Accidental Hypothermia

Chapter 140


Accidental Hypothermia




Perspective


The “reanimations” of profoundly cold victims in prolonged cardiac arrest and the emergence of therapeutic hypothermia after cardiac arrest help explain the contemporary allure of hypothermia. A 29-year-old Norwegian physician was successfully resuscitated from accidental hypothermia at 13.7° C after a 9-hour resuscitation.1 This included cardiopulmonary resuscitation initiated at the scene and 179 minutes of cardiopulmonary bypass.2


Medical uses of cold were not scientifically evaluated until the 18th century, although it has been used for medical purposes for millennia. The hemostatic, analgesic, and therapeutic effects of cold were well known. Accidental hypothermia was also common and its treatment controversial. Biblical references cite truncal rewarming of King David by a damsel, and various remedies, including rubbing of the extremities with hot oil, were mentioned by Hippocrates, Aristotle, and Galen.


Cold weather has had a major impact on military history.3,4 Hannibal lost nearly half of his army of 46,000 while traversing the Alps in 218 BCE. The winter of 1777 took its toll on Washington’s troops at Valley Forge. Napoleon’s chief surgeon, Baron Larrey, reported that only 350 of the 12,000 men in the 12th division survived the cold during their retreat from Russia in 1812. Those soldiers who were rapidly rewarmed closest to the campfire died. The French subsequently suffered heavy losses in the Crimean War (1845-1855). These lessons were relearned during both world wars. Many pilots and U-boat crews perished from the cold water in the North Atlantic. Approximately 10% of the U.S. casualties in Korea were cold related.


Innumerable cold-related tragedies affect both military personnel and civilians, in particular hunters, sailors, skiers, climbers, boaters, swimmers, and survivors of some natural disasters. Widespread participation in outdoor winter sports increases the number of patients who have hypothermia. Hypothermia is geographically and seasonally pervasive.5–7 Most cases occur in urban settings. “Primary” hypothermia fatalities are classified as accidental, homicidal, or suicidal. Death certificate data, however, under-report secondary hypothermia deaths, in which cold complicates many systemic diseases. The effect of cold on mortality from cardiovascular and neurologic disorders is greatly underestimated.8


Hypothermia is defined as a core temperature below 35° C. Many variables contribute to the development of accidental hypothermia. Exposure, age, health, nutrition, medication, and intoxicants can decrease heat production, increase heat loss, or interfere with thermostability.9 The healthy individual’s compensatory responses to heat loss through conduction, convection, radiation, and evaporation are often overwhelmed by exposure. Medications can also interfere with thermoregulation. Central nervous system (CNS) problems commonly decrease the efficiency of thermoregulation.10



Principles of Disease



Physiology of Temperature Regulation


Human basal heat production increases with food ingestion, muscle activity, fever, and acute cold exposure. Cold stress increases preshivering muscle tone, potentially doubling heat production. Maximal heat production lasts only a few hours because of fatigue and glycogen depletion.


Shivering thermogenesis increases the basal metabolic rate two to five times. Shivering, which markedly increases oxygen consumption, is modulated by the posterior hypothalamus and the spinal cord.


The preoptic anterior hypothalamus orchestrates nonshivering heat conservation and dissipation. Serotonergic and dopaminergic neurons are pivotal. They exert immediate control through the autonomic nervous system and delayed control through the endocrine system. Thermal suppression or activation of the sympathetic nervous system with cold-induced release of norepinephrine also occurs. Cold stimulates the hypothalamus to release thyrotropin-releasing hormone. This activates the anterior pituitary gland, which releases thyroid-stimulating hormone and results in the release of thyroxine from the thyroid gland.11


Heat loss occurs through five mechanisms: radiation, conduction, convection, respiration, and evaporation. Assuming an average basal metabolic rate in a normally clothed person at room temperature, 55 to 65% of this loss is through radiation. Heat loss by radiation is greatest when one is spread out nude and least when one is curled up and insulated. Radiative heat loss depends on the temperature gradient between the environment and the exposed body surface area. Conduction normally accounts for only approximately 2 to 3% of the heat loss, but this may increase up to five times in wet clothing. Convection in cold water can increase heat loss by a factor of 25.


