Hypothermia describes a state in which the body's mechanism for temperature regulation is overwhelmed in the face of a cold stressor. Hypothermia is classified as accidental or intentional, primary or secondary, and by the degree of hypothermia.
Accidental hypothermia generally results from unanticipated exposure in an inadequately prepared person; examples include inadequate shelter for a homeless person, someone caught in a winter storm or motor vehicle accident, or an outdoor sport enthusiast caught off guard by the elements. Intentional hypothermia is an induced state generally directed at neuroprotection after an at-risk situation (usually after cardiac arrest, see Therapeutic Hypothermia). Primary hypothermia is due to environmental exposure, with no underlying medical condition causing disruption of temperature regulation. Secondary hypothermia is low body temperature resulting from a medical illness lowering the temperature set-point.
Many patients have recovered from severe hypothermia, so early recognition and prompt initiation of optimal treatment is paramount. See Treating Hypothermia: What You Need to Know, a Critical Images slideshow, to help recognize the signs of hypothermia as well as the best approach for hypothermic patients.
Systemic hypothermia may also be accompanied by localized cold injury (see Emergent Management of Frostbite). See the image below.
Osborne (J) waves (V3) in a patient with a rectal core temperature of 26.7°C (80.1°F). ECG courtesy of Heather Murphy-Lavoie of Charity Hospital, New ....
The body's core temperature is tightly regulated in the "thermoneutral zone" between 36.5°C and 37.5°C, outside of which thermoregulatory responses are usually activated. The body maintains a stable core temperature through balancing heat production and heat loss. At rest, humans produce 40-60 kilocalories (kcal) of heat per square meter of body surface area through generation by cellular metabolism, most prominently in the liver and the heart. Heat production increases with striated muscle contraction; shivering increases the rate of heat production 2-5 times.
Heat loss occurs via several mechanisms, the most significant of which, under dry conditions, is radiation (55-65% of heat loss). Conduction and convection account for about 15% of additional heat loss, and respiration and evaporation account for the remainder. Conductive and convective heat loss, or direct transfer of heat to another object or circulating air, respectively, are the most common causes of accidental hypothermia. Conduction is a particularly significant mechanism of heat loss in drowning/immersion accidents as thermal conductivity of water is up to 30 times that of air.
The hypothalamus controls thermoregulation via increased heat conservation (peripheral vasoconstriction and behavior responses) and heat production (shivering and increasing levels of thyroxine and epinephrine). Alterations of the CNS may impair these mechanisms. The threshold for shivering is 1 degree lower than that of vasoconstriction and is considered a last resort mechanism by the body to maintain temperature. The mechanisms for heat preservation may be overwhelmed in the face of cold stress and core temperature can drop secondary to fatigue or glycogen depletion.
Hypothermia affects virtually all organ systems. Perhaps the most significant effects are seen in the cardiovascular system and the CNS. Hypothermia results in decreased depolarization of cardiac pacemaker cells, causing bradycardia. Since this bradycardia is not vagally mediated, it can be refractory to standard therapies such as atropine. Mean arterial pressure and cardiac output decrease, and an electrocardiogram (ECG) may show characteristic J or Osborne waves (see the image below). While generally associated with hypothermia, the J wave may be a normal variant and is seen occasionally in sepsis and myocardial ischemia.
Osborne (J) waves (V3) in a patient with a rectal core temperature of 26.7°C (80.1°F). ECG courtesy of Heather Murphy-Lavoie of Charity Hospital, New ....
Atrial and ventricular arrhythmias can result from hypothermia; asystole and ventricular fibrillation have been noted to begin spontaneously at core temperatures below 25-28°C.
Hypothermia progressively depresses the CNS, decreasing CNS metabolism in a linear fashion as the core temperature drops. At core temperatures less than 33°C, brain electrical activity becomes abnormal; between 19°C and 20°C, an electroencephalogram (EEG) may appear consistent with brain death. Tissues have decreased oxygen consumption at lower temperatures; it is not clear whether this is due to decreases in metabolic rate at lower temperatures or a greater hemoglobin affinity for oxygen coupled with impaired oxygen extraction of hypothermic tissues.
The term "core temperature after drop" refers to a further decrease in core temperature and associated clinical deterioration of a patient after rewarming has been initiated. The current theory of this documented phenomenon is that as peripheral tissues are warmed, vasodilation allows cooler blood in the extremities to circulate back into the body core. Other mechanisms may be in operation as well. Some believe that after drop is most likely to occur in patients with frostbite or long-standing hypothermia.
