Emp-Hypothermia and Frostbite

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Hypothermia And Other Cold-Related Emergencies

The young woman is wheeled through the door at nearly midnight on New Years Eve. The paramedic gives the report: Apparently she has a psych history. Family says shes depressedleft the house a few hours ago and might have taken an overdose. The police found her in a snow bank. Thought she was dead at first, but we got some kind of rhythm on the monitor and I think I felt a pulse. Looking at the gurney, you see no obvious signs of life. As shes transferred onto the hospital bed, the monitor begins alarmingher rhythm has just converted to ventricular fibrillation.
December 2003
Volume 5, Number 12
Authors Luke Hermann, MD Assistant Professor, Department of Emergency Medicine, Mount Sinai School of Medicine, New York, NY. Scott Weingart, MD Chief Resident, Mount Sinai School of Medicine, Department of Emergency Medicine, New York, NY. Peer Reviewers Wyatt W. Decker, MD, FACEP Chair, Department of Emergency Medicine, Mayo Clinic and Mayo Medical School, Rochester, MN. Scott Gallagher, MD, FACEP Aspen Valley Hospital, Aspen, CO. Charles Stewart, MD, FACEP Colorado Springs, CO. CME Objectives Upon completing this article, you should be able to: 1. describe common environmental conditions and physical conditions that predispose a patient to hypothermia; 2. describe the diagnosis and management of frostbite; 3. discuss the prehospital management of coldrelated emergencies; 4. discuss salient points in the history and physical examination that can help identify conditions that can precipitate and/or complicate hypothermia; and 5. list indications and contraindications of rewarming techniques for hypothermia.
YPOTHERMIA develops when more heat is lost than the body can generate. While typically considered a wintertime condition, hypothermia can occur in any weather, and its cause is not limited solely to environmental exposure. Hypothermia can both complicate and even be precipitated by many patient conditions, such as metabolic or circulatory disorders, substance abuse, trauma, age, or even medication use. Rapid identification, careful selection of rewarming strategies, and attention to comorbid illness are required for optimal care of the hypothermic patient. Furthermore, the ED treatment of other cold-related disorders, such as frostbite, plays an important role in long-term outcomes. This issue of Emergency Medicine Practice reviews the evidence regarding the assessment and treatment of hypothermia and other coldrelated disorders.
Critical Appraisal Of The Literature

There are few randomized, controlled trials to guide the clinician on the treatment of hypothermia and cold-related disorders. Hypothermia is difficult to study in a rigorous, prospective manner outside of the laboratory. Most of our knowledge of accidental hypothermia comes from case reports and retrospective analysis, often giving variable results. Many of the studies that elucidated the pathophysiology of hypothermia were performed decades ago and have not been repeated. Human studies are limited to mild hypothermia because of ethical concerns. Animal models have certainly furthered our understanding of the condition, but the results must
Associate Editor
Andy Jagoda, MD, FACEP, ViceChair of Academic Affairs, Department of Emergency Medicine; Residency Program Director; Director, International Studies Program, Mount Sinai School of Medicine, New York, NY. Director, Emergency Department, San Gabriel Valley Medical Center, San Gabriel, CA. Francis M. Fesmire, MD, FACEP, Director, Heart-Stroke Center, Erlanger Medical Center; Assistant Professor of Medicine, UT College of Medicine, Chattanooga, TN. Valerio Gai, MD, Professor and Chair, Department of Emergency Medicine, University of Turin, Italy. Michael J. Gerardi, MD, FAAP, FACEP, Clinical Assistant Professor, Medicine, University of Medicine and Dentistry of New Jersey; Director, Pediatric Emergency Medicine, Childrens Medical Center, Atlantic Health System; Department of Emergency Medicine, Morristown Memorial Hospital. Michael A. Gibbs, MD, FACEP, Chief, Department of Emergency Medicine, Maine Medical Center, Portland, ME. Gregory L. Henry, MD, FACEP, CEO, Medical Practice Risk Assessment, Inc., Ann Arbor, MI; Clinical Professor, Department of Emergency Medicine, University of Michigan Medical School, Ann Arbor, MI; President, American Physicians Assurance Society, Ltd., Bridgetown, Barbados, West Indies; Past President, ACEP. Jerome R. Hoffman, MA, MD, FACEP, Professor of Medicine/Emergency Medicine, UCLA School of Medicine; Attending Physician, UCLA Emergency Medicine Center; Co-Director, The Doctoring Program, UCLA School of Medicine, Los Angeles, CA.
