Identifying and Managing Accidental Hypothermia

Learning Objectives

  • Explain the four different ways a body can lose heat.
  • Define the four stages of hypothermia and understand the assesment considerations.
  • Understand the treatment strategies for accidental hypothermia.

Key Terms

  • Conduction: Transfer of heat to a solid object or a liquid by direct contact.
  • Convection: Mechanism by which body heat is picked up and carried away by moving fluid currents.
  • Core body temperature: The temperature in the part of the body comprising the heart, lungs, brain and abdominal viscera.
  • Evaporation: The conversion of a liquid to a gas.
  • Hypothermia: Condition in which the core body temperature falls significantly below normal.
  • Radiation: Emission of heat in the form of electromagnetic energy.

Medic 15 is dispatched on a cold winter morning to the parking lot behind a local gas station for a third-party report of a subject down. You arrive to find a middle-age male lying supine on the ground with a stellate laceration on his forehead. He’s unresponsive, appears to be breathing slowly, is very pale and is noticeably cold to the touch. As you run through the ABCs (i.e., airway, breathing and circulation), you start to think about prioritizing the patient’s problems and how the cold might affect the patient.

Hypothermia

Hypothermia is commonly defined as a core temperature that’s less than 95 degrees F (35 degrees C).1 In emergency medicine, there are two general types of hypothermia: therapeutic hypothermia (i.e., the intentional use of hypothermia in post-cardiac arrest patients to optimize neurological recovery) and accidental hypothermia.

Accidental hypothermia, the focus of this article, is a common condition that carries the risk of substantial morbidity and mortality. It can either be a primary cause of death or contribute to making almost any other medical or traumatic condition worse. Consequently, it’s difficult to know how many deaths should be attributed to hypothermia each year in the United States, with estimates varying from 600 to more than 1,500.2-4 Always be aware of the possibility of hypothermia; it’s seen in all 50 states and during every month of the year.5

Heat Balance

The human body produces heat through metabolism and exercise. In order to maintain a constant temperature, that heat production must balance out the multiple ways in which the body can lose heat to the environment: conduction, convection, radiation and evaporation. (See Figure 1.)

In conduction, heat is lost from direct contact with a solid or liquid that’s colder than the patient’s body, such as when a patient is in cold water or has fallen and cannot get up from a cold tile floor. To stop conductive heat loss, simply insulate the patient from the cold medium. For example, replace their wet clothing with blankets or move them from the ground to the stretcher.

Convection is just an extension of conduction, when air or liquid heated by the patient’s body flows away and is replaced by colder matter. A blanket keeps a person warm by limiting convective heat loss-it traps a layer of air around the body that then gets warmed up by conduction. Limit convective heat loss with clothing and blankets, or by moving the patient into an ambulance or building.

Using a space blanket (known by many other names, including foil blanket, survival blanket and heat sheet), decreases heat loss due to radiation. Humans emit energy in the form of infrared light, a form of radiation, which doesn’t require physical contact to transfer heat. Under most conditions, radiation accounts for around 60% of lost heat.6 Even if special reflective blankets aren’t available, normal cloth can significantly decrease radiation losses.

The final mechanism of heat loss, evaporation, is most noticeable in the form of sweat. Even in colder temperatures, evaporation takes place in the respiratory system. This lost moisture is what appears as foggy breath. Though it’s more commonly an in-hospital intervention, evaporative heat loss can be limited by the administration of heated humidified oxygen.

Compensation for Heat Loss

In order to maintain a constant temperature in even mildly cold conditions, the body has multiple ways to increase the amount of heat that it produces. If fuel is available, the rate of metabolism increases and shivering generates heat via the rapid action of skeletal muscles.7 Since infants can’t shiver, they compensate by metabolizing brown fat (which is unique to infants) and entering a mildly hyperthyroid state.8

Perhaps the most important physiologic response to cold is vasoconstriction in the skin and extremities. Distal and superficial vasoconstriction serves two major purposes. First, it keeps more warm blood around the vital organs in the head and torso. Second, it insulates a larger portion of the blood supply from the cooling effect of running through the extremities and skin, each of which can dissipate heat by acting like a vehicle’s radiator.9

As a person gets cold, they also exhibit a standard set of behavioral responses to avoid hypothermia. These include seeking shelter, putting on warm clothes, consuming hot food and drink, engaging in physical activity (e.g., rubbing hands or arms to create friction, jumping in place), and changing position to minimize the amount of exposed skin (e.g., crouching, crossing arms over chest).8 Our unresponsive patient found outside is losing heat through all four mechanisms, and can’t act to protect himself from the cold.

