Accidental hypothermia occurs when there is an unintentional drop in the body’s core temperature below 35°C (95°F). At this temperature, many of the compensatory physiologic mechanisms that conserve heat begin to fail. Primary accidental hypothermia is a result of the direct exposure of a previously healthy individual to the cold. The mortality rate is much higher for patients who develop secondary hypothermia as a complication of a serious systemic disorder.
Primary accidental hypothermia is geographically and seasonally pervasive. Although most cases occur in the winter months and in colder climates, this condition is surprisingly common in warmer regions as well. Multiple variables render individuals at the extremes of age—both the elderly and neonates—particularly vulnerable to hypothermia (Table 478e-1). The elderly have diminished thermal perception and are more susceptible to immobility, malnutrition, and systemic illnesses that interfere with heat generation or conservation. Dementia, psychiatric illness, and socioeconomic factors often compound these problems by impeding adequate measures to prevent hypothermia. Neonates have high rates of heat loss because of their increased surface-to-mass ratio and their lack of effective shivering and adaptive behavioral responses. At all ages, malnutrition can contribute to heat loss because of diminished subcutaneous fat and as a result of depleted energy stores used for thermogenesis.
TABLE 478e-1Risk Factors for Hypothermia ||Download (.pdf) TABLE 478e-1 Risk Factors for Hypothermia
|Age extremes ||Endocrine-related |
| Elderly || Diabetes mellitus |
| Neonates || Hypoglycemia |
|Environmental exposure || Hypothyroidism |
| Occupational || Adrenal insufficiency |
| Sports-related || Hypopituitarism |
| Inadequate clothing ||Neurologic |
| Immersion || Cerebrovascular accident |
|Toxicologic and pharmacologic || Hypothalamic disorders |
| Ethanol || Parkinson’s disease |
| Phenothiazines || Spinal cord injury |
| Barbiturates ||Multisystemic |
| Anesthetics || Trauma |
| Neuromuscular blockers || Sepsis |
| Antidepressants || Shock |
Hepatic or renal failure
Burns and exfoliative dermatologic disorders
Immobility or debilitation
Individuals whose occupations or hobbies entail extensive exposure to cold weather are at increased risk for hypothermia. Military history is replete with hypothermic tragedies. Hunters, sailors, skiers, and climbers also are at great risk of exposure, whether it involves injury, changes in weather, or lack of preparedness.
Ethanol causes vasodilation (which increases heat loss), reduces thermogenesis and gluconeogenesis, and may impair judgment or lead to obtundation. Phenothiazines, barbiturates, benzodiazepines, heterocyclic antidepressants, and many other medications reduce centrally mediated vasoconstriction. Up to 25% of patients admitted to an intensive care unit because of drug overdose are hypothermic. Anesthetics can block shivering responses; their effects are compounded when patients are not insulated adequately in the operating or recovery units.
Several types of endocrine dysfunction can lead to hypothermia. Hypothyroidism—particularly when extreme, as in myxedema coma—reduces the metabolic rate and impairs thermogenesis and behavioral responses. Adrenal insufficiency and hypopituitarism also increase susceptibility to hypothermia. Hypoglycemia, most commonly caused by insulin or oral hypoglycemic drugs, is associated with hypothermia, in part because of neuroglycopenic effects on hypothalamic function. Increased osmolality and metabolic derangements associated with uremia, diabetic ketoacidosis, and lactic acidosis can lead to altered hypothalamic thermoregulation.
Neurologic injury from trauma, cerebrovascular accident, subarachnoid hemorrhage, and hypothalamic lesion increases susceptibility to hypothermia. Agenesis of the corpus callosum (Shapiro syndrome) is one cause of episodic hypothermia; in this syndrome, profuse perspiration is followed by a rapid fall in temperature. Acute spinal cord injury disrupts the autonomic pathways that lead to shivering and prevents cold-induced reflex vasoconstrictive responses.