Close correlation exists between subcutaneous fat thickness and cooling rates. Individuals with greater insulation lose heat more slowly. Conduction and convection normally account for about 15% of the body’s heat loss, but convective losses increase with shivering. Respiration and evaporation account for the remainder of the loss, with 2 to 9% lost in heating of inspired air and 20 to 27% lost to insensible evaporation from the skin and lungs.


Cutaneous and respiratory heat loss is markedly influenced by the ambient temperature, air motion, and relative humidity. Greater losses occur in a cool, dry, windy environment (windchill index). When the body is not perspiring, most heat loss is through radiation and convection. Convective losses become significant in immersion-induced hypothermia. Children cool faster than adults do because of the elevated ratios of surface area to mass. Chronic cold exposure may result in gradual evolutionary adaptations and thermal acclimation (Fig. 140-1).



When core temperature is between 37 and 32° C, vasoconstriction, shivering, and nonshivering basal and endocrinologic thermogenesis generate heat. From 30 to 24° C, a progressive depression of the basal metabolic rate occurs without shivering thermogenesis. At temperatures below 24° C, autonomic and endocrinologic mechanisms for heat conservation become inactive.



Pathophysiology


The physiologic characteristics of hypothermia are described in Table 140-1.




Cardiovascular


After initial tachycardia, progressive bradycardia develops. The pulse usually decreases by 50% at 28° C. If an observed tachycardia is inconsistent with a patient’s temperature, associated conditions such as hypoglycemia, drug ingestion, and hypovolemia should be considered.


The bradycardia of hypothermia results from decreased spontaneous depolarization of the pacemaker cells. As a result, the bradydysrhythmia is refractory to atropine. The electrocardiographic features of hypothermia are unique.12,13 Initially described by Tomaszewski in 1938, the Osborn (J) wave is seen at the junction of the QRS complex and ST segment (Fig. 140-2). J waves are potentially diagnostic but not prognostic. They may appear at any temperature below 32° C. The size of the J wave is not related to arterial pH but does increase with temperature depression.



image


Figure 140-2 Hypothermic J waves.


J waves are normally upright in the aVL, aVF, and left precordial leads.14 The J deflection may be a result of hypothermic ion flux alterations, with delayed depolarization or early repolarization of the left ventricular wall. It can also be seen during local cardiac ischemia and with sepsis or CNS lesions, hypercalcemia, and the Brugada syndrome.


Some J waveform abnormalities simulate a myocardial injury current. Hypothermic electrocardiographic changes are not easily recognized by computer programs. Reliance on computer interpretations can result in mistaken thrombolysis, which would be expected to exacerbate preexistent coagulopathies.15


All atrial and ventricular dysrhythmias are common in moderate or severe hypothermia. Reentrant dysrhythmias result from decreased conduction velocity with increased myocardial conduction time and a decreased absolute refractory period. Because the conduction system is more sensitive to the cold than the myocardium is, cardiac cycle prolongation occurs. Fluctuations of available oxygen, pH, electrolytes, and nutrients also alter conduction. As hypothermia worsens, the PR interval, then the QRS interval, and finally (and most characteristically) the QTc interval become prolonged. In the absence of obvious shivering, thermal muscle tone may obscure P waves or produce artifacts.


Atrial fibrillation is common when the core temperature is below 32° C. Other rhythms are sinus, atrial, or junctional. Atrial fibrillation usually converts spontaneously during rewarming, but mesenteric embolization is a hazard.


The development of ventricular fibrillation (VF) or asystole in hypothermia is multifactorial. Putative explanations include tissue hypoxia, physical jostling, electrophysiologic or acid-base disturbances, and autonomic dysfunction. Asystole and VF can occur spontaneously when the core temperature falls below 25° C.16,17 Hypothermia causes a decrease in transmembrane resting potential, which in turn decreases the threshold for ventricular dysrhythmias. VF can also result from an independent focus or a reentrant phenomenon. When the heart is cold, a large dispersion of repolarization exists, which facilitates the development of a conduction delay. The action potential is also prolonged.


The term core temperature afterdrop refers to a further decline in an individual’s core temperature after removal from the cold. The two processes that contribute to afterdrop are simple temperature equilibration across a gradient and circulatory changes. Countercurrent cooling of the blood, which is perfusing cold tissues, results in a temperature decline until the gradient is eliminated.18


Active external rewarming of the extremities obliterates peripheral vasoconstriction and reverses arteriovenous shunting. This was most vividly demonstrated by Hayward, who measured his own esophageal, rectal, tympanic, and cardiac temperatures (by use of a flotation tip catheter) after cooling in 10° C water on three different days.19 Warm bath immersion rewarming caused a 30% fall in mean arterial pressure coupled with a 50% decline in peripheral vascular resistance.


