Page 126 - 2020 JSOM Winter
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improved clothing ensembles, 9,10  and leadership emphasis on   skin tissues.  Chilblains (also called pernio) is a more serious
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          cold-injury prevention.  Nonetheless, cold-weather injuries   condition associated with repeated exposure to near-freezing,
                            11
          still occur, and there are reasons to assume that military op-  dry environmental conditions. Individuals experience burning
          erations in colder areas of the world might increase. Climate   sensations, pruritus, swelling, and erythema. Blisters and ul-
          change has resulted in the melting of arctic ice.  There will   cerations may occur in more severe cases. 18–20  Histologic stud-
                                                12
          likely be competition for natural resources in Arctic areas,   ies indicate  inflammatory infiltrates (mainly lymphocytes),
          including oil reserves that were previously inaccessible and   necrotic keratinocytes, and microthrombi in the dermis. 19
          where national boundaries are not clearly delineated. Sea lanes
          across the Arctic Ocean are opening, and their use can reduce   Frostbite is the most serious injury on this spectrum. It occurs
          ocean transit times and avoid Panama Canal and Suez Canal   when body tissues are exposed to temperatures below freez-
          fees, but these areas are largely in Russian territory. 13,14  These   ing and the tissues are damaged through direct and indirect
          facts increase the likelihood that US forces will be deployed to   mechanisms associated with freezing body fluids. Lower tem-
          colder areas of the world for peacekeeping, handling of natu-  peratures, wind, and moisture exacerbate this process.  Patho-
                                                                                                      21
          ral disasters, and other national security operations. It is ex-  physiologic changes are depicted in Figure 1 and involve two
          pected that cold-weather training operations will increase and   different mechanisms: (1) direct cellular damage and (2) effects
          that the United States will partner with coalition allies in these   from vascular inflammation, thrombosis, and ischemia. 15,22
          efforts.  Medical personnel planning for cold-weather opera-  When peripheral tissues (e.g., fingers, toes, ears, nose) are
               14
          tions should emphasize cold-injury prevention and prepare for   first exposed to cold temperatures, they respond with cycles
          the treatment of cold-related injuries.            of vasoconstriction and vasodilation. Cold-induced vasodi-
                                                             lation (CIVD) warms the tissue by allowing blood from the
          Among the most serious cold weather–related injuries is frost-  warmer body core to enter the peripheral circulation, while
          bite. Low temperature exacerbated by wind and surface mois-  vasoconstriction promotes cooling. When heat loss is great
          ture results in body cooling and the shunting of blood away   enough, the vasodilation/vasoconstriction cycles cease, and ice
          from the extremities. If the blood flow to the extremities is   crystals begin to form in the extracellular fluids. This increases
          restricted long enough and skin temperatures fall low enough,   osmotic pressure and draws free water from cellular spaces,
          ice crystals will form in the blood, and tissues will freeze.   resulting in intracellular dehydration, hyperosmolality, de-
          Frostbite will occur, with the resulting tissue necrosis and the   creased pH, and denaturing of lipids and proteins that damage
          potential for catastrophic amputation in the affected parts. 15,16    cell membranes and result in cellular necrosis. Ice crystals also
          This article covers the pathophysiology, epidemiology, diagno-  mechanically damage cell membranes and slow blood flow.
          sis, treatment, and prevention of frostbite.       These factors initiate an inflammatory response and release
                                                             of the inflammatory mediators (prostaglandins, thromboxane,
                                                             bradykinin, histamine) that cause platelet and leukocyte ag-
          Pathophysiology
                                                             gregation and thrombosis in affected tissue, leading to isch-
          Frostbite is part of a spectrum of cold temperature–induced   emia and cell death. 17,21–23
          local injury that ranges from minimal chilling of the skin with-
          out impairment to major tissue damage from the development   Once exposed to a warmer environment, vasodilation re-
          of extracellular ice crystals.  Frostnip is the least severe con-  sumes, resulting in reperfusion injury and a further increase in
                                17
          dition on this spectrum. Frostnip generally involves a drop in   the inflammatory response. The thin layer of endothelial cells
          the local temperature of the epidermal and dermal skin layers,   separates from blood vessels. Capillary leakage from damaged
          with some local pain and/or numbness but no injury to the   endothelial cells can form epidermal blisters. An increase in the
















                                                                                FIGURE 1  Pathophysiology of frostbite.

















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