Date of original release: December 1, 2003. Date of most recent review: November 10, 2003. See Physician CME Information on back page.
of Emergency Medicine, Thomas Jefferson University, Philadelphia, PA. Corey M. Slovis, MD, FACP, FACEP, Professor of Emergency Medicine and Chairman, Department of Emergency Medicine, Vanderbilt University Medical Center; Medical Director, Metro Nashville EMS, Nashville, TN. Mark Smith, MD, Chairman, Department of Emergency Medicine, Washington Hospital Center, Washington, DC. Charles Stewart, MD, FACEP, Colorado Springs, CO. Thomas E. Terndrup, MD, Professor and Chair, Department of Emergency Medicine, University of Alabama at Birmingham, Birmingham, AL.
Francis P. Kohrs, MD, MSPH, Lifelong Medical Care, Berkeley, CA. Michael S. Radeos, MD, MPH, Attending Physician, Department of Emergency Medicine, Lincoln Medical and Mental Health Center, Bronx, NY; Assistant Professor in Emergency Medicine, Weill College of Medicine, Cornell University, New York, NY. Steven G. Rothrock, MD, FACEP, FAAP, Associate Professor of Emergency Medicine, University of Florida; Orlando Regional Medical Center; Medical Director of Orange County Emergency Medical Service, Orlando, FL. Alfred Sacchetti, MD, FACEP, Research Director, Our Lady of Lourdes Medical Center, Camden, NJ; Assistant Clinical Professor
Editorial Board
Judith C. Brillman, MD, Residency Director, Associate Professor, Department of Emergency Medicine, The University of New Mexico Health Sciences Center School of Medicine, Albuquerque, NM. W. Richard Bukata, MD, Clinical Professor, Emergency Medicine, Los Angeles County/USC Medical Center, Los Angeles, CA; Medical
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be applied cautiously to humans as physiology differs. The most recent iteration of the American Heart Association/International Liaison Committee on Resuscitation (AHA/ILCOR) guidelines offers an evidencebased consensus opinion on the treatment of hypothermia.1,2 While a good portion of the guidelines deals with the treatment of cardiac arrest in the setting of hypothermia, there are recommendations for the treatment of various core temperatures. For instance, in mild hypothermia (34C-36C), passive rewarming and active external warming are recommended. In moderate hypothermia (30C-34C), passive rewarming and active external rewarming of the truncal areas only is recommended. (The latter recommendation is based on the supposition that rewarming only the trunk will decrease the possibility of afterdrop.) For severe hypothermia (<30C), active internal rewarming is recommended. The strength of evidence, and its limitations, supporting these consensus recommendations is presented later in this review. The state of Alaska has also released consensusbased guidelines, which are posted at http:// www.hypothermia.org.3 These guidelines have rewarming protocols similar to the AHA/ILCOR guidelines. It is interesting to note that the Alaskan protocols also give strong warning regarding afterdrop despite disagreement among experts as to the clinical relevance of this phenomenon.
35C with a non-perfusing rhythm.) Typical manifestations of severe hypothermia include shallow breathing, weak pulse, a progressive decline in consciousness, and, ultimately, death. Although a few cases of extreme cold resuscitation have been reported, most patients whose core temperature drops to less than 23C will not survive. (See also Table 1.)
