Hypothermia is defined as a core temperature of less than 35 degrees C. Below this temperature the body systems for thermoregulation begin to fail. The body’s ability to minimize heat loss through radiation, convection, respiration, conduction, and evaporation are very limited. The very young and the very old are the most susceptible to hypothermia as a result of their impaired thermoregulatory capacity. This article will present an overview of the pathogenesis of hypothermia, as well as the clinical features and the treatment modes available.
Each year approximately 750 people die in the United States from hypothermia (range 550 to 1000). The true incidence of hypothermia is probably much higher because of reporting bias; many cases are not reported as due to hypothermia because of the wide clinical variability and complicating medical conditions. Most of these deaths occur in three distinct geographic regions: northern states with severely cold winters (Illinois and New York), the mid-Atlantic states because of drastic changes in weather conditions (the Carolinas and Virginia), and Western states (New Mexico and Arizona) because of the large drops in temperature that occur at night. Hypothermia can occur in any season however, and in almost any weather.
Groups At Risk
Those at increased risk for hypothermia include the very young and the very old. Small children are at risk because of the relatively increased surface area of the skin and a decreased ability to generate heat. The elderly are at increased risk because of underlying medical problems, impaired heat regulation, and decreased heat production. Those with alcohol or drug related illness or endocrine abnormalities, like diabetes or adrenal insufficiency, are at increased risk as well. Practically speaking, most cases of hypothermia result from prolonged cold exposure without adequate clothing, sustaining an injury in a cold environment, or prolonged submersion in cold water.
Hypothermia results from a mismatch of heat generated versus heat lost. There are several means by which the body can lose more heat or produce less heat and thereby upset the balance.
Decreased heat production
Endocrine disease, insufficient fuel stores, and impaired physical exertion can all result in decreased heat production. Endocrine abnormalities like adrenal insufficiency, hypopituitarism and hypothyroidism all cause a generalized metabolic slowing, with a resulting decrease in heat production. Hypoglycemia or malnutrition can lead to insufficient fuel reserves with the same result. Impaired physical exertion, either inactivity or inadequate shivering, also may result in an altered heat balance. Shivering is normal as the body temperature decreases, but it may be suppressed by benzodiazepines, phenothiazines, tricyclic antidepressants, and alcohol. Shivering is also dependent on glycogen stores and will stop when stores are exhausted.
Increased heat loss
Increased heat loss can result from increased vasodilation, skin abnormalities, iatrogenic causes, or environmental causes. Ingestion of drugs, such as some antihypertensives, or alcohol can cause increased vasodilation of the small capillary beds in the dermis. This leads to increased heat loss through radiation and convection. Normal shivering also causes increased heat lost directly to the surrounding air or water. Inflammation, or burns, of the skin increases the amount of heat lost as well. Iatrogenic causes include infusion of cold IV fluids and exposure during multiple trauma resuscitations or operative procedures. Immersion-type environmental exposures in cold water causes direct conductive heat loss to the water.
Impaired temperature regulation
Neurological abnormalities, both central and peripheral, as well as general medical and metabolic abnormalities, can lead to impaired temperature regulation. Diabetic neuropathy and spinal cord injury (acute or chronic) results in the loss of innervation of the peripheral circulation, and thus impaired vasodilation and constriction. Central nervous system dysfunction, from a stroke, intracerebral hemorrhage, tumor or trauma, may result in loss of hypothalamic temperature regulation.
Other causes, with various combinations of the above mechanisms, include multisystem trauma, shock, acidosis, pancreatitis, uremia, systemic infections, and cancer.
Physiological Response To Cold
The human body functions best within a narrow range of temperatures, between 36 and 38 degrees Centigrade. Any deviation from this range affects all organ systems, some more than others. Hypothermia, like hypocapnia, shifts the oxygen-dissociation curve to the left, resulting in decreased oxygen release from hemoglobin into the tissues. Increased blood viscosity, ventilation-perfusion mismatch, and peripheral vasoconstriction all contribute to tissue hypoxia. Tissue hypoxia, impaired liver metabolism of lactate, and cold-induced diuresis together lead to the development of metabolic acidosis.
The earliest stages of hypothermia begin at a temperature less than 35° C., down to about 32 degrees. A generalized increase in muscle tone and shivering are the first mechanisms to increase heat production. Peripheral vasoconstriction helps to minimize heat lost from the skin.
Moderate hypothermia (28°- 32° C.) leads to further depression of the metabolic rate and the loss of shivering.
Severe hypothermia, less than 28° C., results in inactivity of the endocrine and autonomic nervous systems. It is characterized by a decline in cerebral blood flow and by markedly decreased metabolism and oxygen utilization. Insulin loses its effectiveness, resulting in hyperglycemia.
Initially, tachycardia and increased peripheral resistance lead to an increase in cardiac output. A progressive decrease in temperature causes bradycardia, decreased cardiac output, impaired electrical conduction, increased myocardial irritability, dysrhythmias (atrial and ventricular fibrillation), hypotension, ECG abnormalities, and eventually, asystole.
