Classifications

Accidental hypothermia is best defined as the unintentional decrease of around 2° C (3.6° F) in the “normal” core temperature of 37.2° to 37.7° C (99.0° to 99.9° F) without disease in the preoptic and anterior hypothalamic nuclei (Table 5-1). Classically, hypothermia is defined as a core temperature below 35° C (95° F). Hypothermia is both a symptom and a clinical disease entity. When sufficient heat cannot be generated to maintain homeostasis and core temperature drops below 30° C (86° F), the patient becomes poikilothermic and cools to the ambient temperature.^204,306

TABLE 5-1 Fahrenheit-to-Celsius Conversion Scale

* C = (F − 32) × 5/9

† F = 9/5 C + 32

Among clinical classifications, the most practical division includes healthy patients with simple environmental exposure (primary), those with specific diseases that produce hypothermia (secondary), and those with predisposing conditions. Other divisions that reflect the etiology of hypothermia include immersion versus nonimmersion, and acute versus chronic heat loss.^225,249

Various physiologic stressors and other factors can impair thermoregulation.³⁰⁷ Age extremes, state of health and nutrition, type of exposure, and a multitude of intoxicants or medications can jeopardize thermostability by decreasing heat production or increasing heat loss. Physiologic stressors also include dehydration, sleep deprivation, and fatigue. These challenges increase heat loss via evaporation, radiation, conduction, and convection, and compensatory responses often fail.²²⁵ The resulting mortality rates range to well over 50% in many clinical series, depending largely on the severity of risk factors and on patient selection criteria.^{59,244,289,363}

For safety, experimental investigations of induced hypothermia in human volunteers usually terminate cooling at about 35° C (95° F). Naturally, this precludes analysis of some of the more significant pathophysiologic features of moderate or severe hypothermia. Design limitations also occur in studies of anesthetized animals, because the results of these experiments require varying degrees of extrapolation to humans. For example, large differences exist both in the cardiovascular responses to interventions and in the amounts of peripheral musculature that are present, particularly in nonporcine animal models. As a result, clinical treatment recommendations must be predicated on the degree and duration of hypothermia and on the predisposing factors that are subsequently identified.¹²⁵

Nervous System

Numbing cold depresses the central nervous system, producing impaired memory and judgment, slurred speech, and decreased consciousness. During cold-weather expeditions, leaders are prone to risk-taking behavior and its attendant trauma. Temperature-dependent enzyme systems in the brain do not function properly at cold temperatures that are well tolerated by the kidneys. As a result, most patients are comatose below 30° C (86° F), although some remain amazingly alert.¹⁴⁷

Neurons are initially stimulated by a 1° C (1.8° F) drop in temperature, but the brain does not always cool uniformly during accidental hypothermia. After the initial increase, there is a linear decrease in cerebral metabolism by 6% to 10% per degree Celsius from 35° C (95° F) to 25° C (77° F). Hypothermia can afford cerebral protection because of the diminished cerebral metabolic requirements for oxygen.¹⁰⁸

The electroencephalogram is abnormal below 33.5° C (92.3° F) and becomes silent at 19° to 20° C (66.2° to 68° F). The triphasic waves commonly noted in hypothermia are also observed in various metabolic, toxic, and diffuse encephalopathies. Visual evoked potentials, another objective measure of cerebral function, become smaller as the mercury drops. After cerebral cortical function becomes impaired, lower brainstem functions are also deranged.

Cerebrovascular autoregulation is protectively intact until the temperature drops below 25° C (77° F). Although vascular resistance is increased, blood flow is disproportionately redistributed to the brain. In canine studies, blood flow in the brain, muscle, kidneys, and myocardium recovers quickly to control levels after rewarming. Flow deficits persist in the pulmonary, digestive, and endocrine systems for up to 2 hours after rewarming.

Chilling the peripheral nervous system increases muscle tension and preshivering tone, eventually leading to shivering. Shivering, which is also centrally controlled, is a much more efficient heat producer than are voluntary muscle contractions of the extremities.

