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Military dermatology

The topic of cold injuries caused by cold is quite relevant in the conditions of the war unleashed by Russia against Ukraine, since a large number of cold injuries usually occur only during the war. These injuries often require months of rehabilitation or result in permanent disability. The <a href="https://pro.bhub.com.ua/cosmetology/voenna-dermatologia-travma-spricinena-holodom-prakticnij-aspekt">previous article</a> dealt with indirect cold injuries. The source of such specific information is the textbook on military dermatology Textbook of Military Medicine, which was provided by Tetyana Svyatenko, professor of the Dnipro Medical University, MD, member of the EAHV. (Source: <a href="https://derma.school/clinical-studies/disaster_medicine">Military Dermatology</a> . Translation: Galina Prit. Photo by Pexels Dmitrii Ageev.) DIRECT COLD INJURY Direct cold injuries are caused by the influence of low temperatures and are not associated with an exacerbation of the underlying disease. Examples are astheatic eczema and frostbite. Asteatotic eczema Asteatotic eczema is characterized by the following conditions: the skin becomes dry, rough and less elastic than usual, flaky, often cracked. Dermatosis is a consequence of cold damage, aggravated by a cold. Dry pruritus leads to scratches, excoriations, and often secondary infection. The most common location is the front of the lower leg. Therefore, these symptoms should not be neglected. Etiology. Dry skin with asteatotic eczema is due to a decrease in the moisture content of the stratum corneum. Decreased secretion of the sebaceous glands leads to an insufficient amount of lipids to maintain water in the stratum corneum. Atmospheric conditions, cold and low humidity play a role in the development of dry skin. Poor nutrition is also a predisposing factor. Clinical manifestations. Peeling and itching with asteatotic eczema are noticeable especially on the legs, but any part of the body can be affected. As the complexity of the condition increases, string-like fissures and follicular hyperkeratosis eventually occur. Rubbing and scratching can lead to lichenification of the affected areas. Treatment. Moisturizing is the mainstay of treatment for dry skin associated with asteatotic eczema. Any moisturizer is acceptable, and regular petroleum jelly is excellent and usually readily available. Applying in a cream after a shower will help retain moisture in the skin. frostbite The mechanism of frostbite is the destruction of local tissue caused by temperatures below zero. ( Fortunately, on the territory of Ukraine, the temperature as a whole no longer drops below zero, so we will consider frostbite only in the general context of cold injuries. - Note ed .) Etiology. Frostbite occurs as a result of the actual freezing of tissues, and subsequent changes in blood vessels. The human body&#39;s initial reaction to exposure to cold is vasoconstriction of the skin, which occurs to reduce heat loss and maintain core temperature. Vasoconstriction persists with prolonged exposure to cold. The walls of blood vessels and endothelial cells change with increased permeability and blood stasis. Subsequently, arteriovenous shunting occurs, and the affected tissue areas are bypassed and devitalized. Rapid freezing leads to the formation of intracellular ice crystals and, consequently, to cell damage. Proteins are denatured and enzyme systems are disrupted. Cells become dehydrated when cold damages them and water flows into the extracellular spaces. Clinical manifestations. Frostbite is divided into four categories, which will be discussed in order of increasing severity: first-degree frostbite or frostbite; frostbite of the second stage, or superficial; and frostbite of the third and fourth degrees, or deep frostbite. First-degree frostbite (Frostnip) is superficial freezing of the skin, often the skin of the face or fingertips, which becomes pale and numb. If there is no further exposure to cold and the area is warmed up again, no permanent damage or tissue changes occur. Redness, itching and mild swelling may occur within 3 hours of thawing. Frostbite of the second stage (superficial frostbite Superficial Frostbite). Superficial frostbite freezes the skin and subcutaneous tissue but preserves deep structures that remain soft on deep palpation. There is blanching and numbness. As the tissues thaw, the patient develops pain, erythema, and swelling of the affected areas. The skin may take on a mottled cyanotic appearance. Bubbles can usually form within 24-48 hours, but sometimes up to 6 hours after thawing. These blisters are clear and often extend to the fingertips, which is considered a good prognostic sign. Only broken blisters should be removed. Within weeks, the tissue may mummify, blacken, and flake, revealing red, atrophic new skin. Hyperhidrosis often occurs in the second or third week, and prolonged cold sensitivity may also occur. Frostbite of the third and fourth degree (deep frostbite Deep Frostbite). Frostbite of the third and fourth degree is associated with damage to deep tissues. Frostbite of the third degree is frostbite of the skin and subcutaneous tissue with tissue damage and ulceration. Vesicles may form on thawing, but are often smaller, hemorrhagic, and do not extend to the fingertips. Severe pain may begin within a few days. Hard black scabs form and peel off over several weeks, leaving a granular base. Healing time averages 68 days, and hyperhidrosis, which may appear at 4-10 weeks, may persist for months. Frostbite of the fourth degree leads to complete necrosis and loss of deep tissues, including bone. On deep palpation, the deeper tissues are rigid. When warmed, the skin may turn purple to red and become insensitive. The edema is usually proximal to the area of the fourth degree injury, reaching a peak after 6-12 hours. Then dry-type gangrene can rapidly