Frostbite
Frostbite is a disease of prolonged exposure to the cold. Military personnel, the homeless, participants in recreational winter activities, and those with outdoor occupations are all at risk.4 Cofactors for risk of frostbite include inadequate clothing, alcohol use, substance abuse, mental illness, and contact with metal or moisture.5,6 Urban civilian studies show a high incidence of alcohol intoxication and psychiatric illness in frostbite cases.6,7 Individuals who are acclimated to cold environments may have more effective defenses against frostbite, possibly because they are more aware of how to prepare for the cold.4
Pathophysiology
Accidental hypothermia can be classified as either primary or secondary. Primary hypothermia occurs when an otherwise healthy subject is exposed to temperatures cold enough to overcome the bodys ability to appropriately thermoregulate. While this type of hypothermia is frequently associated with prolonged activity in a cold environment, it is important to note that it can occur in any setting, even when ambient temperatures are relatively mild.8 Interestingly, in the largest prospective study of accidental hypothermia to date, 69 of 428 cases occurred in Florida.5 Annual mortality due to primary hypothermia in the United States averages slightly over 700 cases per year, with most occurring in urban settings.9 Primary hypothermia may be complicated by drug and alcohol use, and/or concurrent homelessness, which may contribute to increased mortality in urban at-risk populations. Secondary hypothermia occurs in patients whose underlying medical conditions disrupt adequate thermoregulatory mechanisms. As these patients are typically admitted to the hospital with a primary diagnosis other than hypothermia (e.g., sepsis), the incidence of secondary hypothermia may very well be grossly underreported.
Epidemiology
Hypothermia is typically defined as a core body temperature of 35C (95F) or less. While texts propose different definitions, core temperatures of 30C-35C with a perfusing rhythm are generally defined as mild-tomoderate hypothermia. Symptoms include shivering, confusion and disorientation, memory loss, drowsiness, exhaustion, fumbling hands and poor coordination, slurred speech, and numbness. A core temperature of less than 30Cdefined as severe hypothermiais often associated with cardiac dysrhythmias. (Severe hypothermia may also be defined as a core temperature of 30C-
Table 1. Physiologic Responses To Core Temperature Changes.

Normothermia Mild hypothermia Ataxia, confusion Shivering ceases Severe hypothermia Ventricular fibrillation risk No response to pain Cardiac output severely reduced Loss of corneal reflexes; only isolated cases of survival below this level 37C 35C 33C 31C 30C 28C 26C 25C 23C 98.6F 95F 91.4F 87.8 86F 82.4F 78.8F 77F 73.4F
Thermoregulation
While exposure to an environment colder than body temperature is the common denominator to all forms of hypothermia, an individuals capacity to compensate for cold stress determines in part whether the patient will become hypothermic. Body temperature is controlled by a balance between heat loss and heat production. Thermoregulation is a complex process with overall control mediated by the anterior hypothalamus.10 When exposed to a cold environment, peripheral receptors transmit stimuli through the spinal cord to the hypothalamus, initiating a number of
Emergency Medicine Practice
www.empractice.net December 2003
responses aimed at both heat production and conservation. The bulk of the bodys heat production is a result of shivering, which raises the basal metabolic rate two to five times.11 Inhibition of shivering in one controlled study caused a 37% decrease in rewarming rates when compared to shivering controls.12 Release of epinephrine and thyroid hormones during cold exposure, as well as other physiologic factors, act to increase nonshivering thermogenesis.13 Heat conservation is facilitated initially via peripheral vasoconstriction, which redirects blood from the skin into the deeper tissues. Vasoconstriction is most pronounced in the extremities and can lead to a sixfold increase in insulating capacity.14 Additionally, behavioral responses limit heat loss via mechanisms such as adding layers of clothing and seeking shelter. There are many predisposing factors for the development of hypothermia. (See also Table 2.) They can loosely be broken down into four categories: factors that impede circulation, increase heat loss, decrease heat production, or cause impairment of thermoregulation. Significant overlap between these categories exists. Adequate circulation may be impaired by mechanical obstruction (such as tight-fitting clothing), certain medications, smoking, or underlying disease processes (e.g., diabetes or peripheral vascular disease). Dehydration can impede circulation by reducing overall volume. Net heat loss occurs anytime environmental exposure overcomes the bodys ability to generate and conserve heat. Though this can occur in surprisingly temperate conditions, it is most dramatic in cold, windy environments and immersion scenarios. Multiple medications and recreational drugs, particularly alcohol, can predispose to heat loss by impairing vasoconstriction. Infants have a high surfacearea-to-body-mass ratio, which speeds heat loss. All patients with disruption of normal skin function are at risk for increased heat loss. This predisposition is most dramatic in burn patients but is also present in any patient with an exfolialitive dermatitis.