 

Classification

Before discussing what hypothermia does to the body, it’s useful to be able to categorize its severity. The most common scheme1,10 recognizes four categories of hypothermia based on core temperature: mild (90-95 degrees F; 32-35 degrees C), moderate (82-90 degrees F; 28-32 degrees C), severe (68-82 degrees F; 20-28 degrees C), and profound (below 68 degrees F; below 20 degrees C). There are other systems,11 but memorization isn’t critical; general familiarity is more important.

Clinical management should be guided by the patient’s overall presentation, especially since the prehospital determination of core body temperature is often problematic. Although each category of hypothermia generally correlates with certain symptoms, the correspondence isn’t absolute.

Physiologic Effects of Hypothermia

Hypothermia affects every organ system of the human body. The central nervous system (CNS) is initially protected from hypothermia by the body’s autoregulatory mechanisms, as described previously, but the CNS becomes depressed as core temperature falls. Even in mild hypothermia, patients can experience slurred speech, confusion, impaired judgement and amnesia.12 As hypothermia worsens, patients progress from lethargic to comatose, their reflexes disappear, and the CNS stops regulating the cardiovascular system.

The cognitive symptoms are especially dangerous, since they prevent patients from taking the actions necessary to save themselves. The most extreme example of bizarre decision-making in hypothermia is paradoxical undressing. A significant number (more than 20% in one case series) of moderately to severely hypothermic patients begin to feel strangely warm and take off their clothes while still exposed to the elements.13

As tissue temperature drops, cellular metabolism slows down. A cold brain is sluggish and doesn’t function optimally, but it also requires less oxygen and metabolic fuel to stay alive. It’s been recognized for decades that hypothermia can slow the progression of anoxic brain injury.14

Targeted temperature management (TTM), also called therapeutic hypothermia, is now a standard part of in-hospital care for cardiac arrest patients who are comatose after return of spontaneous circulation. TTM has been shown to decrease mortality and improve functional recovery in these patients due to the protective effect of hypothermia on the brain. As of the latest guidelines, TTM isn’t recommended as part of prehospital care.15

The next two most important systems in terms of prehospital care are the cardiovascular and respiratory systems. In mild hypothermia, heart rate, cardiac output and systemic vascular resistance all increase. After this initial peak, there’s a roughly linear decrease in heart rate. At a core temperature of 82.4 degrees F (28 degrees C), the heart rate has usually decreased by about half. Because hypothermic bradycardia is a direct consequence of slowed cellular metabolism in the heart’s pacemaking centers, it’s often refractory to atropine.1 As hypothermia progresses, there are corresponding drops in blood pressure and cardiac output.

Many ECG changes are seen as a patient gets colder. Even in mild hypothermia, the PR, QRS and QTc intervals start becoming prolonged.16 The J wave (also called the Osborn wave or hypothermic hump) is a classic ECG finding associated with hypothermia. Though it’s the go-to electrical abnormality associated with hypothermia, it can be seen in other conditions like head injury and sepsis. J waves can be widespread and increase in size as temperature decreases.1 Since they occur at the beginning of the ST segment, it’s important to differentiate J waves from ST elevations. Generally, ECG acquisition and interpretation are difficult in the violently shivering patient and even the application of electrodes to frozen or near frozen skin can be difficult.

In moderate and severe hypothermia, almost any atrial or ventricular arrhythmia can be seen. Spontaneous v fib can be expected below 82.4 degrees F (28 degrees C), and asystole below 68 degrees F (20 degrees C).12 Cold myocardium is very sensitive to stress, including the physical shock of being moved around. Hypothermic patients should be handled and moved as gently as possible.17

The respiratory system responds to decreasing temperature in the same way as the cardiovascular system: initial tachypnea followed by a decline in function. Breathing slows, and in severe hypothermia the respiratory drive from the brainstem is shut down. Tissue stiffens as it cools, and this is particularly noticeable in the chest wall and lungs.1

A few other effects of hypothermia are important to the prehospital provider. In mild hypothermia, patients shiver in an attempt to generate heat. At core temperatures around 90 degrees F (32 degrees C), shivering becomes less effective.10 As temperature continues to drop, a patient will stop shivering completely. Mild and moderate hypothermia lead to diuresis, so patients can easily become dehydrated. Finally, hypothermia induces coagulopathy;12 in fact, hypothermia, coagulopathy and acidosis are known as the trauma triad of death.18

To stop conductive heat loss, insulate the patient from the cold by replacing their wet clothing with blankets or move them from the ground to the stretcher. AP Photo/Brennan Linsley

Special Populations

Patients at both extremes of age are especially vulnerable to the cold. Infants and the elderly have less physiologic reserve and decreased ability to ramp up heat production when needed.17 Elderly patients often have started to lose their ability to sense ambient temperature, which blunts their behavioral response to cold environments. In the winter, an older patient might be hypothermic simply from sitting for a long time in a home that’s just slightly too cold. Because of their decreased compensatory ability, this can happen in temperatures that wouldn’t even register as cold to rescuers coming into the house for a short time.

