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CHAPTER 209:  Hypothermia      1337 below 90% (>4000 m or 13,000 ft), the use of supplemental oxygen or a portable hyperbaric device should be considered. 48 Recent case series proposed the use of systemic thrombolytic therapy and/or prostacyclin therapy in these environments if transfer is not possible in time to pro vide potentially definitive management. 48 These cases include severe frostbite of the digits, when amputation risk is high (significant periph eral cyanosis that extends proximally above metacarpophalangeal joints after rewarming), if unable to transfer to higher levels of care within 24 hours. 48 The field use of IV prostacyclin therapy (iloprost) has also been proposed and may be less risky for lower grades of frostbite and if the patient cannot be transferred to a higher level of care within 48 hours. Sequelae Up to 65% of persons with frostbite injuries experience sequelae from their injuries. 4 Sequelae may be seen in patients with mild injuries but are generally more intense with more severe frostbite. The most typical sequelae are hypersensitivity to cold, pain, ongoing numbness, and increased risk for developing future frostbite injury. The clinical and functional limitations associated with late sequelae are dependent on the type and severity of the frostbite injury and the related anatomic deformities and amputations. Disposition and Follow-Up Because it is difficult to determine the extent of frostbite on initial examination, it is best to be conservative when contemplating admission. Consider age and social and medical issues when planning disposition. Undomiciled patients should not be discharged back into subfreezing temperatures with an active injury, and a special consideration for admission or discharge to a local shelter is warranted. If the frostbite is extensive and the hospital and staff are not equipped to treat injury of that degree of severity, consider transfer to a tertiary hospital after initial rewarming and treatment. Patients with only superficial local frostbite may be discharged home if social circumstances allow. Patients with deeper frostbite injuries should be hospitalized. At discharge from the ED, patients must be provided with sufficient guidelines for self-care as well as clear instruc tions for short-term and long-term follow-up, preferably with local burn center or plastic surgery providers. Patients who are discharged from the ED should be treated with topical aloe vera cream and oral ibuprofen and encouraged not to smoke or drink alcohol to maximize healing potential. REFERENCES The complete reference list is available online at www.TintinalliEM.com.

y with local burn center or plastic surgery providers. Patients who are discharged from the ED should be treated with topical aloe vera cream and oral ibuprofen and encouraged not to smoke or drink alcohol to maximize healing potential. REFERENCES The complete reference list is available online at www.TintinalliEM.com. TABLE 209-1 Causes of Secondary Hypothermia Predominantly Increased Heat Loss •   Burns •   Iatrogenic (i.e., blood transfusions and other cold infusions, cooling blankets, inadequate insulation) •   Recent birth Predominantly Impaired Thermogenesis •   Impaired shivering (i.e., advanced or very young age, malnutrition, physical exhaustion, neuromuscular disease) Multifactorial •   Medications and toxins (i.e., alcohol, anesthetic agents, narcotics, sedatives, vasodilators) •   Metabolic and endocrine disorders (i.e., alcoholic or diabetic ketoacidosis, hypoadrenalism, hypoglycemia, hypopituitarism, hypothyroidism lactic acidosis, Wernicke’s encephalopathy) •   Neurologic (i.e., space-occupying lesion, stroke, spinal cord injury) •   Sepsis (small subset of sepsis cases, more common in the elderly or cachectic patient) •   Shock •   Trauma Hypothermia Douglas J.A. Brown INTRODUCTION AND EPIDEMIOLOGY Accidental hypothermia is an involuntary drop in core temperature below 35°C (<95°F) and can often be associated with significant morbidity and mortality. 1 Therapeutic hypothermia, also called targeted tem perature management, is a purposeful drop in core temperature usually performed with the hope of ameliorating tissue damage associated with an ischemic event. 2,3 Accidental hypothermia can be subclassified as primary, due to simple environmental exposure, or secondary, due to impaired thermoregulation ( Table 209-1 ). Primary accidental hypothermia is commonly seen in cold climates, whereas secondary accidental hypothermia can be seen worldwide. The true incidence of accidental hypothermia and its related morbidity and mortality remains unknown, but estimates suggest it is 0.1 to 5 cases per 100,000 inhabitants in nontropical climates. CHAPTER  HYPOTHERMIA CLASSIFICATION Historically, hypothermia has been classified as mild, moderate, severe, and profound, based on core temperature, shivering, level of consciousness, and vital signs. 6-8 Unfortunately, there is considerable variation in clinical features at any given temperature, and a reliable core temperature is sometimes unavailable during initial assessment. Shivering is particularly unreliable because it may be present or absent across a wide temperature range. The modified staging system (mild, moderate, severe, and hypothermic cardiac arrest) 6-8 described in Table 209-2 is a hybrid of the Swiss 8 and classical systems 6 that is based primarily on level of consciousness, the presence or absence of vital signs, and core temperature (when available). PATHOPHYSIOLOGY Body temperature is tightly regulated by a combination of behavioral, neuroendocrinologic, and cardiovascular responses to cold stress. Core temperature will fall when the amount of heat lost to the environment exceeds the amount of heat produced.  HEAT LOSS Heat is lost from a warm body by conduction, convection, evaporation, and radiation. Conduction occurs when a warm body makes direct contact with a cold object. Conductive heat loss can be minimized by avoiding contact with cold or poorly insulated objects (e.g., metal backboards or stretchers). Convective cooling occurs when a fluid (usually air or water) comes in contact with a warm body. The amount of heat lost via convection can be considerable and is proportional to the amount of fluid that flows around the body, the specific heat capacity of the fluid, and the temperature difference between the fluid and the body.