Hypothermia associated with sepsis is a poor prognostic sign. Hepatic failure causes decreased glycogen storage and gluconeogenesis as well as a diminished shivering response. In acute myocardial infarction associated with low cardiac output, hypothermia may be reversed after adequate resuscitation. With extensive burns, psoriasis, erythrodermas, and other skin diseases, increased peripheral-blood flow leads to excessive heat loss.
Heat loss occurs through five mechanisms: radiation (55–65% of heat loss), conduction (10–15% of heat loss, much increased in cold water), convection (increased in the wind), respiration, and evaporation; both of the latter two mechanisms are affected by the ambient temperature and the relative humidity.
The preoptic anterior hypothalamus normally orchestrates thermoregulation (Chap. 23). The immediate defense of thermoneutrality is via the autonomic nervous system, whereas delayed control is mediated by the endocrine system. Autonomic nervous system responses include the release of norepinephrine, increased muscle tone, and shivering, leading to thermogenesis and an increase in the basal metabolic rate. Cutaneous cold thermoreception causes direct reflex vasoconstriction to conserve heat. Prolonged exposure to cold also stimulates the thyroid axis, leading to an increased metabolic rate.
In most cases of hypothermia, the history of exposure to environmental factors (e.g., prolonged exposure to the outdoors without adequate clothing) makes the diagnosis straightforward. In urban settings, however, the presentation is often more subtle, and other disease processes, toxin exposures, or psychiatric diagnoses should be considered.
After initial stimulation by hypothermia, there is progressive depression of all organ systems. The timing of the appearance of these clinical manifestations varies widely (Table 478e-2). Without knowing the core temperature, it can be difficult to interpret other vital signs. For example, tachycardia disproportionate to the core temperature suggests secondary hypothermia resulting from hypoglycemia, hypovolemia, or a toxin overdose. Because carbon dioxide production declines progressively, the respiratory rate should be low; persistent hyperventilation suggests a central nervous system (CNS) lesion or one of the organic acidoses. A markedly depressed level of consciousness in a patient with mild hypothermia raises suspicion of an overdose or CNS dysfunction due to infection or trauma.
TABLE 478e-2Physiologic Changes Associated with Accidental Hypothermia ||Download (.pdf) TABLE 478e-2 Physiologic Changes Associated with Accidental Hypothermia
|Severity ||Body Temperature ||Central Nervous System ||Cardiovascular ||Respiratory ||Renal and Endocrine ||Neuromuscular |
|Mild ||35°C (95°F)– 32.2°C (90°F) ||Linear depression of cerebral metabolism; amnesia; apathy; dysarthria; impaired judgment; maladaptive behavior ||Tachycardia, then progressive bradycardia; cardiac cycle prolongation; vasoconstriction; increase in cardiac output and blood pressure ||Tachypnea, then progressive decrease in respiratory minute volume; declining oxygen consumption; bronchorrhea; bronchospasm ||Diuresis; increase in catecholamines, adrenal steroids, triiodothyronine, and thyroxine; increase in metabolism with shivering ||Increased preshivering muscle tone, then fatiguing |
|Moderate ||<32.2°C (90°F)–28°C (82.4°F) ||EEG abnormalities; progressive depression of level of consciousness; pupillary dilation; paradoxical undressing; hallucinations ||Progressive decrease in pulse and cardiac output; increased atrial and ventricular arrhythmias; suggestive (J- wave) ECG changes ||Hypoventilation; 50% decrease in carbon dioxide production per 8°C (46°F) drop in temperature; absence of protective airway reflexes ||50% increase in renal blood flow; renal autoregulation intact; impaired insulin action ||Hyporeflexia; diminishing shivering-induced thermogenesis; rigidity |
|Severe ||<28°C (<82.4°F) ||Loss of cerebrovascular autoregulation; decline in cerebral blood flow; coma; loss of ocular reflexes; progressive decrease in EEG abnormalities ||Progressive decrease in blood pressure, heart rate, and cardiac output; reentrant dysrhythmias; maximal risk of ventricular fibrillation; asystole ||Pulmonic congestion and edema; 75% decrease in oxygen consumption; apnea ||Decrease in renal blood flow that parallels decrease in cardiac output; extreme oliguria; poikilothermia; 80% decrease in basal metabolism ||No motion; decreased nerve- conduction velocity; peripheral areflexia; no corneal or oculocephalic reflexes |
Physical examination findings can also be altered by hypothermia. For instance, the assumption that areflexia is solely attributable to hypothermia can obscure and delay the diagnosis of a spinal cord lesion. Patients with hypothermia may be confused or combative; these symptoms abate more rapidly with rewarming than with chemical or physical restraint. A classic example of maladaptive behavior in patients with hypothermia is paradoxical undressing, which involves the inappropriate removal of clothing in response to a cold stress. The cold-induced ileus and abdominal rectus spasm can mimic or mask the presentation of an acute abdomen (Chap. 20).