progress in this area, demarcation lines are noted already 72 hours after thawing. Slow progression can also occur, with the formation of a scab and gangrene appearing no earlier than 2-3 weeks after thawing. Severe pain and intense burning will occur during thawing, and large amounts of analgesics may be required. Paresthesias appear 3-13 days after rewarming, lasting at least 6 months in more than 50% of frostbite victims. The line of demarcation appears on average after 36 days and extends to the bones 60-80 days after injury. Long-term effects of frostbite include sensitivity to cold, paresthesia, numbness, pain, and hyperesthesia. Other problems, such as arthritis from frostbite, occur later, weeks to years, and resemble osteoarthritis. Treatment. Frostbite prevention is the best treatment. Frostbite can be treated immediately in the field. Warming can be done by placing your fingers in the armpit, blowing warm air on frozen surfaces, or placing your hand on a warm area. Recovery usually occurs quickly, and long-term therapy is not required. Frozen parts should not be thawed until final care is available (i.e. there is no risk of refreezing). After thawing, this part becomes painful, and if the legs are sore, the person will not be able to walk. The thaw-thaw-refreeze cycles are also very harmful and should be avoided. When treating military personnel, the availability of definitive care must be taken into account. If transportation is not available, a soldier with frostbite may have to continue fighting or move out of the combat zone. No action is applicable until the frostbitten feet have thawed. More severe types of frostbite are treated by rapidly warming the affected area in a warm water bath at 40 to 42°C until the most distal area is red. Rewarming is painful and anesthesia is needed. It is necessary to observe bed rest, raise the affected limb and protect the damaged area with two antiseptic hot tubs for gentle cleaning. Tetanus toxoid should be given to all victims. Secondary infection is common, but not all sources recommend prophylactic antibiotics. No smoking. Early heparinization, started within 36 hours and stopped after 2-3 days, appears to be beneficial, but anticoagulant therapy in humans in the field may not be possible, and there may be other injuries to watch out for. Low molecular weight dextran, 1.5 g/kg IV on the first day, then 0.75 mg/kg IV daily for 5 days has been shown to reduce blood viscosity and increase tissue perfusion in limited studies. Intra-arterial reserpine, 0.25 to 0.5 mg, may be used if vasospasm is noted on angiogram around day 10, with repeat angiogram 2 days later. Surgical sympathectomy has been used late in the healing process in severe cases, but its use is not universally recommended. Both major debridement and amputation should be avoided until dead tissue is clearly demarcated and spontaneous detachment occurs, which can take months. Wet gangrene with infection is, of course, an exception to this rule. LITERATURE<ol><li> Wayne TF, DeBakey ME. Cold Injury, Ground Type, in World War II. Washington, DC: Medical Department, US Army, Office of The Surgeon General; 1958.</li><li> US offices from the army, Novi, and the airport. Cold Injury. Washington, DC: D.O.D.; TB MED 81, NAVMED P-5052-29, AFP 161-11. September 30, 1976: 1–15.</li><li> Hanson H, Goldman R. Fatal injury in man: A review of its etiology and discussion of its speculation. Milit Med. October 1969;134(11):1307-1316.</li><li> Orr K, Fainer D. Mortal exhaustion in Korea during the winter of 1950–1951. Medicine. 1952;39:177-220.</li><li> Reuler J. Hypothermia: Paphophysiology, clinical settings, and management. Ann Intern Med. 1978;89:519–527.</li><li> Vaughn B. Local cold injury - menace to military operations: A review. Milit Med. 1980;145(5):305-310.</li><li> Sumner D, Criblez T, Doolittle W. Host factors in human frostbite. Milit Med. 1974;139:454-461.</li><li> Demis DJ. clinical dermatology. 17th ed. Philadelphia: JB Lippincott, 1990.</li><li> Page E, Shear N. Temperature-dependent skin disorders. J Am Acad Dermatol. 1988;18(5):1003-1019.</li><li> Marzella L, Jesudass R, Manson P, Myers R, Bulkley G. Morphological characterization of aggressive decline into space endothelium skin by frostbite. Plast Reconstr Surg. 1989;83(1):67-75.</li><li> Leecost T. Frostbite, diagnosis and treatment. Journal of the American Podiatry Association. November 1981;71(11):599-603.</li><li> Taylor M, Kulungowski M. Frostbite injuries during winter maneuvers: Long-term disability. Milit Med. 1989;154(8):411-412.</li><li> Glick R, Parnami N. Frostbite arthritis. J Rheumatol. 1979;6(4):456-460. Cold-Induced Injury 37</li><li> Bangs C, Boswick J, Hamlet M, Sumner D, Weatherley-White RCA. Winter problems: When your patient suffers frostbite. Patient care. 1 Feb 1977:132–157.</li><li> Cohen P. Cutis marmorata telengiectatica congenita: Clinopathological characteristics and differential diagnosis. cutis. 1988;42:518–522.</li><li> Fleischer A, Resnick S. Livedo reticularis. Dermatol Clin. 1990;8(2):347–354.</li><li> Corbett D. Cold injuries. J Assoc Military Dermatologists. Fall 1982; 8:34–40.</li><li> Coffman J. The enigma of primary Raynaud&#39;s disease. circulation. 1989;80(4):1089-1090.</li><li> Freedman R, Mayes M, Sabharwal S. Induction of vasospastic attacks despite digital nerve block in Raynaud&#39;s disease and phenomenon. circulation. 1989; 80(4): 859-862.</li><li> Surwit R, Gilgor R, Alain L, Duvik M. Bilateral personis studio in the course of Ryanaude phenomenon in scleroderma. Arch Dermatol. March 1984;120:329–331.</li><li> Rodeheffer R, Rommer J, Wigley F, Smith C. Nifedipine-driven bilateral blind trif in Rheinaud phenomenon outcome. N engl J Med. 1983;308(15):880-883.</li><li> Kleckner M, Allen E, Wakim K. Efficacy of topical glyceryl trinitrate (nitroglycerin) on Rheinaud&#39;s disease and Rheinaud&#39;s phenomenon,</li></ol>

Military dermatology: direct cold injuries