Deep Frostbite Treated With Hyperbaric and Thrombolytics
Deep Frostbite Treated With Hyperbaric and Thrombolytics
The authors present a case of deep frostbite treated with both hyperbaric oxygen and thrombolytic therapies. Both of these therapies are experimental and have not yet achieved widespread clinical use. The patient described in this paper sustained frostbite after becoming intoxicated and falling unconscious in a snowy field. He was treated acutely for hypothermia and came into the authors' care for wound management. Of his 6 digits with extensive, deep frostbite, 1 digit eventually required partial amputation, and another had protracted osteomyelitis treated with intravenous antibiotics. The authors present a case history in the context of current research and provide a listing of previous case reports of hyperbaric oxygen therapy for frostbite.
Frostbite is defined as the freezing of tissue, leading to the formation of extracellular ice crystals that damage cell membranes and osmotically dehydrate cells. Upon rewarming, frostbite results in extensive blistering, edema, and ischemia of the affected tissues and can become necrotic and gangrenous, sometimes requiring amputation. The pathophysiological mechanisms of frostbite damage have been described as taking place in 2 phases. The first phase is during the time of cold exposure, when cellular damage is caused by the formation of extracellular ice crystals. As crystals form, the remaining fluid becomes hyperosmotic, leading to the dehydration and shrinking of surrounding cells. Ice crystals also cause direct damage to plasma membranes and proteins. As endothelial cells shrink and are otherwise damaged, the structural integrity and function of microvasculature is compromised. Rapidly rewarming the injured tissues using warm water—a well-proven treatment for frostbite—is believed to limit the amount of damage caused by these ice crystals. The second phase of the pathophysiology of frostbite is the progressive dermal ischemic damage that begins upon rewarming, as a result of the damage to endothelial cells and the resulting release of inflammatory mediators including prostaglandins and thromboxanes, leading to thromboses, edema, and other vascular sequela. Hyperbaric oxygen (HBO) and thrombolytics, along with prostacyclin and sympathetic nerve blocks have all been used experimentally to address dermal ischemic damage related to frostbite, but have yet to receive widespread support.
Hyperbaric oxygen therapy has been used to treat frostbite injuries for more than 50 years. Beginning in 1963, there were several case reports published that described favorable outcomes. In response to these case reports, laboratory studies were conducted on mouse and rabbit models, but these yielded mixed results. For 25 years, no new case reports were published. Beginning in 1997, many more case reports on HBO therapy for frostbite injuries were published, all with favorable outcomes. In addition to these recent case reports, a laboratory study was conducted on a rabbit model that yielded favorable results. There have been no controlled trials of HBO for frostbite published to date.
Thrombolytic therapy using tissue plasminogen activator (tPA) has more recently been suggested as a treatment for frostbite, and some initial clinical studies have had promising results. One study, using a historical control group, found a significant reduction of digital amputations with use of tPA therapy. Earlier studies, using frostbitten animal models, also demonstrated positive outcomes using other thrombolytic agents.
The purpose of this report is to add a unique case to the growing literature on HBO and thrombolytic therapies for frostbite, and to provide a listing of other case reports on HBO for frostbite published to date (Table 1).
Abstract and Introduction
Abstract
The authors present a case of deep frostbite treated with both hyperbaric oxygen and thrombolytic therapies. Both of these therapies are experimental and have not yet achieved widespread clinical use. The patient described in this paper sustained frostbite after becoming intoxicated and falling unconscious in a snowy field. He was treated acutely for hypothermia and came into the authors' care for wound management. Of his 6 digits with extensive, deep frostbite, 1 digit eventually required partial amputation, and another had protracted osteomyelitis treated with intravenous antibiotics. The authors present a case history in the context of current research and provide a listing of previous case reports of hyperbaric oxygen therapy for frostbite.
Introduction
Frostbite is defined as the freezing of tissue, leading to the formation of extracellular ice crystals that damage cell membranes and osmotically dehydrate cells. Upon rewarming, frostbite results in extensive blistering, edema, and ischemia of the affected tissues and can become necrotic and gangrenous, sometimes requiring amputation. The pathophysiological mechanisms of frostbite damage have been described as taking place in 2 phases. The first phase is during the time of cold exposure, when cellular damage is caused by the formation of extracellular ice crystals. As crystals form, the remaining fluid becomes hyperosmotic, leading to the dehydration and shrinking of surrounding cells. Ice crystals also cause direct damage to plasma membranes and proteins. As endothelial cells shrink and are otherwise damaged, the structural integrity and function of microvasculature is compromised. Rapidly rewarming the injured tissues using warm water—a well-proven treatment for frostbite—is believed to limit the amount of damage caused by these ice crystals. The second phase of the pathophysiology of frostbite is the progressive dermal ischemic damage that begins upon rewarming, as a result of the damage to endothelial cells and the resulting release of inflammatory mediators including prostaglandins and thromboxanes, leading to thromboses, edema, and other vascular sequela. Hyperbaric oxygen (HBO) and thrombolytics, along with prostacyclin and sympathetic nerve blocks have all been used experimentally to address dermal ischemic damage related to frostbite, but have yet to receive widespread support.
Hyperbaric oxygen therapy has been used to treat frostbite injuries for more than 50 years. Beginning in 1963, there were several case reports published that described favorable outcomes. In response to these case reports, laboratory studies were conducted on mouse and rabbit models, but these yielded mixed results. For 25 years, no new case reports were published. Beginning in 1997, many more case reports on HBO therapy for frostbite injuries were published, all with favorable outcomes. In addition to these recent case reports, a laboratory study was conducted on a rabbit model that yielded favorable results. There have been no controlled trials of HBO for frostbite published to date.
Thrombolytic therapy using tissue plasminogen activator (tPA) has more recently been suggested as a treatment for frostbite, and some initial clinical studies have had promising results. One study, using a historical control group, found a significant reduction of digital amputations with use of tPA therapy. Earlier studies, using frostbitten animal models, also demonstrated positive outcomes using other thrombolytic agents.
The purpose of this report is to add a unique case to the growing literature on HBO and thrombolytic therapies for frostbite, and to provide a listing of other case reports on HBO for frostbite published to date (Table 1).