Table 2. Thermoregulatory Risk Factors For Cold-Related Illnesses.

Extremes of age (early childhood or age greater than 65) Mental or physical disability Psychiatric disorders (e.g., Alzheimers disease) Dehydration Factors that result in poor circulation (e.g., age, tight clothing or boots, cramped positions, fatigue, certain medications, smoking, alcohol, and diseases that affect the blood vessels, such as diabetes) Factors that decrease the bodys ability to produce heat (e.g., neuromuscular disease, arthritis, hypothyroidism, malnutrition, beta-blocker use, neuroleptic use) Factors that can result in increased body heat loss (e.g., psoriasis, dermatitis, burns, dehydration, decreased subcutaneous fat, alcohol use) Factors that can contribute to loss of body thermoregulation (e.g., central nervous system pathology, trauma, stroke, Parkinsons disease, neuropathies, spinal cord injuries)
Factors that predispose to inadequate heat production include endocrinologic failure (hypothyroidism, hypoadrenalism), inadequate fuel stores (hypoglycemia, malnutrition), certain pharmacologic agents (beta-blockers, neuroleptics), and decreased ability for physical exertion and shivering (common to infants and the elderly). Impaired thermoregulation may occur as a result of central nervous system pathology (stroke, tumor, bleed), toxin exposure (particularly alcohol), or because of inadequate peripheral sensory function (peripheral neuropathies, spinal cord transsection). Multiple drugs can impair central thermoregulation. Benzodiazapines, opioids, barbiturates, phenothiazines, atypical antipsychotics, and tricyclic antidepressants all impair central thermoregulation and, via alpha blockade, inhibit vasoconstriction.15-17 Ethanol use predisposes to hypothermia in multiple ways. It impairs judgment and thermal perception, which increases the risk of exposure, and it also causes peripheral vasodilation, impedes shivering, and predisposes to hypoglycemia.18 Additionally, it has a direct effect on the hypothalamus, which in turn results in a lowering of the thermoregulatory set point, resulting in a reduction of the core temperature.19 The elderly deserve special mention because of their predisposition to develop hypothermia. This is a reflection of age-related impairment of many of the systems that allow appropriate thermoregulation. Heat production may be impaired because of a reduced shivering response, decreased mobility, malnutrition, and diminished lean body mass.20-22 The elderly are less able to discriminate temperature changes and when exposed to cold environments are less able to vasoconstrict adequately.23 They may also be on multiple medications, particularly cardiac medications, that may increase their risk. Additionally, the elderly are more prone to cold exposure because of falls or illness. The importance of infection as a source of hypothermia in the elderly is well-documented in the literature. Several studies have noted that the incidence of sepsis in this group is approximately 80%.24,25 Sepsis should be of particular concern if the hypothermic patient was found indoors.26 Social factors such as living with inadequate heating due to low income must also be considered.
Environmental Heat Loss

Heat loss occurs through four primary mechanisms: radiation, conduction, evaporation, and convection. The ratios by which these mechanisms produce heat loss vary in different exposure situations.27 The four environmental conditions through which these mechanisms cause coldrelated stress are low temperatures, high/cool winds, dampness, and cold water. Radiation is the transfer of particulate energy through space. Radiation of heat occurs in all environments and is roughly proportional to the difference between skin and ambient temperature.27 Loss of body heat through radiation occurs when the ambient temperature is below 98.6F. Important factors in radiant heat loss are the surface area and
December 2003 www.empractice.net
the temperature gradient.28 Conduction refers to heat transfer between two objects in direct contact. The most obvious example occurs during immersion. Water conducts heat away from the body 25 times faster than air because it has a greater density (and therefore a greater heat capacity).28 Survival times in ocean water immersion have been estimated to be about 4.5 hours in 15C water and less than two hours in 0C water.29 Patients with a lower body mass (including children) and a lower fat content are likely to cool down more rapidly.30 Wet clothes increase heat loss by five times over dry clothes.28 The importance of other substances thermal conductivity should not be overlooked; for instance, granite has four times the conductivity of water, a salient point in an elderly patient who has spent several hours on a cold tile floor after a fall.31 Evaporation is heat loss that results from converting water from a liquid to a gas. In the hypothermic patient, this occurs through insensible perspiration (the body sweats to maintain a humidity level of about 70% next to the skin; in cold, dry environments, a great deal of moisture and heat can be lost this way) and respiration (as water vapor during exhalation). While evaporation can result in significant heat loss, another important effect is that these processes reduce the overall circulating volume, which can lead to dehydration (which in turn makes the body more susceptible to hypothermia and other cold-related illnesses).28 Convection is heat transfer that is facilitated by movement of air or liquid across an object. The rate of convective heat loss depends on the density of the moving substance (water convection occurs more quickly than air convection) and the velocity of the moving substance.28 When convection combines with evaporation (e.g., wet clothes on a cold, windy day), extreme heat loss can occur. Wind chill, a combination of temperature and velocity, is a crucial factor to evaluate.
