Best Review Article
hypoglycemia, malnutrition, ETOH, Addison’s, infection, and Myxedema (especially if failure to rewarm)
Do not need to worry until temp hits 30-32° C, <90 F. Stop shivering at 31°.
People die from poor judgment from the hypothermia, not hypothermia itself.
Sudden immersion in cold water kills not b/c of hypothermia, but b/c reflex gasp. Muscle weakness and tetany can cause drowning, abates in 5 minutes. Also cardiac dysrhythmia from huge catecholamine surge. Reflex can be attenuated by splashing cold water on face for a minute or two.
If you place patients in rewarming bath, will get afterdrop b/c warming is surface to core. Also will stop shivering as soon as placed in bath. Warming far safer if done core to surface.
Paradoxical undressing: at end stages of hypothermia, vessels can no longer maintain vasoconstriction and will dilate causing pt to feel quite warm, just like ETOH.
If your feet are cold, put on a hat because the vasoconstriction 2° to exposed skin is systemic not local. Note: Our perception of our body temperature is based on our skin temperature not our core.
Bradycardia (refractory to atropine), but should not be treated anyway as it is appropriate to body temperature.
Cold diuresis is seen
Lidocaine works poorly, Bretylium works well as prophylaxis, not treatment. Randomized trial of amiodarone and bretylium vs. placebo showed no benefit in dogs (Acad Emerg Med 2003;10 187-191)
Crit should increase 2% for each decrease in degree Celsius
Must be greater than 35 degrees to be considered dead
Place rectal probe in 15 cm.
FS, ABG, CBC, Lytes, LFTS/Lipase, PT/PTT, Tox, TFTs, Cortisol
Shivering 1.5 C/hr
Warming Blanket 2-3 C/hr
Active rewarming if pt temp <32, CNS sx, or age extremes
Warm O2-1 C/hr with mask, 1.5-2 C/hr ET tube
IV Fluids-do not add, but do not take away either (1.5 min on high in microwave)
Peritoneal Lavage-3 C/hr
Chest Tubes-3 C/hr
Cardiac Bypass-9 C/hr
Therma-STAT/Thermarescue-hand vacuum 3 C/hr
Osborn (J) Waves-diagnostic only, usually seen at 32 or less, II,V6. Not pathognomonic. Simply early repolarization effect.
If K>10, pt is not coming back, even if cold and dead.
Environmental Emergencies: Cold Illness Eric B. Tulley, MD Madigan Army Medical Center – University of Washington Affiliated Program in Emergency Medicine Fort Lewis, Washington David A. Townes, MD, MPH Assistant Professor and Associate Residency Director Division of Emergency Medicine University of Washington School of Medicine Seattle, Washington Introduction Under ideal circumstances, the human body maintains its temperature within a range permitting normal physiology to occur (approximately 97-99°F). Small deviations from this normal range may result in dramatic changes in physiology manifesting clinically as heat and cold illness. Heat and cold illness include a spectrum of conditions from very mild to life threatening. It is important for the emergency medicine physician to be able to recognize and treat all types of heat and cold illness. This discussion outlines the basic epidemiology, clinical presentation, prehospital, and emergency department management of hypothermia, the most severe form of cold illness. Heat production is primarily a function of metabolism and a by-product of muscular activity while heat loss occurs by radiation, conduction, convection, and evaporation (1). Hypothermia results from an imbalance between heat production and heat loss. Hypothermia is defined as the pathologic state in which the core body temperature falls below 35°C (95°F) (1-3). Hypothermia may be further divided into mild (35°-32°C), moderate (32°- 28°C), severe (28°-20°C), and profound (< 20°C) (Table 1). Table 1: Hypothermia Core Body Temperature (°C/°F) Mild Moderate Severe Profound 35°-32°C 32°- 28°C 28°-20°C < 20°C 95°-89.6°F 89.6°F-82.4°F 82.4°F-68°F <68°F It is also helpful to distinguish between primary and secondary hypothermia. Primary hypothermia, or accidental hypothermia, occurs when an otherwise healthy individual is exposed to environmental circumstances, such as adverse weather or cold-water immersion that causes his/her core temperature to drop. Secondary hypothermia, or urban hypothermia, occurs when the drop in core temperature is a secondary complication of a primary disease process such as ethanol intoxication, trauma or acute myocardial infarction. Epidemiology In the United States, hypothermia is seen in both urban and rural/wilderness settings with a majority occurring in urban areas. In the wilderness, the typical victim of hypothermia is an outdoor enthusiast who is either not prepared for the conditions or becomes lost, ill, or injured preventing him from reaching adequate shelter. In urban settings, hypothermia typically affects individuals who are unable to obtain adequate shelter due to illness or circumstance. Hypothermia may be seen in a variety of settings during any time of the year. In one study of 428 cases of hypothermia, 69 occurred in Florida (6). In the United States, between 1979-1995 there were an average of 723 deaths due