Be especially aware of conductive heat loss in immobile patients. A patient who falls and is unable to get up will lose significantly more heat to being in contact with the ground than they will to the air. Approximately half of hypothermia deaths in the U.S. each year involve patients who are 65 or older.3

Neonates have almost no defense against the cold, which is why warming is such an important part of neonatal resuscitation.19 Infants at least five days old have a few ways to metabolically compensate, but are still very prone to heat loss. Their high surface-to- volume ratio, lack of much subcutaneous tissue for insulation, and total lack of behavioral defenses combine to make infants very sensitive to ambient temperatures.1

Trauma patients are also very vulnerable to hypothermia. In various studies, hypothermia was found to be present in 29-66% of patients with major trauma. This is problematic, since hypothermia is associated with greater mortality and worse outcomes for patients who survive.20,21 There are multiple factors that contribute to the high incidence of hypothermia in this population. Injuries to the CNS, depressed levels of consciousness, burns, large open wounds and shock all disrupt the body’s ability to regulate temperature. Major trauma patients are also more likely than average to be immobile and exposed to the elements. If a patient isn’t fully stripped by EMS, they will have their clothes taken off at the hospital.

History, Exam & Diagnosis

There are two basic types of accidental hypothermia: primary and secondary. Primary hypothermia is caused by exposure to a cold environment, not underlying disease. Secondary hypothermia is due to a condition that either disrupts the body’s ability to properly regulate heat balance or decreases the body’s capacity to generate or conserve heat. There are many conditions that can contribute to secondary hypothermia. (See Table 1.) It’s often more difficult to recognize hypothermia than it is to treat it, and maintaining a high index of suspicion is very important.

The most obvious cases of hypothermia will be those in which the patient is found outside or in an unheated space in cold weather. Unfortunately, identifying hypothermia isn’t always so easy. Have a lower threshold for considering hypothermia if a patient has a history of any predisposing condition or falls into one of the special populations discussed earlier. Depending on their comorbidities and environment, patients can present with almost any chief complaint and also happen to have a low core temperature. In these cases, hypothermia can still contribute to morbidity and mortality. Since it’s straightforward to treat, makes almost any chief complaint worse and makes patients less comfortable, hypothermia should be sought out and treated whenever possible.

The oral and tympanic thermometers commonly carried on ambulances aren’t very reliable. Many thermometers don’t work below 93 degrees F (34 degrees C), so unless a crew is specially equipped it may not be possible to obtain a correct temperature.10 Rectal temperature is generally more accurate, but can be thrown off by the presence of cold or frozen feces. If available, an esophageal temperature probe can be used in the unresponsive and intubated patient.

As with every patient, assess level of consciousness and the need for airway management. In order to get a clinical idea of how hypothermic a patient is in the absence of an accurate core temperature, note signs that indicate moderate and severe cooling: mydriasis, difficulty with speech and memory, depressed vital signs, paradoxical undressing or other behavioral disturbances, and lack of shivering in somebody who’s obviously cold. Remember that sepsis can present with decreased temperature instead of fever.

The physical exam for potentially hypothermic patients should focus on obtaining an accurate set of vitals and identifying the most dangerous sequelae of hypothermia. Perform the exam in a warm area, and keep the patient as dry and covered as possible. In significantly hypothermic patients, pulse and respirations may be present but difficult to detect; they should be checked carefully for a full 60 seconds.22

Evaluate the patient’s vitals in relation to their approximate degree of hypothermia. For example, suppose our patient appears severely hypothermic and has a blood pressure of 128/72 mmHg. This might look normal, but is hypertensive in such a hypothermic patient. Critical causes of hypertension, such as head injury or drug use, should be considered.

Prehospital Treatment

If the patient is found to be in the water or on ice above a body of water, appropriately trained personnel should be dispatched for rescue. Water and ice rescue are very dangerous and shouldn’t be attempted without careful preparation, but a crew can throw flotation devices or ropes towards the patient from a safe location. Technical, mountain and wilderness rescue resources should be utilized as needed.

