Humans as homeothermic mammals must maintain a stable internal body temperature within narrow range to allow function of enzymes within this narrow range. Regional and seasonal variations in the environment mandate the ability to either loose or generate heat in order to maintain temperature within this range. Mechanisms to either conserve heat (surface vasoconstriction, shivering, and piloerection) or lose heat (surface vasodilation, sweating with evaporation) allow adaptation to a colder or warmer environment. Three specific adaptive behaviors permit existence in a cold environment and have allowed the spread of human kind across six of the seven continents. These are fabrication of clothing, shelter-building, and control of fire. However, environmental extremes, abnormal endocrine function, or infection and injury can result in the inability of the organism to maintain body temperature within the normal range, leading to significant functional disturbances.

It is important to understand the distinction between environmental hypothermia (due to exposure to cold), and hypothermia associated with injury. Hypothermia due to exposure can be lethal when it is severe and ongoing (consider Napoleon’s Army during the retreat from Moscow¹), but with modern medical care, hypothermia without injury has a significant survival rate even in the setting of cardiac arrest (50%).² In patients after injury, however, the effects of hypothermia are profound, with hypothermia being an important component of the “bloody vicious cycle” first described by Kashuk and colleagues.³ In one large historical series there were no survivors of hypothermia and serious trauma if initial core body temperature was less than 32^°C.⁴ This distinction mandates a different approach for patients with hypothermia and injury.

Definitions

The normal core body temperature for humans is 37^°C, with a circadian variation of approximately 0.5–1^°C.⁵ The standard definition of hypothermia, developed for environmental hypothermia, defines mild hypothermia above 32^°C, moderate from 28 to 32^°C, and a core body temperature of less than 28^°C as severe. The lowest reported temperature for an adult survivor of hypothermia is 13.7^°C. In trauma patients with hypothermia, the scale is shifted due to significant changes in mortality, with temperatures of 34–36^°C defined as mild, 32–34^°C as moderate, and less than 32^°C as severe.

Measurement of temperature should be performed using a reliable technique. The most readily available and accurate techniques include a bladder catheter with thermistor tip, tympanic thermometer (although many tympanic thermometers do not read below 34^°C), or esophageal monitoring (not as widely available). Rectal temperature measurements are not as responsive to changes in core body temperature as the previously noted techniques. Oral and axillary temperature measurements are not reliable in hypothermic patients and should not be utilized.

Environmental Hypothermia

Environmental hypothermia (also known as accidental hypothermia), occurs if a normal person is exposed to cool temperatures with inadequate clothing or shelter. The incidence of environmental hypothermia in both the United States and Europe is increasing with risk factors including advanced age, mental illness, male sex, and alcohol intoxication.^6,7 Unsurprisingly, hypothermia is highly associated with the winter season.⁷ Cooling is accelerated in the presence of windy conditions, and submersion in cold water can result in heat loss of more than 30 times that of the same air temperature.⁸ Although exceptional athletes can swim for hours in cold water, an unconditioned person may become unconscious within 30 minutes of immersion in 4^°C water. Case reports and small series suggest improved survival of children with cold water immersion undergoing cardiopulmonary resuscitation.⁹ with a major issue being anoxic brain injury.¹⁰

The physiology of hypothermia is significantly dependent on the variation from normal body temperature¹¹ (Table 49-1). Initially there is an intense cutaneous vasoconstriction to reduce heat loss, and the exposed skin can rapidly cool to the ambient temperature. The patient experiences thermogenic shivering, which markedly increases oxygen consumption and depletes glycogen stores.¹² As the temperature drops, metabolism progressively slows and shivering ceases. The patient becomes confused, lethargic, and cold to the touch. Urine production is profuse due to impaired production of antidiuretic hormone (ADH) and increased vascular tone. The patient exhibits bradycardia, ECG changes.¹³ hypotension, hypovolemia, and metabolic acidosis with elevated blood lactate. Agitation, irrational behavior, and combativeness are replaced by obtundation and finally coma. When cardiac arrest occurs, death is not immediate, but is inevitable without medical intervention.

Management of Environmental Hypothermia

Warming Techniques:

There are a variety of techniques available for prevention and treatment of hypothermia. These include both passive and active warming techniques (Table 49-2). Passive techniques, consisting of warmed blankets and environment are more applicable for prevention of hypothermia and for treatment of patients with cold stress (temperature >35^°C). Active methods can be defined as either external or internal. One of the most common external methods in use is forced-air rewarming (Bair-Hugger, 3M, St Paul, MN or similar). Current broadly-used internal methods include use of arterial-venous rewarming through catheters placed in femoral artery and vein with the blood passed through a fluid warmer, or continuous venovenous rewarming (using continuous hemofiltration dialysis unit). A more recently developed option is use of a femoral venous catheter designed for therapeutic hypothermia (Thermogard XP, Zoll Medical, Minneapolis, MN) which circulates warmed or cooled fluid through the catheter. For unstable patients or those who have developed cardiac arrest, extracorporeal membrane oxygenation (ECMO) or cardiopulmonary bypass (CPB) are appropriate options.