Accurately estimating the incidence of hypothermia is impossible, as hospital encounters only represent the "tip of the iceberg" in that they reflect the more severe cases. Even so, the number of emergency department encounters for hypothermia is growing, as ever-growing numbers of people take to the outdoors in search of adventure. Hypothermia is also a disease of urban settings. Societal problems with alcoholism, mental illness, and homelessness create a steady stream of these cases to inner-city hospitals. Although most cases occur in regions of the country with severe winter weather, other areas with milder climates also experience cases on a regular basis. This is especially true in milder climates that experience rapid climate changes either due to seasonal changes or day-to-night changes secondary to altitude. According to current data, states with the highest overall death rates for hypothermia are Alaska, New Mexico, North Dakota, and Montana.
The greatest number of cases of hypothermia occur in an urban setting and are related to environmental exposure attributed to alcoholism, illicit drug use, or mental illness, often exacerbated by concurrent homelessness. This is simply due to the fact that more people are found in the urban regions rather than rural areas.
A second affected group includes people in an outdoor setting for work or pleasure, including hunters, skiers, climbers, boaters/rafters, and swimmers.
The US Centers for Disease Control and Prevention (CDC) report the following statistics for deaths by excessive natural cold in the period 1999-2011 :
The overall mortality rate from hypothermia is similar between men and women. Because of a higher incidence of exposure among males, men account for 65% of hypothermia-related deaths.
Very young and elderly persons are at increased risk and may present to the emergency department with symptoms that are not clinically obvious or specific for hypothermia, such as altered mental status.
Older patients appear to be more likely to present with chronic or secondary hypothermia. Half of the recorded deaths from accidental hypothermia occurred in individuals older than 65 years.
The risk of morbidity and mortality depends on the severity of the degree of hypothermia and the underlying cause. Recovery is usually complete for previously healthy individuals with mild or moderate hypothermia (mortality rate < 5%). The mortality rate for patients with severe hypothermia, especially with preexisting illness, may be higher than 50%.
According to one study, overall in-patient mortality in hypothermic patients was 12%. Most people tolerate mild hypothermia (32-35°C body temperature) fairly well, which is not associated with significant morbidity or mortality. In contrast, a multicenter survey found a 21% mortality rate for patients with moderate hypothermia (28-32°C body temperature). Mortality is even higher in severe hypothermia (core temperature below 28°C). Despite hospital-based treatment, mortality from moderate or severe hypothermia approaches 40%. Patients experiencing concurrent infection account for most deaths due to hypothermia. Other comorbidities associated with higher mortality rates include homelessness, alcoholism, psychiatric disease, and advanced age.
"Indoor hypothermia" is more likely to occur in patients with significant medical comorbidities (alcoholism, sepsis, hypothyroidism/hypopituitarism) and tends to carry worse outcomes than exposure hypothermia.
According to current records, approximately 700 people die in the United States from accidental primary hypothermia each year.
For patient education resources, see the First Aid and Injuries Center. Also, see the patient education article Hypothermia.
Hypothermia is usually readily apparent in the setting of severe environmental exposure. In elderly patients or "indoor" patients, or for a patient—particularly a wet patient, with exposure to less extreme cold, the history may be subtle and less obvious. These patients may have a higher mortality rate secondary to a longer time to diagnosis and increased age and fragility. Mild or moderate hypothermia can present with misleading symptoms, such as confusion, dizziness, chills, or dyspnea.
A patient's companions often note initial symptoms in the field. Symptoms can include mood change, irritability, poor judgment, and lassitude. Companions may note the patient to demonstrate paradoxical undressing (a severely hypothermic person removes clothing in response to prolonged cold stress) or rhythmic or repeated motions such as rocking. Slurred speech and ataxia may mimic a stroke, alcohol intoxication, or high-altitude cerebral edema. Similarly, profound hypothermia may present as coma or cardiac arrest.
In an urban environment, the use of alcohol or illicit drugs, overdose, psychiatric emergency, and major trauma all are associated with an increased risk of hypothermia.
