Temperature-Related Syndromes: Hyperthermia, Hypothermia, and Frostbite

David H. Ahrenholz

As humans, we are homeothermic mammals who maintain our core temperature within a very narrow range, with a normal diurnal variation of about 1.5°C.¹ Temperate climates present a range of temperatures that cause rapid loss of body heat to the environment, and three specific behaviors—fabrication of clothing, shelter-building, and control of fire—have allowed us to populate the earth. But hypothermia occurs when external heat loss exceeds the rate of endogenous thermogenesis. In the initial stages there are no irreversible changes as the metabolic rate slows about 50% for each 10°C drop in core temperature (Arrhenius’ law).² Under rigidly controlled anesthesia, asystolic arrest occurs between 15–20°C, and a brief state of “suspended animation” can facilitate the completion of otherwise impossible surgical procedures in a relatively bloodless field.³

SYSTEMIC HYPOTHERMIA

Primary Accidental Hypothermia

Accidental nontraumatic hypothermia, with a core temperature below 35°C, occurs if a normal person is exposed to cool temperatures with inadequate clothing or shelter, and is most common during winter months.⁴ 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.⁵ As the temperature drops, metabolism progressively slows and shivering ceases. The patient becomes confused, lethargic, and cold to the touch. Urine production is profuse as the kidneys lose the ability to transport sodium and other ions. The patient exhibits bradycardia, 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.

Cooling is accelerated in windy conditions, but immersion in cold water will remove heat up to 25 times faster than air at the same temperature. 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. Children immersed in cold water quickly become hypothermic and comatose, but if the glottis closes and excludes water from the lungs, they may be resuscitated even if vital signs are undetectable. If a rescued child is given cardiopulmonary resuscitation (CPR) and rapidly rewarmed, survival without neurologic impairment is possible.⁶

For the responsive hypothermic patient with a core temperature above 34°C, passive rewarming measures with convective warming blankets and warm fluids are adequate.⁵ Severely hypothermic patients require warmed parenteral fluids to correct the cold-induced diuresis. Urine output will 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 easily trigger ventricular fibrillation of the cold myocardium. A Foley catheter with an integral temperature probe is optimal to monitor the core temperature. Comatose patients 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.

If no perfusing cardiac activity is noted, begin CPR, and continue until the patient is rewarmed to a temperature that permits successful defibrillation (>30°C) (Figure 49-1). During rewarming monitor the patient for electrolyte imbalances, respiratory and renal complications, which may have delayed onset. Mortality of 17–27% is reported.^7,8

FIGURE 49-1 Management algorithm for treatment of hypothermia. All patients should also be closely monitored for physiologic complications associated with hypothermia. (Reproduced with permission from Reed RL III, Gentilello LM. Temperature associated injuries and syndromes. In: Mattox KL, Moore EE, Feliciano DV, eds. Trauma. 6th ed. New York: McGraw-Hill; 2008:1071.)

Patients with hypothermia routinely present with a skin temperature more than 15°C lower than the core temperature,⁵ so that even in a warmed environment, the core temperature can continue to fall, a phenomenon referred to as “afterdrop.” Once shivering stops the patient has little capacity for thermogenesis.⁵ Immersion of the patient in 40°C water is the most rapid rewarming technique,⁹ but is contraindicated if the patient requires CPR, emergency surgery, or treatment of open wounds or unstable fractures. Extremely cold or even frozen extremities are not rewarmed until the core temperature reaches 33°C. Then each affected extremity is sequentially immersed as the patient is monitored for any temperature decrease.¹⁰

If immersion is not possible, the patient can be rewarmed by extracorporeal bypass¹¹ or with a multiport central venous catheter designed to induce therapeutic hypothermia, usually placed via the femoral vein into the inferior vena cava. Balloons integral to the catheter are irrigated with warm saline via a closed circuit.

Secondary Metabolic Hypothermia

A number of pathophysiologic states can interfere with mechanisms to maintain normothermia. These occur in debilitated or elderly patients secondary to hypothyroidism, adrenal insufficiency, sepsis, or stroke.¹² Trauma profoundly disrupts temperature homeostasis and is the most common cause of secondary hypothermia.

Hypothermia in Trauma

Hypothermia increases the mortality across all trauma age groups. Jurkovich et al.¹³ reported a 40% mortality in trauma patients with a core temperature <34°C, which increased to 100% in those patients with a core temperature <32°C. A larger retrospective study from the National Trauma Databank using stepwise logistic analysis found that hypothermia independently predicted mortality after trauma (odds ratio 1.54, 95% CI 1.40–1.71).¹⁴ Wang et al. reported similar data from analysis of 38,520 patients in Pennsylvania Trauma Outcome Study (odds ratio 3.03, 95% CI 2.62–3.51).¹⁵ Inaba et al. reviewed the mortality of trauma patients undergoing cavitary surgery. Postoperative hypothermia was an independent predictor of mortality (odds ratio 3.2 CI 1.9-5.3).¹⁶ Mortality was increased 7-fold for patients with a temperature <33°C versus >35°C. Gentilello et al. showed that hypothermic trauma patients who were aggressively rewarmed had a markedly improved survival compared to those treated with less aggressive methods (Figure 49-2).¹⁷

FIGURE 49-2 Adjusted cumulative survival (Kaplan–Meier) trauma of patients randomized to rapid or slow rewarming, demonstrating an increase in mortality during resuscitation with slow rewarming. (Reproduced with permission from Gentilello LM, Jurkovich GJ, Stark MS, et al. Is hypothermia in the victim of major trauma protective or harmful? A randomized, prospective study. Ann Surg. 1997;226:439.)

Hypothermia and Metabolic Reserves

It is unclear if hypothermia causes increased mortality or if a falling core temperature is a preterminal event as the energy stores are exhausted. Blood adenosine triphosphate (ATP) levels are lower and remain depressed longer in hypothermic trauma patients compared to persons with hypothermia following elective surgery¹⁸ or patients with therapeutic hypothermia induced under anesthesia.¹⁹ This depletion may be hormonally mediated. Trauma and hypothermia induce profound stress by activating the adrenomedullary hormonal system, hypothalamic–pituitary–adrenocortical axis, and sympathetic nervous system.²⁰

Hypothermia and Immunity

Hypothermia impairs immune function by a direct effect on leukocyte-mediated microbial killing. Intraoperative hypothermia is associated with an increase in superficial wound infections following elective surgery.²¹

Hypothermia and Cardiac Function

Hypothermia causes bradycardia, and cardiac output decreases about 7% for each 1°C drop in temperature. The cold myocardium is irritable and ventricular fibrillation is common if chest compressions are used in the presence of bradycardia. Defibrillation is difficult until the heart is rewarmed.²²

Hypothermia and Coagulation

Cold exerts its most profound adverse effect on the coagulation system, with a marked increase in clinical bleeding even before a change in coagulation test values, which are routinely performed on blood samples warmed to 37°C.²³ A host of mechanisms have been implicated including depressed platelet function,²⁴ impaired platelet delivery,²⁵ slowed coagulation enzyme activation,²⁶ activation of protein C,²⁷ and activation of fibrinolysis.²⁸ All of these can contribute to traumatic bleeding, depending upon the temperature and degree of acidosis. The “trauma triad of death” has been defined as hypothermia, acidosis, and massive bleeding following trauma.²⁹ The resulting exsanguination depletes calcium, platelets, and clotting factors and requires early replacement with whole blood. Trauma control laparotomy is optimal in these patients.³⁰

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