When a patient in hypothermic cardiac arrest is first discovered, cardiopulmonary resuscitation is indicated unless (1) a do-not-resuscitate status is verified, (2) obviously lethal injuries are identified, or (3) the depression of a frozen chest wall is not possible. As the resuscitation proceeds, the prognosis is grave if there is evidence of widespread cell lysis, as reflected by potassium levels >10–12 mmol/L (10–12meq/L). Other findings that may preclude continuing resuscitation include a core temperature <10–12°C (<50–54°F), a pH <6.5, and evidence of intravascular thrombosis with a fibrinogen value <0.5 g/L (<50 mg/dL). The decision to terminate resuscitation before rewarming the patient past 33°C (91°F) should be predicated on the type and severity of the precipitants of hypothermia. There are no validated prognostic indicators for recovery from hypothermia. A history of asphyxia with secondary cooling is the most important negative predictor of survival.
DIAGNOSIS AND STABILIZATION
Hypothermia is confirmed by measurement of the core temperature, preferably at two sites. Rectal probes should be placed to a depth of 15 cm and not adjacent to cold feces. A simultaneous esophageal probe should be placed 24 cm below the larynx; it may read falsely high during heated inhalation therapy. Relying solely on infrared tympanic thermography is not advisable.
After a diagnosis of hypothermia is established, cardiac monitoring should be instituted, along with attempts to limit further heat loss. If the patient is in ventricular fibrillation, it is unclear at what core temperature ventricular defibrillation (2 J/kg) should first be attempted. One attempt below 30°C is warranted. Further defibrillation attempts should be deferred until some rewarming (1°–2°C) is achieved and ventricular fibrillation is coarser. Although cardiac pacing for hypothermic bradydysrrhythmias is rarely indicated, the transthoracic technique is preferable.
Supplemental oxygenation is always warranted, since tissue oxygenation is affected adversely by the leftward shift of the oxyhemoglobin dissociation curve. Pulse oximetry may be unreliable in patients with vasoconstriction. If protective airway reflexes are absent, gentle endotracheal intubation should be performed. Adequate preoxygenation will prevent ventricular arrhythmias.
Insertion of a gastric tube prevents dilation secondary to decreased bowel motility. Indwelling bladder catheters facilitate monitoring of cold-induced diuresis. Dehydration is encountered commonly with chronic hypothermia, and most patients benefit from an intravenous or intraosseous bolus of crystalloid. Normal saline is preferable to lactated Ringer’s solution, as the liver in hypothermic patients inefficiently metabolizes lactate. The placement of a pulmonary artery catheter can cause perforation of the less compliant pulmonary artery. Insertion of a central venous catheter deeply into the cold right atrium should be avoided since this procedure can precipitate arrhythmias.
Arterial blood gases should not be corrected for temperature (Chap. 66). An uncorrected pH of 7.42 and a Pco2 of 40 mmHg reflect appropriate alveolar ventilation and acid-base balance at any core temperature. Acid-base imbalances should be corrected gradually, since the bicarbonate buffering system is inefficient. A common error is overzealous hyperventilation in the setting of depressed CO2 production. When the Pco2 decreases by 10 mmHg at 28°C (82°F), it doubles the pH increase of 0.08 that occurs at 37°C (99°F).
