The skin has an important thermoregulatory function, controlled by variation of blood flow, which can be reduced to about 10% of baseline without ischaemia, as the metabolic requirements of skin are low. Maximum skin vasoconstriction occurs in the extremities when cooled to around , with further cooling causing an increased perfusion due to the "hunting response", or<unk> -induced vasodilation, which occurs in 5 to 10 minute cycles, which may adapt in strength and cycling rate with repeated exposures. A strong response is thought to improve resistance to NFCI, but evidence is not conclusive. The mechanism of NFCI is poorly understood. Reduced control of circulation and damage to the microcirculation are characteristic. Although some authorities consider the cause to be only prolonged vasoconstriction, others think it likely to be more complex. There is evidence suggesting that extent and severity of tissue damage is due to a combination of temperature and duration, and that repeated exposures may cause more damage than a single longer exposure. Damage to nerves and to the microvascular blood supply of nerves may be reversible or irreversible. The duration of a single exposure at a given temperature that is likely to cause NFCI is not known, and the quantitative effects of multiple exposures are similarly unclear. The presence of a wet environment appears to be important, and immobility and malnutrition appear to be contributory. Experimental evidence suggests a complex mode of<unk>  with microvascular disruption, cyclic ischaemia, reperfusion<unk>  and direct damage to nerves due to<unk> . Large, myelinated nerve fibres appear to be more susceptible. Tissue loss may occur in severe cases, but is thought to be caused by pressure<unk> , with or without compartment syndrome, and mechanical<unk> , and not by the<unk> .
Non-freezing cold injury
Uremic frost
NSAID hypersensitivity reactions
Simulator sickness
Foreign body reaction
Aerotoxic syndrome
Bullous drug reaction
High pressure injection injury