For the responsive patient with a core temperature above 35^°C, passive rewarming measures and support care are adequate. For patients with mild hypothermia (32–35^°C), normal mentation, and preserved vital signs, passive or active external warming techniques can be effectively utilized. Trauma patients with mild hypothermia should be transported to a trauma center if feasible, and should receive active warming. Patients with hypothermia should receive warmed parenteral fluids only. In patients with moderate hypothermia, a foley catheter with an integral temperature probe is optimal to monitor core temperature and measure urine output. Urine output will typically remain brisk during rewarming and is NOT an indicator of adequate intravascular volume. Subclavian or internal jugular catheter placement is avoided because the guide wire can trigger ventricular fibrillation of the cold myocardium. Rewarming can be performed using either active internal or external techniques. Patients with severe hypothermia require endotracheal and nasogastric tubes to protect the airway and prevent aspiration. If any perfusing rhythm can be detected, administer pressor agents, but avoid chest compressions that may trigger intractable ventricular fibrillation. In patients showing signs of severe hypothermia in the field (eg, unconsciousness, minimal vital signs) consideration should be given for transport to a center with the ability to perform extracorporeal membrane oxygenation (ECMO) or cardiopulmonary bypass (CPB), as these are the most effective techniques for both support of the cardiopulmonary system and rewarming, with survival in small series of 50–100%.^14,15 Figure 49-1 presents an algorithm of the above management strategies, adapted from a number of society guidelines.^16,17,18

The classic adage for the hypothermic trauma patient is that the patient is not dead until they are warm and dead. However, there are a number of identified markers strongly correlated with death despite aggressive resuscitation. These include elevated serum K of more than 12 mEq/L, lethal traumatic injury, core temperature less than 10^°C, unwitnessed cardiac arrest, or chest wall too stiff to permit cardiopulmonary resuscitation (CPR).^17,18

There are a number of potential complications associated with rewarming. These include core temperature afterdrop, rewarming-associated hypotension, pulmonary edema, hypoglycemia, electrolyte imbalances, renal failure, disseminated intravascular coagulation (DIC), and rhabdomyolysis.¹⁹ An expected major sequela of rewarming of patients with hypothermic cardiac arrest is potential for anoxic brain injury.²⁰ Mortality of 0–50% is reported.^14,15,19,20

Patients with hypothermia routinely present with an extremity temperature more than 15^°C lower than the core temperature, so that even in a warmed environment, the core temperature can continue to fall, a phenomenon referred to as “afterdrop.”²¹ Afterdrop may be clinically relevant in the setting of a patient with borderline severe hypothermia. In this setting a further drop in cardiac temperature may result in cardiac arrest. An afterdrop of up to 5^°C has been reported.²² For this reason, until rewarming is achieved, patients with moderate or severe hypothermia should not be mobilized to minimize return of cold peripheral blood to the central circulation.

Hypothermia in Trauma

Hypothermia is associated with increased risk of death after serious trauma. A classic study performed by Jurkovich et al.²³ in 1987 reported a 40% mortality in trauma patients with a core temperature less than 34°C, which increased to 100% in those patients with a core temperature less than 32^°C. Wang et al reported data from analysis of 38,520 patients in Pennsylvania Trauma Outcome Study, with an odds ratio for death of 3.03 associated with hypothermia.²⁴ In an effort to determine whether or not hypothermia was a risk factor for death or a marker of complications, Shafi and coauthors evaluated nearly 40,000 patients in the National Trauma Data Bank, and found that hypothermia was independently associated with increased mortality.²⁵ In one large multicenter, prospective evaluation, hypothermia in severely injured trauma patients was found to be independently associated with multiple organ failure but not mortality.²⁶ In a randomized trial of active internal versus external rewarming techniques, Gentilello et al noted improved early survival in patients receiving active internal rewarming. However, this early benefit did not lead to improved survival to discharge.²⁷

In contrast to these results in humans, there are a number of animal studies showing benefit to hypothermia in animal models of traumatic injury and shock.^28,29,30 The discrepancy between animal and human studies is initially puzzling, but is key to understanding the differences between accidental and traumatically-induced hypothermia. The primary driver of hypothermia after injury is insufficient intrinsic heat generation due to mitochondrial anoxia during anaerobic metabolism, resulting in a drop of the organisms’ core temperature toward that of the ambient environment. This is in distinction to induced hypothermia, which is sparing of adenosine triphosphate (ATP) levels, resulting in protection of the cellular environment during anaerobic conditions. For example, ATP levels are lower and remain depressed longer in hypothermic trauma patients compared to persons with hypothermia following elective surgery³¹ or patients with therapeutic hypothermia induced under anesthesia.³²

In the case of animal models, most involve induction of hypothermia over a short period of time, close to the time of injury/shock, and frequently in the setting of a standardized single-organ model whereas in the human condition, hypothermia develops over a variable period of time, with the patient in shock, and with varied periods of transport and exposure to environmental cooling prior to arrival for definitive medical care. Until more evidence exists defining appropriate patient populations for therapeutic hypothermia, we recommend aggressively warming multiply-injured patients to normothermic levels.

Hypothermia and Coagulation

Coagulation disorders are the most concerning physiologic abnormality in trauma patients and hypothermia exerts profound effects on the coagulation system. It is difficult to separate the effects of hypothermia alone in the setting of the “bloody vicious cycle” of traumatic coagulopathy. However, the effects of hypothermia on the intrinsic and extrinsic coagulation systems, and their laboratory measures, have been extensively evaluated. Cosgiff and coauthors identified coagulopathy in massively transfused patients and noted in multivariate analysis that hypothermia was a significant risk factor, with an odds ratio of 8.7.³³ These clinical results have been confirmed in a number of animal and human ex vivo studies,^34,35 demonstrating significant impairments of coagulation measurements with plasma or blood in cold conditions that resolve with warming of the plasma. This is relevant for clinicians, as coagulation tests are performed after warming of the plasma to 37^°C, suggesting that these tests in hypothermic trauma patient are likely to underestimate the degree of coagulopathy. These results were confirmed clinically in a group of 112 seriously injured trauma patients in which core body temperature was correlated with coagulation studies.³⁶ They noted that coagulation enzyme activity decreased below a threshold temperature of 34^°C.