Cardiovascular System

Many cardiovascular responses caused by or associated with hypothermia are well described.^206,207 Cold stress increases consumption of myocardial oxygen. Autonomic nervous system stimulation causes tachycardia and peripheral vasoconstriction, both of which increase systemic blood pressure and cardiac afterload.

As core temperature drops, there is a fairly linear decrease in pulse rate. After premonitory tachycardia, decremental bradycardia produces a 50% decrease in heart rate at 28° C (82.4° F). Because this bradycardia is caused by decreased spontaneous depolarization of pacemaker cells, it is refractory to atropinization. If there is a “relative” tachycardia not consistent with the degree of hypothermia, the clinician should be concerned. Associated conditions include occult trauma with hypovolemia, drug ingestion, and hypoglycemia.

During hypothermic bradycardia, unlike normothermia, systole is prolonged longer than diastole. In addition, the conduction system is much more sensitive to cold than is the myocardium, so the cardiac cycle is lengthened. Cold-induced changes in pH, oxygen, electrolytes, and nutrients also alter electrical conduction.²²⁴

Hypothermia progressively decreases mean arterial pressure and cardiac index. Cardiac output drops to about 45% of normal at 25° C (77° F). Systemic arterial resistance, determined by invasive hemodynamic monitoring, is increased. Even after rewarming, cardiovascular function may remain temporarily depressed, with impaired myocardial contractility, metabolism, and peripheral vascular function.³⁴¹

Mild, steady hypothermia in patients with poikilothermic thermoregulatory disorders causes electrocardiographic (ECG) alterations and conduction abnormalities.⁶⁸ First the PR, then the QRS, and most characteristically the QTc intervals are prolonged. Clinically invisible increased preshivering muscle tone can obscure the P waves; ST-segment and T-wave abnormalities are inconsistent.^9,347 Of note, ordinary surface ECG electrodes, when attached to dry skin, will accurately reflect cardiac electrical activity. Needle electrodes are not necessary to detect weak ECG signals.¹⁸⁷

The J wave (Osborn wave or hypothermic hump; (Figure 5-2), first described by Tomaszewski in 1938, occurs at the junction of the QRS complex and the ST segment. It is not prognostic but is potentially diagnostic.^112,197 J waves occur at any temperature below 32.2° C (90° F) and are most frequently seen in leads II and V₆. When core temperature falls below 25° C (77° F), J waves are found in the precordial leads (especially V₃ or V₄). The size of the J waves also increases with temperature depression, but is unrelated to arterial pH.³⁷³ J waves are usually upright in aVL, aVF, and the left precordial leads.^3,175,262

FIGURE 5-2 The J or Osborn wave of hypothermia. Note that the obvious J waves were not properly interpreted by the computer.

J waves may represent hypothermia-induced ion fluxes, resulting in delayed depolarization or early repolarization of the left ventricle, or there may be an unidentified hypothalamic or neurogenic factor. J waves are not pathognomonic of hypothermia but occur also with central nervous system lesions, focal cardiac ischemia, and sepsis. They may also be present in young, healthy persons. When pronounced, J waveform abnormalities can simulate myocardial infarction. Computer software is not widely available that can successfully recognize and suggest the diagnosis of hypothermia.^202,235,255

The prehospital capability to differentiate between J waves and injury current is important in rural and wilderness settings.⁵⁷ Thrombolysis is unstudied in hypothermia but would be expected to exacerbate coagulopathies.¹¹⁰

Below 32.2° C (90° F), all types of atrial and ventricular arrhythmias are encountered.⁷⁵ The His-Purkinje system is more sensitive to cold than is the myocardium. As a result, conduction velocity decreases and electrical signals can disperse. Because conduction time is prolonged more than the absolute refractory period, reentry currents can produce circus rhythms that initiate ventricular fibrillation (VF).

In addition to causing bradycardia, widening the QRS complex, and prolonging the QT interval, hypothermia increases the duration of action potentials (Figure 5-3, online).^21,22 During rewarming, nonuniform myocardial temperatures can disperse conduction and further increase the action potential duration, another mechanism to develop the unidirectional blocks that facilitate reentrant arrhythmias. At temperatures between 25° and 20° C (77° and 68° F), myocardial conduction time is prolonged further than the absolute refractory period. Another arrhythmogenic mechanism is development of independent electrical foci that precipitate arrhythmias.

