Frostbite was reported as early as 5000 years ago in a Chilean mummy with the right foot exhibiting loss of digits ascribed to cold injury [1]. Current management of the disorder dates back to treatment of military casualties, witnessed during the invasion of Russia in 1812, as described by Baron Dominique Larrey, Napoleon’s military surgeon. He recognized the importance of rewarming and the injurious effects of the freeze-thaw-freeze cycle [2, 3]. Prophylactic measures to prevent frostbite were introduced by Munroe during First World War. In 1915, R.H. Jocelyn Swan, writing in the British Medical Journal, used the term “frost-bite” in soldiers and described symptoms of paresthesias and pain. He advocated painting the wounds with 2 % iodine solution and delaying amputation to await a natural separation at the junction of necrotic and viable tissue [4]. These recommendations remain just as true today.

When the temperature is less than 15 °C, the body undergoes an auto-thermoregulatory response with cycles of vasoconstriction and vasodilation, known as “the hunting reaction of Lewis.” This preferentially decreases blood flow intermittently to the extremities to maintain core body temperature. Prolonged hypothermia leads to persistent vasoconstriction with hypoxia, acidosis, stasis of blood flow, and thrombosis [2, 5].

As tissue freezes parallel mechanisms act synergistically resulting in injury. The formation of extracellular ice crystals damages cell membranes, causing a change in the osmotic gradient, intracellular dehydration, electrolyte shifts, and ultimately cell death. As the temperature of the tissue continues to fall, formation and expansion of intracellular ice crystals also mechanically disrupt cells [2, 5]. Additionally progressive dermal ischemia augments the injury by an ischemia reperfusion response [2, 3]. Endothelial injury, tissue hypoxia, and thrombosis of blood vessels lead to a massive inflammatory cascade (Fig. 30.1). This triggers the release of prostaglandins and thromboxanes that lead to further vasoconstriction, platelet aggregation, and thrombosis, which is amplified during rewarming and recurrent freezing [2, 5]. Effective treatment must be aimed at prevention, rewarming to halt freezing, increasing blood flow to decrease hypoxia, and blocking the release of inflammatory mediators.