and fibrils by scar tissue. Wet feet Wet feet can be seen as a counterbalance to the soldiers&#39; trench feet of sailors. The term &quot;wet feet&quot; was first used during the Second World War to describe a syndrome of clinical conditions occurring in extremities exposed to prolonged immersion in water of varying temperatures, from 0 to 15 o C. It was most clearly observed during the Second World War, as As a rule, a wet foot was found in persons who were shipwrecked, adrift, in the water, or in rescue boats partially filled with water. This has also been reported in Vietnam as a result of prolonged immersion in rice fields. Clinical manifestations in soldiers with wet feet: the same stages of prehyperemia, hyperemia and posthyperemia as in classic trench feet. However, in wet feet, the injury can extend higher up to include the knees, hips, and buttocks, depending on the depth of the dive. Also, due to prolonged exposure, the condition of wet foot may begin on the first day of negative exposure, whereas trench foot usually begins to develop over several days of lesser and perhaps intermittent exposure. The histological findings observed in wet foot are similar to those seen in trench foot. Comparison table for trench foot symptoms<table border="1" cellpadding="0" cellspacing="0"><tbody><tr><td style="width:121px;"> Syndrome</td><td style="width:246px;"> Trench foot</td><td style="width:246px;"> Wet foot</td></tr><tr><td style="width:121px;"> Affected area</td><td style="width:246px;"> Feet</td><td style="width:246px;"> Feet, in some cases knees, thighs or buttocks</td></tr><tr><td style="width:121px;"> Symptoms</td><td style="width:246px;"> Prehyperemic:<ul><li> early - numbness, pain, paresthesia;</li><li> later – anesthesia, “walking on a piece of wood.”</li></ul> Hyperemic:<ul><li> tingling turning into pulsation;</li><li> burning pain;</li><li> hypersensitivity, distal anesthesia may occur.</li></ul> Posthyperemic:<ul><li> deep pain in the joints;</li><li> continued loss of sensation</li></ul></td><td style="width:246px;"> The same</td></tr><tr><td style="width:121px;"> Manifestations</td><td style="width:246px;"> Prehyperemic:<ul><li> pallor, swelling;</li><li> vesiculobulous lesions;</li><li> distal cyanosis.</li></ul> Hyperemic:<ul><li> increased swelling, warmth;</li><li> dryness, erythemosis;</li><li> pulsation, vesicles, blisters, ecchymosis.</li></ul> Posthyperemic:<ul><li> early – cold, humidity, spots, cyanosis, decreased pulse;</li><li> late – skin and muscle atrophy, osteoporosis, deformities</li></ul></td><td style="width:246px;"> The same</td></tr><tr><td style="width:121px;"> Systematic influence</td><td style="width:246px;"> No</td><td style="width:246px;"> No</td></tr><tr><td style="width:121px;"> Recovery time</td><td style="width:246px;"><ul><li> Visible changes – within 4 weeks-5 months;</li><li> neurological and structural changes after months (may be permanent)</li></ul></td><td style="width:246px;"> The same</td></tr><tr><td style="width:121px;"> Pathological changes</td><td style="width:246px;"> Prehyperemic: thrombosis, edema, vasoconstriction. Hyperemic: thrombosis, capillary rupture, hemorrhage, vasodilation, edema, subepidermal vesiculation. Posthyperemic: fibrin deposition on vascular walls, muscles, swelling of nerve axons, various lymphatic lesions.</td><td style="width:246px;"> The same</td></tr><tr><td style="width:121px;"> Pathogenesis</td><td style="width:246px;"> Direct damage to blood vessels by cold</td><td style="width:246px;"> The same</td></tr><tr><td style="width:121px;"> Exposure to water</td><td style="width:246px;"> 2-14 days wet (not necessarily submerged)</td><td style="width:246px;"> 1 day or more continuous diving</td></tr><tr><td style="width:121px;"> Water temperature</td><td style="width:246px;"> 15 o C</td><td style="width:246px;"> 15 o C</td></tr><tr><td style="width:121px;"> Impact of temperature</td><td style="width:246px;"> A decrease in temperature accelerates damage</td><td style="width:246px;"> The same</td></tr><tr><td style="width:121px;"> Treatment</td><td style="width:246px;"> Stopping exposure to water, avoiding stress, warming the body by