The severity of anemia may be underestimated because the hematocrit increases 2% for each 1°C drop in temperature. White blood cell sequestration and bone marrow suppression are common, potentially masking an infection. Although hypokalemia is more common in chronic hypothermia, hyperkalemia also occurs; the expected electrocardiographic changes can be obscured by hypothermia. Patients with renal insufficiency, metabolic acidoses, or rhabdomyolysis are at greatest risk for electrolyte disturbances.
Coagulopathies are common because cold inhibits the enzymatic reactions required for activation of the intrinsic cascade. In addition, thromboxane B2 production by platelets is temperature dependent, and platelet function is impaired. The administration of platelets and fresh-frozen plasma is therefore not effective. The prothrombin or partial thromboplastin times or the international normalized ratio can be deceptively normal and contrast with the observed in vivo coagulopathy. This contradiction occurs because all coagulation tests are routinely performed at 37°C (99°F), and the enzymes are thus rewarmed.
The key initial decision is whether to rewarm the patient passively or actively. Passive external rewarming simply involves covering and insulating the patient in a warm environment. With the head also covered, the rate of rewarming is usually 0.5°–2°C (1.10°–4.4°F) per hour. This technique is ideal for previously healthy patients who develop acute, mild primary accidental hypothermia. The patient must have sufficient glycogen to support endogenous thermogenesis.
The application of heat directly to the extremities of patients with chronic severe hypothermia should be avoided because it can induce peripheral vasodilation and precipitate core temperature “afterdrop,” a response characterized by a continual decline in the core temperature after removal of the patient from the cold. Truncal heat application reduces the risk of afterdrop.
Active rewarming is necessary under the following circumstances: core temperature <32°C (<90°F) (poikilothermia), cardiovascular instability, age extremes, CNS dysfunction, hormone insufficiency, and suspicion of secondary hypothermia. Active external rewarming is best accomplished with forced-air heating blankets. Other options include devices that circulate water through external heat exchange pads, radiant heat sources, and hot packs. Monitoring a patient with hypothermia in a heated tub is extremely difficult. Electric blankets should be avoided because vasoconstricted skin is easily burned.
There are numerous widely available options for active core rewarming. Airway rewarming with heated humidified oxygen (40°–45°C [104°–113°F]) via mask or endotracheal tube is a convenient option. Although airway rewarming provides less heat than do some other forms of active core rewarming, it eliminates respiratory heat loss and adds 1°–2°C (1.1°–4.4°F) to the overall rewarming rate. Crystalloids should be heated to 40°–42°C (104°–108°F), but the quantity of heat provided is significant only during massive volume resuscitation. The most efficient method for heating and delivering fluid or blood is with a countercurrent in-line heat exchanger. Heated irrigation of the gastrointestinal tract or bladder transfers minimal heat because of the limited available surface area. These methods should be reserved for patients in cardiac arrest and then used in combination with all available active rewarming techniques.
Closed thoracic lavage is far more efficient in severely hypothermic patients with cardiac arrest. The hemithoraxes are irrigated through two inserted large-bore thoracostomy tubes. Thoracostomy tubes should not be placed in the left chest of a spontaneously perfusing patient for purposes of rewarming. Peritoneal lavage with the dialysate at 40°–45°C (104°–113°F) efficiently transfers heat when delivered through two catheters with outflow suction. Like peritoneal dialysis, standard hemodialysis is especially useful for patients with electrolyte abnormalities, rhabdomyolysis, or toxin ingestion. Another option involves the central venous insertion of a rapid endovascular warming device.
Extracorporeal blood rewarming options (Table 478e-3) should be considered in severely hypothermic patients, especially those with primary accidental hypothermia. Cardiopulmonary bypass should be considered in nonperfusing patients without documented contraindications to resuscitation. Circulatory support may be the only effective option in patients with completely frozen extremities or those with significant tissue destruction coupled with rhabdomyolysis. There is no evidence that extremely rapid rewarming improves survival in perfusing patients. The best strategy is usually a combination of passive, truncal active, and active core rewarming techniques.