to hypothermia per year (2). In Canada between 1992-1996, there were 411 deaths or approximately 102 deaths per year due to hypothermia (3). Since hypothermia may be unreported or unrecognized as a contributing cause of death in trauma and medical illness, the actual incidence of mortality due to hypothermia is undoubtedly higher. While primary hypothermia more frequently affects young males and infants, secondary hypothermia is seen more commonly in individuals who are elderly, homeless, mentally ill, trauma victims, or those with multiple co-morbid conditions or chronic illness (2). Risk factors for hypothermia include any state or condition that increases heat loss, decreases heat production or thermogenesis, impairs thermoregulation or inhibits the individuals ability to seek insulation or shelter (Table 2). Table 2: Hypothermia Risk Factors Increased Heat Loss Burns Environmental exposure/immersion Exfoliative dermatitis Iatrogenic Ichthyosis Pharmacological Psoriasis Toxicological Decreased Heat Production/Thermogenesis Extreme exertion Extremes of age Kwashiorkor Hypoadrenalism Hypoglycemia Hypopituitarism Hypothyroidism Impaired shivering Inactivity Malnutrition Marasmus Impaired Thermoregulation Acute spinal cord transection Anorexia nervosa Cerebral vascular accident CNS trauma Diabetes Hypothalmic dysfunction Metabolic Multiple sclerosis Neoplasm Neuropathy Parkinsons disease Pharmacological Subarachnoid hemorrhage Toxicological Miscellaneous Episodic hypothermia Giant cell arteritis Pancreatitis Recurrent hypothermia Sarcoidosis Sepsis Shaken baby syndrome Uremia Clinical Presentation Patients with hypothermia may present in a variety of ways. The diagnosis may be obvious when there is a history of cold exposure. Primary hypothermia in a patient after a prolonged search and rescue in a wilderness setting is one example where the diagnosis is fairly straightforward. The diagnosis however may be more elusive causing a delay in diagnosis or an incorrect diagnosis. Patients with altered mental status, a history of trauma, and those with no obvious history of cold exposure may all be hypothermic. Often in cases of secondary hypothermia, there is a delay in diagnosis due to the underlying medical condition that complicates the picture. In the patient with mild to moderate hypothermia, the patient may complain of nausea, dizziness, fatigue, or hunger. He may exhibit poor judgment, slurred speech, or altered mental status. In severe cases of hypothermia, the patient may present with altered mental status including coma, as well as depression of cardiac, respiratory and renal function. While in both hyperthermia and hypothermia there is correlation between the patients core temperature and signs and symptoms, the correlation appears to be more linear in hypothermia. Patients with hypothermia present with a spectrum of illness that correlates well with their degree of hypothermia. The pathophysiologic response to hypothermia is outlined in Table 3 (1-6). Table 3: Correlation of Core Temperature and Physiologic Changes Grade °C °F Physiologic Changes Mild 35 95.0 Maximum shivering, impaired judgment, confusion 34 93.2 Tachycardia, tachypnea, increased SVR, cold diuresis 33 91.4 Bradycardia, respiratory depression, hyperglycemia, dysarthria, ataxia Moderate 32 89.6 Stupor, lethargy, arrest of shivering thermogenesis 31 87.8 Atrial arrhythmia, Osborn J-waves on EKG, worsening bradycardia 30 86.0 Insulin ineffective, decreased oxygen consumption 29 85.2 Progressive decreased level of consciousness, pulse, respiratory rate Severe 28 82.4 Increased susceptibility for ventricular fibrillation, pulse rate and oxygen consumption decreased by 50% 27 80.6 Loss of reflexes and voluntary movement, hypoglycemia 26 78.8 Acid-base disturbances, no response to pain 25 77.0 Cerebral blood flow decreased by 2/3, pulmonary edema, apnea 24 75.2 Hypotension 23 73.4 Corneal and oculocephalic reflexes absent 22 71.6 Maximum risk for ventricular fibrillation, oxygen consumption 25% of normal Profound 20 68.0 Lowest resumption of cardiac activity, pulse 20% of normal 19 66.2 Asystole Hypothermia affects multiple systems of the body including cardiac, nervous, respiratory, and coagulation. In general, the initial response to cold is an increase in metabolic rate with tachycardia, tachypnea, and diuresis. As the body continues to cool, there is a reversal of this process with bradycardia, respiratory and mental depression, and renal shutdown. Hypothermia should be thought of as a progressive pathologic state that without intervention will lead to death. In mild hypothermia, patients present with shivering, ataxia, cyanosis, dysarthria, tachycardia, and tachypnea. Once the patients temperature drops below 32°C (89.6°F) , heat production via shivering stops and the progression to moderate and severe hypothermia may hasten. In moderate hypothermia, the body loses its compensatory mechanisms and the patient becomes increasingly lethargic, bradycardic, bradypneic with worsening enzymatic dysfunction with