cooling occurs when a fluid (usually air or water) comes in contact with a warm body. The amount of heat lost via convection can be considerable and is proportional to the amount of fluid that flows around the body, the specific heat capacity of the fluid, and the temperature difference between the fluid and the body. Practically, the emergency physician needs to understand that exposure to cool air or water will result in heat loss, that water can absorb a large amount of heat in a short period of time, and that windy conditions or flowing water can significantly increase the rate of cooling. Evaporative heat loss occurs due to the energy required for water to phase change from a liquid to a gas. The amount of heat lost to evaporation is pro portional to the temperature difference between the body and the air and the wind speed over the body and is inversely proportional to the humidity. Therefore, a warm, moist body exposed to cold, dry, windy air will lose a significant amount of heat. A vapor barrier (e.g., a plastic bag or sheet) placed around the patient effectively prevents evaporative cooling but is often not practical when repeated access to the patient’s skin is required. Radiant cooling occurs because all warm bodies “radiate” heat in the form of electromagnetic waves. Increasing the temperature Tintinalli_Sec16_p1333-1418.indd 1337 8/2/19 8:22 PM

ound the patient effectively prevents evaporative cooling but is often not practical when repeated access to the patient’s skin is required. Radiant cooling occurs because all warm bodies “radiate” heat in the form of electromagnetic waves. Increasing the temperature Tintinalli_Sec16_p1333-1418.indd 1337 8/2/19 8:22 PM 1338 SECTION 16: Environmental Injuries TABLE 209-2 Staging and Treatment of Accidental Hypothermia Stage Clinical Symptoms Typical Core Temperature Treatment Mild (HT I) Conscious, shivering 35–32°C Warm environment and clothing, warm sweet drinks, and active movement (if possible) HT I patients with significant trauma or comorbidities or those suspected of secondary hypothermia should receive HT II treatment Moderate (HT II) Impaired consciousness* (may or may not be shivering) <32–28°C Active external and minimally invasive rewarming techniques (warm environment; chemical, electrical, or forced air heating packs or blankets; warm parenteral fluids) Cardiac and core temperature monitoring Minimal and cautious movements to avoid dysrhythmias Full-body insulation, horizontal position, and immobilization Severe (HT III) Unconscious*, vital signs present <28°C HT II management plus: Airway management as required Preference to treat in an ECLS center, if available, due to the high risk of cardiac arrest Consider ECLS in cases with cardiac instability that is refractory to medical management Consider ECLS for comorbid patients who are unlikely to tolerate the low cardiac output associated with HT III Hypothermic cardiac arrest (HT IV) Vital signs absent Cardiac arrest is possible below 32°C; the risk increases substantially below 28°C and continues to increase with ongoing cooling CPR and up to three doses of epinephrine and defibrillation (further dosing guided by clinical response) Airway management Transport to ECLS† Prevent further heat loss (insulation; warm environment; do not apply heat to head) Active external and minimally invasive rewarming (see HT II) during transport is recommended but controversial; do not apply heat to head Abbreviations: ECLS = extracorporeal life support; HT = hypothermia. *Consciousness may be impaired by comorbid illness (e.g., trauma, CNS pathology, toxic ingestion) independent of core temperature. †Transfering an HT IV patient to an ECLS center may reduce mortality by 40% to 90% (number needed to treat, ∼2); if ECLS is not available within a few hours of transport,7,9 consider on-site rewarming with hot packs or forced air blankets, warm IV fluid, ± warm thoracic lavage, ± warm bladder lavage, and ± warm peritoneal lavage; do not apply heat to the head. of the room can minimize radiant heat loss, and some losses can be recovered using special reflective fabrics (likely low yield in most clini cal situations). In summary, it is important to minimize heat loss in the hypothermic patient, and a basic understanding of the physics of heat transfer can be helpful. Practically, heat loss can be minimized by heat ing the room, removing wet clothes, drying the patient (or wrapping the patient in a vapor barrier), providing insulation, and protecting the patient from wind.  HEAT CONSERVATION AND PRODUCTION The most important responses to cold include behavior (e.g., putting on warm clothing, seeking a warm environment), peripheral vasoconstric tion, increased metabolic rate, and muscular thermogenesis (voluntary or shivering). Shivering is a remarkably efficient method of heat pro duction, and care is required to preserve this important source of heat.

