In the United States, hypothermia should be a preventable disease, yet between 1999 and 2011, an average of 1301 people per year die of excessive natural cold.1,2 The majority of reported mortality cases involve victims older than 19 years and two thirds of all victims are male. Predisposing factors that increase the risk for hypothermia are listed in Table 173-1.
TABLE 173-1Risk Factors Predisposing to Hypothermia ||Download (.pdf) TABLE 173-1 Risk Factors Predisposing to Hypothermia
| Extreme ages: neonates and geriatrics
| Neuromuscular disorders
Maintaining the body’s core temperature is essential for human life. It is dependent on basal metabolism and physical activity. The human body can lose heat by four mechanisms: (1) radiation, or transfer of heat through infrared energy; (2) evaporation, which includes respiration; (3) convection, or transfer of heat by the movement of air currents; and (4) conduction, or heat loss through direct contact with another object. When conduction and convection are combined, heat loss may be as high as 10% to 15%, which is why removing cold and wet clothes is essential in the initial management.
Hypothermic patients are traditionally classified into three categories according to core temperature: mild (32°C to 35°C), moderate (30°C to 31.9°C), and severe (less than 30°C). The lower the core temperature, the more organ systems are affected and the greater the potential for morbidity and mortality. In the pre-hospital setting, obtaining an accurate core temperature is impractical. Thus, clinical criteria were developed by wilderness search and rescue teams and emergency medical services providers. The criteria are as follows: HT I—Conscious and shivering (core temperature 35°C to 32°C); HT II—Impaired consciousness, not shivering (<32°C to 28°C); HT III—Unconscious, not shivering, vital signs present (<28°C 24°C); HT IV—No vital signs (<24°C).3
Another form of morbidity that is not solely related to hypothermia is frostbite. Frostbite represents a continuum from tissue injury to irreversible tissue damage. Two mechanisms are responsible.4,5 The first is cellular death at the time of cold exposure and involves ice crystal formation in the extracellular space, which induces an osmotic shift, the end result is intracellular dehydration and cell death. As the tissue is continually exposed to cold temperatures, intracellular ice crystals are formed and cause more cellular destruction. The body’s response to this localized trauma is to alternate vasoconstriction and vasodilation. As a whole, the process of thawing and refreezing causes most of the cellular damage. The second mechanism of injury is very similar to thermal burns and is a result of prolonged, progressive dermal ischemia. Cold exposure induces inflammatory mediators: thromboxanes, prostaglandins, histamine, and bradykinins. These mediators promote edema that results in the formation of blisters.5
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