resultant acid base abnormalities. Patients with severe hypothermia demonstrate signs of physiologic derangement including coma, absence of reflexes, profound metabolic disturbances, apnea, hypotension, and dysrhythmias. Cardiovascular System The cardiovascular system, similar to other systems of the body, responds to hypothermia with an initial increase in activity followed by depression and eventual loss of activity. Tachycardia and vasoconstriction, the initial response to cold stress, result in an increase in blood pressure and cardiac output. With worsening hypothermia, there is a reversal of this process, bradycardia occurs, oxygen demand decreases, and cardiac output falls. Eventually, severe bradycardia, ventricular fibrillation, or asystole ensues. Coagulation System The patient with moderate to severe hypothermia may develop a coagulopathy. The likely explanation is that lower temperatures adversely affect enzymes responsible for the coagulation cascade. This will not be reflected in laboratory studies such as PT, PTT that may be normal. Hypothermic patients will also be thrombocytopenic and may develop physiologic hypercoagulability similar to DIC. Nervous System The nervous system is especially intolerant of hypothermia. The response to mild hypothermia may include impaired judgment and memory. As the severity of hypothermia worsens, slurred speech, ataxia and decreased level of consciousness may be observed. Patients may exhibit foot stomping and paradoxical undressing. Finally, in severe hypothermia, there may be a shut down of the nervous system resulting in coma and death. Renal System The initial response of the renal system to hypothermia is increased activity resulting in diuresis. This may result from peripheral vasoconstriction and relative central hypervolemia. Many people have experienced this cold weather diuresis. More severe hypothermia results in renal failure and renal shutdown. Respiratory System The initial response to hypothermia is an increase in respiratory rate and a resultant respiratory alkalosis. As the body cools, the respiratory rate falls and the patient develops carbon dioxide retention, respiratory acidosis and ultimately respiratory arrest. Diagnosis The diagnosis of hypothermia is simple. A low temperature recorded on an accurate thermometer is all that is needed. Hypothermia may be missed by the simple mistake of either not obtaining a complete set of vital signs or being misled by an inaccurate external auditory or oral reading. In the emergency department, if hypothermia is suspected, a rectal temperature should be performed to confirm the diagnosis. The diagnosis of hypothermia may also be supported by the finding of Osborn J waves on EKG. This upward deflection of the terminal S wave (at the junction of the QRS complex and the ST segment) occurs at or near 32°C. It is initially seen in leads II and V6. As the core temperature drops, Osborn J waves develop in the precordial leads. Osborn J wave Prehospital Care In the prehospital setting, the initial approach to the hypothermic patient is similar to any potentially critically ill or injured patient. The assessment should begin with a primary and secondary survey. If hypothermia is suspected or is a concern to develop, all wet clothing should be removed and the patient placed in warm, dry, insulating material such as a sleeping bag. It is important to place something between the patient and the ground rather than just cover the patient to minimize heat loss. While exercise may generate heat, it should be avoided in the hypothermic patient as it may exacerbate core temperature afterdrop by increasing peripheral dilation (see below). For this reason, the patient should be maintained in a horizontal position as much as possible. Massaging cold extremities is also contraindicated as it may suppress shivering and increase peripheral vasodilation. Further prehospital care will depend on the resources available and the distance and time to definitive care. There are a variety of devices used by search and rescue personnel to begin rewarming in the field. If possible, an intravenous line should be established and warmed intravenous fluids given. This may prove difficult secondary to peripheral vasoconstriction. Heated, humidified air or oxygen should be administered if available. The severely hypothermic patient must be handled with extreme caution, as the hypothermic myocardium is sensitive to ventricular fibrillation. The treatment of ventricular fibrillation in the hypothermic patient remains unclear but it has been recommended that defibrillation be attempted in the prehospital setting if available. If there is no response after three attempts, the patient should be aggressively rewarmed prior to subsequent attempts. Emergency Department Management General Approach Once the diagnosis of hypothermia has been established, the appropriate intervention depends on the severity of hypothermia and the clinical state of the patient. There is no algorithm for the treatment of hypothermia. Due to the