The key to establishing a diagnosis of hypothermia is rapid determination of true core temperature. In the emergency department, core temperature is best measured using a low-reading temperature probe in the bladder or rectum or an esophageal probe. In the field, core temperature may be more difficult to establish reliably. A special low-reading thermometer can be used orally or rectally, but it may not reflect a true core temperature. Care should be taken not to rely on a temperature from a rectal thermometer lodged in stool because an inaccurately low core temperature can be recorded; the probe's reading will also lag behind the core temperature during rewarming. Additionally, a thermometer may become dislodged; be suspicious if a core temperature reading is identical to the room temperature.
Obtaining a core temperature may help prevent erroneous diagnosis for patients with an altered mental status due to stroke, drug overdose, alcohol intoxication, or mental illness. Standard temperature measuring devices commonly used for triage may lack the capability to report unusually low temperature; obtain a core temperature reading for any patient suspected of being significantly hypothermic.
At a given temperature, specific physical examination findings vary among patients. However, an examination does provide a frame of reference for dividing presenting symptoms into mild, moderate, and severe hypothermic signs.
Between 34°C and 35°C, most people shiver vigorously, usually in all extremities.
As the temperature drops below 34°C, a patient may develop altered judgment, amnesia, and dysarthria. Respiratory rate may increase.
At approximately 33°C, ataxia and apathy may be seen. Patients generally are stable hemodynamically and able to compensate for the symptoms.
In this temperature range, the following may also be observed: hyperventilation, tachypnea, tachycardia, and cold diuresis as renal concentrating ability is compromised.
Oxygen consumption decreases, and the CNS depresses further; hypoventilation, hyporeflexia, decreased renal flow, and paradoxical undressing may be noted.
Most patients with temperatures of 32°C or lower present in stupor.
As the core reaches temperatures of 31°C or below, the body loses its ability to generate heat by shivering.
At 30°C, patients develop a higher risk for arrhythmias. Atrial fibrillation and other atrial and ventricular rhythms become more likely. The pulse continues to slow progressively, and cardiac output is reduced. J wave may be seen on ECG in moderate hypothermia.
Between 28°C and 30°C, pupils may become markedly dilated and minimally responsive to light, a condition that can mimic brain death.
At 28°C, the body becomes markedly susceptible to ventricular fibrillation and further depression of myocardial contractility.
Below 27°C, 83% of patients are comatose.
Pulmonary edema, oliguria, coma, hypotension, rigidity, apnea, pulselessness, areflexia, unresponsiveness, fixed pupils, and decreased or absent activity on EEG are all seen.
Several etiologies related to endocrine derangements may cause decreased heat production. These include hypopituitarism, hypoadrenalism, and hypothyroidism. Consider all these conditions in patients presenting with unexplained hypothermia who fail to rewarm with standard therapy.
Other causes include severe malnutrition or hypoglycemia and neuromuscular inefficiencies seen in the extremes of age.
This category includes accidental hypothermia due to both immersion etiologies and nonimmersion etiologies and is the most common form of hypothermia encountered in the emergency department.
Patients may present with induced vasodilatation from pharmacologic or toxicologic agents.
Hypothermia due to increased heat loss can occur in conditions with erythroderma, such as burns or psoriasis, which decrease the body's ability to preserve heat. In addition, iatrogenic etiologies, such as cold infusions, overenthusiastic treatment of heatstroke, or emergency deliveries, may cause hypothermia due to increased heat loss.
A variety of causes may be associated with impaired thermoregulation, but, generally, it is associated with failure of the hypothalamus to regulate core body temperature.
This may occur with CNS trauma, strokes, toxicologic and metabolic derangements, intracranial bleeding, Parkinson disease, CNS tumors, Wernicke disease, and multiple sclerosis.
Miscellaneous causes include sepsis, multiple trauma, pancreatitis, prolonged cardiac arrest, and uremia.
Hypothermia may be related to drug administration; such medications include beta-blockers, clonidine, meperidine, neuroleptics, and general anesthetic agents. Ethanol, phenothiazines, and sedative-hypnotics also reduce the body’s ability to respond to low ambient temperatures.
Arterial blood gas determination includes the following:
Many hypothermic patients are volume contracted because of cold diuresis. As a result, hematocrit level may be deceptively high. Hematocrit levels may increase 2% for each 1°C drop in core temperature.
