Hypothermia is a core body temperature below 95 ºF (35 ºC). Stages include mild hypothermia (90–95 ºF/32–35 ºC), moderate hypothermia (82–90 ºF/28–32 ºC), and severe hypothermia (below 82 ºF/28 ºC). Measuring a “true” core body temperature can be a challenge in the hospital, let alone in the prehospital environment, and individual physiological responses to cold can vary widely. From a practical perspective, hypothermia is best defined from a physiological standpoint: cold stress exceeding the body’s ability to produce sufficient heat to maintain body temperature [2]. The stages can then be based on clinical presentation and a patient’s ability to self-rewarm if the cold stress is eliminated (Table 48.1). In this approach, the core temperature is adjunctive but the clinical picture guides the provider’s actions.

Types

From 1999 to 2011, there were on average 1301 deaths annually in the United States attributed to hypothermia [3]. While the classic image of hypothermia is the lost hiker huddled in the snow, EMS providers are more likely to encounter urban hypothermia, a multifactorial hypothermia resulting from cold exposure and some combination of medical conditions, medications, changes in temperature perception, substance abuse, inadequate nutrition, and inadequate social circumstances [4–7]. Urban hypothermia is a chronic disease and while the clinical presentation of hypothermia may precipitate the call for EMS and may well be the immediate life threat, it is rarely the only active disease process. It is often considered to be secondary hypothermia.

Wilderness or environmental hypothermia, by contrast, is primary hypothermia caused by exposure to cold stress that exceeds the body’s heat production capacity. It is either acute, as in immersion, or subacute hypothermia (over days), as seen in the inadequately prepared hiker in a cold (although not necessarily freezing) environment.

Mechanisms of thermoregulation

Humans maintain a core temperature within a narrow range of (95–100.7 ºF/35–38 ºC) for optimal metabolic functioning. Four mechanisms, radiation, conduction, convection, and evaporation, contribute to heat loss from the body; homeostasis is maintained by balancing these mechanisms against heat production.

Infrared radiation emission accounts for up to 40% of all heat loss. The greater the temperature difference between the individual and the environment, the greater the rate of heat loss [8]. This can occur even when the air temperature is warm if the surrounding environmental features (such as a cave or concrete structure) are colder.

Evaporation via sweating dissipates excess heat, with approximately 575 calories of heat lost for each cubic centimeter of evaporated sweat [8]. Unfortunately, this mechanism is just as effective at removing heat during periods of cold stress. Individuals who become wet will rapidly lose heat via evaporation in a cold environment.

In conduction, direct transfer of heat from one object to another, a colder object becomes an important source of heat loss for the recumbent ill or injured individual. The greater the area of uninsulated contact, the more heat is lost.

Convection, particularly combined with evaporation, also contributes to heat loss. The body heats a small local environment to minimize heat transfer. If this buffer zone is lost, the body is constantly reheating new air (or water) and heat losses increase dramatically. Moving air (wind) augments this effect. Heat loss is a function of the square of wind velocity so doubling the wind speed quadruples heat loss [8] up to a maximum speed of 40 mph (64 km/h), after which the air is moving too quickly to absorb heat [9]. This phenomenon is referred to as wind chill (Figure 48.1). Wind chill describes the rate of heat loss from exposed skin. This has implications for how urgently a rescue must be effected. Use of windproof garments or shelters eliminates the wind chill effect.

Two primary defenses guard against heat loss. First, in response to cold stress, there is a behavioral imperative to add additional layers of clothing and to seek sources of warmth [8]. The second defense is heat production. Any muscular activity produces heat. The body can uncouple heat production from useful activity via shivering [3]. While shivering will produce additional heat to counter cold stress, it will not prevent worsening hypothermia if the environmental conditions don’t change. Shivering should serve as a signal to take other actions to decrease the environmental cold stress. Performing useful activity that increases the chances of survival also generates heat and is the preferred method of muscular heat production.