cold include behavior (e.g., putting on warm clothing, seeking a warm environment), peripheral vasoconstric tion, increased metabolic rate, and muscular thermogenesis (voluntary or shivering). Shivering is a remarkably efficient method of heat pro duction, and care is required to preserve this important source of heat. Unfortunately, shivering can be suppressed by medications (e.g., analgesics, sedatives), by the application of warming devices (e.g., hot packs, forced air blankets, warm humidified air), if energy stores are exhausted, or if the core temperature drops below a critical level (∼31°C). 6 The suppression of shivering by various warming methods is one of the reasons why the rewarming literature is so controversial.  CONTINUED CORE COOLING Core temperature may continue to drop after a patient is removed from the cold environment, 10,11 a process often referred to as after drop. The amount of continued core cooling will depend on the stage of hypothermia, the degree of thermoregulatory dysfunction, the ongoing cold stress (often significant in the prehospital care envi ronment), and the physics of heat transfer (heat from the relatively warmer core will be transferred to the cooler periphery by direct conduction or by convection from blood flow). Careful experimen tal studies have demonstrated an approximately 1°C drop in core temperature during minimally invasive rewarming when shivering is inhibited with narcotics 12 or during exercise, 13 but case series have not demonstrated any clinically significant afterdrop or morbidity when minimally invasive rewarming is used. 7,14 In general, healthy uninjured patients who are able to shiver and have adequate fuel reserves (or can drink warm sweet drinks) will be able to self-rewarm once removed from further cold stress. In contrast, patients who have lost the ability to shiver are at significant risk of further temperature decline unless active rewarming is used. 7,15,16 The use of aggressive immersion rewarming techniques such as hot baths or showers should likely be avoided due to the potential risks of vasodilatory hypoten sion or convective cooling.  SECONDARY HYPOTHERMIA Cases of secondary hypothermia can be conveniently organized into those caused predominantly by increased heat loss, those caused pre dominantly by impaired thermoregulation, and those caused by multiple factors (Table 209-1). This classification is somewhat arbitrary, but in general, the multifactorial cases have a higher risk of missed diagnosis and are less likely to fully resolve with rewarming and supportive care. Iatrogenic causes of hypothermia deserve special attention, particularly in trauma patients, where the loss of just a few degrees of core temperature can create a profound coagulopathy and more than double patient mortality. 18 Massive transfusion and large-volume crystalloid resus citation are common iatrogenic causes of hypothermia unless proper fluid warmers are used. Inadequate insulation, repeated or prolonged exposure to the cool air of the resuscitation or operating room, and inadequate core temperature monitoring all contribute to iatrogenic heat loss, which may increase morbidity and mortality.  COLD PHYSIOLOGY The body attempts to preserve normothermia through mechanisms such as increased metabolic rate, peripheral vasoconstriction, increased preshivering muscle tone, or shivering. As the core temperature drops Tintinalli_Sec16_p1333-1418.indd 1338 8/2/19 8:22 PM

which may increase morbidity and mortality.  COLD PHYSIOLOGY The body attempts to preserve normothermia through mechanisms such as increased metabolic rate, peripheral vasoconstriction, increased preshivering muscle tone, or shivering. As the core temperature drops Tintinalli_Sec16_p1333-1418.indd 1338 8/2/19 8:22 PM CHAPTER 209:  Hypothermia      1339 FIGURE 209-1. ECG strip from a patient with a temperature of 25°C (77°F) showing atrial  fibrillation  with  a  slow  ventricular  response,  muscle  tremor  artifact,  and  Osborn  (J) wave (arrow). below approximately 35°C, progressive impairment occurs, affecting all of the body’s organ systems. CNS impairment can progress from poor judgment, amnesia, and dysarthria to ataxia, apathy, unconsciousness, areflexia, and eventually electroencephalographic arrest. 6 Paradoxical undressing is a potentially deadly behavior that occurs in up to 30% of fatal hypothermia cases. 19 Below approximately 29°C, the pupils may become dilated and fixed, and below approximately 23°C, corneal reflexes may be absent; neither is reliable for neurologic prognosis in hypothermia. Cardiorespiratory Responses Cardiovascular responses to cold include profound peripheral vasoconstriction and an initial increase in heart rate and blood pressure, usually followed by progressive bradycardia, hypotension, and myocardial irritability. Below approximately 32°C, the risk of cardiac arrest increases as malignant cardiac dysrhythmias become more common, particularly below 28°C. 20 The term rescue collapse is used to describe cardiac arrest that can commonly occur during extrication, transport, or treatment of a deeply hypothermic patient. The cause of rescue collapse is multifactorial, but ultimately related to the profound irritability of the cold myocardium. Atrial fibrillation and flutter are expected dysrhythmias and not necessarily markers of cardiac instability. 7 ECG changes in hypothermia are variable but classically include bradycardia with prolonged PR, then QRS widening, and then prolonged QT c. ECGs are often complicated by muscle tremors or shivering, and hypothermia can cause almost any heart block or atrial or ventricular dysrhythmias. The classic Osborn J waves (Figure 209-1) usually occur below 32°C, can be misdiagnosed as ST-elevation myocardial infarction, and can also be caused by intracranial pathology or sepsis. Occasionally patients may be in a low-flow state, with a very difficult to detect pulse that may provide some oxygen delivery. Asystole is the common final dysrhythmia, but in accidental hypothermia, it does not exclude the possibility of a successful resuscitation. Respiratory changes include initial tachypnea, followed by a progressive decrease in minute ventilation and eventual respiratory arrest. Pulmonary edema is an inconsistent complication of hypothermia, but is common after resuscitation from stage IV hypothermia. The gradi ent between end-tidal carbon dioxide (ETCO 2) and uncorrected partial pressure of arterial carbon dioxide increases variably in severe hypothermia, making the interpretation of ETCO 2 and titration of ventilation parameters challenging in the absence of blood gas measurements.21 Metabolic Responses The renal response to hypothermia is termed cold diuresis and is a response to vasoconstriction-induced hypervol emia. It results in significant fluid losses, which may be further increased in patients with a history of cold water immersion or alcohol intoxication. Rhabdomyolysis is a potential complication of hypothermia 22; however, the clinician should always exclude a missed compartment syndrome or extensive frostbite when an elevated creatine kinase is detected.