The first priority is to move the patient to an environment in which they’re no longer losing heat. Usually, this can be as simple as getting the patient into the back of the ambulance and making sure that the heat is turned up. Remove wet or cold clothing, since water conducts heat away 25 times faster than air,7 and cover the patient with blankets. Remember that overly rough care can shock cold myocardium into an arrhythmia, so moderately and severely hypothermic patients should be handled as gently as possible. Placement of an advanced airway isn’t likely to induce arrhythmia, and should be done without delay if indicated.22

For the patient with mild hypothermia (either by temperature or by having no concerning vitals or exam findings), passive rewarming with blankets and a heated ambulance compartment should suffice. When combined with removing wet clothing, these simple steps mitigate all four mechanisms of heat loss. Cardiac monitoring can be considered, and the administration of cold or room-temperature IV fluids should be avoided if possible.

For moderately and severely hypothermic patients, all of the above steps should be taken. If there are available options for active external rewarming, such as heating pads or warm forced air, they can be used. When using active external rewarming, make sure to frequently reassess the patient to avoid burns. Active rewarming should begin with the trunk and not the extremities. If the extremities are warmed first, distal vasodilation can cause the rapid return of cold blood to the heart. This can lead to a decrease in core temperature, called afterdrop. If permitted by local protocols and equipment, administer IV fluids warmed to 40-42 degrees C.10

Many arrhythmias can be seen in hypothermia, but most don’t need any treatment and disappear as the patient’s core temperature rises. The bradycardia that often accompanies hypothermia tends to be resistant to atropine since the low heart rate isn’t due to a specific problem with the sinoatrial or atrioventricular nodes.1

If the patient is found to be unresponsive, spend a full 60 seconds assessing for pulse and respirations; unnecessary chest compressions can easily send a profoundly hypothermic patient into a potentially lethal arrhythmia. Hypothermic cardiac arrest care should focus on excellent CPR while not exposing the patient to more heat loss than necessary. If the patient is in v fib, one shock and one round of medications should be delivered. It’s reasonable to delay further defibrillation attempts and medications until the patient is rewarmed to 86 degrees F (30 degrees C), since it’s long been suspected that these interventions are less effective on cold myocardium. It’s often useful to be in contact with medical command in these cases.23

Due to the neuroprotective effects of hypothermia, patients have survived long periods of CPR after hypothermic cardiac arrest. As the saying goes: A patient isn’t dead until they’re warm and dead. Patients have survived 6.5 hours of cardiac arrest, and from an initial core temperature of 58 degrees F (14.2 degrees C).24,25

The use of mechanical CPR devices can be very helpful to reduce rescuer fatigue and assure continuous high-quality chest compressions for the hours it may take to bring the hypothermic cardiac arrest patient back up to temperature for successful resuscitation or to be pronounced dead.

Return to Case

Not knowing the mechanism of injury, your crew places the patient in a cervical collar and logrolls him onto a long backboard before moving him to the stretcher and loading him into the rig. In the back of the ambulance, you turn up the heat while your partner places the patient on high-flow oxygen and connects the patient to the monitor. A quick glance at lead 2 shows atrial fibrillation at a rate of 28 bpm, and you palpate a correspondingly slow carotid pulse.

During the eight-minute transport time to the closest trauma center, you place an IO in the left tibia and begin to infuse a saline bolus per protocol. As you offload the patient and the stretcher locks in the up position, you see on the monitor that the patient’s rhythm has suddenly changed to v fib. You quickly charge the defibrillator, deliver a shock, and begin CPR and BVM ventilations as you roll into the trauma bay.

In the trauma bay, the initial ECG shows asystole and CPR is continued as the patient is intubated. An esophageal probe shows the patient has a temperature of 84.6 degrees F (29.2 degrees C). The trauma team places two chest tubes in the patient’s left chest and begins lavage of the thoracic cavity with warmed saline.

After 65 minutes of CPR and continuous left chest lavage, the patient re-develops v fib as his core temperature reaches 93.5 degrees F (34.2 degrees C) and he’s shocked into sinus tachycardia with pulses. Laboratory testing reveals that his blood ethanol level was four times the DUI limit at the time of his ED arrival. His head CT scan shows no intracranial injury and he’s admitted to the ICU.

After a weeklong hospitalization, the patient is discharged to a rehab facility for intense therapy. He remains moderately cognitively impaired, but is able to perform normal daily activities such as feeding and bathing himself.

 

References

1. Danzl D: Accidental hypothermia. In Auerbach P (Ed.), Wilderness medicine, 5th edition. Mosby Elsevier: Philadelphia, pp. 125-160, 2007.