Core temperature afterdrop is a clinically relevant consideration in the treatment of patients with a large temperature gradient between the core and the periphery. This is common in patients who are dehydrated after chronic exposure. Major afterdrop can also occur in severely hypothermic patients if frostbitten extremities are thawed before thermal stabilization of the core.






Predisposing Factors


Predisposing factors that contribute to the pathophysiologic changes accompanying core temperature depression can be categorized as those that decrease heat production, increase heat loss, or impair thermoregulation (Box 140-1).



BOX 140-1   Factors Predisposing to Hypothermia







Decreased Heat Production


Decreased thermogenesis is often secondary to an endocrinologic failure, such as hypopituitarism, hypoadrenalism, or myxedema. Myxedema coma is several times more common in women; up to 80% of these persons are hypothermic. Hypothyroidism is often occult in this setting. There is usually no available history of lassitude, dry skin, arthralgias, or cold intolerance.


Hypoglycemia with central neuroglycopenia also predisposes to hypothermia. Another cause of decreased heat production is malnutrition, which causes a decrease in subcutaneous fat. Severe malnutrition, as with marasmus, contributes to heat loss. Kwashiorkor is less commonly associated with hypothermia because of the insulating effect of the hypoproteinemic edema.11


The young and the old are commonly at risk. The neonate has a large surface area–to–mass ratio, a relatively deficient subcutaneous tissue layer, and an inefficient shivering mechanism. Neonates lack behavioral defense mechanisms.


Acute neonatal hypothermia is common after emergency deliveries or resuscitations. Many neonates are lethargic, fail to thrive, and have a weak cry. Half have deceptively rosy cheeks. Late-onset hypothermia, which occurs after 72 hours of life, is commonly a result of septicemia. Hypothermia can occur in the shaken baby syndrome and may be a factor in some cases of apparent sudden infant death syndrome.


Homeostatic capability progressively decreases with aging. Thermal perception is altered and elderly people manipulate the indoor ambient temperature less precisely. Most elderly patients are capable of normal thermoregulation but are prone to conditions, including immobility and systemic diseases, that interfere with heat production and conservation. Inability to sense cold, abnormal adaptive behavioral responses, and decreased peripheral blood flow reflect geriatric autonomic dysfunction.22



Increased Heat Loss


Patients with erythrodermas, including psoriasis, exfoliative dermatitis, ichthyosis, eczema, and burns, can have increased peripheral blood flow. Iatrogenic causes of heat loss include exposure during resuscitations, massive cold or room temperature infusions, overcooling of patients with heat stroke, and overzealous burn treatment.


Ethanol is metabolized at a slower rate in hypothermic individuals and interacts with every putative thermoregulatory neurotransmitter. It may directly suppress the activity of the posterior hypothalamus and the mammillary bodies. Cutaneous heat loss increases through vasodilation, and shivering thermogenesis is decreased.23


Ethanol is the most common cause of excessive heat loss in urban settings.7,16 Intoxicated persons often lack protective adaptive behavior to avoid the cold. “Paradoxical undressing,” which is the removal of clothing in response to a cold stress, is common.24 Aging is associated with an increased sensitivity to the hypothermic actions of ethanol. Hypothermic alcoholic ketoacidosis also occurs. Hypothermia is common in patients with Wernicke’s encephalopathy. Hypothermia can mask the usual clinical triad of ophthalmoplegia, confusion, and truncal ataxia. Intravenous thiamine can be both diagnostic and therapeutic.



Impaired Thermoregulation


Thermoregulation can be impaired centrally, peripherally, or metabolically. Skull fractures, particularly basilar fractures, and chronic subdural hematomas are implicated in central impairment. Other causes include cerebrovascular accidents, neoplasms, anorexia nervosa, and Hodgkin’s and Parkinson’s diseases. The final common pathway in these disorders may be centrally mediated vasodilation. Cerebellar lesions produce choreiform, less efficient shivering.


