Hypothermia

Hypothermia

Author: James Li, MD; Chief Editor: Joe Alcock, MD, MS more...

Updated: Aug 25, 2014

Background

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).[1] Primary hypothermia is due to environmental exposure, with no underlying medical condition causing disruption of temperature regulation.[2] 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 Orleans.

Pathophysiology

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.[3] 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 Orleans.

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.

Epidemiology

Frequency

United States

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[4] :

Total deaths: 16,911

Average deaths per year: 1,301

Highest yearly total: 1,536 (2010)

Lowest yearly total: 1,058 (2006)

Approximately 67% were among males

Mortality/Morbidity

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.

Sex

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.

Age

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.

Contributor Information and Disclosures

Author

James Li, MD Former Assistant Professor, Division of Emergency Medicine, Harvard Medical School; Board of Directors, Remote Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

Wyatt Decker, MD Vice President and Chief Executive Officer, Mayo Clinic Campus, Arizona

Wyatt Decker, MD is a member of the following medical societies: American College of Emergency Physicians

Disclosure: Nothing to disclose.

Mark A Silverberg, MD MMB, FACEP, Assistant Professor, Associate Residency Director, Department of Emergency Medicine, State University of New York Downstate College of Medicine; Consulting Staff, Department of

Emergency Medicine, Staten Island University Hospital, Kings County Hospital, University Hospital, State University of New York Downstate Medical Center

Mark A Silverberg, MD is a member of the following medical societies: American College of Emergency Physicians, Society for Academic Emergency Medicine, Council of Emergency Medicine Residency Directors, American Medical Association

Disclosure: Nothing to disclose.

Jamie Alison Edelstein, MD Staff Physician, Department of Emergency Medicine, State University of New York, Kings County Hospital Center

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment.

James Steven Walker, DO, MS Clinical Professor of Surgery, Department of Surgery, University of Oklahoma College of Medicine

James Steven Walker, DO, MS is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Osteopathic Emergency Physicians, American Osteopathic Association

Disclosure: Nothing to disclose.

Chief Editor

Joe Alcock, MD, MS Associate Professor, Department of Emergency Medicine, University of New Mexico Health Sciences Center

Joe Alcock, MD, MS is a member of the following medical societies: American Academy of Emergency Medicine

Disclosure: Nothing to disclose.

Additional Contributors

Dan Danzl, MD Chair, Professor, Department of Emergency Medicine, University of Louisville Hospital

Dan Danzl, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, Kentucky Medical Association, Society for Academic Emergency Medicine, Wilderness Medical Society

Disclosure: Nothing to disclose.

References

1.Polderman KH. Mechanisms of action, physiological effects, and complications of hypothermia. Crit Care Med. 2009 Jul. 37(7 Suppl):S186-202. [Medline].

2.Long WB 3rd, Edlich RF, Winters KL, Britt LD. Cold injuries. J Long Term Eff Med Implants. 2005. 15(1):67-78. [Medline].

3.Sessler DI. Thermoregulatory defense mechanisms. Crit Care Med. 2009 Jul. 37(7 Suppl):S203-10. [Medline].

4.Centers for Disease Control and Prevention. Number of Hypothermia-Related Deaths, by Sex - National Vital Statistics System, United States, 1999–2011. Available at http://www.cdc.gov/mmwr/preview/mmwrhtml /mm6151a6.htm. Accessed: August 22, 2014.

5.McCullough L, Arora S. Diagnosis and treatment of hypothermia. Am Fam Physician. 2004 Dec 15. 70(12):2325-32. [Medline].

6.Buckley JJ, Bosch OK, Bacaner MB. Prevention of ventricular fibrillation during hypothermia with bretylium tosylate. Anesth Analg. 1971 Jul-Aug. 50(4):587-93. [Medline].

7.Murphy K, Nowak RM, Tomlanovich MC. Use of bretylium tosylate as prophylaxis and treatment in hypothermic ventricular fibrillation in the canine model. Ann Emerg Med. 1986 Oct. 15(10):1160-6. [Medline].