FIGURE 5-3 Example of the effects of temperature on action potentials in cardiac cells.

Various electrolyte abnormalities can further complicate the situation during hypothermic conditions, because they exacerbate the effects of prolonged action potentials. Most conspicuously, hypothermia-induced cellular calcium loading mimics digitalis toxicity and may predispose to a forme fruste of torsades de pointes.

Hypothermia-induced VF and asystole often occur spontaneously below 25° C (77° F). The VF threshold and transmembrane resting potential are decreased. Because the heart is cold, the conduction delay is facilitated by the large dispersion of repolarization, and the action potential is prolonged. The increased temporal dispersion of the recovery of excitability is linked to VF. Nature’s model of resistance to VF is the heart of hibernating animals during rewarming.¹⁶³ Animals with this capacity seem to be protected by a shortened QT duration and a calcium channel handling system that prevents intracellular calcium overload.

Asystole and VF may both result from hypovolemia, tissue hypoxia, therapeutic manipulations, acid–base fluxes, autonomic dysfunction, and coronary vasoconstriction coupled with increased blood viscosity. Other causes may include rough handling or jostling, sudden vertical positioning, and acute metabolic stress from exertion or very rapid rewarming.

Core Temperature Afterdrop

Core temperature afterdrop refers to the continued decline in a hypothermic patient’s temperature after removal from the cold (see also Chapter 6). Contributing to afterdrop is the simple temperature equilibration between the warmer core and cooler periphery. Circulatory changes account for another set of observations. The countercurrent cooling of blood that perfuses cold extremities results in core temperature decline until the existing temperature gradient is eliminated. In cold-water immersion, post-rescue collapse may also result from abrupt hypotension after loss of hydrostatic squeeze contributed by the water.

The incidence and magnitude of core temperature afterdrop vary widely in clinical experiments and in surgically induced hypothermia.^103,104,125 Hayward¹²⁸ measured his own esophageal, rectal, tympanic, and cardiac temperatures (via flotation tip catheter) during rewarming after being cooled in 10° C (50° F) water. On three different days, rewarming was achieved via shivering thermogenesis, heated humidified inhalation, and warm bath immersion. Coincident with a 0.3° C (0.5° F) afterdrop during warm bath immersion, his mean arterial pressure fell 30% and his peripheral vascular resistance fell 50%. Therefore the circulatory mechanism is another major contributor to afterdrop.

A human study of peripheral blood flow during rewarming from mild hypothermia suggests that minimal skin blood flow changes can also lead to afterdrop (Figure 5-4). The largest core temperature afterdrops occur when subjects are rewarmed with plumbed garments and heating pads.

FIGURE 5-4 Infrared scan of the palmar hand surface. Blue, 43° C (109.4° F); red, 68° C (154.4° F). A, At room temperature. B, After 5 minutes in a cold room, with evidence of vasoconstriction.

(Courtesy Naval Health Research Center, San Diego, Calif.)

In summary, core temperature afterdrop appears to become most clinically relevant when a large temperature gradient exists between the periphery and the core, particularly in dehydrated, chronically cold patients. Both conductive and convective mechanisms are responsible for afterdrop.¹⁰⁴ Stimulating peripheral blood flow can increase afterdrop. Major afterdrops are also observed when frostbitten extremities are thawed before crystalloid volume resuscitation and thermal stabilization of the core temperature.

Respiratory System

Any exposure to a big chill initially stimulates respiratory drive, which is followed by progressive depression of respiratory minute volume as cellular metabolism is depressed. The respiratory rate often falls to 5 to 10 breaths/min below 30° C (86° F), and ultimately brainstem neurocontrol of ventilation fails. An important physiologic observation is that carbon dioxide production drops 50% for each 8° C (14° F) fall in temperature. In severe hypothermia, carbon dioxide retention and respiratory acidosis reflect the aberrant responses to normothermic respiratory stimuli.⁹⁹

Other pathophysiologic factors contributing to ventilation–perfusion mismatch include decreased ciliary motility, increased quantity and viscosity of secretions, hypothermic acute respiratory distress syndrome, and noncardiogenic pulmonary edema.³³² The thorax loses elasticity, and pulmonary compliance drops. The respiratory “bellows” stiffen and fail because contractile efficiency of the intercostal muscles and diaphragm declines.