Systemic Effects Of Hypothermia Cardiovascular System

The cardiovascular effects of hypothermia can be divided into two categories: electrical effects (conduction abnormalities and arrhythmias) and hemodynamic effects. The initial cardiac response to cold stress is tachycardia, which is replaced by progressive bradycardia as temperatures decline. This is a result of both decreased spontaneous depolarization and slowing of the conduction system. It is refractory to atropine.32 In one review of 22 hypothermic patients, both bradycardia and the amount of QT interval prolongation were found to correlate significantly with declines in temperature.33 The observation of a relative tachycardia in the hypothermic patient should prompt the clinician to search for associated conditions, such as occult traumatic bleeding, sepsis, or drug ingestion. As heart rates decline, there is a progres-
sive reduction in cardiac output that mirrors the bradycardia so that at 20C, cardiac output has declined approximately 80%.34 Interestingly, oxygen consumption as a result of metabolism declines by approximately 6% per degree C, essentially matching the decline in cardiac output.35 This may explain why pulseless, profoundly hypothermic patients have been resuscitated without evidence of ischemic injury to vital organs. In addition to rate-related changes, one animal model study suggests both systolic and diastolic dysfunction in severe hypothermia.36 In this study, eight dogs were cooled to 25C, resulting in a significant decline in stroke volume and an increase in ventricular wall stiffness. Similarly, data from the surgical literature have noted a decrease in ventricular contractility when hypothermia is induced for surgical procedures.37 Peripheral resistance progressively increases as body temperature declines. One study of 11 dogs documented an increase of 310% over normothermic controls at 20C.34 This increase is likely multifactorial, related to increased blood viscosity, hemoconcentration, and sympathetic tone.38-40 Osborn or J waves (see Figure 1) are one of the more well-known ECG findings associated with hypothermia and appear as an elevation at the junction of the QRS and ST segments. They typically occur at core temperatures less than 32C. In one prospective study of 43 hypothermic patients, all patients whose temperature at presentation was below 32.2C had J waves present, while 38% of those with temperatures above 32.2C did not.41 The exact etiology of the J wave is unknown but may be related to injury current, delayed depolarization, or early repolarization that occurs in one area of the ventricle prior to completion of depolarization in another area.42,43 Although J waves are not pathognomonic for hypothermia and have been reported in other disease states such as subarachnoid hemorrhage, normothermic normal patients, and hypercalcemia, their presence is highly suggestive of a significant decrease in core temperature. Aside from the observation that their size appears inversely related to temperature, they do not appear to have any prognostic value.44 Hypothermia is associated with a wide array of atrial and ventricular dysrhythmias. Atrial fibrillation, the most commonly cited hypothermic dysrhythmia, has been noted in the surgical literature for decades. In patients undergoing cardiac and neurosurgical procedures, hypothermia is often induced for protective benefit. The incidence of atrial fibrillation in these patients increases with temperature drop and is frequently encountered at
Figure 1. The J wave.