losses, which may be further increased in patients with a history of cold water immersion or alcohol intoxication. Rhabdomyolysis is a potential complication of hypothermia 22; however, the clinician should always exclude a missed compartment syndrome or extensive frostbite when an elevated creatine kinase is detected. Hypothermia can also cause muscle rigidity, termed pseudo-rigor mortis; hence, rigor mortis cannot be used as a reliable marker of death in the cold patient. Hypothermia has a somewhat dramatic impact on coagulation and blood viscosity, and these effects are often underrecognized by clinicians because blood samples are heated to 37°C prior to analysis. Coagulopathy is a concern below 34°C, particularly in trauma patients in whom hypothermia can compromise the chance for a surgical cure and exponentially increase mortality, 18 partly due to poor activity of clotting factors and platelet dysfunction. 23 Hypothermic patients can also be hypercoagulable from a combination of increased viscosity, hemo concentration, and an inflammatory cascade similar to disseminated intravascular coagulation; these factors can put hypothermic patients at an increased risk for venous thromboembolic disease as well as coronary and cerebral artery occlusion. Cellular oxygen consumption decreases as core temperature drops and, in an otherwise healthy patient who has adequate oxygen delivery prior to cooling, may provide protection against ischemia. It is estimated that cerebral oxygen requirements are approximately 50% at 28°C, 19% at 18°C, and 11% at 8°C. 6,24 This neuroprotective effect of hypothermia is exploited in certain cardiac surgeries. The most dramatic technique is deep hypothermic circulatory arrest, where patients are cooled to approximately 18°C and cardiac arrest is induced and maintained for up to approximately 30 minutes. 25 The combination of the potential to survive prolonged periods of ischemia, with the uncertainty of knowing if a patient has been in a low-flow state (difficult to detect cardiac activ ity that provides some oxygen delivery) versus cardiac arrest, increases the complexity of termination of resuscitation decisions for hypothermic patients unless the history clearly indicates death prior to cooling. CLINICAL FEATURES Patients with hypothermia will feel cold to touch; they will have a core temperature less than 35°C and may have a history of cold exposure or a history of a condition associated with secondary hypothermia (Table 209-1). Hypothermia can be staged clinically using level of consciousness and vital signs (Table 209-2). Measure the core temperature as soon as possible. If the core temperature deviates significantly from the clinical features of the stage, then consider alternative diagnoses. For example, if a patient has a core temperature of 33°C but is unconscious, hypothermia is unlikely the main cause of coma.  CORE TEMPERATURE MEASUREMENT Make sure that the device being used to measure core temperature is capable of extreme measurements and is properly calibrated (thermis tor devices are usually preferred). Temperature measurement at differ ent body sites will yield different readings depending on local perfusion and environmental conditions. In the intubated patient, the lower third of the esophagus (∼24 cm below the larynx in an adult) is the preferred site for core temperature measurement, because it closely mirrors the cardiac temperature. 6 In the absence of an esophageal probe, a rectal probe inserted to a depth of 15 cm or a bladder probe is adequate, but realize that these temperatures often lag behind true core temperature during rewarming and that bladder or peritoneal lavage may falsely elevate the reading.

closely mirrors the cardiac temperature. 6 In the absence of an esophageal probe, a rectal probe inserted to a depth of 15 cm or a bladder probe is adequate, but realize that these temperatures often lag behind true core temperature during rewarming and that bladder or peritoneal lavage may falsely elevate the reading. Oral and infrared tympanic temperature measure ments do not correlate well with core temperature and should not be used. When an accurate core temperature measurement is not available, management decisions should be made based on clinical staging (Table 209-2). Ongoing core temperature monitoring should be implemented as soon as possible for all moderate to severe hypothermia patients (stages II to IV). DIAGNOSIS Hypothermia causes dysfunction of every organ system, so the potential list of differential diagnoses is broad. A practical approach is to focus the differential diagnosis using a combination of history, physical exam, and expected degree of dysfunction for the clinical stage and measured core temperature. For the patient with absent vital signs, if the history indicates normothermic cardiac arrest prior to cooling, then hypother mia can be excluded as the cause of cardiac arrest, regardless of the patient’s core temperature (Figure 209-2). Similarly, in the patient with absent vital signs, asystole, and an accurate core temperature above 32°C, accidental hypothermia is not the cause of cardiac arrest. Classic diagnostic dilemmas in relation to accidental hypothermia often revolve around impaired cognitive function, level of consciousness, or declara tion of death. Intoxication, head injury, and CNS infection are three Tintinalli_Sec16_p1333-1418.indd 1339 8/2/19 8:22 PM

ypothermia is not the cause of cardiac arrest. Classic diagnostic dilemmas in relation to accidental hypothermia often revolve around impaired cognitive function, level of consciousness, or declara tion of death. Intoxication, head injury, and CNS infection are three Tintinalli_Sec16_p1333-1418.indd 1339 8/2/19 8:22 PM 1340 SECTION 16: Environmental Injuries Patient’s trunk feels cold on examination or core temperature <35°C? Vital signs present Obvious signs of irreversible death Valid DNR order Conditions unsafe for rescuer Avalanche burial >35 min and airway packed with snow Consider termination of CPR Cardiac arrest from alternate cause prior to cooling Major trauma Witnessed normothermic arrest Avalanche burial <35 min Transport to nearest appropriate hospital or manage as per supervising MD Consider tests to confirm need for ECMO/CPB Core temperature <32°C Serum potassium <12 mmol/L Impaired consciousness Prehospital cardiac instability SBP <90 mm Hg Ventricular dysrhythmias Core temperature <28°CTransport to nearest appropriate hospital Trauma Comorbidities Suspected secondary hypothermia YesN o YesNo No to all Yes to any No to all Yes to any HT I, II, or III Active external and minimally invasive rewarming (insulation, hot packs, or forced air blankets, warm IV fluid, allow shivering) Minimal and cautious movements to avoid arrhythmias Airway management if required Start CPR; do not delay transport Prevent further heat loss Airway management and up to 3 doses of medication/ defibrillation HT IV Do NOT terminate CPR Transport to ECMO Prevent further heat loss (insulation, warm environment, do not apply heat to head) Active external and minimally invasive rewarming during transport is recommended but controversial; do not apply heat to head If ECMO not available within 6 h consider on-site rewarming with hot packs or forced air blankets, warm IVF +/– warm thoracic lavage, +/– warm bladder lavage; do not apply heat to head Rewarm to ≥32 °C HT I Warm environment and clothing Warm sweet drinks Active movement No to all Yes to an yN o to all Yes to any Consider termination of CPR Prepare for multiorgan failure and need for ECMO respiratory support Provide postarrest management Consider targeted temperature management Yes to all No to any No ROSCROSC Transport to ECMO hospital FIGURE 209-2. Transport  and management  of accidental  hypothermia. 7 CPB = cardiopulmonary  bypass;  DNR = do not resuscitate;  ECMO = extracorporeal  membrane  oxygenation; HT = hypothermia; MD = physician; ROSC = return of spontaneous circulation; SBP = systolic blood pressure. Tintinalli_Sec16_p1333-1418.indd 1340 8/2/19 8:22 PM