8.[Guideline] ECC Committee, Subcommittees and Task Forces of the American Heart Association. 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2010 Nov. 122(18):Suppl 3.

9.Brown DJ, Brugger H, Boyd J, Paal P. Accidental hypothermia. N Engl J Med. 2012 Nov 15. 367(20):1930-8. [Medline].

10.Boué Y, Payen JF, Brun J, Thomas S, Levrat A, Blancher M, et al. Survival after avalanche-induced cardiac arrest. Resuscitation. 2014 Sep. 85(9):1192-6. [Medline].

11.Laniewicz M, Lyn-Kew K, Silbergleit R. Rapid endovascular warming for profound hypothermia. Ann Emerg Med. 2008 Feb. 51(2):160-3. [Medline].

12.Abella BS, Rhee JW, Huang KN, Vanden Hoek TL, Becker LB. Induced hypothermia is underused after resuscitation from cardiac arrest: a current practice survey. Resuscitation. 2005 Feb. 64(2):181-6. [Medline].

13.Alam HB, Rhee P, Honma K, et al. Does the rate of rewarming from profound hypothermic arrest influence the outcome in a swine model of lethal hemorrhage?. J Trauma. 2006 Jan. 60(1):134-46. [Medline].

14.Casas F, Alam H, Reeves A, Chen Z, Smith WA. A portable cardiopulmonary bypass/extracorporeal membrane oxygenation system for the induction and reversal of profound hypothermia: feasibility study in a Swine model of lethal injuries. Artif Organs. 2005 Jul. 29(7):557-63. [Medline].

15.Elbaz G, Etzion O, Delgado J, Porath A, Talmor D, Novack V. Hypothermia in a desert climate: severity score and mortality prediction. Am J Emerg Med. 2008 Jul. 26(6):683-8. [Medline].

16.Headdon WG, Wilson PM, Dalton HR. The management of accidental hypothermia. BMJ. 2009 Jun 10.

338:b2085. [Medline].

17.Jurkovich GJ. Environmental cold-induced injury. Surg Clin North Am. 2007 Feb. 87(1):247-67, viii. [Medline].

18.Launay JC, Savourey G. Cold adaptations. Ind Health. 2009 Jul. 47(3):221-7. [Medline].

19.Schewe JC, Heister U, Fischer M, Hoeft A. [Accidental urban hypothermia. Severe hypothermia of 20.7 degrees C]. Anaesthesist. 2005 Oct. 54(10):1005-11. [Medline].

20.Spencer SM, Roeseler J, Verschuren F, Reynaert M, Thys F. Metabolism study in an 88-year-old woman with severe hypothermia during rewarming procedures. Am J Emerg Med. 2007 Oct. 25(8):986.e1-3. [Medline].

21.Windsor JS, Firth PG, Grocott MP, Rodway GW, Montgomery HE. Mountain mortality: a review of deaths that occur during recreational activities in the mountains. Postgrad Med J. 2009 Jun. 85(1004):316-21. [Medline].

Medscape Reference © 2011 WebMD, LLC

Hypothermia Clinical Presentation

Author: James Li, MD; Chief Editor: Joe Alcock, MD, MS more...

Updated: Aug 25, 2014

History

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.

Physical

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.[5]

Mild hypothermia (32-35°C)

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.

Moderate hypothermia (28-32°C)

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.

Severe hypothermia (< 28°C)

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.

Causes

Decreased heat production

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.

Increased heat loss

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.

Impaired thermoregulation

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.

Other causes

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.

Contributor Information and Disclosures

Author

James Li, MD Former Assistant Professor, Division of Emergency Medicine, Harvard Medical School; Board of Directors, Remote Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

Wyatt Decker, MD Vice President and Chief Executive Officer, Mayo Clinic Campus, Arizona

Wyatt Decker, MD is a member of the following medical societies: American College of Emergency Physicians

Disclosure: Nothing to disclose.