The J wave (or Osborn wave) is associated with moderate hypothermia but has no prognostic significance.
temperatures below 32C. In one prospective study of 29 patients undergoing cardiac surgery, 68% of patients developed atrial fibrillation as core temperatures declined from 35C to 28C.45 In another study, atrial fibrillation occurred in six of 10 patients at a mean temperature of 29C.46 In a review of 60 patients presenting with accidental hypothermia, atrial fibrillation was found in over 50% of cases with a core temperature less than 33C.47 Given the coagulopathies associated with hypothermia, and the observation that most cases of atrial fibrillation will resolve with rewarming, routine anticoagulation is generally not recommended.47 Ventricular fibrillation becomes more likely as temperatures decline below 28C, though its incidence may have been overestimated in the past.15,33 The potential for ventricular fibrillation increases as core temperature declines. This is partially due to a decrease in the fibrillation threshold. There are multiple theories to explain this observation, related to acid-base disturbances, ischemia, and myocardial temperature gradients.48,49 Traditional teaching is that induction of ventricular fibrillation can occur with rough handling, endotracheal intubation, or as a consequence of core afterdrop. There is no convincing evidence to substantiate the myth regarding induction of ventricular fibrillation with moving or caring for the hypothermic patient. Data from one multicenter study of accidental hypothermia refute the claim that intubation is likely to induce ventricular fibrillation.5 Once present, ventricular fibrillation is typically resistant to defibrillation until core temperatures are above 28C. An isolated case report of successful defibrillation at 25.6C does exist, supporting the current recommendation for an initial trial of defibrillation once ventricular fibrillation is identified.50
rewarming control arms, suggesting that convection is likely not the issue.59 Conductive heat transfer offers an alternative explanation for observed afterdrop. The hypothermic patient cools from the outside in. Consequently, a heat gradient is established from the relatively warm core to the cool periphery. This heat gradient does not reverse immediately upon initiation of rewarming. Until the gradient is reversed, further heat transfer occurs from the warmer core to cooler peripheral tissues. This mechanism is supported by the observation that afterdrop has been demonstrated in a frozen leg of beef and a cooled bag of gelatin.62 Regardless of the mechanism, it is important to note that afterdrop has not been shown to be of any clinical importance in rewarming the hypothermic patient.
Rewarming Shock
Rewarming shock refers to cardiovascular collapse that can occur as the patient is warmed. It is attributed to the increases in the metabolic rate of peripheral tissue and the peripheral vasodilation that accompany external rewarming.63 Cardiac output from the cool heart is unable to match tissue demand, and a clinically apparent shock state ensues. Clinical experience with successful rewarming of severely hypothermic patients using primarily external rewarming techniques has refuted this observation.64-66
Neurologic System
The neurologic manifestations of hypothermia are welldescribed in the literature. As with most of hypothermia, the bulk of our knowledge comes from case reports; no controlled studies exist. In the largest study specifically addressing the neurologic manifestations of accidental hypothermia, several findings were observed to correlate significantly with reduction in core temperature.67 This review of 97 patients found that as the patients temperatures decreased, the level of consciousness declined, pupillary light response and deep tendon reflexes diminished, and muscular tone increased. In severe hypothermia, this frequently resulted in patients who were unresponsive to noxious stimuli and were areflexic with fixed pupils and stiff bodiesa clinical picture that could easily be misinterpreted as death. These observations are consistent with other reports and align with the pathophysiologic changes of nerve tissue that accompany hypothermia. Animal studies have demonstrated that peripheral nerve conduction progressively decreases as temperatures decline.68 Additionally, muscle contraction has been shown to be temperature dependent, as is synaptic delay time, which may partially explain the dysarthria commonly observed in the hypothermic patient.69,70 Electroencephalograms performed on patients with induced hypothermia for surgical procedures demonstrate a progressive decrease in the frequency and amplitude of electrical activity, with electrocerebral silence occurring in the range of 13.5C-21.5C.71,72
Afterdrop