After the initial tachypnea, the respiratory rate and tidal volume progressively decrease, with resulting respiratory acidosis, to apnea. Bronchospasm, loss of protective airway reflexes, and decreased oxygen consumption also occur with moderate hypothermia.
Initially altered mental status and impaired judgement lead to confusion, dilated pupils, lethargy, and hyporeflexia. Progressive decreases in core temperature result in severe CNS depression, hallucinations, areflexia and coma.
Even in profound hypothermia, less than 20° C., the brain is relatively protected from ischemia. Total cardiovascular collapse may be tolerated by the brain for up to one hour. Patients with hypothermia should, therefore, not be pronounced brain dead until they have been rewarmed and their CNS reevaluated by EEG.
The initial cold diuresis results from central shunting of blood flow and suppression of antidiuretic hormone. This, together with fluid sequestration, can lead to profound dehydration. Decreased cardiac output and hypotension lead to decreased renal blood flow, oliguria and renal failure.
Prompt diagnosis is important to ensure a satisfactory outcome. All Emergency Departments should have a thermometer capable of registering temperatures below 30 degrees C. The best estimates of core temperatures are measured internally, either rectal, esophageal, or in the bladder. Infrared ear devices are clearly not adequate and should not be used. Because severe drops in core temperature can lead to apnea, areflexia, coma, hypotension, and cardiac arrest, hypothermic patients may appear clinically dead. They should not be pronounced dead, however, unless they remain unresponsive to resuscitation efforts after adequate rewarming. In other words, nobody is dead until they are warm and dead.
Emergency Medical Service personnel should maintain a high index of suspicion for hypothermia in any patient with an altered mental status who may have been exposed to even a moderately cold environment. Prehospital treatment is limited to removal from the cold environment, removing wet clothing, wrapping the victim in warm blankets, and stabilizing any obvious signs of trauma. Patients should be moved carefully during transport because the cold heart is prone to fibrillation. Cardiac monitoring is essential along with routine vital signs. Warmed IV fluids should be started, if available, because dehydration may be severe.
Treatment priorities, as in any emergency, include immediate attention to the airway and breathing; patients in respiratory failure should be intubated and artificially ventilated. If there is any history or sign of trauma, especially in the setting of near-drowning, cervical spine immobilization is mandatory. The circulation is next in importance; at least two large-bore IV lines should be placed, and central access should be considered, especially if central warming is to be undertaken. Femoral lines are felt to be better than subclavian or jugular to avoid any possible ventricular stimulation that could potentially precipitate fibrillation.
The IV fluid given should be D5W or Normal Saline; Ringer’s Lactate should be avoided because the liver cannot metabolize lactate in the presence of hypothermia.
The cold heart, in addition to being refractory to pharmacotherapeutic measures, is very resistant to pacing and defibrillation. Chest compressions may need to be performed for an extended time period until the core temperature is high enough for the heart to respond to drugs and/or electricity.
As in any patient with altered mental status, glucose, thiamine, and naloxone should be considered and given if appropriate. Warm, humidified oxygen should also be given by face mask. A Foley catheter should be placed to monitor urine output. Pulse oximeters do not work well in hypothermic patients because of the peripheral vasoconstriction.
There are basically three methods for rewarming: passive external, active external, and active internal. Patients with only mild hypothermia, temperature greater than 32 C., can usually be managed with removal of any wet clothing and wrapping in insulating blankets. This, of course, is limited to patients who can generate their own heat. Active external rewarming exposes the body directly to an exogenous heat source. This can be a circulating air blanket, electric blanket, or total body immersion in warm water. Immersion in warm water is somewhat controversial because of afterdrop, a continued decrease in core temperature related to increased peripheral circulation and return of cold blood to the central circulation. Immersion also makes cardiac and vital sign monitoring more difficult. It should be used only for otherwise healthy patients who can tolerate the procedure and for whom complete recovery is likely. The ideal method and rate of rewarming are somewhat controversial. There are no controlled studies examining either issue. Patients with normal cardiac rhythm can probably be rewarmed over a period of several hours, but those with cardiac instability should be warmed promptly. The choice of rewarming strategy should be based on the clinical status of the patient.
Patients with severe hypothermia, temp. less than 24 C., should be treated aggressively with active internal, or core, rewarming. This includes giving warmed IV fluids and warmed, humidified oxygen in addition to invasive procedures. IV fluids should be warmed to 40 degrees C. Inhaled, warmed oxygen by mask can raise the body temperature by about 2 degrees C. per hour. It also eliminates loss of heat from the respiratory tract.
Invasive techniques include warm fluid lavage and extracorporeal methods. Any body cavity can be lavaged with warm water or saline: the stomach, chest, colon, or peritoneum. Gastric and colonic irrigation are more easily performed and are the least invasive. Gastric lavage is performed by using a normal nasogastric tube. Warmed saline or water (40 to 45 degrees C.) is instilled in 500 ml aliquots and left in for 15 minutes; the water is then suctioned out and the process repeated. Peritoneal lavage is performed using peritoneal access catheters with warmed isotonic dialysate. Thoracic lavage has shown some promise in the treatment of severe hypothermia, but it should be limited to those patients in cardiac arrest and only if extracorporeal rewarming is unavailable. It involves placing two large-bore thoracostomy tubes, one anterior and one axial, on the right side of the chest and instilling warm water anteriorly. The left chest should be avoided to reduce stimulation of the heart.
