Deep frostbite is a thermal injury associated with significant morbidity. Historically, this has been associated with military personnel; however, increasingly it is becoming an injury that afflicts the civilian population. The use of intravenous iloprost or intra-arterial thrombolytics has led to promising tissue salvage. This article provides an up-to-date understanding of frostbite pathophysiology, classification, prevention, and management. It also highlights the role of telemedicine in optimizing patient outcomes. To further the understanding of optimal frostbite management, larger, likely multicenter, high-quality trials are required. An international frostbite register would facilitate data gathering.
Frostbite is associated with significant morbidity, and prevention is key.
Freeze-thaw-freeze cycles must be avoided.
New therapies, such as parenteral iloprost or thrombolytics, offer significant promise in the management of deep frostbite injury.
Expert opinion is now readily available via telemedicine.
Frostbite injury can result in debilitating long-term irreversible morbidity. Despite this, frostbite management strategies remained constant and unchanged until recent years, when novel therapies have led to promising, tissue-saving, outcomes. This article gives a background understanding of frostbite and its pathophysiology and reviews the current evidence and latest frostbite management strategies to educate clinicians to maximize the outcomes of their patients.
The first physical evidence of frostbite injury is in a 5000-year-old pre-Columbian mummy discovered in the Andes. In military medicine, cold injuries, including frostbite, have long been recognized as a significant cause of mortality and morbidity. Examples of this include Hannibal crossing the Alps in 218 bc , when only 19,000 survived out of 38,000, or the American War of Independence, in which cold casualty rates in George Washington’s army were described as being as high as 10%. Napoleon Bonaparte’s Surgeon in Chief, Dominique Jean Larrey, during the failed invasion of Russia in the winter of 1812 to 1813, wrote the first authoritative report on frostbite and cold injury. Frostbite continues to afflict modern militaries.
Within the civilian environment, frostbite can affect a myriad of individuals. One civilian subgroup is that of mountaineers. A cross-sectional questionnaire found a mean incidence of 366 per 1000 population per year. The British Antarctic Survey found an incidence for cold injury of 65.6 per 1000 per year; 95% of this was for frostbite, with recreation being a risk factor. On Denali, frostbite was found to be the most common (18.1%) individual diagnosis made at the medical facilities. An epidemiologic review of the first 10 years of the so-called Everest ER (emergency room) found that cold exposure accounted for 18.4% of all trauma visits, of which 83.7% were attributable to frostbite.
In the nonadventurer civilian population, there are certain recognized risk factors for frostbite injury. These risk factors include alcohol consumption, smoking, vagrancy, psychiatric disturbance, unplanned exposure to cold with inadequate protection, previous cold injury, several medications (eg, β-blockers), and working with equipment that uses NO 2 or CO 2 . Alongside the aforementioned, there seem to be important genetic risk factors that include African American ethnicity and O group blood typing. Possession of the angiotensin-converting enzyme DD allele may also increase risk.
Frostbite is a freezing cold thermal injury that occurs when tissues are exposed to temperatures below their freezing point. Pathologic changes can be divided into direct cellular injury and indirect cellular injury, also referred to as progressive dermal ischemia.
Direct cellular injury
Direct cellular injury occurs because of a variety of mechanisms. These mechanisms can be summarized as ice crystal formation (intracellular and extracellular), cell dehydration and shrinkage, electrolyte disturbances, denaturation of lipid-protein complexes, and thermal shock. These mechanisms result in cell injury and death.
Indirect cellular injury (progressive dermal ischemia)
Indirect cellular injury is secondary to progressive microvascular insult and is more severe than the direct cellular effect. Following thawing, microvascular thrombosis occurs, resulting in continued cell injury and death. Endothelial damage, intravascular sludging, increased levels of inflammatory mediators and free radicals, reperfusion injury, and thrombosis all play a role in contributing to progressive dermal ischemia and positively reinforce each other.
There have been several proposed classifications for frostbite and historically the degrees classification has been favored. This system divided frostbite into frostnip, first-degree, second-degree, third-degree, and fourth-degree frostbite depending on depth of injury. Others clinicians have opted for a simpler classification of superficial (first-degree and second-degree) and deep (third-degree and fourth-degree). Because bone loss is always distal to the observed extent of frostbite, these classifications often fail to predict likely amputation levels, which only become apparent at subsequent mummification.
Over recent years there has been an effort to formulate a reproducible and prognostic classification system rather than the established observational systems. Cauchy and colleagues proposed a classification system of 4 grades for frostbite of the hand or foot based on the appearance of the lesion after rapid rewarming, appearance at day 2, and radioisotope uptake on bone scan at day 2. The advantage of this classification is that it gives an early prognostic indicator of bone and tissue loss and the likely anatomic level of loss. This grading system relies on isotope bone scanning. In the field, Cauchy and colleagues suggest the use of portable Doppler or the clinical stigmata of soft tissue cyanosis as surrogate markers for amputation risk.