Pertinent potentially protective or detrimental factors that affect tissue oxygenation in endothermic humans are listed in Box 5-1.

Renal System

The kidneys respond briskly to hypothermia-induced changes in the vascular tree’s capacitance. Peripheral vasoconstriction can result initially in a relative central hypervolemia, producing diuresis, even with mild dehydration. In addition, renal blood flow is depressed by 50% at 27° to 30° C (80.6° to 86° F), which decreases glomerular filtration rate. Nevertheless, there is an initial large diuresis of this dilute glomerular filtrate, which does not efficiently clear nitrogenous wastes.

The etiology of the cold diuresis is multifactorial.^114,115 Some of the suggested mechanisms include inhibition of antidiuretic hormone (ADH) release and decreased renal tubular function. Neither hydration nor ADH infusions seem to influence the diuretic response, which appears to be an attempt to compensate for initial relative central hypervolemia caused by vasoconstrictive overload of capacitance vessels.

The diuresis may also be pressure related, caused by impaired autoregulation in the kidneys. Cold diuresis has circadian rhythmicity and correlates with periods of shivering. Cold water immersion increases urinary output 3.5 times, and the presence of ethanol impressively doubles that diuresis.

Coagulation

Coagulopathies often develop in hypothermic patients because the enzymatic nature of the activated clotting factors is depressed by cold.⁸⁸ In vivo, prolonged clotting is proportional to the number of steps in the cascade. For example, at 29° C (84.2° F), a 50% to 60% increase in the partial thromboplastin time (PTT) would be expected. Kinetic tests of coagulation, however, are performed in the laboratory at 37° C (98.6° F). As the blood warms in the machine, the enzymes between the factors in the cascade are activated. The sample of warmed in vitro blood then clots normally.⁷⁷

The reversible hemostatic defect created by hypothermia may not be reflected by the “normal” prothrombin time (PT), PTT,²⁹² or international normalized ratio (INR). This coagulopathy is basically independent of clotting factor levels and cannot be confirmed by laboratory studies performed at 37° C (98.6° F). Treatment is rewarming and not simply administration of clotting factors.²⁸⁸ When rapid rewarming is difficult, concentrations of 0.01 to 1 nM of desmopressin may partially reverse hypothermia-induced coagulopathy in vitro.³⁷⁶

Thrombocytopenia as a cause of bleeding becomes progressively significant in severe hypothermia. Proposed mechanisms include direct bone marrow suppression and splenic or hepatic sequestration. Thromboxane B₂ production by platelets is also temperature dependent, so cooling skin temperature produces reversible platelet dysfunction. Thrombocytopenia is a common but poorly recognized corollary of hypothermia in older adults and neonates.

Coagulopathy in trauma patients is attributed to enzyme inhibition, platelet alteration, and fibrinolysis.³²⁰ The critical temperature at which enzyme activity slows significantly is 34° C (93.2° F).³⁵⁸ In addition, clot strength weakens as a result of platelet malfunction. Fibrinolysis is not significantly affected at any temperature in the range measured (33° to 37° C [91.4° to 98.6° F]) (see Trauma, later).

Physiologic hypercoagulability also develops during hypothermia, with a sequence similar to that seen in disseminated intravascular coagulation (DIC). This produces a higher incidence of thromboembolism during hypothermia. Causes include thromboplastin release from cold tissue, simple circulatory collapse, and release of catecholamines and steroids. Because fibrin split-product levels can be normal, bleeding is not always considered a hematologic manifestation of DIC.²⁸²

Whole blood viscosity increases with the hemoconcentration seen after diuresis and the shift of fluid out of vascular compartments. Red blood cells (RBCs) simply stiffen and have diminished cellular deformity when chilled.²⁷⁶ The elevated viscosity of hypothermia is also exacerbated by cryoglobulinemia. Cryofibrinogen is a cold-precipitated fibrinogen occasionally seen with carcinoma, sepsis, and collagen vascular diseases. Blood viscosity is also increased by the transient increases in platelet and RBC counts seen with mild surface cooling. This could explain the increased mortality from coronary and cerebral thromboses that occur in winter.²²⁵

