Vascular Atlas

62 year old homeless man presents to the emergency department after he developed black toes. He states that after a particularly cold week his toes initially became numb with the sensation of “pins and needles” followed by weakness and eventually to complete loss of sensation. Evaluation reveals multiple ischemic digits.
Frostbite is described as severe, localized, cold-induced tissue injury typically involving the fingers, toes, cheeks, nose, and ears, although frostbite of the cornea has also been described. Common symptoms include parethesias and poikilothermia of the effected area. The pathophysiology of frostbite lies along a spectrum of cold-induced tissue injury including frontnip, pernio, trench foot, and Raynaud’s phenomena.

Physiology of frostbite

The physiology of frostbite centers on the formation of extra-cellular ice crystals resulting in damage to the cellular membrane. Further exposure causes a shift of intracellular fluid resulting in intracellular volume loss and eventual intracellular crystal formation. Damage caused by ice crystal expansion is irreversible. Vascular shunting results in alternating vasoconstriction and vasodilation, known as the hunting reaction, causing rewarming of peripheral tissue with core blood. This cycling causes the release of cellular mediators and platelet aggregation leading to vascular thrombosis. Continued exposure slows the vasodilation response leaving unopposed vasocontriction ultimately causing ischemia.

Frostbite treatment

The varying degrees of frostbite have been described similarly to that of thermal burns:

  • First degree describes superficial distribution with a central pallor and surrounding edema. The surrounding skin typically experiences sensory changes.
  • Second degree is characterized by blister formation of tissue exposure. There is usually no tissue loss at this stage. Eschar may form and slough revealing healthy granulation tissue beneath it.
  • Third degree reveals more extensive blistering expanding past the superficial layer of skin. Blisters may at this point be hemorrhagic and skin may form eschar within weeks.
  • Finally, fourth degree frostbite describes extension into the deeper layers including muscle, tendon and bone. This stage is characterized by tissue necrosis and irreversible tissue loss.
    Treatment begins with removing from cold exposure and prompt rewarming. Fire heat should be avoided due to sensory loss which can result in thermal burns. Rewarming is most effective through immersion of the affected tissue into water heated to 40-42 degrees Celsius for 15 to 30 minutes. Due to its potential association with vascular thrombosis, intravenous or intra-arterial tissue plasminogen activator (tPA) along with intravenous heparin has been shown to improve outcome.
  • Frostbite References:

    1. Legmuskallio E, Lindholm H, Koskenvuo K, et al. Frostbite of the face and ears: epidemiological study of risk factors in Finnish conscripts. BMJ 1995; 311:1661
    2. Cauchy E, Chetaille E, Marchand V, Marsigny B. Retrospective study of 70 cases of severe frostbite lesions: a proposed new classification scheme. Wilderness Environ Med 2001; 12:248
    3. McIntosh SE, Hamonko M, Freer L, Grissom CK, Auerbach PS, Rodway GW, et al. Wilderness Medical Society practice guidelines for the prevention and treatment of frostbite. Wilderness Environ Med. Jun 2011;22(2):156-66
    4. Bruen KJ, Ballard JR, Morris SE, Cochran A, Edelman LS, Saffle JR. Reduction of the incidence of amputation in frostbite injury with thrombolytic therapy. Arch Surg. Jun 2007;142(6):546-51

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About Author

Ari J. Mintz, DO

Ari J. Mintz, DO is an internal medicine resident at Lahey Hospital and Medical Center in Burlington, MA. His clinical interests include peripheral arterial disease, noninvasive imaging, and advanced therapeutic approaches to venous thromboembolism. 

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