Not surprisingly, the ambient temperature, as well as the duration over which tissues are exposed to it, has a strong environmental influence on tissue surface temperature and thus can initiate frostbite injury. Thus, the skin and its circulation are generally affected first. Opposing the effect of ambient cold temperatures on the extremity skin is heat generated from the deeper tissues, whose effect is proportional to the muscle mass of the extremity. Thus, hands are particularly vulnerable due to their distance from the body core as well as their relatively large surface area and small muscle mass.

Water and moisture can conduct heat 25 times faster than air, and because of this, wet and windy environmental conditions (particularly when moisture is in contact with the skin) amplify the effect of the ambient temperature and accelerate heat loss.

There is evidence from human and animal studies that subjects can adapt to relatively cold climates with prolonged exposure, and that this acclimation is protective in the face of intermittent extreme cold exposure. One putative mechanism for this acclimatization, observed in Alaskan Eskimos, is increased peripheral blood circulation, particularly in the hand.

Although young age is not associated with immature homeostatic function, frostbite is more common in healthy children compared to healthy adults. A majority of frostbite injuries in children are preventable and attributed to improper clothing and lack of supervision during outdoor activity. Furthermore, frostbite most often affects the fingers and hands of children, while adults more often suffer from cold injury to the toes and feet.

The risk of these injuries is further increased by

Vasoconstrictive processes, from static vasoocclusive atherosclerosis (primarily in the lower extremities) to vasospastic phenomena such as Raynaud disease (upper extremities), represent significant risk factors for frostbite as well.

The severity of the injury is furthermore affected by dependency, body position, presence of open wounds, and constrictive clothing.

There is intermittent cold-induced peripheral vasodilation, together with transient arteriovenous shunting in the extremity. This is known as the “hunting response,” a physiologic strategy to rewarm an extremity at the cost of core body temperature.

However, if prolonged cold exposure leads to hypothermia (35°C), the response becomes dampened, sacrificing the extremity to preserve life.

Tissue freezing begins with crystallization of the extracellular water, leaving behind a relatively hypersomolar extracellular solution.

This alteration in osmotic balance induces fluid shifts out of cells. Destruction of cells thus occurs through dehydration as well as mechanical trauma from expanding crystals.