Hypothermia

Morgan Eutermoser and Jay Lemery

BACKGROUND

In 2005, the Centers for Disease Control and Prevention (CDC) Morbidity and Mortality Weekly Report disclosed that 689 deaths per year in the United States were attributable to accidental hypothermia, defined as an involuntary or unintentional drop in core body temperature to <35°C (95°F).¹^,² Heat loss from environmental exposure occurs through four well-known mechanisms: radiation, conduction (which can significantly increase in water and/or wet clothes), convection, and evaporation.³ Conversely, heat generation occurs through skeletal muscle use as well as through involuntary hypothalamic-mediated shivering.⁴ The latter is a neuroendocrine response to mild hypothermia mediated through serotonin, dopamine, norepinephrine, thyroid-stimulating hormone, and thyrotropin-releasing hormone, all of which affect the autonomic nervous system.³

Primary hypothermia occurs when an individual’s intrinsic compensatory capacity is overwhelmed by cold stress and thus unable to maintain temperature homeostasis. Patients with chronic disease or physiologic vulnerability—such as advanced age, alcohol or drug abuse, and mental impairment—have diminished compensatory capacity and are at greater risk for primary hypothermia.³^,⁵

Secondary hypothermia occurs when a person with a systemic illness (e.g., myxedema coma or sepsis) becomes hypothermic due to a pathologic lack of autoregulation. Clinicians should be aware that this may occur even in a warm environment and is a sign of severe physiologic decompensation. This chapter describes the clinically relevant parameters of hypothermia and outlines an appropriate organ system–based approach to diagnosis and management.

DEFINITIONS

Hypothermia is a sign of severe illness and/or significant environmental exposure. Prompt identification is critical for optimal clinical management. Degree of hypothermia is generally stratified to four categories: mild (35°C to 32°C), moderate (32°C to 28°C), severe (28°C to 20°C), and profound (<20°C).⁶ In the absence of an ability to quantify temperature, the Swiss staging system (Table 53.1) may be used to categorize hypothermia severity based on clinical presentation.⁷

TABLE 53.1 Swiss Staging System

Adapted from Brown Douglas JA, Brugger H, Boyd J, et al. Accidental hypothermia. N Engl J Med. 2012;367:1930–1938.

PATHOPHYSIOLOGY AND CLINICAL PRESENTATION

Cardiovascular

The initial response to cold stress and mild hypothermia (>33°C) is a norepinephrine (NE)-mediated increase in mean arterial pressure (MAP) and heart rate (HR).⁶ These physiologic signs reverse, with a decrease in MAP and HR, when the core temperature falls below 33°C.⁶ Sinus bradycardia is an expected finding in hypothermic patients, due to a combination of decreased sympathetic tone and a slowing of spontaneous depolarization of cardiac pacemaker cells.³ This bradycardia is not vagally mediated, and thus atropine will have limited efficacy in resuscitation. The hypothermic state significantly lowers metabolism, and therefore marked bradycardia is not as detrimental to the body’s needs as in a euthermic patient. The hypothermic effect on the myocardium is known to produce an “irritable” state, in which the use of pacing wires and antiarrhythmic drugs during resuscitation has been shown to trigger significant dysrhythmias. These interventions are not supported by available evidence and are not recommended in the current American Heart Association (AHA) guidelines.

The classic ECG finding of hypothermia (<33°C) (Fig. 53.1)—the “J-wave” or “Osborn wave”—is a marked with a dome configuration at the R-ST junction.⁸ First characterized in 1953, this EEG morphology was associated by Osborn with the risk of impending ventricular arrhythmias; however, this has since been refuted.⁹ J-waves can also be seen in myocardial ischemia, sepsis, and CNS lesions and can be a normal ECG variant in young people.³ The formation of the J-wave in hypothermia is thought to be due to delayed depolarization or early repolarization of the left ventricular wall.

Figure 53.1 ECG from a hypothermic patient demonstrating Osborn waves and bradycardia. Reprinted with permission from Dr. Steve Lowenstein, University of Colorado Hospital.