In therapeutic or toxic doses, antidepressants, antimanic agents, antipsychotics, anxiolytics, and general anesthetics interfere with thermoregulation by impairing centrally mediated vasoconstriction. Overdosage of these medications and others (e.g., the organophosphates, heroin, glutethimide, and carbon monoxide) predisposes to hypothermia.25


Peripheral thermoregulatory failure classically occurs in neurogenic shock after acute spinal cord transection. The interruption of the autonomic nervous system eliminates vasoconstrictive control. The patient effectively becomes poikilothermic and can rapidly become hypothermic. Neuropathies and diabetes are additional peripheral causes of heat loss. An abnormal plasma osmolality may explain hypothalamic interference in uremia, lactic acidosis, diabetic ketoacidosis, and hypoglycemia.26




Traumatic Factors


After trauma, hypotension and hypovolemia jeopardize thermostability.27 In patients with major injuries, a fall in core and skin temperature with no compensatory shivering thermogenesis occurs. Thermoregulation is impaired, and heat production decreases.


Hypothermia may exacerbate blood loss by inducing a coagulopathy through three mechanisms: the coagulation cascade of enzymatic reactions is impaired, plasma fibrinolytic activity is enhanced, and platelets are sequestered and poorly functional.28


Traumatic injuries may be overlooked if hypotension or neurologic findings such as areflexia or paralysis are misattributed to hypothermia. Major risk factors for hypothermia in trauma patients include age, type of injury, level of intoxicants, transfusion requirements, and elapsed time spent in the field, emergency department, and operating room.


Hypothermia can protect the brain from ischemia only when it is induced before shock develops. This reduces adenosine triphosphate (ATP) use while the ATP stores are nearly normal. In traumatized patients, the ATP stores are already depleted.29



Clinical Features


Appreciation of subtle presentations helps facilitate the early diagnosis of mild to moderate hypothermia. Vague symptoms include hunger, nausea, confusion, dizziness, chills, pruritus, and dyspnea (Box 140-2). During outdoor activities, individuals may simply become uncooperative, uncoordinated, moody, or apathetic. Indoors, elderly patients may exhibit confusion or simply become less communicative and display lassitude or a peculiar “flat” affect. Subtle progression of mental deterioration or motor skill impairment may mimic dementia. Symptoms such as slurred speech and ataxia may resemble symptoms of a cerebrovascular accident or intoxication.26



BOX 140-2   Presenting Signs of Hypothermia











Some elderly people have a decreased ability to sense cold and thus fail to take appropriate adaptive action. The maladaptive phenomenon of paradoxical undressing is not uncommon.24 This last preterminal effort of the victim may be related to the peripheral vasoconstrictive changes of profound hypothermia. The patient can be mistaken for a victim of sexual assault.


In urban settings, hypothermia is most commonly associated with ethanol ingestion or underlying illness. Other common causes include strokes, overdoses, psychiatric emergencies, and coexistent major trauma.16


Neurologic manifestations vary widely. A progressive decrease in the level of consciousness is usually proportional to the degree of hypothermia. Some patients, however, continue to be verbally responsive and display intact reflexes at 27 to 25° C.


Eye movement abnormalities and extensor plantar responses do not correlate directly with the degree of hypothermia. Cranial nerve signs may be seen with bulbar damage from central pontine myelinolysis. Above 22° C, it should be assumed that nonreactive dilated pupils reflect inadequate tissue perfusion and not hypothermia.


The rest of the neuromuscular examination may suggest the diagnosis. The patient’s posture ranges from stiff to pseudo–rigor mortis to opisthotonos. Reflexes are usually hyperactive down to 32° C, then become hypoactive until they disappear around 26° C. Cremasteric reflexes are absent because the testicles are already retracted. The plantar response usually remains flexor until 26° C. The knee jerk is the last reflex to disappear and the first to reappear with rewarming. The diagnosis of an antecedent CNS disorder, including spinal cord lesions, may be obscured by hypothermia.


Between 30 and 26° C, both contraction and relaxation phases of the reflexes are equally prolonged. If it is intact, the ankle jerk is helpful in diagnosis of hypothermic myxedema. Myxedema prolongs the relaxation phase more than the contraction phase.