elevating and cooling the feet, nutritious nutrition, asepsis, tetanus prophylaxis, prophylactic antibiotics, conservative surgical approach, smoking cessation</td><td style="width:246px;"> The same</td></tr><tr><td style="width:121px;"> Prevention</td><td style="width:246px;"> Individual training in first aid and identification of lesions, constant rotation from cold wet areas, nutritious nutrition, awareness of management personnel</td><td style="width:246px;"> Closed rescue boats, personal protective suits</td></tr><tr><td style="width:121px;"> Perception factors</td><td style="width:246px;"> Dependency loss of movement, injury, oxygen deprivation, poor nutrition, inappropriate heating</td><td style="width:246px;"> The same</td></tr></tbody></table> WEALTH MANAGEMENT Treatment of lesions not associated with hypothermia, such as trench and wet foot, is based on reversing ischemia and, at the same time, preventing increased edema, extravasation of red blood cells, or inflammation during the hyperemic stage. When heated, affected tissue cells have an increased need for effective blood circulation to remove necrosis products. Since reflex vasodilation occurs, preliminary thrombosis and direct damage to endothelial cells by cold and anoxia causes massive transudation of plasma and red blood cells, which leads to varying degrees of edema, vasiculation and hemorrhage. To reduce metabolism and reflex vasodilation, the physician must raise the patient&#39;s body temperature while keeping the affected limb cold. As a rule, it helps if you elevate the patient&#39;s bare legs, directing cold air from a fan onto them, while simultaneously keeping the body warm. The patient feels a decrease in pain, swelling, hyperemia and a decrease in vasiculation. Cooling of the extremities continues until the stage of hyperemia subsides and circulation resumes. The practice of rubbing the affected limb with snow or ice results in further injury to the affected tissue and has no place in modern therapy. Other general interventions include avoidance of exercise, direct trauma, aseptic techniques, prophylactic antibiotics, smoking cessation, tetanus prophylaxis, analgesics, a high protein diet, and possible plasma transfusion if necessary. Surgery should be delayed as long as possible to allow natural demarcation of the damaged tissue, and amputation should therefore be conservative. Other forms of treatment suggested for frostbite have not been studied for non-frostbite lesions and are not recommended - treatments such as rapid rewarming, low molecular weight dextran, sympathetic blockade, ultrasound, continuous epidural anesthesia, anticoagulant, local sympathectomy. Treatment of the posthyperemic stage is mainly symptomatic, including physical therapy, exercises and surgical correction of the deformity. Early sympathictomy in more severe cases may prevent long-term sequelae such as fibrosis, contractures, and scarring, but such intervention awaits further study. Preventing trench foot and wet foot is difficult, especially during military operations. The correct selection, use and care of safety footwear is essential. Individual training in premedical first aid and identification of lesions, attention to personal hygiene, frequent rotation from wet and cold areas, support for adequate nutrition and psychological state, and commander awareness are necessary to prevent the occurrence of trench foot. Wet feet can be prevented at sea by the use of enclosed lifeboats and the provision of protective suits on ships. P._S._Several measures available _ After the material was translated, the initiators of the publication brainstormed and offered some advice.<ul><li> For prevention, use sanitary pads for shoes.</li><li> You can dry your shoes or socks by pouring chalk, crushed brick fragments, salt, and rice into them.</li><li> You can dry the skin with tooth powder or toothpaste (only without menthol!).</li><li> Brew oak bark and make baths or moisten a rag and wrap your foot for a few minutes.</li><li> Flour and butter cannot be used!</li></ul> We will continue to publish chapters of the book as they are translated.

Military dermatology: trench foot