Atrial fibrillation is quite common at core temperatures below 32°C and will commonly convert spontaneously with rewarming.³ At 28°C, severe bradycardia (30 to 40 bpm) can be expected.¹⁰ As moderate to severe hypothermia set in, decreased conduction velocity, increased myocardial conduction time, and decreased refractory time can result in the sinus bradycardia degenerating into atrial and ventricular dysrhythmias.³ Below 25°C, asystole and ventricular fibrillation occur spontaneously and may be hastened by the jostling of patients by caregivers; therefore, care must be taken when handling these patients.³

As previously noted, MAP drops in severe hypothermia, producing an associated significant decrease in global sympathetic tone. Peripheral vasodilation occurs at this time and can result in a warming sensation. When combined with an altered mental status (see neurologic effects below), this warming sensation can lead to “paradoxical undressing,” whereby patients may remove clothing in an effort to cool down, compounding environmental hypothermia.¹¹ During hypothermic resuscitation, IV arterial vasopressor therapies such as vasopressin or phenylephrine may be used to improve peripheral vasomotor tone during rewarming. Careful attention to and correction of any intravascular volume deficit are also important for appropriate resuscitation.

Pulmonary

The initial response to hypothermia is tachypnea driven by the increased metabolic demand from shivering. However, once basal metabolism begins to slow (50% decrease in CO₂ production with an 8°C drop in core temperature), there is a commensurate decrease in minute ventilation. This physiologic change highlights the need to be aware of possible overventilation and subsequent iatrogenic hypocapnia during a hypothermic resuscitation. Direct cold exposure affects pulmonary mechanics through airway congestion, bronchoconstriction, increased secretions, and decreased mucociliary clearance. The primary ventilatory response to cold air is a decrease in baseline ventilation and respiratory chemosensitivity. These responses are thought to provide significant protection against heat loss in animals, although the effect on human physiology is minimal. Cold exposure also elicits an increase in pulmonary vascular resistance. This stimulus is synergistic with hypoxia and may mediate pulmonary hypertension and edema at altitude.¹²

Neurologic

For every 1°C decrease in core body temperature, cerebral metabolism is decreased by 6% to 7%, with EEG silencing typically found at 19°C to 20°C.³^,¹³ Loss of pupillary light reflex and deep tendon reflexes can be seen in moderate hypothermia.¹⁴ However, in one series of 97 patients with accidental hypothermia, level of consciousness, pupillary reflex, and deep tendon reflexes could not be correlated with temperature even in severe hypothermia.¹⁵ This illustrates an important clinical pearl —patients may appear dead, yet be profoundly hypothermic. Indeed, there have been many case reports of patients who have survived with extremely low core temperatures—as low as 14.2°C in a child and 13.7°C in an adult—thus supporting the maxim patients are not dead until they are warm and dead.¹⁶^,¹⁷

Renal

Renal pathology in hypothermia is most commonly due to prerenal failure from cold-induced diuresis and fluid shifts (primary hypothermia) and may be coupled with underlying systemic diseases affecting renal function (secondary).¹⁸ The initial systemic autonomic response to cold stress is that blood flow shifts to the core and away from the periphery.¹⁹ The resulting increased central blood volume and perfusion produce a reduction in CNS release of antidiuretic hormone resulting in renal free water diuresis, a process known as “cold diuresis.” This is important to understand during a hypothermic resuscitation, as the patient may have markedly reduced blood volume yet maintain a normal blood pressure due to significant concomitant vasoconstriction. Likewise, when rewarming begins, peripheral vasodilation may lead to core blood redistribution and cardiovascular collapse in the hypothermic dehydrated patient.