Hypothermia may present with wide fluctuations in electrolytes, and no clear trend or predictability exists as to when a patient's electrolytes will be abnormal or how large swings may be. Plasma potassium levels can be useful in evaluating prognosis. A level of 10 mmol/L or greater is associated with a very low likelihood of recovery. Classic ECG changes of hyperkalemia may be absent or diminished. Chronic hypothermia occasionally can lead to hypokalemia.
Acute hypothermia can result in hyperglycemia, while chronic hypothermia or secondary hypothermia may present with low blood glucose level.
The body's coagulation mechanism is often disrupted in moderate or severe hypothermia, and a disseminated intervascular coagulation–type syndrome can be present.
Coagulopathy has several causes. The primary issue is disruption of enzymatic reactions of the clotting cascade caused by protein denaturization at decreased temperature.
Because the kinetic tests of coagulation are performed at 37°C in the laboratory, a clinically evident coagulopathy may not be reflected by deceptively normal laboratory values.
A chest radiograph is indicated in patients with hypoxia. Aspiration pneumonia and pulmonary edema are common findings.
Patients with trauma or altered mental status of indeterminate cause may need a noncontrast head CT scan and further imaging for a standard trauma evaluation.
The ECG may show prolonged PR, QRS, and QT intervals, and atrial or ventricular arrhythmias. The length and height of the respective QT-interval prolongation and characteristic J (Osborne) waves are often proportional to the degree of hypothermia.
Prehospital management focuses on preventing further heat loss, rewarming the body core temperature, and avoiding precipitating ventricular fibrillation or another malignant cardiac rhythm. This should be the preeminent concern. Conscious patients can develop ventricular fibrillation suddenly; prehospital workers, particularly those operating in remote search-and-rescue operations, should avoid inadvertent jerky movement of severely hypothermic patients. Patients who develop hypothermia-induced dysrhythmia in the field may be beyond resuscitation. How the hypothermic heart deteriorates into the rhythm of ventricular fibrillation remains under debate.
Patients developing hypothermia from cold-water immersion appear to be at high risk of ventricular fibrillation; rescuers probably are justified in instructing such patients to minimize motion and to await careful extrication.
Anecdotal reports of sudden cardiac death associated with tracheal intubation appear to be exaggerated, particularly if a patient is adequately preoxygenated.
Both cardiac pacing and atropine are generally ineffective for bradyarrhythmia.
Lidocaine is ineffective in preventing hypothermia-induced ventricular dysrhythmias.
Many authors have advocated prophylactic bretylium in cases of severe hypothermia when spontaneous conversion to ventricular fibrillation is possible.[6, 7] This recommendation was due to limited success of such therapy both in controlled animal studies and in anecdotal human reports. A 2014 review makes no recommendation regarding bretylium or other antidysrhythmics, owing to inadequate evidence. Cardiac dysrhythmias begin to develop at a core temperature of 30°C. Ventricular fibrillation susceptibility is greatest below the core temperature of 22°C. Bretylium (5 mg/kg initially) has been recommended by some authors for any hypothermic patient manifesting significant new ventricular ectopy or frank dysrhythmia. However, bretylium has been discontinued by all manufacturers resulting in a worldwide shortage and has been unavailable to many centers since 1999. The optimal dosage and ideal infusion rate for bretylium are unknown. Whether bretylium is effective for prophylaxis in patients with core temperatures below 30°C is also unknown.
To prevent cardiac dysrhythmia with continued hypothermia, rescuers or paramedics should attempt rewarming in the field. (A notable exception would be isolated frostbite injury in which limb rewarming would preclude self-rescue because of pain.) Gently place patients in an environment most favorable to reducing further heat loss from evaporation, radiation, conduction, or convection. Remove wet clothing, and replace it with dry blankets or sleeping bags. Initiate active external rewarming with heat packs (eg, hot water bottles, chemical packs) placed in the axillae, on the groin, and on the abdomen. Be aware of the risk of causing body surface burns from exuberant active external rewarming. In dire circumstances, rescuers may provide skin-to-skin contact with patients when heat packs are unavailable and such therapy would not delay evacuation.
Ventricular fibrillation in a cold patient is a desperate event. Generally, defibrillation is ineffective at hypothermic core temperatures and when equipment for heroic attempts at resuscitation is unavailable. In such circumstances, attempt a round of chemical conversion with intravenous bretylium (if available), followed by extended cardiopulmonary resuscitation (CPR) until rescuers can begin active rewarming and perform successful defibrillation.
