Cold Crisis, Hot Solutions: Navigating the Complex Terrain of Hypothermic Resuscitation

Introduction

As temperatures fall and w­inter takes hold, the likelihood of seeing a patient presenting to the emergency department with hypothermia climbs. However, depending on the etiology of hypothermia, a hypothermic patient can certainly present to the ED amid a summer heat wave as well. Because there are slight variations in temperature that define hypothermia, accidental hypothermia is defined here as a core temperature less than 35ºC (95ºF) and can be associated with significant morbidity and mortality (1). Accidental hypothermia can be further characterized as primary, due to environmental exposure, or secondary, due to impaired thermoregulation (2).

 
 

A complex array of homeostatic interactions occurs to maintain the widely accepted definition of normal body temperature of approximately 37ºC (98.6ºF) (3). The body’s core temperature will fall when the body experiences an amount of heat loss that exceeds heat production. As you may (or may not) recall from your high school and college physics courses, heat loss can occur through a variety of mechanisms including conduction, convection, evaporation, and radiation (Table 2) An elderly patient who had an unwitnessed fall with a prolonged downtime can experience conductive heat loss with the floor. This can be further exacerbated if the patient fell outside on a cool breezy day where they will also lose heat via convection as the wind goes across their skin. Conductive and convective heat loss are the most common mechanisms of accidental hypothermia (4).

 
 

Classification

The European Resuscitation Council guidelines classifies hypothermia as mild (core temperature 32-35ºC [90-95ºF]); moderate (core temperature 28-32ºC [82-90ºF]); and severe (core temperature <28ºC [82ºF] (5). Profound hypothermia is classified as a core temperature <24ºC (75ºF) (6). When an accurate temperature measurement is unobtainable such as the prehospital setting, there have been various attempts to create an accurate clinical staging system to estimate the extent of hypothermia. Several studies evaluating the Swiss system developed by the International Commission for Mountain Emergency Medicine revealed a relatively high degree of misclassification of hypothermia severity (7,8). The Swiss system has since been modified to the Revised Swiss System (figure 1) and is more like the Danish system, which has been used by prehospital personnel for several years. Both systems stage hypothermia based on the level of consciousness and the subsequent risk of cardiac arrest rather than core temperature (9).

 
 

Pathophysiology

Various central and peripheral thermal receptors monitor the body’s temperature. Through numerous hypothalamic pathways to other organs such as the thyroid and adrenal glands, the body can both produce and conserve heat through behavior modification, peripheral vasoconstriction, increasing metabolic rate, and muscular thermogenesis or shivering (10). When the heat loss exceeds the body’s abilities to produce and conserve heat, the body’s core temperature drops, which leads to a multitude of other physiologic changes including decreased tissue metabolism, central nervous system impairment, myocardial irritability, respiratory impairment, and coagulopathy (2).

Studies have revealed various temperatures that correlate with specific pathologies. The pupils may become fixed and dilated below approximately 29ºC (84.2ºF) and corneal reflexes absent below 23ºC (73.4ºF). As the core temperature falls below 32ºC (89.6ºF), Osborn J waves typically show up on ECG, which are roughly proportional to the degree of hypothermia, and the risk of cardiac arrest increases drastically below 28ºC (82.4ºC) (10). Other ECG changes visible include bradycardia with progressively prolonging intervals (PR, QRS, QTc). When a patient is hypothermic, some ECG findings (T-wave abnormalities associated with hyperkalemia) may be masked, therefore it would be prudent to consider these patients as sick. Given the myocardial irritability and lower threshold to develop dysrhythmia associated with a low core temperature, it is important for patients to be handled especially carefully and kept in a horizontal position. Within the hematological system, when core temperature falls below 34ºC (93.2ºF), activity of clotting factors and platelets can be affected resulting in a hypercoagulable coagulopathy. Hypothermia also results in decreased oxygen consumption by the brain due to decreased metabolic activity and cerebral oxygen requirements are estimated to be around 50% at a core temperature of 28ºC (82.4ºF) and just 11% at 8ºC (46.4ºF) (2).

Clinical Presentation & Evaluation

When patients with suspected hypothermia present to the ED, it is important to not only expedite the time to rewarming, but also obtain vital signs and an accurate core temperature with a low-reading thermometer. If using a pulse oximeter to monitor oxygen, consider using a forehead or earlobe probe due to the delayed response time (11). Because of the extent of vasoconstriction present in hypothermia, peripheral pulses may not be palpable. In these cases, continuous-wave doppler should be used for a full minute to evaluate for a pulse (10). Point-of-care echocardiography can also be utilized to assess for cardiac motion. The various clinical presentations of hypothermia are listed in the table below (table 3).