ransport  and management  of accidental  hypothermia. 7 CPB = cardiopulmonary  bypass;  DNR = do not resuscitate;  ECMO = extracorporeal  membrane  oxygenation; HT = hypothermia; MD = physician; ROSC = return of spontaneous circulation; SBP = systolic blood pressure. Tintinalli_Sec16_p1333-1418.indd 1340 8/2/19 8:22 PM CHAPTER 209:  Hypothermia      1341 examples of conditions that impair neurologic function directly, but can also cause secondary hypothermia and cold-related neurologic dysfunction. Vigilance is required with any decreased level of consciousness, particularly if the degree of neurologic impairment does not match the stage of hypothermia. Areflexia or paralysis should not be attributed to hypothermia until spinal injury has been ruled out. Carefully consider secondary causes of accidental hypothermia, par ticularly if the measured core temperature is lower than expected based on the cold exposure history or the patient is slow or fails to rewarm with appropriate therapy. Tachycardia or tachypnea can be a marker of secondary pathology in moderate and severe hypothermia (stages II and III), because bradycardia with or without bradypnea is the normal response to hypothermia below a core temperature of approximately 32°C. Intoxication and sepsis are two common causes of secondary hypothermia, and depending on the patient presentation, routine screening and, in some cases, empiric therapy may be reasonable. Classic causes such as adrenal failure and myxedema coma are comparatively rare, and empiric testing or therapy is likely unwarranted in the absence of good historical or laboratory evidence. Hyperglycemia that persists after rewarming may indicate secondary pathology such as diabetic ketoacidosis or pancreatitis. The appropriate breadth of workup will vary considerably depending on the particular patient and the degree of clinical uncertainty.  DECLARATION OF DEATH Declaration of death in the presence of hypothermia is particularly challenging due to the ability of hypothermia to mimic death (can cause fixed and dilated pupils, stiffness resembling rigor mortis, absent reflexes, or respiratory arrest) or cause death that may be reversible. Figure 209-3 provides a triage tool for stage IV (absent vital signs) patients to assist with clinical decision making. In general, patients with obvious signs of irreversible death or who are frozen solid, have a history of normothermic arrest with subsequent cooling, or have a potassium level >12 mmol/L are extremely unlikely to benefit from resuscitative efforts, and death can be declared without rewarming. 7 An exception to the above statement is the child with simultaneous normothermic cardiac arrest and very rapid accidental cooling (e.g., a child pinned underwater in an icy creek); in such a case, prolonged resuscitation and expert consultation may be appropriate (see “Children” under the “Special Considerations/Special Populations” section).  LABORATORY TESTING AND IMAGING Laboratory testing and imaging studies should be targeted based on history, physical examination, and the differential diagnosis. It seems reasonable that every hospitalized hypothermia patient undergo pointof-care glucose testing, but additional routine tests are not necessarily required. An ECG should be obtained for moderate and severe hypo thermia (stages II and III) patients, and a chest radiograph is likely reasonable depending on the suspicion for conditions such as aspira tion or pulmonary edema.

ient undergo pointof-care glucose testing, but additional routine tests are not necessarily required. An ECG should be obtained for moderate and severe hypo thermia (stages II and III) patients, and a chest radiograph is likely reasonable depending on the suspicion for conditions such as aspira tion or pulmonary edema. For cases where secondary hypothermia is suspected, measuring CBC, serum electrolytes, creatinine, glucose, lactate, lipase, thyroid-stimulating hormone, random cortisol level, osmolality, and levels of potential intoxicants (e.g., ethanol, aspirin, acetaminophen) and calculation of the anion and osmolar gap may be reasonable depending on clinical suspicion. Patients with suspected sepsis may benefit from blood culture. For patients with suspected compartment syndrome, frostbite, or prolonged immobility, measure serum creatine kinase. Severe hypothermia (stages III and IV) patients should be considered critically ill, and therefore, expanded laboratory testing including CBC, electrolytes, pH, lactate, blood gas levels, and creatine kinase may be considered. For patients in cardiac arrest (stage IV), a serum potassium level ≥12 mmol/L is strongly associated with nonsurvival.  HYPOTHERMIA EFFECTS ON LABORATORY VALUES Laboratory results from hypothermic patients can be difficult to interpret due to the fact that high, low, or “normal” values may be appropriate in different patients. In an otherwise healthy patient with primary hypothermia, most laboratory values will normalize with rewarming; therefore, treat the patient, not the numbers. For complex cases or those that do not respond to usual therapy, it may be help ful to have a sense of the “expected” abnormalities associated with hypothermia. Hematocrit classically increases approximately 2%/°C, secondary to decreased circulating plasma volume. 6 WBC counts may be normal or decreased due to sequestration or secondary causes such as sepsis. Electrolyte abnormalities are inconsistent, and cold blood may be prone to sampling hemolysis; hence, rewarming and ongoing monitoring are often the best strategy. Glucose levels are somewhat unpredictable, with an early rise being common secondary to catechol amine-induced gluconeogenesis and hypothermia-induced insulin resistance. This increase is classically followed by a drop with the onset of resource depletion and metabolic failure. 6 Acid-base disturbances in hypothermia are complex; some hypothermic patients will be acidotic, whereas others may be alkylotic, and both conditions may be an appro priate physiologic response to cooling 6 or may be a marker of second ary pathology. Blood gas analyzers rewarm samples to 37°C, and in rewarmed samples, the partial pressure of gases increases and the pH is lower, compared with the cold in vivo sample (correction usually not required; see stage III treatment for details). It is also important to note that the coagulopathy of hypothermia (see earlier section, “Cold Physi ology”) will not be apparent on laboratory results due to the warming of samples prior to testing. TREATMENT Treatment of accidental hypothermia varies depending on the clinical stage, but the general principles include basic or advanced life support, prevention of further heat loss, transport to an appropriate facility if indicated, 27 rewarming (Table 209-2 and Figure 209-2), and in second ary hypothermia, treatment of the underlying cause.  MILD HYPOTHERMIA (STAGE I) Otherwise healthy stage I patients (conscious, shivering, core tempera ture ≥32°C) can often be rewarmed locally using a warm environment, provision of dry clothes, warm sweet drinks, and active movement.

