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.

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

The signs and symptoms of a hypothermic patient are inherently associated with the person’s core temperature. Table 173-2 outlines the core temperatures associated with clinical findings.^6,7

CENTRAL NERVOUS SYSTEM

Hypothermia results in decreased metabolism and blood flow to the brain. Brain function, thought processes, and motor skills decline as the body’s core temperature drops below 35°C. Fine motor skills decline, which leads to frank clumsiness. Dysarthria and ataxia follow. As hypothermia worsens, a phenomenon known as “paradoxical undressing” may occur whereby victims undress themselves. It is thought that this phenomenon signifies impending thermoregulatory collapse. By 32°C, confusion and drowsiness become evident. Below 32°C, the person becomes unconscious.⁶

CARDIOVASCULAR SYSTEM

The early cardiovascular response to hypothermia is tachycardia. However, as the body cools below 35°C, heart rate slows and cardiac output decreases. Hypotension may occur secondary to decreased cardiac output, cardiac contractility, and intravascular volume. Electrocardiographic findings are nonspecific and include prolongation of the PR, QRS, and QTc intervals as well as ST-segment and T-wave changes. As the core temperature drops to 32°C, roughly 30% of hypothermic victims will demonstrate the J wave or Osborn wave, on electrocardiograms.⁸ The Osborn wave is an upward deflection after the QRS complex (Figure 173-1). There are no arrhythmias specific to hypothermia, but atrial and ventricular fibrillations are well documented.^8-10

RESPIRATORY SYSTEM

Tachypnea is initially seen in mild hypothermia, but as the core temperature continues to decline, hypopnea will follow. Hypoxia and hypercapnia ensue and produce both metabolic and respiratory acidosis. Ciliary function ceases as hypothermia intensifies, thus predisposing the victim to pneumonia.¹¹

MUSCULAR AND PERIPHERAL VASCULAR SYSTEM

Shivering produces heat as a means to maintain core temperature. This mechanism of heat production stops when the core temperature drops below 32°C. Cessation of shivering signifies the body’s inability to combat hypothermia.^6,11

Arteriolar vasoconstriction decreases blood flow to the skin. A slight increase in blood pressure may be noted. However, as the body’s temperature drops, blood pressure also declines as a result of loss of sympathetic tone. Conversely, intense peripheral vasoconstriction leads to pallor. Facial puffiness may ensue secondary to increased capillary permeability with subcutaneous edema.¹²

SKIN

Blisters may be found with prolonged cold exposure. They are typically superficial or deep dermal injuries. Superficial injuries portend a good prognosis and on examination include normal-colored skin and blisters filled with clear fluid. In addition, the skin will have the ability to deform with palpation. The physical findings after deep dermal injury suggest long-term morbidity and include dark, hemorrhagic blisters, and hard, non-deforming skin on palpation.⁵

Frostbite is classified into four categories—first to fourth degree—based on severity. First-degree frostbite is characterized by an anesthetic central white area with peripheral erythema. Second-degree injury represents blisters filled with either clear or milky fluid, surrounded by erythema or edema, and appears in the first 24 hours (Figure 173-2). Third-degree frostbite is associated with hemorrhagic blisters that progress over a course of 2 to 4 weeks, with the end result being a thick, black eschar (Figure 173-3). Fourth-degree frostbite produces complete tissue necrosis and autoamputation.⁵

RENAL SYSTEM

Peripheral vasoconstriction increases blood flow to the kidneys, which induces diuresis. In addition, there is a decrease in circulating antidiuretic hormone. These two factors, along with insensible water loss (sweating and respiration) and tissue third spacing, lead to a decrease in intravascular volume and prerenal failure.⁴