Patients with respiratory failure should be endotracheally intubated and placed on a mechanical ventilator. Intubation and insertion of vascular catheters should not be delayed but performed gently while closely monitoring cardiac rhythm for ventricular fibrillation.
Measure core temperatures using a low-reading esophageal, rectal, or bladder thermometer. Tympanic thermometers are unreliable in a setting of profound hypothermia and should not be used. If using a rectal probe, insertion into stool can yield falsely low readings.
Determine whether a cold patient is profoundly or mildly hypothermic. Profoundly hypothermic patients present with stupor or cardiac dysrhythmia (regardless of the recorded temperature) and a core temperature of 30°C or lower. Mildly hypothermic patients may be rewarmed in any available manner (eg, warm blankets, removal of cold, wet clothing) since their risk for cardiac dysrhythmia is low. Surface rewarming is adequate in these cases, but it is ineffective in very low body temperatures and carries an additional risk of temperature after drops and shock secondary to peripheral vasodilation.
Remove any wet clothing, and replace it with warm, dry materials.
Profound hypothermia is a true emergency, warranting the same resource-intensive resuscitation as myocardial infarction. Direct treatment at maintaining or restoring cardiac perfusion; maximizing oxygenation is indicated for a prolonged period of time until the core temperature is at least 32°C.
Do not attempt resuscitation on the patient with a frozen chest where compressions are not possible.
Gingerly handle patients identified with profound hypothermia, and take immediate measures to prevent degeneration of cardiac activity into malignant dysrhythmia.
Profoundly hypothermic patients who demonstrate cardiac ectopy may be ideal candidates for bretylium, if available. Administer an initial dose of 5 mg/kg IV (repeated at 10 mg/kg, as needed) to prevent ventricular fibrillation. Lidocaine is ineffective for treatment of hypothermia-induced dysrhythmias. While no randomized human trials have been reported, at least 4 animal trials and 2 human case reports support using bretylium for any patient with profound hypothermia. Based on such evidence, the US Wilderness Emergency Medical Services Institute recommends using empiric bretylium for profound hypothermia.
Initiate warmed, humidified oxygen; provide heated intravenous saline; and place warmed blankets or heat lamps around a hypothermic patient.
Although many texts suggest that intravenous fluids be heated to 45°C, this temperature choice is based on convenience of previous study designs rather than any hard evidence. A trial using fluids heated to 65°C demonstrated more efficacy in treating severe hypothermia. Emergency departments that routinely treat hypothermia can keep blankets and intravenous fluid bags in a shared heater. In urgent situations, intravenous fluids that contain no dextrose or blood can be heated in a microwave oven. Once these simple measures have been applied, consider more difficult rewarming therapies.
A patient who is not becoming progressively colder, is conscious, and has a perfusing cardiac rhythm may not require intensive intervention beyond the methods already discussed.
Debate centers on interventions for patients who are worsening, are comatose, have nonperfusing rhythms, or appear dead. Most texts advocate aggressive therapy for severely hypothermic patients, basing the recommendation on anecdotal reports of success.
Researchers recently confirmed justification for aggressive treatment in a 16-year longitudinal review of profound hypothermia. In this series of 32 Swiss patients presenting with hypothermia and cardiac arrest, 15 patients were resuscitated with aggressive techniques, and all 15 patients showed full neurologic recovery.
In an older review, rewarming at rates faster than 2°C/h was noted to reduce mortality when compared with slower rates.
An optimal warming strategy is elusive. Some have postulated that rapidly warming a patient to 33°C and maintaining him or her at that temperature, using hypothermia therapeutically as though he or she was a cardiac arrest patient might be beneficial.
Optimal rewarming techniques depend on a patient's condition, the capabilities of providers, and the availability of in-hospital care and warming devices. If core body temperature does not respond to warming efforts, underlying infection or endocrine derangements must be considered.
For simplicity, aggressive rewarming methods can be categorized as slow, moderate, or rapid. Slow rewarming provides heat from 17-30 kcal/h, corresponding to increasing temperature by 0.3-1.2°C/h. (Comparisons are somewhat difficult since different study groups used different measurements of heat gain.) Slow rewarming methods include IV solutions heated to 45°C (17 kcal/h); heated, humidified oxygen by mask (30 kcal/h or 0.7°C/h); warmed blankets (0.9°C/h); and heated, humidified oxygen via endotracheal tube (1.2°C/h). If intact, a patient's endogenous physiologic mechanisms (other than shivering) provide similar rates of rewarming (30 kcal/h).