Decreased Heat Production

Thermogenesis is decreased at both extremes of age. In older adults, neuromuscular inefficiency and decreased physical activity impair shivering. Aging progressively diminishes homeostatic and cold adaptive capabilities. Although most older adults have normal thermoregulation, they tend to develop conditions that impair heat conservation.^283,286

Older adults are physiologically less adept at increasing heat production and the respiratory quotient (the ratio of the volume of carbon dioxide produced to the volume of oxygen consumed per unit of time). Impaired thermal perception, possibly caused by decreased resting peripheral blood flow, leads to poor adaptive behavior. Metabolic studies also demonstrate that in severely hypothermic older adults, lipolysis occurs in preference to glucose consumption.^256,271

Neonates have a large surface area–to–mass ratio, relatively deficient subcutaneous tissue layer, and virtually no behavioral defense mechanisms. Newborn “unadapted” infants attempt to thermoregulate with initial vasoconstriction and acceleration of metabolic rate. In contrast, “adapted” infants who are older than 5 days can increase lipolysis immediately and burn oxidative brown adipose tissue.

No cause-and-effect relationship has been found between hypothermia and the mortality rate of premature infants.^129,301 Although the smaller infants in a neonatal intensive care unit are at the greatest risk for hypothermia, mortality is related to hypothermia only in larger neonates.

Emergency deliveries and resuscitations are responsible for most acute neonatal hypothermia. Other common risk factors are prematurity, low birth weight, inexperienced mother, perinatal morbidity, and low socioeconomic status. In babies with more chronically induced subacute hypothermia, lethargy, a weak cry, and failure to thrive are common.³³⁵

Many cold infants have “paradoxical rosy cheeks,” looking surprisingly healthy. After the first few days of life, hypothermia frequently indicates septicemia and carries a high mortality rate. Low weight and malnutrition are common. Hypothermia in a low-birth-weight neonate should suggest the possibility of intracranial hemorrhage; hypothermia is also observed in shaken baby syndrome.

Endocrinologic failure, including hypopituitarism, hypoadrenalism, and myxedema, commonly decreases heat production. Interestingly, congenital adrenal hyperplasia with mineralocorticoid insufficiency is more common in cold climates, possibly an adaptive response to prolonged exposure to cold temperatures, because “normal” cold diuresis is reduced in these patients.

Hypothyroidism is often occult, with no history of cold intolerance, dry skin, lassitude, or arthralgias. The physician should check for a thyroid scar or any history of thyroid hormone replacement. The degree of temperature depression correlates fairly directly with mortality. Eighty percent of patients in myxedema coma, which is several times more common in female patients, are hypothermic.

The effects of insufficient nutrition extend from hypoglycemia to marasmus to kwashiorkor. Kwashiorkor is less often associated with hypothermia than is marasmus, because of the insulating effect of hypoproteinemic edema. Central neuroglycopenia distorts hypothalamic function. Many alcoholic patients with hypothermia are hypoglycemic. Malnutrition decreases insulative subcutaneous fat and directly alters thermoregulation. Poor nutrition predisposes to hypothermia and its attendant clumsiness in older adult women with femoral neck fractures. Partly because of fuel depletion, hypothermia is as great a threat as hyperthermia in marathon races run in cool climates. Runners slowing from fatigue or injury late in a race are at serious risk of hypothermia.¹⁷⁰

Increased Heat Loss

Poorly acclimated and insulated individuals often have high diaphoretic, convective, and evaporative heat losses during exposure to cold. Because the skin functions as a radiator, any dermatologic malfunction increases heat loss. Such erythrodermas include psoriasis, exfoliative dermatitis, and toxic epidermal necrolysis. Hypothermia with hypernatremic dehydration is also seen in congenital lamellar ichthyosis.