2 and Figure 209-2), and in second ary hypothermia, treatment of the underlying cause.  MILD HYPOTHERMIA (STAGE I) Otherwise healthy stage I patients (conscious, shivering, core tempera ture ≥32°C) can often be rewarmed locally using a warm environment, provision of dry clothes, warm sweet drinks, and active movement. Stage I patients with traumatic injuries or significant medical comor bidities or in whom secondary hypothermia is suspected should be transported to the nearest appropriate hospital and managed as per stage II guidelines.  MODERATE HYPOTHERMIA (STAGE II) Stage II patients (impaired consciousness, may or may not be shivering, core temperature ∼28°C to 32°C) require careful handling, prevention of further heat loss, active external and minimally invasive rewarming (warm environment; forced air, electrical, or chemical warming blankets; warm parenteral fluids), cardiac monitoring, and core temperature monitoring ( Figure 209-4). Careful handling to decrease the risk of cardiac dysrhythmia becomes important for stage II and III patients, due to the increasing irritability of the cold myocardium. For all stages of hypothermia, warmed crystalloids (38°C to 42°C) should be titrated based on clinical volume status. Significant volume might be required during rewarming. Warmed IV fluids do not provide significant heat, but do prevent iatrogenic cooling. Atrial fibrillation, atrial flutter, and bradycardia are common in accidental hypothermia, do not usually require specific therapy, and typically resolve with rewarming. Vas opressors are usually not indicated in early resuscitation because hypothermia already provides maximal vasoconstriction and the addition of vasopressors may increase the risk of dysrhythmia. Vasopressors may be indicated later in resuscitation if rewarming-induced vasodilation cannot be managed with fluids and is contributing to significant hypo tension. Special care is required when assessing the risk-to-benefit ratio of sedatives and analgesics. Many medications will inhibit shivering, decrease sympathetic tone, and/or cause vasodilatation, all of which can contribute to a further drop in core body temperature. 13 Depending on the stage of hypothermia, the degree of thermoregulatory dysfunction, Tintinalli_Sec16_p1333-1418.indd 1341 8/2/19 8:22 PM

analgesics. Many medications will inhibit shivering, decrease sympathetic tone, and/or cause vasodilatation, all of which can contribute to a further drop in core body temperature. 13 Depending on the stage of hypothermia, the degree of thermoregulatory dysfunction, Tintinalli_Sec16_p1333-1418.indd 1341 8/2/19 8:22 PM 1342 SECTION 16: Environmental Injuries Obvious signs of irreversible death: Decapitation, decomposition, truncal transection Body frozen solid (not compressible) Valid DNR order Note: Fixed and dilated pupils, areflexia, and stiffness that resembles rigor mortis are not reliable indicators of death in hypothermia. Consider standard TOR (termination of resuscitation guidelines) Cardiac arrest from alternate cause prior to cooling Major trauma, hypoxia, or medical condition Witnessed normothermic arrest Consider standard TOR Consider tests to exclude need for ECMO/CPB Core temperature >32°C Serum potassium >12 mmol/L No to all Yes to any Yes to any Transport to closest hospital with ECMO/CPB Yes to any Special Circumstances Drowning, avalanche, or trauma No to all Drowning: Submersion (patient goes underwater and has a hypoxic cardiac arrest prior to cooling): poor prognosis unless very young with rapid cooling, consider standard TOR Immersion (patient breathing air during cooling and then has a hypothermic cardiac arrest): consider transfer to ECMO/CPB Avalanche: <35 min burial: hypoxia or trauma likely caused the cardiac arrest; consider standard TOR >35 min burial and airway packed with snow: hypoxia likely caused the cardiac arrest; consider standard TOR >35 min burial and airway patent: hypothermia may have caused the cardiac arrest; consider transfer to ECMO unless signs of traumatic arrest Trauma: Hypothermia generally increases the mortality in trauma patients; consider standard TOR for patients with signs of traumatic arrest Yes to any Consider standard TOR >6-h transport time to ECMO* Yes Transport to nearest appropriate hospital HT IV Do NOT terminate CPR Prevent further heat loss (insulation, warm environment, do not apply heat to head) Airway management and up to 3 doses of epinephrine/defibrillation Transport to ECMO If ECMO not available within 6 h, consider on-site rewarming with hot packs or forced air blankets, warm IV fluids, +/– warm thoracic lavage, +/– warm bladder lavage; do not apply heat to head Rewarm to 32°C *Geographic location, vehicle/aircraft availability, and weather and road conditions will all impact transport time. In exceptional cases, >6-h transport time may be considered. FIGURE 209-3. Triage tool for hypothermia (HT) patients with absent vital signs. CPB = cardiopulmonary bypass; DNR = do not resuscitate; ECMO = extracorporeal membrane oxygenation. [© Doug Brown, MD, FRCPC.] the cold stress, and the physics of heat transfer, continued core cooling is possible despite appropriate treatment, particularly in the prehospital care setting. Such a failure to rewarm should trigger the clinician to reconsider secondary causes of hypothermia and ensure that ongoing heat losses have been ameliorated (uninsulated backboard, wet clothing, cool or windy environment) and that rewarming techniques are actually delivering significant heat.  SEVERE HYPOTHERMIA (STAGE III) Stage III (unconscious, vital signs present, core temperature < ∼28°C) patients require the same treatment as stage II patients and may require intubation for airway protection (Table 209-2). The role of invasive vascular rewarming methods that do not support circulation (dialy sis, venovenous extracorporeal membrane oxygenation (ECMO), and Tintinalli_Sec16_p1333-1418.indd 1342 8/2/19 8:22 PM

