Freezing cold injury, also known as frostbite, is an example of local peripheral cold injury. The pathological process can be divided into two discrete entities: freezing and thawing. The freezing component is due to a combination of extracellular ice crystal formation with a subsequent development of intracellular osmotic pressure gradient differences resulting in cellular membrane disruption, dehydration and death. The thawing process causes microvascular changes including erythrocyte sludging, microthrombus formation, increasing compartment pressures and decreased blood flow leading to tissue hypoxia and necrosis [6].

There have been two methods of describing the extent of freezing cold injury: one describing the degree of injury [7] (Table 30.1) and the other describing the depth of injury.

Because of the difficulty in assessing the differing degrees of injury, Mills and associates [8] proposed the terms superficial and deep injury instead of the traditional degrees:

Nonfreezing cold injury is an injury of the hands and feet that results from prolonged exposure to wet conditions and temperatures just above freezing. It is predominantly due to microvascular endothelial damage, stasis and vascular occlusion. At first, the tissue is cold and sensate, progressing to anaesthesia in 24–48 h. The hyperaemic phenomenon is accompanied by an intense burning sensation as well as blisters and possible ulceration [9].

The present view is that nonfreezing cold injury is brought about by prolonged vasoconstriction. In the normal human physiological response, peripheral vasoconstriction is brought about by a sympathetic response. When cutaneous blood vessels are cooled, they become more sensitive to catecholamines, and the arterioles and venules constrict [10]. It is also worth noting that this response is mediated by genetic components as well as acclimatisation. Native peoples in the arctic show much less vasoconstriction than European settlers with cold water exposure. It would be natural to assume that this process would continue in prolonged cold exposure. However, the body endeavours to prevent prolonged peripheral ischemia by a complex series of pathways resulting in a protective cold-induced vasodilation [11]. This phenomenon disappears quite quickly in the initial cold exposure in individuals who obtain nonfreezing cold injury.

Clinical and experimental studies have also demonstrated that cold exposure can be a direct cause of peripheral nerve injury. A widespread, predominantly distal degeneration of axons has been documented, leading to nerve dysfunction and damage to sympathetic nerve fibres [12]. There has been no conclusive evidence that certain types of nerve fibres are more at risk than others. Various studies have hypothesised that small unmyelinated fibres are more at risk than large myelinated ones and vice versa [13, 14].