No psychiatric disorder improves when the patient is cold. Mental status alterations include anxiety, perseveration, neurosis, and psychosis. Many individuals who are functional in temperate climates decompensate in colder weather. Hypothermia-induced psychiatric presentations and suicide attempts are commonly misdiagnosed.11



Diagnostic Strategies



Laboratory Evaluations



Acid-Base Balance


Blood gas analyzers warm blood to 37° C, which increases the partial pressure of dissolved gases. This results in an arterial blood gas report showing higher oxygen and carbon dioxide levels and a lower pH than the patient’s in vivo values.30–32 In fact, attempting to maintain a corrected pH at 7.4 and arterial partial pressure of carbon dioxide (PaCO2) at 40 mm Hg during hypothermia depresses cerebral and coronary blood flow and cardiac output and increases the incidence of VF.33 The ideal acid-base strategy is the ectothermic alpha-stat approach.10 Simply put, the goal is an uncorrected pH at 7.4 and PaCO2 at 40 mm Hg.


Cold blood buffers poorly. In normothermia, when the PaCO2 increases 10 mm Hg, the pH decreases 0.08 unit. At 28° C, the decrease in pH doubles. Because the neutral point of water at 37° C is a pH of 6.8, the normal 0.6-unit pH offset between blood and intracellular water should be maintained at all temperatures (Fig. 140-3).



Intracellular electrochemical neutrality ensures optimal enzymatic function at all temperatures.31 Relative alkalinity affords myocardial protection and improves the heart’s electrical stability.33 Carbogen could prove valuable in the treatment of accidental hypothermia because it flattens and shifts the oxyhemoglobin dissociation curve to the right.



Hematologic Evaluation


A patient’s hematocrit can be deceptively high as the result of the decreased plasma volume. The hematocrit level increases 2% for every 1° C fall in temperature. A low-normal hematocrit level in a moderately to severely hypothermic patient should suggest acute or chronic blood loss.


A normal white blood cell count never excludes infection, especially if the patient is debilitated, alcoholic, myxedematous, or at either age extreme. Splenic, hepatic, and splanchnic sequestration in hypothermia decreases leukocyte and platelet counts.


Frequent evaluation of serum electrolytes during rewarming is essential. There are no safe predictors of their values or trends.16 Changes occur in membrane permeability and in the sodium-potassium pump. The patient’s preexisting physiologic status, the severity and chronicity of hypothermia, and the method of rewarming alter the serum electrolyte values.


The plasma potassium level is independent of the primary hypothermic process. Hyperkalemia is often associated with metabolic acidosis, rhabdomyolysis, or renal failure. An important caveat is that hypothermia enhances the cardiac toxicity of hyperkalemia and obscures the premonitory electrocardiographic changes associated with it.


Hypokalemia is most common with chronic hypothermia. It results from potassium’s entering muscle, not a kaliuresis. A discrepant decline in serum potassium level despite a decreasing serum pH is caused by intracellular pH fluxes greater than extracellular pH fluxes.


Conditions associated with hypokalemia include preexisting diabetic ketoacidosis, hypopituitarism, inappropriate secretion of antidiuretic hormone, previous diuretic therapy, and alcoholism. If the potassium level is less than 3 mEq/L, supplementation may be necessary during rewarming.


The blood urea nitrogen and creatinine levels are elevated with preexisting renal disease or decreased clearance. Because of hypothermic fluid shifts, the hematocrit and blood urea nitrogen levels are poor indicators of a patient’s actual fluid status.


The blood glucose level may also provide a subtle clue to the type of hypothermia. Acute hypothermia initially elevates blood glucose levels through catecholamine-induced glycogenolysis, diminished insulin release, and inhibition of cellular membrane glucose carrier systems. On the other hand, subacute and chronic hypothermia produce glycogen depletion, leading to hypoglycemia. Symptoms of hypoglycemia can be masked by hypothermia. A cold-induced renal glycosuria does not imply hyperglycemia or guarantee normoglycemia.26


When hyperglycemia persists during rewarming, one should suspect hemorrhagic pancreatitis or diabetic ketoacidosis. Patients with diabetic ketoacidosis should be actively rewarmed past 30° C because insulin is ineffective below that temperature. Correction of hypoglycemia corrects the level of consciousness only to that of the corresponding level of hypothermia.


Severe hypothermia also causes serum enzyme elevation because of the ultrastructural cellular damage. Rhabdomyolysis is commonly associated with cold exposure.


Ischemic pancreatitis may result from the microcirculatory shock of hypothermia. The decreased pancreatic blood flow then activates proteolytic enzymes.7

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