Core temperature afterdrop refers to the observation that as some patients are warmed, their core temperature continues to decline. In the past, this continued drop of core temperature was believed to predispose the patient to the development of ventricular fibrillation, and rewarming strategies that were thought to minimize afterdrop were encouraged. There is little evidence to substantiate these concerns, leading several experts to question the importance of afterdrop.51,52 There are two explanations for the phenomenon of afterdrop; one is based on a conductive mechanism, and the other on a convective mechanism. The convective theory holds that the return of cool blood from peripheral circulation to the core leads to afterdrop. Historically, this has led many authors to caution against active external rewarming for the moderately-to-severely hypothermic patient. As at least one author has pointed out, this makes little intuitive sense given the extreme peripheral vasoconstriction that typifies significant hypothermia.49 In fact, active external rewarming has been shown in multiple studies to have little impact on afterdrop.53-61 In this group of studies, the largest recorded afterdrop occurred in one of the passive
Hematologic System
Hypothermia causes a multitude of hematologic changes,
the etiology of which is not entirely understood. With a decline in temperature, there is a progressive hemoconcentration, resulting in an increase of the hematocrit by approximately 2% for each 1C drop.73 This is likely secondary to an increase in vascular permeability with resultant third spacing of fluids as well as free water loss via cold-induced diuresis.74 Animal studies suggest that splenic contraction may play a role as well.75 As blood cools, there is a concomitant increase in blood viscosity that can lead to microinfarction.74 Hypothermia affects coagulation and hemostasis in several ways. Lowering blood temperatures inhibits enzymatic reactions of the clotting cascade, leading to a progressive coagulopathy. If a tube of blood is cooled to 28C, prothrombin times and partial thromboplastin times increase an average of 5 and 20 seconds, respectively.76 As blood specimens are typically warmed to 37C in the lab, this coagulopathy will not be apparent in recorded prothrombin times or partial thromboplastin times. Impaired hemostasis may be encountered because of thrombocytopenia or a decrease in platelet activity. Thrombocytopenia can reflect splenic or hepatic sequestration, marrow depression, or disseminated intravascular coagulopathy.77,78 Platelet inhibition is believed to be related to a temperature-mediated decline in thromboxane B2.79 Alternately, impaired synthesis of prostacyclin at low temperatures can lead to platelet aggregation and thrombosis, another catalyst for the development of disseminated intravascular coagulopathy.80 Disseminated intravascular coagulopathy in the hypothermic patient is also believed to be related to a release of thromboplastin from poorly perfused tissue.81
glucose and hydrogen ions, contributing to the hyperglycemia and acidosis associated with hypothermia.88
Gastrointestinal System
Hepatic dysfunction can occur with hypothermia and is generally attributed to decreased perfusion.74 Clearance of lactate is impaired, contributing to metabolic acidosis.74 Additionally, the livers ability to detoxify toxins is reduced, which complicates overdoses.89 Pancreatitis is noted at autopsy in 20%-30% of hypothermia-related deaths, with asymptomatic elevations of serum amylase levels occurring even more frequently.90,91 The cause is not known, though it may be related to thrombotic-related microinfarcts.92
Endocrine System
In hypothermia of abrupt onset in a healthy host, hyperglycemia should be expected. There are multiple contributing mechanisms, including cold-related inhibition of insulin secretion and increases in sympathetic tone and glucagon levels that lead to an increase in glycogenolysis and gluconeogenesis.93,94 As core temperatures decline, insulin secretion by the pancreas decreases and insulin resistance of target cells increases, leading to serum hyperglycemia.95 Insulin resistance makes its use ineffective until temperatures are above 32C.14 Attempts to lower the blood sugar of the hypothermic patient can result in significant iatrogenic hypoglycemia once rewarming occurs.9 If the patient remains hyperglycemic after rewarming, diabetic ketoacidosis, hyperosmolar syndrome, and pancreatitis should all be considered. If hypothermia has developed over a longer period of time and in debilitated patients, hypoglycemia may be present. Increased metabolism associated with shivering can deplete glycogen stores, predisposing to the development of hypoglycemia.14 Thyroid, adrenal, and pituitary function is generally believed to be normal in simple exposure hypothermia but may impair thermogenesis in patients with preexisting deficiencies. If the patient is resistant to rewarming, empiric administration of hydrocortisone or thyroid hormone should be considered.