Moderate rewarming methods provide heat at approximately 3°C/h. Methods include warmed gastric lavage (2.8°C/h), intravenous solutions heated to 65°C (2.9°C/h), and peritoneal lavage with 45°C fluid at 4 L/h (70 kcal/h or 3°C/h).
Rapid rewarming methods provide heat at levels higher than 100 kcal/h. Methods include thoracic lavage at 500 mL/min (6.1°C/h), cardiopulmonary bypass (400 kcal/h or 18°C/h), thoracic lavage at 2 L/min (19.7°C/h), ECMO, and AV dialysis (1-4 degrees per hour, and warm-water immersion [1500 kcal/h]).
In comparison, endogenous shivering provides rewarming at a rate of 300 kcal/h. No noninvasive technique rewarms as rapidly as full-body immersion in warm water. Known as the Hubbard tank technique, immersion has successfully rewarmed humans with severe hypothermia. Important, however, the effectiveness of warm water baths for hypothermic patients is controversial. Immersion in warm water was not recommended by a 2014 expert panel review because of concerns for core temperature afterdrop and the risk of cardiovascular collapse.
Defibrillation also is difficult; however, defibrillation is likely futile once a patient's core temperature falls below 30°C.
Initiate CPR for hypothermic patients who deteriorate into ventricular fibrillation. These patients also warrant immediate weight-based defibrillation (2 J/kg), along with prompt administration of high-dose bretylium (10 mg/kg).
Consider initiating cardiopulmonary bypass for any case of ventricular fibrillation or profound hypothermia with deterioration. Patients with this degree of hypothermia have optimized outcomes with procedures such as cardiopulmonary bypass and pleural lavage. However, these methods are invasive, often unavailable, and infrequently used and as such are subject to user-inexperience.
Ventricular fibrillation should be treated immediately with defibrillation, despite the fact that most other dysrhythmias will correct with warming alone. If initial attempts at defibrillation are unsuccessful, further attempts at defibrillation and antiarrhythmic intravenous medications should be held until the patient is warmed to above 30°C. During this interval, basic life support is continued. If ventricular fibrillation persists despite rewarming, current AHA guidelines recommend administration of amiodarone.[9, 10]
Although studies in emergency medicine are lacking, cardiothoracic surgeons who induce hypothermia to perform open-heart procedures rewarm patients on a daily basis using open cardiac massage with warmed saline solution. Therefore, a desperate case of severe hypothermia may warrant consideration of direct cardiac rewarming via open emergency department thoracotomy with open cardiac massage.
Cardiothoracic bypass has been used successfully to treat cases of hypothermia presenting in cardiac arrest. To be successful, bypass must be performed rapidly. If a delay is expected, the physician can expedite bypass during an interim period by placing cordis catheters in the patient's femoral vein and artery. Groin cutdowns may be necessary to facilitate such placement; if cutdowns are needed, perform them without hesitation. If bypass is unavailable or delayed, 2 previously described methods of internal rewarming are available: heated thoracic lavage and arteriovenous (AV) heated countercurrent exchange.
Extracorporeal membrane oxygenation (EMCO) blood rewarming is available in some emergency departments in Europe and may become a viable alternative to other methods of cardiopulmonary bypass if emergency physicians become proficient in their use. If available, venoarterial ECMO is preferred to other methods of bypass because it provides blood oxygenation with circulation.
The literature describes 2 methods of thoracic lavage; the simplest method uses available equipment and provides rewarming rates equivalent to cardiopulmonary bypass.
The technique involves placing 2 left-sided, 38 French chest tubes (third intercostal space midclavicular line and sixth intercostal space midaxillary line). Isotonic saline, in 3-liter bags heated to at least 41°C, is infused through the anterior tube at 2 L/min, then drained by gravity via the posterior tube. When warmed saline was not available, physicians successfully infused warmed tap water.
The AV heating method, developed at the University of Washington, uses a modified bypass technique for rapid blood rewarming using a level one fluid warmer that is familiar to physicians experienced in trauma resuscitation. The treatment is preferred for patients with profound hypothermia and markedly depressed hemodynamic status or cardiac arrest. AV heating requires a spontaneous pulse, since the patient's intrinsic blood pressure drives flow through the countercurrent module. (In true cardiothoracic bypass, an external pump is built into the machine.) Catheters are placed into the femoral artery and venous cordis.