progressive physiologic instability associated with greater degrees of hypothermia, as the severity of hypothermia increases, the treatment should be more aggressive. As noted, it is important to be very careful when moving the severely hypothermia patient due to the increased susceptibility of the myocardium to ventricular fibrillation. It is important to remember other clinical factors including underlying medical illness, intoxication, central nervous system disease, trauma, and infection that must be considered in the patient with hypothermia. In any patient with a core temperature measurement of less than 35°C (95°F), treatment begins with evacuation of the patient from the cold environment and removal of any wet or cold clothing if not already done in the prehospital setting. The patient should be placed on a cardiac monitor, intravenous access established, and warming measures initiated. Of note, pulse oximetry may be inaccurate in the hypothermic patient. While the management of hypothermia involves supportive care, the definitive treatment is rewarming. For example, many of the arrhythmias associated with hypothermia resolve when the patients core temperature normalizes. Bradycardia in the hypothermic patient does not respond to atropine, rather rewarming. The treatment for coagulopathies is rewarming rather than administration of clotting factors. There is a wide spectrum of rewarming methods and the correct one will depend on the severity of hypothermia, the clinical state of the patient and the experience of the individual practitioner. Rewarming methods discussed below may be divided into active and passive as well as non-invasive and invasive. Additional Diagnostic Measures There are no laboratory studies specific for hypothermia. Laboratory evaluation should be driven by the clinical situation. In any patient with significant hypothermia, it is reasonable to obtain a complete blood count, a basic chemistry panel, a coagulation panel, arterial blood gas, creatinine kinase, ethanol level, and toxicology panel. These should be monitored/repeated during warming of the hypothermic patient. Physiologic changes associated with hypothermia include a shift in the oxyhemoglobin dissociation curve to the left, an increase in hematocrit due to reduced plasma volume and a low or normal white blood cell count even in the setting of infection (6). There is some controversy surrounding the interpretation of arterial blood gases in the hypothermic patient. It has been suggested that arterial blood gas samples need to be corrected for temperature because they are warmed to 37° C for analysis. A mathematical formula was developed to correct the change in pH for every ° C. In clinical practice however, one need only to compare results with normal results at a given temperature. Thus, samples warmed to 37° C may be compared to normal results at 37° C. At any temperature, an uncorrected pH of 7.4 and a PCO2 of 40 mm Hg represent normal acid-base balance (6). As noted earlier, the initial respiratory response to hypothermia is hyperventilation resulting in a respiratory alkalosis. The subsequent respiratory depression results in a respiratory acidosis. This pattern, combined with a variety of other metabolic changes associated with hypothermia make prediction of acid-base balance difficult (6). In one case series of 135 hypothermic patients, 30% were acidotic and 25% were alkalotic (7). Imaging should also be directed by the clinical situation. A chest x-ray may be helpful if infectious or aspiration pneumonia is suspected. If the patient has sustained any trauma, imaging studies should be done based on the clinical situation. Temperature Monitoring It is important to monitor the core temperature of the hypothermic patient to assess the effectiveness of re-warming. This may be accomplished either by continuous or serial monitoring by a rectal or esophageal probe. Both have their advantages and disadvantages. The rectal probe may lag significantly behind core temperature changes due to cold fecal material. The esophageal probe may give falsely elevated temperature readings due to heated ventilation used for core rewarming. It also requires the patient be intubated. It may be of benefit to have both types of temperature monitoring available to most accurately assess effectiveness of rewarming. Afterdrop Afterdrop, or core temperature afterdrop, is a fall in the patients core temperature as rewarming is instituted. While there is some controversy over the exact mechanism of afterdrop, one theory is that the warming of peripheral sites and abated vasoconstriction results in cool peripheral blood returning back to the circulation lowering the patients core temperature. It is most dramatic when a large temperature gradient exists between the cool periphery and the relatively warm core. Afterdrop may occur when a frostbitten extremity is warmed prior to thermal stabilization of the patient. Afterdrop may cause worsening physiologic derangements and increase the chance of dysrhythmia and cardiac