Burns and inappropriate burn treatment cause excessive heat loss, as do other iatrogenic factors, including massive cold intravenous (IV) infusions and overcooling heatstroke victims.¹⁸⁸ When carbon dioxide is used for abdominal insufflation before laparoscopy, warming the gas before administration helps prevent hypothermia. Environmental immersion exposure is discussed in detail in Chapter 6.¹⁰²

Many pharmacologic and toxicologic agents both increase heat loss and impair thermoregulation.^165–167343 The most common is ethanol, which interacts with every putative thermoregulatory neurotransmitter. Although ingestion of ethanol produces a feeling of warmth and perhaps visible flushing, it is the major cause of urban hypothermia.^59,244 In fatal cases of accidental hypothermia, many victims are under the influence of ethanol. In children with ethanol intoxication, hypothermia is common.

Ethanol is also a poikilothermia-producing agent that directly impairs thermoregulation at high or low temperatures.¹⁶⁵ Body temperature is lowered both from cutaneous vasodilation with radiative heat loss and from impaired shivering thermogenesis. Chronic ethanol ingestion damages the mamillary bodies and posterior hypothalamus, which modulates shivering thermogenesis.²⁷⁷ Ethanol also increases the risk for being exposed to the environment, by modifying protective adaptive behavior. The ultimate example is paradoxical undressing, or removal of clothing in response to a cold stress. As an organic solvent, ethanol confers a few theoretically redeeming qualities in freezing cold injuries by lowering the cellular freezing point.^114,115

The neurophysiologic effects of ethanol are modified by duration and intensity of exercise, food consumption, and applied cold stress.⁹⁴ Aging increases sensitivity to the hypothermic actions of ethanol in some primate experiments. Chronic ingestion yields tolerance to its hypothermic effects, and rebound hyperthermia may be seen during withdrawal. Conditions associated with ethanol ingestion that adversely affect heat balance include immobility and hypoglycemia.³⁶⁸

Inhibited hepatic gluconeogenesis coexists with malnutrition. Hypothermic alcoholic ketoacidosis is reported.³⁶³ Intravenous thiamine is diagnostic and therapeutic for Wernicke’s encephalopathy, another cause of reversible hypothermia. The acute triad of global confusion, ophthalmoplegia, and truncal ataxia is often masked by hypothermia, and temperature depression may persist for weeks.

Impaired Thermoregulation

Various conditions that impair thermoregulation can be considered as having central, peripheral, metabolic, and pharmacologic or toxicologic effects.

Recurrent Hypothermia

Recurrent and episodic hypothermias are widely reported. The recurrent variety is more common and is usually secondary to ethanol abuse, with one person having survived 12 episodes.⁵⁶ Severe, recurrent presentations are also caused by self-poisoning and anorexia nervosa.

Persons with episodic hypothermia can be divided into two groups, albeit with significant overlap, as follows:

Group 1: Diaphoretic episodes precede the temperature decline, which lasts several hours. This group includes those with hypothalamic lesions and agenesis of the corpus callosum (Shapiro syndrome) and persons with spontaneous periodic hyperthermia. Resultant hyperhidrosis and hypothermia are successfully treated with clonidine, a centrally acting α-adrenergic agonist. The hypothermia of corpus callosum agenesis is also seen with hypercalcemia and status epilepticus. Because no hypothermia results from experimental sectioning of the corpus callosum, associated lesions, including lipomas, probably cause thermoinstability. Spontaneous periodic hypothermia may reflect a diencephalic autonomic seizure disorder and can accompany paroxysmal hypertension. Vasomotor and thermoregulatory mechanisms are successfully treated with anticonvulsants. Florid psychiatric symptoms often mask these intermittent hypothermic episodes.

Group 2: The second group consists of persons who remain cold for days to weeks, rather than hours. These people have more seizure disorders, and the central hypothalamic thermostat is set abnormally low.

Patients with intermittent hypothermia usually show some characteristics of both groups.²²⁵ Circadian rhythm disturbances are also seen in persons with neurologic disorders who have chronic hypothermia.

Predisposing Infections or Conditions

Among the infestations and infections that may elevate or depress core temperature are septicemia, pneumonia, peritonitis, meningitis, encephalitis, bacterial endocarditis, typhoid, miliary tuberculosis, syphilis, brucellosis, and trypanosomiasis.²¹⁴ Other diseases, in addition to cerebrovascular and cardiopulmonary disorders, that produce secondary hypothermia include systemic lupus erythematosus, carcinomatosis, pancreatitis, and multiple sclerosis. Hypothalamic demyelination may explain episodic hypothermia observed in some patients with multiple sclerosis.

