Clinical Pearls & Morning Reports

Posted by Carla Rothaus

Published June 8, 2022


What are some of the components of the management of frostbite?

Given a paucity of high-quality data, including data about thrombolytic agents, the practitioner and patient are left with difficult, time-sensitive decisions to make regarding the management of frostbite on the basis of the physical examination, estimated ischemia time, and risk assessment after thorough rewarming. Read the NEJM Review Article here.

Clinical Pearls

Q: Are frostbite cases today more common in wilderness or in urban settings?

A: Today, the majority of frostbite cases are due to exposure to cold in the urban setting, often in conjunction with substance use, trauma, hypothermia, physical disability, and psychosocial issues. Such issues can complicate the process of obtaining consent for treatment.

Q: Describe the pathophysiology of cold injury.

A: The pathophysiology of cold injury is a combination of direct cellular damage from freezing and cellular ischemia from vasospasm and small-vessel thrombosis. Direct cellular damage results from ice-crystal formation and resulting injury to the cell membrane, combined with intracellular metabolic derangements. Ischemic cellular damage follows endothelial disruption of the microcirculation, with vasoconstriction, thrombosis, and poorly characterized inflammatory effects on reperfusion.

Morning Report Questions

Q: What are some of the components of the management of frostbite?

A: An important component of the initial evaluation is identifying patients who have potentially reversible, ongoing, clinically important soft-tissue necrosis that may be ameliorated with thrombolytic intervention. After full rewarming, perfusion can be checked by a physical examination for capillary refill, by detection of Doppler signals in the distal pulp, and by transmission pulse oximetry of the distal digits. Patients with intact distal perfusion should be treated conservatively. Such treatment consists of elevation of the injured extremity, pain control, topical wound care, selective removal or decompression of blisters, avoidance of smoking and repeat cold exposure, excision of clearly necrotic tissue, wound closure by a variety of means, and rehabilitation. If small-vessel flow is absent despite full rewarming, a thoughtful risk–benefit analysis should be promptly undertaken to determine whether angiography and thrombolysis are appropriate. Thrombolytic therapy may ameliorate the terrible long-term burden of frostbite to some extent, although its use must be tempered by the possibility of serious hemorrhagic complications. Anticoagulant therapy after treatment for frostbite (with or without thrombolysis) is controversial. Practices vary widely among programs, from several months of anticoagulant therapy, antiplatelet therapy, or both to no such treatment. Data are not adequate to support guidelines or rational decision making.

Q: Why is iloprost being evaluated for the initial treatment of frostbite in selected patients?

A: Iloprost is a synthetic prostacyclin analogue that is a potent dilator of small-vessel beds in the pulmonary and systemic circulation. The agent is also an inhibitor of platelet aggregation. Iloprost is used primarily for the treatment of pulmonary hypertension and is administered through inhalation with the use of a dedicated system. An intravenous form delivered by pump infusion is available outside the United States. Since vasospasm may play a role in frostbite injury by reducing flow and facilitating the thrombotic process, early trials have evaluated iloprost for the initial treatment of frostbite in otherwise healthy patients. Intravenous iloprost is not available in the United States at present.

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