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Diagnosis: Frostbite and Mild Hypothermia

Flippone, Lisa M. MD

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Dr. Filippone is an assistant professor of emergency medicine at Drexel University College of Medicine and the director of the Division of Emergency Ultrasound at Mercy Hospital of Philadelphia.

This patient has frostbite and mild hypothermia. Removal of wet clothing and applying blankets is sufficient for her hypothermia, but her frostbite needs further management including rewarming, wound and pain management, and tetanus update.

Frostbite is a freezing injury that usually involves the distal extremities, nose, or ears. Frostnip refers to a superficial freezing of the skin with pain and paresthesias that resolves with rewarming. Frostbite involves two phases, the freezing phase and the reperfusion phase. As environmental temperatures decrease, we are able to conserve heat via peripheral vasoconstriction and behavioral mechanisms, such as putting on a coat or coming in from outside. Initial peripheral vasoconstriction may decrease cutaneous blood flow from 200–400 mL/minute to 20–50 mL/minute. As skin temperature continues to decrease to below 50 to 59 degrees Fahrenheit, the body begins a rhythmic cycle of vasoconstriction and vasodilation termed the hunter's response.

The goal is to decrease blood flow to the affected area to conserve heat and to return cooled blood from the extremities. These bursts of vasodilation and vasoconstriction will continue until the core body temperature is threatened at which point blood flow will essentially cease to the affected area. It is at this point that frostbite ensues. Once the skin temperature decreases to 32 degrees Fahrenheit or below, fluid in the extracellular space begins to freeze. The resulting shift of intracellular fluid out of the cells results in cellular dehydration and electrolyte imbalance. Cellular membranes breakdown, proteins become denatured and ultimately intracellular fluid may crystallize. This is termed phase one or the freezing stage of frostbite.

Phase two of frostbite, the reperfusion injury, develops as the affected area is rewarmed. Damaged capillaries and oxidative stress result in activation of the arachidonic acid cascade and production of prostaglandins and thromboxane. Edema, small vessel thrombosis, tissue ischemia, and ultimately tissue necrosis and gangrene result.

The severity of frostbite can be divided into superficial and deep. It also may be described in terms of degrees. First-degree frostbite is a superficial freeze involving only part of the epidermis. The patient experiences burning and numbness. As reperfusion occurs, there may be mild edema and erythema. Symptoms usually resolve within two weeks, and complications are few including cold insensitivity.

Second-degree frostbite is a full thickness injury of the epidermis. Swelling, redness, and pain is more severe and clear blisters often develop which later may desquamate and form blackened eschars. Long-term complications include paresthesias, hyperhidrosis, and cold insensitivity.

Third-degree frostbite involves the epidermis and subcutaneous tissue. The pain is deep and becomes severe with rewarming. Edema and erythema may be severe, and hemorrhagic blisters develop. There may be skin discoloration and tissue necrosis. Long-term complications include tissue loss, severe paresthesias, cold insensitivity, and growth plate abnormities in children.

Fourth-degree frostbite is characterized by involvement of bones, tendons, and joints. Pain and edema may be mild. Skin is discolored, often mottled, and eventually may become black and mummified.

Patients should be removed from the cold environment, have wet cold clothes removed, and have their hypothermia treated initially. Once the patient is hemodynamically stable and her hypothermia is corrected, attention should be paid to rewarming the affected extremity rapidly. The injured area should be submerged in a circulating water bath heated and maintained at 104 to 107 degrees Fahrenheit until the distal area is flushed, soft, and pliable.

Figure. C

Figure. C

As rewarming occurs pain will become severe, and intravenous narcotic analgesia is often required. On average, a superficial injury (first and second degree) will need to be submerged for 30 minutes and a deep injury (third and fourth degree) will need to be submerged for 60 minutes. Once the extremity is soft, warm, and pliable, it should be dried and topical aloe vera should be applied. Digits should be separated and sterile non-adherent bandages applied. The affected extremity should be elevated to decrease edema. Nonsteroidal anti-inflammatory medications should be administered. These along with topical aloe vera act to decrease activation of the arachidonic acid cascade and decrease tissue damage.

Management of blisters is an area of controversy, but most agree that clear blisters rich in thromboxane should be aspirated if not debrided. Hemorrhagic blisters may be left in place unless they interfere with range of motion in which case they may be aspirated or debrided.

Prophylactic antibiotics are generally recommended with two to three days of penicillin. Tetanus should be updated as indicated. Surgery should be withheld until there is full demarcation of viable and necrotic tissue. In general, this takes two to six weeks. Escharotomy may be necessary if limited range of motion occurs. Earlier surgical intervention may be needed if infection develops. Other experimental modalities such as hyperbaric oxygen therapy, intra-arterial recombinant tissue plasminogen activator, and use of prostaglandin analogues should be discussed with a specialist.

In general, most cases of frostbite should be admitted because there is usually some degree of hypothermia involved. Mild cases can be discharged with close follow-up on NSAIDs, topical aloe vera, range of motion exercises, and possible prophylactic antibiotics.

This patient had a few risk factors that are often seen in conjunction with frostbite and hypothermia. She has a history of psychiatric illness and alcohol use, both of which impair judgment. Alcohol causes peripheral vasodilation resulting in increased heat loss, and her wet clothing also increased heat loss.

© 2004 Lippincott Williams & Wilkins, Inc.