Prevention

Preventing wilderness hypothermia requires recognizing cold stress and taking actions to decrease it. Sufficient calorie and water intake is crucial to allow effective metabolism and heat generation. Clothing that maintains a microclimate of trapped air, prevents heat loss though convection, and wicks moisture away through all the layers of the clothing decreases the risk of hypothermia. Avoidance of substances that promote vasodilation (e.g. alcohol) or that impair judgment and temperature perception (e.g. alcohol or illicit drugs) will decrease the risk of primary hypothermia.

Preventing urban hypothermia is a far more complex issue with public health and social welfare implications [10]. Programs such as the Low Income Home Energy Assistance Program likely decrease the incidence of urban hypothermia, as do homeless shelters.

Recognition

While classification based on core body temperatures is useful for research and statistical purposes [1,11–14], an individual’s performance at a given core body temperature can vary widely [15] and so the assessment and treatment should be based on clinical presentation (see Table 48.1).

In the early stages of hypothermia, a perception of being cold and a behavioral imperative to change or exit the cold environment will predominate. Unless sufficient heat is being developed from useful activity, the patient will shiver and may be mildly agitated. Loss of fine motor control follows. At this stage, if the patient has sufficient calorie reserves and is removed from the cold stress, he will be able to rewarm himself.

Left untreated, hypothermia will progress and symptoms will include confusion, slurred speech, loss of gross motor coordination, and loss of judgment. This stage is described as the “-umbles”: the patient stumbles, mumbles, grumbles, fumbles, and tumbles. Eventually as caloric reserves are depleted, shivering stops. At this point, the patient is no longer able to self-rewarm even if cold stress is eliminated.

The patient will progress to a state of unresponsiveness. Cardiac dysrhythmias occur, particularly atrial fibrillation. Metabolic demand decreases and the patient becomes bradycardic. As the myocardium becomes more irritable, the risk of ventricular fibrillation with minimal or no stimulation increases. Respiratory rate decreases and the patient may appear apneic.

Once the patient is comatose, effort must be focused on minimizing physical movements that could trigger ventricular fibrillation, including bumping, dropping, or otherwise physically stimulating the patient.

Treatment

Treatment of hypothermia depends on whether or not the patient is able to self-rewarm if the cold stress is eliminated. Therefore, the most important action is to eliminate the cold stress. This may be as simple as moving the patient to a heated ambulance. If a heated sheltered environment is not readily available, efforts to eliminate further heat loss include insulating the patient from the ground to prevent conduction, removal of wet clothing to minimize evaporation, and sheltering from wind to prevent convection. Although studies have evaluated mechanisms to decrease radiant heat loss [15], to date none have been particularly successful.

Once the cold stress is removed, an assessment must be made of the patient’s ability to self-rewarm. For the patient with mild hypothermia who still has adequate caloric and metabolic reserves (that is, still shivering or recently stopped shivering), elimination of cold stress and feeding the patient should be sufficient to restore normothermia [8,13,16].

For patients who are metabolically depleted and unable to self-rewarm, active interventions will be necessary. The historical dogma has been that out-of-hospital interventions are sufficient only to prevent further heat loss and are not adequate to restore normothermia. Such interventions have included heated IV fluids, heated (and preferably humidified) inhaled oxygen, application of heat packs or heated water bottles to the neck, axilla, and inguinal creases, and rescuer/patient skin-to-skin contact [8,17,18]. More invasive procedures such as warm water irrigation of the stomach, bladder, peritoneal, and pleural cavity as well as heated dialysis and cardiopulmonary bypass have been reserved for the hospital setting [8,19,20].

Over the last decade, research has demonstrated that effective prehospital interventions exist. These include a 600 W heater with a soft rewarming blankets (a forced warm air full-body blanket) [21,22], 600 or 850 W heater with rigid torso cover [21,23], and charcoal vest forced hot air heaters (Figure 48.2

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