Extracorporeal rewarming can be accomplished by either hemodialysis or cardiopulmonary bypass. This is the treatment of choice for the patient in cardiac arrest.
As in any patient with altered mental status, a fingerstick glucose should be measured immediately on presentation and glucose given if necessary. Glucosuria is usually present with hypothermia and does not necessarily reflect serum hyperglycemia. Hyperglycemia is usually present, however, and results from impaired activity of insulin, impaired glucose utilization, and increased cortisol production.
The hematocrit increases 2 percent for every 1 degree C. drop in temperature. This is caused by fluid sequestration and decreased plasma volume.
The most common electrolyte abnormality is hypokalemia; serum potassium levels should be checked frequently because hypothermia can mask potassium-induced changes on the electrocardiogram (ECG). Potassium supplements should be avoided if possible because levels will increase with rewarming. Hyperkalemia is particularly dangerous in the presence of acidosis as well.
Coagulopathies often develop inpatients with hypothermia, in spite of normal levels of coagulation factors. As core temperature decreases, platelet activity also decreases, and there is a cold-induced bone marrow suppression resulting in thrombocytopenia. Serum amylase may be elevated in up to 50% of cases and does not always indicate pancreatitis.
Arterial blood gases should be interpreted using uncorrected values to avoid inappropriate hypoventilation secondary to false elevations in the pCO2. Gradual corrections of acid-base balance is prudent because the normal respiratory and renal compensatory mechanisms gradually become more efficient as the core temperature improves. Sodium bicarb should be used to correct acidosis. There are several ECG changes typical for hypothermia: T-wave inversion, PR, QRS, or QT prolongation, and dysrhythmias (bradycardia, atrial or ventricular fibrillation, AV block, PVCs, and asystole). The pathognomonic sign, however, is the Osborn, or J, wave. It is a small, positive deflection, or shoulder, at the termination of the QRS complex. It usually appears only after the core temperature has decreased to less than 32 degrees C.
Drug therapy for hypothermia should be minimized because the body becomes progressively less responsive to medications as the core temperature drops. Liver metabolism decreases and protein binding of drugs increases.
Even large doses of insulin may be ineffective for hyperglycemia and may, in fact, be dangerous as insulin activity returns with resuscitation and rewarming. Digoxin use for atrial dysrhythmias should likewise be avoided because of decreased effectiveness. Atrial fibrillation usually resolves spontaneously with rewarming.
Low-dose dopamine may be needed for pressure support if IV rehydration is not effective, but high doses should be avoided if possible to avoid undue stimulation of the heart. Hypothermic bradycardia is resistant to atropine. Lidocaine and procainamide are likewise ineffective. Bretylium does seem to be helpful, however, and may actually protect the heart from increased contractility in addition to increasing endogenous catecholamines. Magnesium is also safe and may be effective for ventricular dysrhythmias.
Corticosteroids should be considered, especially if there is any question of steroid dependence (such as an asthmatic) or after successful resuscitation from cardiac arrest. Thyroxine should be considered as well, if there is suspicion of myxedema or profound hypothyroidism.
Empirical antibiotics should be given only to patients with signs of immunocompromise or in neonates with suspected overwhelming infection.
Predisposing, concurrent, or resulting factors must be considered, such as sepsis or overwhelming infection, endocrine crisis, trauma, stroke, alcohol intoxication, or drug overdose. For example, the 80 year-old woman found on the floor of her inadequately heated apartment may have collapsed because of a stroke and then become hypothermic after many hours. Conversely, the 65 year-old alcoholic found passed out on the street may sustain a myocardial infarction as a result of the increased strain on his heart from being hypothermic.
Underlying disorders must be aggressively sought and treated because they contribute to the mortality associated with hypothermia.
Prognosis and Postresuscitation Complications
The following are considered to be markers of poor outcome: out-of-hospital cardiac arrest, severe hypotension, the need for endotracheal intubation, an elevated potassium (over 10 mEq/L) and an elevated BUN.
Rewarming shock is the main postresuscitation complication and results from reversal of peripheral vasoconstriction if insufficient IV fluids are given. Other problems include pulmonary edema, disseminated intravascular coagulation, myoglobinuria, and adrenal insufficiency.
Prevention of hypothermia remains imperative and educational programs should be targeted to both high-risk populations (the urban poor) and the general public. During cold weather, healthcare professionals and public health agencies can help reduce the incidence of hypothermia by monitoring groups at risk.
Hypothermia remains a serious problem in the United States, particularly in high-risk groups, such as the homeless, alcoholics, and the elderly. The range of severity is very broad and includes many subtle findings. Predisposing factors include impaired thermoregulation from drugs, alcohol, CNS abnormalities, infections, and endocrine disease. Multiple laboratory abnormalities are characteristic for hypothermia. Treatment is based on supportive care, as well as various passive and active interventions, depending on the degree of temperature depression.