arrest. Continuous core temperature monitoring is thus imperative in anyone with significant symptoms or who has a core temperature less than 32°C (89.6°F). Fluid Resuscitation In general, hypothermic patients will be dehydrated and volume depleted. The patient should be given a challenge of normal saline or preferably, saline with 5% dextrose as hypothermic patients may be hypoglycemic. Lactated ringers may be used but since the hypothermic liver cannot metabolize lactate, should be avoided when possible. The patient should be monitored carefully for signs of fluid overload. Passive Rewarming In passive rewarming, the patient is moved from the cold environment and their own thermogenesis slowly warms them. No external heat is added to the patient. Any wet or cold garments should be removed and the patient surrounded with dry material that provides insulation such as a blanket or sleeping bag. It is important to cover the patients head to reduce heat loss. Passive rewarming should be reserved for the patient with mild hypothermia who is still able to generate heat by shivering. Active External Rewarming As the name implies, in active external rewarming, heat is added to the patient from an external source. It is the method of choice in the patient with mild to moderate hypothermia whose thermogenesis mechanisms may be impaired or inadequate due to level of hypothermia (especially below 32°C), illness, intoxication, or medication. Active external rewarming may be accomplished by a variety of methods including heat packs, heat lamps, blankets, warm water immersion, warmed blankets, and forced air systems. During active external rewarming the provider must monitor presumptively for afterdrop resulting from the return of cool peripheral blood to the core in response to peripheral vasodilation. This inappropriate warming of distal extremities and worsening hypothermia is just one of the concerns in active external rewarming. Other problems of active external rewarming include difficulty monitoring patients in an immersion bath and tissue injury from radiant heat sources. Forced air systems are one of the most widely accepted means of active external rewarming in current use. Forced air systems are easy to apply, allow for patient monitoring, and seem to limit afterdrop. Rates of warming with these systems approach 1.0-2.5 °C/hr (2,3). The Bair Hugger (Augustine Medical, Inc.) is a well-known example. Active Core Rewarming Patients who present with moderate to severe hypothermia may require active core rewarming. Active core rewarming includes a variety of techniques that vary in terms of complexity and invasiveness. Perhaps the simplest and least invasive form of active core rewarming is the administration of warm intravenous fluids and warm inhaled humidified air/oxygen. This may be an effective method of rewarming the moderately hypothermic but stable patient. It is necessary to warm fluids to 44°C/111°F (1 liter warmed in a conventional microwave for approximately 2 minutes) and run the fluid through large bore, short tubing. An alternative is the use of an inline heating device such as the Hot Line and Level 1 infuser (Level 1 Technologies, Inc.). Warmed humidified air/oxygen should also be heated to 42-44 °C. This may require special equipment or modification to the existing heating circuit. There are systems available for the purpose of heating oxygen for delivery to the hypothermic patient. These heating systems reportedly increase the core temperature at a rate of 1-2.5 °C /h (2,3). Active core rewarming also includes more invasive methods including cavity lavage with warm fluids (gastric, bladder, peritoneal, and pleural), extracorporeal blood rewarming and mediastinal lavage. These methods achieve the most rapid rewarming rates but due to their invasiveness and potential complications, they should be reserved for only the most severe cases of hypothermia including hypothermic cardiac arrest, failure to respond to other rewarming techniques, completely frozen extremities and in rhabdomyolysis with electrolyte abnormalities (6). Recent experience suggests an expanded role for closed pleural irrigation through large-bore thoracostomy tubes (9). Sterile saline warmed to 40-42°C is infused anteriorly and continuously drained from the efferent posterior midaxillary tube. Mediastinal heat transfer is directed more strategically and approximates that achieved with peritoneal lavage. The insertion of a tube on the left side of the chest should be avoided, since it may induce ventricular fibrillation. The data of the use of these invasive modalities remains limited. Extacorporeal Blood Rewarming Extracorporeal blood rewarming is used to aggressively rewarm blood in the severely hypothermic patient who has been refractory to other methods of rewarming. There are several methods of extracorporeal blood rewarming including hemodialysis, arteriovenous, veno-venous, and cardiopulmonary bypass. The biggest advantage of these methods is that the blood and thus the patient can be rewarmed