About Frostbite That Occurs in the Cold Winter

Frostbite refers to tissue damage that occurs when the physiological compensatory mechanisms fail in body parts exposed to a cold environment.

The duration of exposure to cold, humidity, ventilation, air pressure, clothing, the medical condition of the body, and individual susceptibility all play a role in the development of frostbite. When the human body is exposed to a cold environment, homeostatic mechanisms act to maintain the body’s core temperature. In other words, when the extremities are exposed to a cold environment, blood must be diverted to maintain core temperature, and the blood vessels in the cooled extremities constrict to divert blood. However, as a result, the extremities sustain damage due to vasoconstriction, and this is one of the factors involved in frostbite.

Peripheral cold injury includes both freezing injury and non-freezing injury (which occurs at temperatures above freezing in conditions with high humidity). These can occur either together with systemic hypothermia or independently.

A representative example of freezing injury is frostbite, and representative examples of non-freezing injury are trench foot and chilblains.

Pathophysiology

The development of frostbite can be divided into two stages.

First, in the pre-freezing stage, when a body part is exposed to a cold environment, the temperature of the epidermal layer of the skin decreases, and when tissue temperature falls below 10˚C, sensation in the skin is lost. As the temperature drops, blood viscosity increases. Meanwhile, due to the homeostatic mechanism for maintaining body temperature, the blood vessels in the exposed area constrict, and plasma leaks out of the blood vessels, causing tissue edema.

Second, in the freezing stage, if the surrounding temperature drops further, the tissue fluid freezes and forms ice crystals. This increases the osmotic pressure within the tissue, moving water from inside the cells to the outside and causing cellular dehydration. Cellular dehydration increases intracellular osmotic pressure and leads to necrosis, while cell damage in the surrounding capillaries causes blood stasis and blockage of blood flow.

As blood flow is blocked, cells within the blood vessels coagulate and form intravascular thrombi, and ischemic tissue injury gradually progresses. The area affected by cold injury may later suffer additional damage during rewarming, through a mechanism called reperfusion injury.

When tissue that has been affected by cold injury is rewarmed, blood flow increases again in the previously blocked area, and tissue edema worsens due to damage to the vascular endothelial cells. In addition, the dehydrated cells in the ischemically injured area become swollen, and reactive oxygen species are generated, further aggravating damage to the vascular endothelial cells.

Also, inflammatory reactions caused by tissue injury lead to the production of vasoconstrictive factors, which further worsen ischemic tissue injury. Non-freezing injuries similar to frostbite, such as trench foot and chilblains, occur after repeated long-term exposure to a damp, cold environment. Sensory loss occurs due to peripheral nerve damage, and ischemic tissue injury occurs due to microspasms of the blood vessels.

So far, I have explained frostbite that occurs in the cold winter. In the next part, we will look at the symptoms of frostbite, initial response, and first aid.

Source: Korea Disease Control and Prevention Agency, National Health Information Portal