ents require the same treatment as stage II patients and may require intubation for airway protection (Table 209-2). The role of invasive vascular rewarming methods that do not support circulation (dialy sis, venovenous extracorporeal membrane oxygenation (ECMO), and Tintinalli_Sec16_p1333-1418.indd 1342 8/2/19 8:22 PM CHAPTER 209:  Hypothermia      1343 † FIGURE 209-4. Practical tips for rewarming patients with moderate and severe hypothermia. ECLS = extracorporeal life support. [© Doug Brown, MD, FRCPC.] commercial temperature management systems) remains uncertain due to unproven benefits and the potential for procedure- and device-related morbidity. 28 The use of body cavity lavage rewarming has mostly been replaced by minimally invasive rewarming methods for stable patients and by extracorporeal life support (ECLS), where available, for unstable patients or those in cardiac arrest. 7 For stable patients who are slow to rewarm, it is reasonable to use warm saline (38°C to 42°C) bladder lavage because the potential for morbidity is very low, particularly when com pared with peritoneal, thoracic, gastric, or rectal lavage. The use of warm humidified gases for ventilation is recommended; however, it does not contribute significantly to rewarming. 29,30 Other invasive interventions, such as advanced airway management and central line placement, should be performed if required, despite the slight risk of triggering a malignant dysrhythmia (avoid guidewire or catheter tip contact with the heart). Stage III patients are at high risk for cardiac arrest, so patients with a core temperature <28°C, hypotension out of proportion to the degree of hypothermia, or ventricular dysrhythmias should be transferred to an ECLS center if one is available within a few hours of transport 7,9 unless comorbidities, such as major trauma, necessitate transfer to an alternate center. For stage III patients with vital signs, the minimum sufficient circulation is unknown, and there is no accepted threshold to transi tion a potentially unstable patient with vital signs onto ECLS. In studies Tintinalli_Sec16_p1333-1418.indd 1343 8/2/19 8:22 PM

major trauma, necessitate transfer to an alternate center. For stage III patients with vital signs, the minimum sufficient circulation is unknown, and there is no accepted threshold to transi tion a potentially unstable patient with vital signs onto ECLS. In studies Tintinalli_Sec16_p1333-1418.indd 1343 8/2/19 8:22 PM 1344 SECTION 16: Environmental Injuries involving mostly healthy young people, patients with stable vital signs do well with minimally invasive rewarming, 31 but in older comorbid populations (who may have poor tolerance for low cardiac output), there is emerging evidence that ECLS may be beneficial for certain patients with a core temperature <28°C (Table 209-3). 32,33 Treat acid-base disturbances in hypothermic patients primarily by rewarming and reassessment. For the intubated patient, respiratory parameters should target an uncorrected partial pressure of carbon dioxide of 40 mm Hg (this is known as an alpha-stat strategy, where correction factors are not applied to account for the temperature difference between patient temperature and blood gas analysis temperature). 6,34,35 In situations where blood gas measurement is not possible, the role of ETCO 2 measurements to guide ventilation is unclear. Some authors suggest the values should not be used, 21 while others suggest targeting normal ETCO2.7,32 Further research is ongoing, and this author’s current practice is to use blood gas results when available and, in their absence, to follow the recommendations for hypothermic cardiac surgery and titrate ventilation to a temperature-corrected ETCO 2.36,37 Do not give bicarbonate to correct pH, unless there is a clear alternate indication, as in certain toxic ingestions.  HYPOTHERMIC CARDIAC ARREST (STAGE IV) Because hypothermia induces a low-flow state, it can be challenging to detect a pulse in a hypothermic patient, so perform a careful check for signs of life. If any breathing, movement, or pulse is detected, watchful waiting and supportive care are recommended; otherwise, start CPR. High-quality CPR, prevention of further heat loss, and transfer to an ECLS center when possible are the most important priorities for stage IV patients. When transfer to ECLS is definitely not available and the patient is in cardiac arrest, thoracic lavage with normal saline (38°C to 42°C) using a single or dual chest tube method may be the second-best rewarming strategy when combined with ongoing CPR. Controversy exists regarding the use of epinephrine and defibrillation in hypothermic cardiac arrest. The European Resuscitation Council 2010 guidelines recommend up to three defibrillation attempts, to withhold epinephrine until the core temperature exceeds 30°C, and to double the dose frequency until the temperature is above 35°C. 29 In contrast, the American Heart Association 2010 guidelines state that it may be reasonable to use vasopressors during cardiac arrest. 30 Given the conflicting animal and human data that each recommendation is based on, a rea sonable approach is to use standard advanced cardiac life support protocols for up to three cycles and, in the absence of clinical response, defer further defibrillation or epinephrine until core temperature increases significantly or the patient’s clinical status changes. One of the major challenges with stage IV hypothermia is to select the patient with cardiac arrest caused by hypothermia for prolonged resuscitation while avoiding futile resuscitation for patients with nor mothermic cardiac arrest and subsequent cooling. Measuring a serum potassium >12 mmol/L or a core temperature >32°C can help to avoid futile resuscitation, but in their absence, the clinician is dependent on the history and physical to select the patients who may benefit from prolonged resuscitation (Figure 209-3).