2. Baumgartner EA, Belson M, Rubin C, et al. Hypothermia and other cold-related morbidity emergency department visits: United States, 1995-2004. Wilderness Environ Med. 2008;19(4):233-237.

3. Centers for Disease Control and Prevention (CDC): Hypothermia-related deaths: United States, 2003-2004. MMWR Morb Mortal Wkly Rep. 2005;54(7):173-175.

4. Lapostolle L, Couvreur J, Koch F, et al. Hypothermia in trauma victims at first arrival of ambulance personnel: an observational study with assessment of risk factors. Scand J Trauma Resusc Emerg Med. 2017;25(1):43-48.

5. Centers for Disease Control and Prevention (CDC): Hypothermia-related deaths: United States, 1999-2002 and 2005. MMWR Morb Mortal Wkly Rep. 2006;55(10):282-284.

6. Dà­az M, Becker DE. Thermoregulation: Physiological and clinical considerations during sedation and general anesthesia. Anesth Prog. 2010;57(1):25-32.

7. Crawshaw L, Wallace H, Dasgupta S: Thermoregulation. In Auerbach P (Ed.), Wilderness medicine, 5th edition. Mosby Elsevier: Philadelphia, pp. 110-124, 2007.

8. Marieb E, Hoehn K: Human anatomy and physiology, 8th edition. Pearson Benjamin Cummings: San Francisco, pp. 953, 2010.

9. Charkoudian N. Mechanisms and modifiers of reflex induced cutaneous vasodilation and vasoconstriction in humans. J Appl Physiol. 2010;109(4):1221-1228.

10. Zafren K, Mechem CC. (March 30, 2017.) Accidental hypothermia in adults. UpToDate. Retrieved July 16, 2017, from www.uptodate.com/contents/accidental-hypothermia-in-adults.

11. Durrer B, Brugger H, Syme D, et al. The medical on-site treatment of hypothermia: ICAR-MEDCOM recommendation. High Alt Med Biol. 2003;4(1):99.

12. Hanania NA, Zimmerman JL. Accidental hypothermia. Crit Care Clin. 1999;15(2):235-249.

13. Mizukami H, Shimizu K, Shiono H, et al. Forensic diagnosis of death from cold. Legal Med. 1999;1(4):204-209.

14. Ginsberg M, Globus M, Dietrich W, et al. Temperature modulation of ischemic brain injury: A synthesis of recent advances. Prog Brain Res. 1993;96:13-22.

15. Callaway CW, Donnino MW, Fink EL, et al. Part 8: Post-cardiac arrest care: 2015 American Heart Association guidelines update for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation. 2015;132(18 Suppl 2):S465-S482.

16. Doshi H, Giudici M. The EKG in hypothermia and hyperthermia. J Electrocardiol. 2015;48(2):203-209.

17. Bessen H, Ngo B: Hypothermia. In Tintinalli J, Stapczynski JS, Ma OJ, et al. (Eds.), Tintinalli’s emergency medicine: A comprehensive study guide. McGraw-Hill Education: New York, 2016.

18. Gerecht R. Trauma’s lethal triad of hypothermia, acidosis & coagulopathy create a deadly cycle for trauma patients. JEMS. 2014;39(4):56-60.

19. Perlman J, Wyllie J, Kattwinkel J, et al. Part 7: Neonatal resuscitation: 2015 international consensus on cardiopulmonary resuscitation and emergency cardiovascular care science with treatment recommendations. Circulation. 2015;132(16 Suppl 1):S204-S241.

20. Lapostolle F, Sebbah JL, Couvreur J, et al. Risk factors for onset of hypothermia in trauma victims: The HypoTraum study. Crit Care. 2012;16(4):R142-149.

21. Perlman R, Callum J, Laflamme C, et al. A recommended early goal-directed management guideline for the prevention of hypothermia-related transfusion, morbidity, and mortality in severely injured trauma patients. Crit Care. 2016;20(1):107-117.

22. Brown DJ, Brugger H, Boyd J, et al. Accidental hypothermia. N Engl J Med. 2012;367(20):1930-1938.

23. Reuler JB. Hypothermia: Pathophysiology, clinical settings, and management. Ann Intern Med. 1978;89(4):519-527.

24. Lexow K. Severe accidental hypothermia: Survival after 6 hours 30 minutes of cardiopulmonary resuscitation. Arctic Med Res. 1991;50 Suppl 6:112-114.

25. Dobson J, Burgess J. Resuscitation of severe hypothermia by extracorporeal rewarming in a child. J Trauma. 1996;40(3):483-485.

 

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