Core temperature measurements can be done with a rectal thermometer, an esophageal temperature probe in the distal third of the esophagus if they are intubated, and even a temperature-sensing Foley catheter. Because the rectal and bladder temperatures may lag behind the true core temperature, these should be avoided in critical patients and for the purposes of monitoring the rewarming progress.10 When considering laboratory evaluations for patients with hypothermia, one should attempt to identify the presence of lactic acidosis, rhabdomyolysis, and infection. If coagulation studies are ordered, it is important to consider that the study is performed at 37ºC (98.6ºF) and may result as normal despite an obvious coagulopathy in the patient. If resources allow and indicated, thromboelastography (TEG) may provide additional insight to a patient’s coagulopathy for more focused intervention (12). As rewarming is initiated, patients with moderate and severe hypothermia should have labs closely monitored to evaluate for secondary electrolyte derangements due to the rewarming process.

 
 

Management

The primary objectives of managing a patient with hypothermia consist of maintaining airway, breathing, and circulation; preventing further heat loss; initiating an appropriate rewarming strategy; and managing complications as needed (10). Management of concomitant injuries and pathologies should accompany the management of hypothermia, however, will not be discussed here. The rewarming strategy selection should be based on the degree of hypothermia; however, all rewarming strategies begin the same. This includes removal of wet clothing, raise patient’s room temperature, and cover with warm blankets. For patients with mild hypothermia, active external warming should be initiated with forced air warming devices such as a Bair Hugger and application of hot packs. In patients with moderate hypothermia, active external warming will be supplemented with administration of warmed IV fluids and warmed humidified oxygen. For patients with severe hypothermia, the above strategies are implemented with the addition of active internal rewarming procedures, which are selected based on the hemodynamic stability of the patient. If the patient is hemodynamically stable, an endovascular temperature catheter can be placed. If the patient is hemodynamically unstable, extracorporeal membrane oxygenation (ECMO) or cardiopulmonary bypass is the preferred approach. Other strategies such as peritoneal or pleural irrigation with warmed fluids should be reserved for situations where ECMO is not available. 

 
 

Because of the severe dehydration and fluid shifts that can accompany hypothermia, patients should have two large-bore peripheral IVs. Intraosseous lines can be placed if peripheral IV access is not achieved (10). If the decision is made to place a central line, placement of a temporary femoral venous catheter is preferred to avoid arrhythmia, however it is important to reconsider this femoral placement should ECMO be indicated. When placing central lines superior to the diaphragm, the operator should take special care to minimize guidewire contact with the irritable myocardium. Any fluids administered to the patient to address hypotension should also be warmed as room-temperature fluids can decrease core temperature. The resuscitation of a hypothermic patient may persist for hours because of hypothermia’s neuroprotective effects. One case study out of Italy describes a patient who suffered a hypothermic cardiac arrest and made a full neurologic recovery after approximately 9 hours of cardiopulmonary resuscitation with nearly half of the time being managed with mechanical CPR (13). Withholding resuscitative efforts should only occur if there is a nonsurvivable injury or fatal illness, the body is frozen to the point of inhibiting adequate chest compressions, or if the airway is compromised with snow and ice (5).  

As rewarming progresses, patients should be closely monitored for the development of complications. Clinicians should be cognizant of the development of core temperature afterdrop, which is an adverse effect of active external rewarming. If the patient’s extremities and core are warmed simultaneously, pooled blood in the extremities can return to the core circulation due to vasodilation and ultimately drop the core temperature and pH. Additionally, the arterial vasodilation can result in hypotension. To minimize the risk of core temperature afterdrop, the patient’s core should be rewarmed prior to the extremities (10). 

When active internal rewarming strategies are indicated, endovascular temperature-control catheters demonstrate success in rewarming patients according to case reports (14). However, when ECMO is selected, it is important to consider the additional risks associated with the highly invasive procedure. The ICE-CRASH study is a multi-center study out of Japan that evaluated the 28-day survival of nearly 500 individuals with severe accidental hypothermia. They found that ECMO improved the survival and neurologic outcomes in patients who experienced cardiac arrest, however there was no significant difference in 28-day survival in patients who did not experience cardiac arrest (15). Therefore, ECMO should ideally be reserved for those who experience cardiac arrest, especially if the risks outweigh the potential benefit in patients who do not experience cardiac arrest. While these active internal rewarming procedures can increase the core temperature rapidly, rewarming should not be too rapid. A study of over 600 patients on ECMO for rewarming following accidental hypothermia found that rewarming rates less than 5ºC per hour are associated with improved survival with good neurological outcomes (16). 

 
 

Overall, patients who present to the emergency department with hypothermia can require a significant amount of time and resources for resuscitation. It is important to obtain an accurate core temperature early while minimizing the amount of patient movement. While managing the patient, priorities include maintaining airway, breathing, and circulation; preventing further heat loss; initiating appropriate rewarming procedures; and managing complications as necessary. A significant factor that influences the rewarming strategy is the availability of resources. At the very minimum all hypothermia patients should immediately begin active external rewarming with an emphasis of warming the core first, then extremities to minimize the risk of adverse effects such as core temperature afterdrop. If resources allow, ECMO improves 28-day mortality in severe hypothermia patients who experience cardiac arrest. Aim to rewarm the patient at a rate of no more than 5ºC per hour and monitor serial labs for the development of electrolyte derangements.


AUTHORED BY: LUCAS RAPPERT, OMS4

FACULTY EDITING BY: COLIN MCCLOSKEY, MD


References

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