Once catheters are placed, the arterial output is connected to the inflow port of a level one countercurrent warmer, where intravenous fluids are connected. The outflow port is connected to the femoral venous catheter. Water is circulated, at a temperature preset on the level one device, around the blood-containing tubing; the blood warms as it flows through the countercurrent module. The AV method has rewarmed profoundly hypothermic patients 5 times more rapidly (39 min vs 199 min) than standard methods and was demonstrated to decrease the mortality rate.
In an alternative endovascular warming technique, a catheter is advanced into the inferior vena cava and circulates warmed fluids. The catheter acts as indwelling radiator as it is connected to an esophageal temperature probe and uses a feedback loop to attain and maintain programmed patient temperature. By this method, the core body temperature may be elevated at a rate of 3 degrees an hour. Additionally, it is an invasive technique to raise core temperature that utilizes skills that emergency physicians are already well trained and comfortable with.
Vasodilation increases the vascular space; consequently, patients that have been hypothermic for more than 45-60 minutes often require fluid administration. Hypotension should be addressed with volume resuscitation; inotropic agents, such as dopamine, should be avoided unless the hypotension is refractory to intravenous fluids due to the possible cardiac stimulation/ectopy that pressors may induce.
Probes for pulse oximetry placed on the ears or the forehead appear to be less influenced by the peripheral vasoconstriction of the digits associated with decreased body temperature.
Assessment should include a total body survey to exclude local cold-induced injuries.
Controversy surrounds the issue of pronouncing death in a hypothermic patient.
A reasonable approach is to initiate resuscitation on all hypothermic patients unless a patient presents with a frozen chest or other obvious nonsurvivable injuries. A patient can be warmed aggressively and resuscitated until the core temperature rises above 32°C. At that juncture, if no signs of life are present and the patient is not responding to advanced cardiac life support measures, termination of resuscitation may be indicated.
Individual clinical judgment is paramount in these settings, and variables, such as the patient's age and any comorbid conditions, must be taken into account. Serum potassium levels may be useful in determining when to cease resuscitation; patients with potassium levels of 10 mmol/L or higher have very poor outcomes.
Clearly, profound hypothermia can mimic clinical death. However, patients with profound hypothermia can be resuscitated successfully with good neurologic outcomes. The adage that "a patient is not dead until they are warm and dead" is of some use.
In some cases, prologed efforts to bring a patient with no signs of life to a normal body temperature canbe futile. If a patient's chest is frozen, resuscitative efforts are not necessary.
Medical complications from hypothermia often result and necessitate admission to the hospital in moderate and severe hypothermia. Severely hypothermic patients should be admitted to an intensive care unit where their respiratory and cardiac function and temperature may be closely monitored.
Acute pulmonary edema should be treated with oxygen, empirical antibiotics for aspiration pneumonia, and diuretics as necessary. In special cases where ECMO is initiated, pulmonary edema can be concurrently treated while the patient is being rewarmed.
Frostbite and other localized cold injuries result in deep tissue damage. Surgical exploration and debridement may be necessary. Affected body parts may have to be amputated if gangrene develops. Such a procedure is usually performed at some delayed time interval once a line of demarkation has declared itself days to weeks later.
The development of rhabdomyolysis should be monitored.
Complications of hypothermia are as follows:
Complications of treatment of hypothermia are as follows:
Preparation is key to avoiding accidental hypothermia. Appropriate cold weather clothing and survival bags are a necessity if walking or climbing in a cold climate.
Persons should avoid alcohol if anticipating exposure to cold because alcohol can disrupt temperature homeostasis by causing vasodilation. Individuals should remain alert to early symptoms and initiate preventive measures (eg, drinking warm fluids).
Adequate heat in the home should be maintained. Patients should be referred to a social service agency for help with adequate housing, heat, and/or clothing.
The goals of pharmacotherapy are to reduce morbidity and prevent complications.
Clinical Context: Amiodarone has antiarrhythmic effects that overlap all four Vaughn-Williams antiarrhythmic classes. It has a low risk of proarrhythmia, and any proarrhythmic reactions generally are delayed. It is used in patients with structural heart disease.
These agents may be used when ventricular fibrillation persists despite rewarming; current American Heart Association guidelines recommend it.