rapidly when compared to other methods of core rewarming. These methods offer additional advantages including continued delivery of oxygenated blood despite the absence of mechanical cardiac activity (cardiopulmonary bypass). Extracorporeal rewarming should be considered for patients without perfusion who have no documented contraindications to resuscitation, patients with severe hypothermia, and those with completely frozen extremities (9).While no agreed upon criteria exist, several centers reserve this method of rewarming for the patient who presents with a pH above 6.5, a serum potassium below 10 mmol/L, and a core temperature above 53.6°F (8). Hypothermic Cardiac Arrest The treatment of cardiac arrest in the hypothermic patient is difficult. For a variety of reasons including severely depressed cardiac activity and absent peripheral pulses, just establishing the diagnosis of cardiac arrest in the hypothermic patient is not straightforward. It also may be very difficult to delineate asystole from ventricular fibrillation, especially in the prehospital setting. Some stable arrhythmias such as atrial arrhythmias are common and will resolve spontaneously as the patients core temperature is elevated. The treatment of these arrhythmias should focus on rewarming, fluid resuscitation, and correction of electrolyte and acid-base imbalances rather than on the use of anti-arrhythmics. However, preexisting ventricular ectopy is often suppressed by the cold and reappears during rewarming. The use of anti-arrhythmics in ventricular fibrillation is still somewhat unclear. In limited studies, only bretylium has been shown to be of benefit in the hypothermic patient. Further studies are needed to establish the use of these mediations in this clinical setting. Once the diagnosis of cardiac arrest has been established, cardiopulmonary resuscitation (CPR) should be initiated. This however, is another area of controversy. Due to the decreased compliance of the heart and chest wall in the hypothermic patient, it is unclear what rate and force should be used during CPR. It does appear that CPR in the hypothermic patient increases survival in cardiac arrest. Be aware that even though a hypothermia victim may appear dead, full resuscitation and recovery is possible, although unusual. Always act on the premise that “no one is dead until warm and dead”. Disposition The patient with mild hypothermia who responds to passive rewarming may be discharged from the emergency department. Patients with severe or profound hypothermia require admission to a monitored setting. The disposition of the patient with moderate hypothermia should be made depending on the patients age, comorbid factors, social situation, and response to therapy in the emergency department. Conclusion Hypothermia encompasses a wide range of clinical presentations from very mild to life threatening. While it is easy to make the diagnosis, it is important to consider the diagnosis in patients who present with altered mental status, medical illness, multiple trauma, and toxic ingestion. The treatment of hypothermia will depend on the severity. Mild hypothermia may be treated with passive external rewarming while those with moderate and severe disease should be treated with active external rewarming. Active core rewarming should be reserved for those patients with severe and profound hypothermia and those who do not respond too less aggressive methods. The treatment of hypothermia involves supportive care but the definitive treatment is rewarming of the patient. Many of the sequelae of hypothermia including arrhythmia responds to rewarming instead of traditional treatments such as anti-arrhythmics. References 1. Currier J, et al. Hypothermia. In: Harwood-Nuss A, Wolfson AB, Linden CH, Sheperd SM, and Stenklyft PH eds. The Clinical Practice of Emergency Medicine. 3rd ed. Philadelphia, PA: Lippincott Williams & Wilkins Publishers; 2001: 1664-7. 2. Hanania N, Zimmerman J. Environmental emergencies: accidental hypothermia. Crit Care Clin. 1999; 15(2): 235-49. 3. Biem J, Niels K, Dosman J. At the bedside, out of the cold: management of hypothermia and frostbite. CMAJ. 2003; 168(3): 305-11. 4. Danzl D. Accidental hypothermia. In: Rosen P, Barkin RM et al eds. Emergency Medicine: Concepts and Clinical Practice. 5th ed. St. Louis, MO: Mosby-Year Book, Inc.; 2002:1979- 96. 5. Corneli HM. Hot topics in cold medicine: Controversies in accidental hypothermia. Clinical Pediatric Emergency Medicine. 2000; 2:179-191. 6. Aurbach P ed. Accidental hypothermia. In: Wilderness Medicine: Management of Wilderness and Environmental Emergencies. 3rd ed., St. Louis, MO: Mosby-Year Book, Inc.; 1995: 51-103. 7. Miller JW, Danzl DF, Thomas DM. Urban accidental hypothermia: 135 cases. Ann Emerg Med. 1980; 9:456. 8. Aurbach P ed. Accidental hypothermia. In: Wilderness Medicine: Management of Wilderness and Environmental Emergencies. 4th ed., St. Louis, MO: Mosby-Year Book, Inc.; 2001: 135-178. 9. Danzl DF, Pozos RS Accidental hypothermia N Engl J Med 1994;331:1756-60.