Mark A Silverberg, MD MMB, FACEP, Assistant Professor, Associate Residency Director, Department of Emergency Medicine, State University of New York Downstate College of Medicine; Consulting Staff, Department of Emergency Medicine, Staten Island University Hospital, Kings County Hospital, University Hospital, State University of New York Downstate Medical Center

Mark A Silverberg, MD is a member of the following medical societies: American College of Emergency Physicians, Society for Academic Emergency Medicine, Council of Emergency Medicine Residency Directors, American Medical Association

Disclosure: Nothing to disclose.

Jamie Alison Edelstein, MD Staff Physician, Department of Emergency Medicine, State University of New York, Kings County Hospital Center

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment.

James Steven Walker, DO, MS Clinical Professor of Surgery, Department of Surgery, University of Oklahoma College of Medicine

James Steven Walker, DO, MS is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Osteopathic Emergency Physicians, American Osteopathic Association

Disclosure: Nothing to disclose.

Chief Editor

Joe Alcock, MD, MS Associate Professor, Department of Emergency Medicine, University of New Mexico Health Sciences Center

Joe Alcock, MD, MS is a member of the following medical societies: American Academy of Emergency Medicine

Disclosure: Nothing to disclose.

Additional Contributors

Dan Danzl, MD Chair, Professor, Department of Emergency Medicine, University of Louisville Hospital

Dan Danzl, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, Kentucky Medical Association, Society for Academic Emergency Medicine, Wilderness Medical Society

Disclosure: Nothing to disclose.

References

1.Polderman KH. Mechanisms of action, physiological effects, and complications of hypothermia. Crit Care Med. 2009 Jul. 37(7 Suppl):S186-202. [Medline].

2.Long WB 3rd, Edlich RF, Winters KL, Britt LD. Cold injuries. J Long Term Eff Med Implants. 2005. 15(1):67-78. [Medline].

3.Sessler DI. Thermoregulatory defense mechanisms. Crit Care Med. 2009 Jul. 37(7 Suppl):S203-10. [Medline].

4.Centers for Disease Control and Prevention. Number of Hypothermia-Related Deaths, by Sex - National Vital Statistics System, United States, 1999–2011. Available at http://www.cdc.gov/mmwr/preview/mmwrhtml /mm6151a6.htm. Accessed: August 22, 2014.

5.McCullough L, Arora S. Diagnosis and treatment of hypothermia. Am Fam Physician. 2004 Dec 15. 70(12):2325-32. [Medline].

6.Buckley JJ, Bosch OK, Bacaner MB. Prevention of ventricular fibrillation during hypothermia with bretylium tosylate. Anesth Analg. 1971 Jul-Aug. 50(4):587-93. [Medline].

7.Murphy K, Nowak RM, Tomlanovich MC. Use of bretylium tosylate as prophylaxis and treatment in hypothermic ventricular fibrillation in the canine model. Ann Emerg Med. 1986 Oct. 15(10):1160-6. [Medline].

8.[Guideline] ECC Committee, Subcommittees and Task Forces of the American Heart Association. 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2010 Nov. 122(18):Suppl 3.

9.Brown DJ, Brugger H, Boyd J, Paal P. Accidental hypothermia. N Engl J Med. 2012 Nov 15. 367(20):1930-8. [Medline].

10.Boué Y, Payen JF, Brun J, Thomas S, Levrat A, Blancher M, et al. Survival after avalanche-induced cardiac arrest. Resuscitation. 2014 Sep. 85(9):1192-6. [Medline].

11.Laniewicz M, Lyn-Kew K, Silbergleit R. Rapid endovascular warming for profound hypothermia. Ann Emerg Med. 2008 Feb. 51(2):160-3. [Medline].

12.Abella BS, Rhee JW, Huang KN, Vanden Hoek TL, Becker LB. Induced hypothermia is underused after resuscitation from cardiac arrest: a current practice survey. Resuscitation. 2005 Feb. 64(2):181-6. [Medline].