Hematologic

Hypothermia causes an increase in blood viscosity, hematocrit, and fibrinogen levels.¹³ The normal clotting cascade is also impeded, due to the temperature-mediated inhibition of the catalytic function of multiple clotting cascade components.²⁰ Severe hypothermia (often with concomitant frostbite) can lead to fulminant disseminated intravascular coagulation from the release of tissue thromboplastin (responsible for catalyzing the conversion of prothrombin to thrombin) from ischemic tissues.¹³^,²¹ Cold stress also suppresses bone marrow production, which may lead to thrombocytopenia and cause splenic and hepatic sequestration of platelets.³ Hypothermia can have significant impact on the care of trauma patients and is considered part of the “lethal triad of trauma” (metabolic acidosis, coagulopathy, and hypothermia).²²

For every 1°C decline in core temperature, there is a 2% increase in the hematocrit. Anemia in a severely hypothermic patient should therefore raise suspicion and prompt a broader workup.²¹ Caution also should be exercised in interpreting prothrombin time and activated partial thromboplastin times. They will not accurately reflect coagulation status because the values are measured at 37°C in the lab rather than the in vivo core body temperature of the patient.

Gastrointestinal

As temperature declines, gut motility begins to slow, often resulting in an ileus at temperatures below 28°C.¹³ Decreased hepatic blood flow will cause hepatic impairment, which can result in reduced drug metabolism as well as compromised clearing of lactate. Pancreatitis is also commonly seen in hypothermia but can be clinically silent, discovered only through elevation of enzymes. Because of this, glucose should be carefully monitored during rewarming.²³

MANAGEMENT GUIDELINES

Temperature Determination

Optimal clinical management of the hypothermic patient depends on accurate and consistent temperature monitoring. The esophageal probe is the recommended device in a critically hypothermic patient.²⁴ Temperature determination can be falsely elevated if the patient is intubated or ventilated with heated air, or if the probe is placed too proximally in the esophagus. To avoid this problem, it is recommended to place the probe in the lower third of the esophagus.²⁵ Rectal temperature measurement is commonly used but has a greater risk of inaccuracy than the esophageal devices. Specifically, rectal temperatures can lag behind true core body temperatures and thus risk accidental overshoot in core temperature during rewarming.²⁶ Proper placement of the probe is 15 cm into the rectum, avoiding cold feces. Tympanic membrane temperature assessment is cumbersome and not recommended for continuous monitoring, but can effectively and quickly identify core temperature. If used, the ear should be clear of cerumen and shielded from the outside environment.²⁷ Bladder temperature probes are also not recommended in the severely hypothermic patient and may be confounded if warm saline is instilled into the bladder.

Airway and Breathing

Accurately assessing oxygen saturation in a hypothermic patient can be difficult. The skin surface must be warm and well perfused in order to accurately measure transcutaneous oxygen saturation and is therefore poorly suited to this purpose in the hypothermic patient.²⁸ Airway management decisions remain the same as in any critically ill patient. Gentle handling of the patient during airway maneuvers is recommended because of a potentially irritable myocardium; however, a multicenter survey that reviewed 117 intubations of hypothermic patients reported no increased complications.³^,²⁹ Endotracheal intubation has an additional benefit of allowing for the inhalation of humidified, heated air. Hypothermic patients are vulnerable to electrolyte imbalances, and succinylcholine should be avoided given its side effect of transient hyperkalemia.³⁰ In any hypothermic patient with altered mental status, precipitating events, including trauma, infection, and toxic/metabolic disorders, should be carefully assessed.

Medical Therapy

Medications that have temperature-dependent activity may have compromised efficacy in a hypothermic patient. Cold-induced pharmacokinetic changes include increased protein binding and decreased liver metabolism.³¹ Advanced Cardiac Life Support (ACLS) drugs given to a hypothermic patient may remain in circulation and subsequently manifest toxic effects during rewarming. Most hypothermic clinical conditions, however, do not require pharmacologic intervention, as rewarming will resolve the majority of cold-induced pathologies (e.g., atrial fibrillation).

High-risk hypothermic patients merit full infectious workups and consideration of broad-spectrum antibiotics. In a retrospective review of 59 patients with accidental hypothermia, 41% also had serious infections with predominance of respiratory and soft tissue infections.³²

ACLS

ACLS is modified in several protocols. Table 53.2 shows three common transport protocols and recommendations with ACLS modifications. Each patient should be assessed on an individual basis.

TABLE 53.2 ACLS Recommendations in Accidental Hypothermia