TABLE 478e-3Options for Extracorporeal Blood Rewarming ||Download (.pdf) TABLE 478e-3 Options for Extracorporeal Blood Rewarming
|Extracorporeal Rewarming Technique ||Considerations |
|Continuous venovenous (CVV) rewarming ||Circuit: CV catheter to CV, dual-lumen CV, or peripheral catheter |
| ||No oxygenator/circulatory support |
| ||Flow rates 150–400 mL/min |
| ||ROR 2°–3°C (36°–37°F)/h |
|Hemodialysis ||Circuit: single- or dual-vessel cannulation |
| ||Stabilizes electrolyte or toxicologic abnormalities |
| ||Exchange cycle volumes 200–500 mL/min |
| ||ROR 2°–3°C (36°–37°F)/h |
|Continuous arteriovenous rewarming (CAVR) ||Circuit: percutaneous 8.5-Fr femoral catheters |
| ||Requires systolic blood pressure of 60 mmHg |
| ||No perfusionist/pump/anticoagulation |
| ||Flow rates 225–375 mL/min |
| ||ROR 3°–4°C (37°–39°F)/h |
|Cardiopulmonary bypass (CPB) ||Circuit: full circulatory support with pump and oxygenator |
| ||Perfusate-temperature gradient (5°–10°C [41°–50°F]) |
| ||Flow rates 2–7 L/min (average 3–4 L/min) |
| ||ROR up to 9.5°C (49°F)/h |
|Extracorporeal membrane oxygenation (ECMO) ||Decreased risk of post-rewarming cardiorespiratory failure |
When a patient is hypothermic, target organs and the cardiovascular system respond minimally to most medications. Generally, IV medications are withheld below 30°C (86°F). In contrast to antiarrhythmics, low-dose vasopressor medications may improve the intra-arrest rates of return of spontaneous circulation. Because of increased binding of drugs to proteins as well as impaired metabolism and excretion, either a lower dose or a longer interval between doses should be used to avoid toxicity. As an example, the administration of repeated doses of digoxin or insulin would be ineffective while the patient is hypothermic, and the residual drugs would be potentially toxic during rewarming.
Achieving a mean arterial pressure of at least 60 mmHg should be an early objective. If the hypotension does not respond to crystalloid/colloid infusion and rewarming, low-dose dopamine support (2–5 μg/kg per min) should be considered. Perfusion of the vasoconstricted cardiovascular system also may be improved with low-dose IV nitroglycerin.
Atrial arrhythmias should be monitored initially without intervention, as the ventricular response should be slow and, unless preexistent, most will convert spontaneously during rewarming. The role of prophylaxis and treatment of ventricular arrhythmias is problematic. Preexisting ventricular ectopy may be suppressed by hypothermia and reappear during rewarming. None of the class I agents has proved to be safe and efficacious. There is also insufficient evidence that the class III ventricular antiarrhythmic amiodarone is safe.
Initiating empirical therapy for adrenal insufficiency usually is not warranted unless the history suggests steroid dependence or hypoadrenalism or efforts to rewarm with standard therapy fail. The administration of parenteral levothyroxine to euthyroid patients with hypothermia, however, is potentially hazardous. Because laboratory results can be delayed and confounded by the presence of the sick euthyroid syndrome (Chap. 405), historic clues or physical findings suggestive of hypothyroidism should be sought. When myxedema is the cause of hypothermia, the relaxation phase of the Achilles reflex is prolonged more than is the contraction phase.
Hypothermia obscures most of the symptoms and signs of infection, notably fever and leukocytosis. Shaking rigors from infection may be mistaken for shivering. Except in mild cases, extensive cultures and repeated physical examinations are essential. Unless an infectious source is identified, empirical antibiotic prophylaxis is most warranted in the elderly, neonates, and immunocompromised patients.
Preventive measures should be discussed with high-risk individuals, such as the elderly and people whose work frequently exposes them to extreme cold. The importance of layered clothing and headgear, adequate shelter, increased caloric intake, and the avoidance of ethanol should be emphasized, along with access to rescue services.