nor mothermic cardiac arrest and subsequent cooling. Measuring a serum potassium >12 mmol/L or a core temperature >32°C can help to avoid futile resuscitation, but in their absence, the clinician is dependent on the history and physical to select the patients who may benefit from prolonged resuscitation (Figure 209-3). Stage IV patients with return of spontaneous circulation should be rewarmed to ≥32°C and receive standard postarrest management 30 with consideration given to targeted temperature management3 or therapeutic hypothermia2 based on institutional preference. Patients rewarmed to ≥32°C without return of spontaneous circulation who are in asystole can be considered for termination of resuscitation in the absence of other causes of reversible cardiac arrest. DISEASE COMPLICATIONS Early complications are those that develop during the rewarming pro cess, whereas late complications occur after rewarming. Most early complications have been described in the previous “Cold Physiology” section and can be minimized by handling patients carefully and using minimally invasive or extracorporeal rewarming techniques. Early ECLS-related complications are mostly related to cannulation and include bleeding, vessel perforation, dissection, and distal limb ischemia. Possible late complications are numerous and can affect most organ systems. Common respiratory complications include pulmonary edema and infection. Common cardiac complications include prolonged hypotension or dysrhythmias. A variety of neurologic injuries, such as seizure disorders, peripheral neuropathy, impaired cognitive function, or persistent vegetative state, are possible in cases of severe or prolonged ischemia. Similar to other critically ill patients, multiorgan failure is possible, including, but not limited to, acute respiratory distress syndrome, renal failure, liver failure, rhabdomyolysis, disseminated intravascular coagulopathy, bowel ischemia, and adrenal insufficiency. 1 With stage IV hypothermia, colder core temperatures and longer durations of CPR generally predict increased complications. Cardiac stunning 39 and respiratory failure are two important potential late complications of stage IV hypothermia due to the potential need for prolonged ECLS or ECMO. DISPOSITION AND FOLLOW-UP Patients suffering from primary hypothermia who are rewarmed in the ED can be discharged home with routine follow-up by a primary care provider. Patients suffering from secondary hypothermia may require admission or specialized follow-up depending on the nature and severity of the underlying condition. Patients who are unable to be rewarmed within a reasonable period of time will require admission with cardiac and core temperature monitoring (stage III and IV patients require a critical care setting). SPECIAL CONSIDERATIONS/SPECIAL POPULATIONS  CHILDREN Pediatric stage IV hypothermia patients require special consideration, and in general, expert consultation is warranted prior to termination of resuscitation. They have a larger surface area–to–body mass ratio, which means they have the potential to cool more rapidly than adults. Addi tionally, children may have an increased ability to tolerate and recover from hypoxic brain injury. Therefore, prolonged resuscitation may be indicated, even in cases of normothermic hypoxic cardiac arrest, if there is simultaneous very rapid cooling.

means they have the potential to cool more rapidly than adults. Addi tionally, children may have an increased ability to tolerate and recover from hypoxic brain injury. Therefore, prolonged resuscitation may be indicated, even in cases of normothermic hypoxic cardiac arrest, if there is simultaneous very rapid cooling. The classic outlier in the literature is the case of a 2.5-year-old girl who went immediately under the water of a 5°C creek and suffered a normothermic hypoxic cardiac arrest but was rapidly cooled (pinned against a rock under fast-flowing cold water); 66 minutes later, she was removed from the water in cardiac arrest, received 3 hours of CPR, had a core temperature of 19°C, was successfully resuscitated using ECLS, and had a good neurologic outcome.  EXTRACORPOREAL LIFE SUPPORT OR EXTRACORPOREAL MEMBRANE OXYGENATION The use of ECLS/ECMO for the management of stage IV hypothermia can dramatically improve survival for patients, with a number needed to treat of approximately 2 (absolute risk reduction of death, 50% to 90%). 7,9 Well-selected patients treated in an ECLS/ECMO center have an approximately 50% to 100% survival rate, compared with a rate of approximately 10% to 30% if treated in a center without extracorporeal rewarming. 7,40 Hypothermic patients have tolerated prolonged periods of CPR (≥5 hours) with a good neurologic outcome. 9,41,42 The combination TABLE 209-3 Criteria for ECLS Rewarming in Severe Hypothermia (HT III) Endorsed by the International Commission for Mountain Emergency Medicine •   Failure to improve with external active and minimally invasive rewarming methods •   Life-threatening dysrhythmia •   Hypotension (systolic blood pressure <90 mm Hg) •   Respiratory failure •   Refractory acidosis Abbreviations: ECLS    = extracorporeal life support; HT III = hypothermia stage III. Tintinalli_Sec16_p1333-1418.indd 1344 8/2/19 8:22 PM