13.Alam HB, Rhee P, Honma K, et al. Does the rate of rewarming from profound hypothermic arrest influence the outcome in a swine model of lethal hemorrhage?. J Trauma. 2006 Jan. 60(1):134-46. [Medline].

14.Casas F, Alam H, Reeves A, Chen Z, Smith WA. A portable cardiopulmonary bypass/extracorporeal membrane oxygenation system for the induction and reversal of profound hypothermia: feasibility study in a Swine model of lethal injuries. Artif Organs. 2005 Jul. 29(7):557-63. [Medline].

15.Elbaz G, Etzion O, Delgado J, Porath A, Talmor D, Novack V. Hypothermia in a desert climate: severity score and mortality prediction. Am J Emerg Med. 2008 Jul. 26(6):683-8. [Medline].

16.Headdon WG, Wilson PM, Dalton HR. The management of accidental hypothermia. BMJ. 2009 Jun 10. 338:b2085. [Medline].

17.Jurkovich GJ. Environmental cold-induced injury. Surg Clin North Am. 2007 Feb. 87(1):247-67, viii. [Medline].

18.Launay JC, Savourey G. Cold adaptations. Ind Health. 2009 Jul. 47(3):221-7. [Medline].

19.Schewe JC, Heister U, Fischer M, Hoeft A. [Accidental urban hypothermia. Severe hypothermia of 20.7 degrees C]. Anaesthesist. 2005 Oct. 54(10):1005-11. [Medline].

20.Spencer SM, Roeseler J, Verschuren F, Reynaert M, Thys F. Metabolism study in an 88-year-old woman with severe hypothermia during rewarming procedures. Am J Emerg Med. 2007 Oct. 25(8):986.e1-3. [Medline].

21.Windsor JS, Firth PG, Grocott MP, Rodway GW, Montgomery HE. Mountain mortality: a review of deaths that occur during recreational activities in the mountains. Postgrad Med J. 2009 Jun. 85(1004):316-21. [Medline].

Medscape Reference © 2011 WebMD, LLC

Hypothermia Differential Diagnoses

Author: James Li, MD; Chief Editor: Joe Alcock, MD, MS more...

Updated: Aug 25, 2014

Differential Diagnoses

Alcohol Toxicity

Barbiturate Toxicity

Benzodiazepine Toxicity

Carbon Monoxide Toxicity

Ethylene Glycol Toxicity

Gamma-Hydroxybutyrate Toxicity

Opioid Toxicity

Sedative-Hypnotic Toxicity

Stroke, Hemorrhagic

Stroke, Ischemic

Therapeutic Hypothermia

Ventricular Fibrillation in Emergency Medicine

Ventricular Tachycardia

Contributor Information and Disclosures

Author

James Li, MD Former Assistant Professor, Division of Emergency Medicine, Harvard Medical School; Board of Directors, Remote Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

Wyatt Decker, MD Vice President and Chief Executive Officer, Mayo Clinic Campus, Arizona

Wyatt Decker, MD is a member of the following medical societies: American College of Emergency Physicians

Disclosure: Nothing to disclose.

Mark A Silverberg, MD MMB, FACEP, Assistant Professor, Associate Residency Director, Department of Emergency Medicine, State University of New York Downstate College of Medicine; Consulting Staff, Department of Emergency Medicine, Staten Island University Hospital, Kings County Hospital, University Hospital, State University of New York Downstate Medical Center

Mark A Silverberg, MD is a member of the following medical societies: American College of Emergency Physicians, Society for Academic Emergency Medicine, Council of Emergency Medicine Residency Directors, American Medical Association

Disclosure: Nothing to disclose.

Jamie Alison Edelstein, MD Staff Physician, Department of Emergency Medicine, State University of New York, Kings County Hospital Center

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment.

James Steven Walker, DO, MS Clinical Professor of Surgery, Department of Surgery, University of Oklahoma College of Medicine

James Steven Walker, DO, MS is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Osteopathic Emergency Physicians, American Osteopathic Association

Disclosure: Nothing to disclose.