Risk factors for hypothermia include any state or condition that increases heat loss, decreases heat production or thermogenesis, impairs thermoregulation or inhibits the individual’s ability to seek insulation or shelter (Table 2).
Table 2: Hypothermia Risk Factors
Increased Heat Loss
Burns Environmental exposure/immersion Exfoliative dermatitis Iatrogenic Ichthyosis Pharmacological Psoriasis Toxicological
Decreased Heat Production/Thermogenesis
Extreme exertion Extremes of age Kwashiorkor Hypoadrenalism Hypoglycemia Hypopituitarism Hypothyroidism Impaired shivering Inactivity Malnutrition Marasmus
Acute spinal cord transection Anorexia nervosa Cerebral vascular accident CNS trauma Diabetes Hypothalmic dysfunction Metabolic Multiple sclerosis Neoplasm Neuropathy Parkinson’s disease Pharmacological Subarachnoid hemorrhage Toxicological
MiscellaneousEpisodic hypothermia Giant cell arteritis Pancreatitis Recurrent hypothermia Sarcoidosis Sepsis Shaken baby syndrome Uremia
Clinical Presentation Patients with hypothermia may present in a variety of ways. The diagnosis may be obvious when there is a history of cold exposure. Primary hypothermia in a patient after a prolonged search and rescue in a wilderness setting is one example where the diagnosis is fairly straightforward. The diagnosis however may be more elusive causing a delay in diagnosis or an incorrect diagnosis. Patients with altered mental status, a history of trauma, and those with no obvious history of cold exposure may all be hypothermic. Often in cases of secondary hypothermia, there is a delay in diagnosis due to the underlying medical condition that complicates the picture. In the patient with mild to moderate hypothermia, the patient may complain of nausea, dizziness, fatigue, or hunger. He may exhibit poor judgment, slurred speech, or altered mental status. In severe cases of hypothermia, the patient may present with altered mental status including coma, as well as depression of cardiac, respiratory and renal function. While in both hyperthermia and hypothermia there is correlation between the patient’s core temperature and signs and symptoms, the correlation appears to be more linear in hypothermia. Patients with hypothermia present with a spectrum of illness that correlates well with their degree of hypothermia. The pathophysiologic response to hypothermia is outlined in Table 3 (1-6).
Table 3: Correlation of Core Temperature and Physiologic Changes Grade °C °F Physiologic Changes Mild 35 95.0 Maximum shivering, impaired judgment, confusion 34 93.2 Tachycardia, tachypnea, increased SVR, cold diuresis 33 91.4 Bradycardia, respiratory depression, hyperglycemia, dysarthria, ataxia Moderate 32 89.6 Stupor, lethargy, arrest of shivering thermogenesis 31 87.8 Atrial arrhythmia, Osborn J-waves on EKG, worsening bradycardia 30 86.0 Insulin ineffective, decreased oxygen consumption 29 85.2 Progressive decreased level of consciousness, pulse, respiratory rate Severe 28 82.4 Increased susceptibility for ventricular fibrillation, pulse rate and oxygen consumption decreased by 50% 27 80.6 Loss of reflexes and voluntary movement, hypoglycemia 26 78.8 Acid-base disturbances, no response to pain 25 77.0 Cerebral blood flow decreased by 2/3, pulmonary edema, apnea 24 75.2 Hypotension 23 73.4 Corneal and oculocephalic reflexes absent 22 71.6 Maximum risk for ventricular fibrillation, oxygen consumption 25% of normal Profound 20 68.0 Lowest resumption of cardiac activity, pulse 20% of normal 19 66.2 Asystole
Hypothermia affects multiple systems of the body including cardiac, nervous, respiratory, and coagulation. In general, the initial response to cold is an increase in metabolic rate with tachycardia, tachypnea, and diuresis. As the body continues to cool, there is a reversal of this process with bradycardia, respiratory and mental depression, and renal shutdown. Hypothermia should be thought of as a progressive pathologic state that without intervention will lead to death. In mild hypothermia, patients present with shivering, ataxia, cyanosis, dysarthria, tachycardia, and tachypnea. Once the patient’s temperature drops below 32°C (89.6°F) , heat production via shivering stops and the progression to moderate and severe hypothermia may hasten. In moderate hypothermia, the body loses its compensatory mechanisms and the patient becomes increasingly lethargic, bradycardic, bradypneic with worsening enzymatic dysfunction with resultant acid base abnormalities. Patients with severe hypothermia demonstrate signs of physiologic derangement including coma, absence of reflexes, profound metabolic disturbances, apnea, hypotension, and dysrhythmias.