Hypothermia can also result from low cardiac output after a major myocardial infarction, which can be reversed by intra-aortic balloon counterpulsation. Finally, causes include vascular insufficiency, giant cell arteritis, uremia, sickle cell anemia, Paget disease, sarcoidosis, and sudden infant death syndrome. Magnesium sulfate infusion during preterm labor can produce hypothermia with fetal and maternal bradycardia, and hypothyroidism can be manifested as hypothermia after preeclampsia (see Box 5-2).

Trauma

Hypothermia protects the brain from ischemia but can result in arrhythmias, acidosis, and coagulopathies, and it can extract a high metabolic cost during rewarming.⁹⁷ Hypothermia hinders protective physiologic responses to acute trauma and affects pharmacologic and therapeutic maneuvers necessary to treat injuries.^18,27

An inverse relationship usually exists between the Injury Severity Score (ISS) and core temperature of traumatized patients on arrival in the emergency department (ED). This observation does not settle whether hypothermia is just another risk factor for increased mortality or reflects the fact that the most severely injured patients are in hemorrhagic shock.¹³²

One study assessed the impact of hypothermia as an independent variable during resuscitation from major trauma.⁹⁷ Patients not aggressively rewarmed with continuous arteriovenous rewarming (CAVR) had increased fluid requirements, increased lactate levels, and increased acute mortality.

Of the clinical entities associated with hypothermia, traumatic conditions causing hypotension and hypovolemia most dramatically jeopardize thermostability. Hypothermia is often obscured by obvious hemorrhaging and injuries. Liberalized indications for Focused Assessment With Sonography for Trauma (FAST) ultrasound examinations can minimize unnecessary computed tomography (CT) imaging. On the other hand, traumatic neurologic deficits, including paresis and areflexia, can be misattributed to hypothermia. In trauma patients requiring surgery, the mean temperature loss was greater in the ED than in the operating room.¹¹⁷ Thermal insults are often added during a trauma resuscitation. The patient is completely exposed for examination, and resuscitative procedures cause further heat loss.³⁰⁸

In a study stratifying subjects with the anatomic ISS, hypothermic patients had a higher mortality rate than did similarly injured patients who remained normothermic.¹⁷¹ Another study did not corroborate this finding,³²² but those investigators stratified using trauma revised injury severity score (TRISS) methodology, which is probably less valid during hypothermia because its physiologic components overestimate injury severity. To illustrate this point, some component of hypotension is normal for a given degree of hypothermia.

Various adverse physiologic events accompany hypothermia with trauma. Decreased skin and core temperatures without compensatory shivering thermogenesis are reported in patients with major trauma as defined by the ISS.

Hypothermia directly causes coagulopathies in trauma patients through at least three avenues (see Coagulation, earlier).³³ The cascade of enzymatic reactions is impaired, and plasma fibrinolytic activity is enhanced, producing a clinical presentation similar to that of DIC. Also, platelets are poorly functional and become sequestered.

Hypothermia is protective only when induced before shock occurs. This reduces adenosine triphosphate (ATP) utilization while ATP stores are still normal, as during elective surgery. ATP stores in traumatized patients are already depleted. Hypothermia worsens the effects of endotoxins on clotting time in vitro and may synergistically exacerbate the coagulopathy seen in trauma.⁸⁸ The average temperature of 123 initially normothermic trauma patients in whom lethal coagulopathies developed was 31.2° C (88.2° F). In another study, postinjury life-threatening coagulopathy in the seriously injured who require massive transfusion was predicted by persistent hypothermia and progressive metabolic acidosis.^50,89

The appropriate target core temperature for a hypothermic patient with an isolated severe head injury may be 32° to 33° C (89.6° to 91.4° F). This target temperature balances neuroprotection against the adverse hematologic and physiologic consequences of hypothermia^19,231,232 (see Cerebral Resuscitation, later.)