Chief Editor

Joe Alcock, MD, MS Associate Professor, Department of Emergency Medicine, University of New Mexico Health Sciences Center

Joe Alcock, MD, MS is a member of the following medical societies: American Academy of Emergency Medicine

Disclosure: Nothing to disclose.

Additional Contributors

Dan Danzl, MD Chair, Professor, Department of Emergency Medicine, University of Louisville Hospital

Dan Danzl, MD is a member of the following medical societies: American Academy of Emergency Medicine,

American College of Emergency Physicians, American Medical Association, Kentucky Medical Association, Society for Academic Emergency Medicine, Wilderness Medical Society

Disclosure: Nothing to disclose.

References

1.Polderman KH. Mechanisms of action, physiological effects, and complications of hypothermia. Crit Care Med. 2009 Jul. 37(7 Suppl):S186-202. [Medline].

2.Long WB 3rd, Edlich RF, Winters KL, Britt LD. Cold injuries. J Long Term Eff Med Implants. 2005. 15(1):67-78. [Medline].

3.Sessler DI. Thermoregulatory defense mechanisms. Crit Care Med. 2009 Jul. 37(7 Suppl):S203-10. [Medline].

4.Centers for Disease Control and Prevention. Number of Hypothermia-Related Deaths, by Sex - National Vital Statistics System, United States, 1999–2011. Available at http://www.cdc.gov/mmwr/preview/mmwrhtml /mm6151a6.htm. Accessed: August 22, 2014.

5.McCullough L, Arora S. Diagnosis and treatment of hypothermia. Am Fam Physician. 2004 Dec 15. 70(12):2325-32. [Medline].

6.Buckley JJ, Bosch OK, Bacaner MB. Prevention of ventricular fibrillation during hypothermia with bretylium tosylate. Anesth Analg. 1971 Jul-Aug. 50(4):587-93. [Medline].

7.Murphy K, Nowak RM, Tomlanovich MC. Use of bretylium tosylate as prophylaxis and treatment in hypothermic ventricular fibrillation in the canine model. Ann Emerg Med. 1986 Oct. 15(10):1160-6. [Medline].

8.[Guideline] ECC Committee, Subcommittees and Task Forces of the American Heart Association. 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2010 Nov. 122(18):Suppl 3.

9.Brown DJ, Brugger H, Boyd J, Paal P. Accidental hypothermia. N Engl J Med. 2012 Nov 15. 367(20):1930-8. [Medline].

10.Boué Y, Payen JF, Brun J, Thomas S, Levrat A, Blancher M, et al. Survival after avalanche-induced cardiac arrest. Resuscitation. 2014 Sep. 85(9):1192-6. [Medline].

11.Laniewicz M, Lyn-Kew K, Silbergleit R. Rapid endovascular warming for profound hypothermia. Ann Emerg Med. 2008 Feb. 51(2):160-3. [Medline].

12.Abella BS, Rhee JW, Huang KN, Vanden Hoek TL, Becker LB. Induced hypothermia is underused after resuscitation from cardiac arrest: a current practice survey. Resuscitation. 2005 Feb. 64(2):181-6. [Medline].

13.Alam HB, Rhee P, Honma K, et al. Does the rate of rewarming from profound hypothermic arrest influence the outcome in a swine model of lethal hemorrhage?. J Trauma. 2006 Jan. 60(1):134-46. [Medline].

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Medscape Reference © 2011 WebMD, LLC

Hypothermia Treatment & Management

Author: James Li, MD; Chief Editor: Joe Alcock, MD, MS more...

Updated: Aug 25, 2014

Prehospital Care

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 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 is due to the success of such therapy both in controlled animal studies and in anecdotal human reports. Note the following:

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) is recommended 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.

Although the optimal dosage and ideal infusion rate for bretylium are unknown, consider prophylactic bretylium for patients with core temperatures below 30°C.

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.) Note the following:

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, when heat packs are unavailable, rescuers can provide skin-to-skin contact with patients.

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.

Emergency Department Care

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, be careful not to insert it into stool.

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