Methods include thoracic lavage at 500 mL/min (6.1°C/h), cardiopulmonary bypass (400 kcal/h or 18.0°C/h), thoracic lavage at 2 L/min (19.7°C/h), and warm-water immersion (1500 kcal/h).
The literature describes 2 methods of thoracic lavage; the simplest method uses available equipment and provides rewarming rates equivalent to cardiopulmonary bypass. The technique involves placing 2 left-sided, 38 French chest tubes (third intercostal space midclavicular line and sixth intercostal space midaxillary line). Isotonic saline, in 3-liter bags heated to at least 41°C, is infused through the anterior tube at 2 L/min, then drained by gravity via the posterior tube. When warmed saline was not available, physicians successfully infused warmed tap water. The AV heating method, developed at the University of Washington, employs a modified bypass technique for rapid blood rewarming using a Level One fluid warmer that is familiar to physicians experienced in trauma resuscitation. The treatment is preferred for patients with profound hypothermia and markedly depressed hemodynamic status or cardiac arrest. AV heating requires a spontaneous pulse, since the patient’s intrinsic blood pressure drives flow through the countercurrent module. (In true cardiothoracic bypass, an external pump is built into the machine.) Place catheters into femoral artery and venous cordis. Once catheters are placed, connect the arterial output to the inflow port of a level one countercurrent warmer, where IV fluids are connected. Connect the outflow port to the femoral venous catheter. Circulate water, at a temperature preset on the level one device, around the blood-containing tubing; blood warms as it flows through the countercurrent module. The AV method has rewarmed profoundly hypothermic patients 5 times more rapidly (39 min vs 199 min) than standard methods and was demonstrated to decrease mortality rate. Go to source: eMedicine – Hypothermia : Article by James Li, MD
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In urban environments, failure to rewarm at least 1 C per hour. In this study, pts rewarmed at the same rate no matter which method, unless they were infected (Acad Emerg Med 2006;13(9):913)
Rewarming with Chest Tubes
36-38 F Chest tubes one anterior and one posterior lateral
Use 3L bages of 40-41 C saline
attach auto-transfuser to posterior-lat chest tube to allow cont. emptying
or use one chest tube with a y connector 300 cc aliquots with 2 minute dwell time
Review article with two case reports (Resuscitation 2005;66:99-104)
J Trauma 1991;31:1151 and 1992;32:316
both by Gentilello
Crit Care Med 2011;39:1064
you can pace hypothermia internally (Ann Emerg Med 2007;49(5):)
Who Needs Transfer to ECMO Center?
- Cardiac Instability (a-fib and bradycardia are normal)
- Ventricular Dysrhythmia
- Core <28 (especially 24)
If you insert a central line, insert shallow
Who not to Start Resus on
- Clearly dead before cooling rather than cool before dead
- Core >=32
- Frozen Solid
- Trauma-not salvageable (e.g. decapitation)
- Drowning/Submersion (hypoxic arrest from being under water–before cooling)
- Avalanche with No Airspace (35 minutes of survival to come down to temp-so if pulled out before that point=DEAD; is there snow in mouth?)
Submersion vs. immersion. Former is drowning, latter, pt gets cold and eventually succumbs
Afterdrop is a myth
duration of CPR is not a predictor