Respiratory System
Early tachypnea is followed by progressive slowing of the respiratory rate as temperatures decline.15 The decline in respiratory rate correlates to decreasing core temperatures with cessation of spontaneous respirations occurring in dogs at 24C.82 The hypoventilation associated with hypothermia is likely related to two mechanisms. First, as temperature declines, metabolism slows, which results in a 50% reduction of oxygen consumption and carbon dioxide production at 30C.74 Second, cooling of the respiratory centers depresses ventilatory drive, with a response to pCO2 stimulation progressively attenuated below 34C.83 Protective airway mechanisms are impaired because of decreased ciliary motility, bronchorrhea, and coldrelated thickening of respiratory tract secretions.84 Oxygenation may be further compromised by the development of noncardiac pulmonary edema.14
Other Cold-Related Injuries Frostbite

Frostbite occurs when the skin tissue actually freezes. Although frostbite typically occurs at temperatures below 30F (-1C), wind chill effects can cause frostbite at abovefreezing temperatures. Absolute air temperature is not as relevant as the combination of ambient temperature, wind chill, and the presence or absence of precipitation.96 Initial effects of frostbite include uncomfortable sensations of coldness; a tingling, stinging, or aching feeling of the exposed area is followed by numbness. Ears, fingers, toes, cheeks, and noses are primarily affected. Superficial frostbite involves just the skin; the exterior will be white and frozen but the tissue below the surface is soft and resilient before rewarming. Deep frostbite injuries involve underlying structures tissues (muscles, tendons, etc.).97 Before rewarming, the injured
Renal System
As core temperature declines, a progressive diuresis occurs. Initially, this reflects an increase in renal blood flow secondary to peripheral vasoconstriction.85 As temperatures continue to drop, the kidneys are unable to appropriately concentrate the urine because of tubular dysfunction.86,87 This leads to a progressively dilute urine and continued diuresis.87 Tubular dysfunction also limits renal clearance of
part will feel hard and solid, often compared to wood. Any factors that decrease blood flow to a tissue area of the body can contribute to frostbite. The bodys response to the extremes of temperature is to protect the core. The peripheral vasoconstriction that occurs as a result can be localized (e.g., as when one touches cold metal) or generalized (e.g., a cold wind blows across your scalp and the vessels in your hand constrict). The resulting decreased blood flow to the skin can lower the temperature of the tissues and predispose to injury. Since water conducts temperature far better than air, moisture will also dramatically increase the chances of cold-related skin injury. Fractures and muscular skeletal injuries pose further risk of frostbite, as edema can also mechanically obstruct blood flow. The bodys natural vasoconstrictive response to dehydration increases the chances of frostbite. Smoking further exacerbates vasoconstriction in cold exposures.98 The pathogenesis of frostbite is classically divided into four phases.9 In the prefreeze phase, skin temperature falls until maximal vasoconstriction occurs at approximately 15C. At 10C, to counter the deleterious effects of this shunting of blood from the acral areas of the body (ears, nose, fingers, toes), the body allows intermittent blood flow through cold-induced vasodilation, also known as the hunting response. First described in 1830, cold-induced vasodilation is a cycle of constriction and dilation of the vessels that allows warm blood to intermittently flow to distal areas and prevent freezing.99,100 People who are often exposed to a cold environment develop an enhanced coldinduced vasodilation response.100,101 Many other factors affect cold-induced vasodilation, such as diet, alcohol consumption, altitude, race, age, and stress.100 Unfortunately, cold-induced vasodilation can be blunted by dehydration, hypoxia, altitude, or Raynauds phenomenon. Cold-induced vasodilation keeps a minimal level of blood flow to the distal areas. If the temperature drops further, the core will start to be cooled by the returning blood, and the hunting response will cease.97 At this point, the tissue in the distal areas progresses to the next phase of damage. When the skin temperature decreases to -4C or lower, the freeze phase begins with the formation of extracellular ice crystals. This causes relative extracellular dehydration, resulting in the flow of cellular water out to the interstitial space; eventually, cells will crenate and lyse. Intracellular ice crystal formation will also destroy cells by direct mechanical damage. (Touching cold metal, certain chemicals like nitrous oxide, or certain supercooled liquids, such as gasoline or white gas used in camping, can result in instant frostbite. In this type of flash freezing, intra- and extracellular ice crystals form simultaneously, resulting in the rapid destruction of large amounts of tissue.9) The vascular stasis phase is accompanied by rising concentrations of the breakdown products of dead cells and the buildup of inflammatory mediators.102 Prostaglandins, histamine, thromboxane, and bradykinin all play a role in progressive tissue ischemia.103 Stasis causes inflammatory edema that further compromises blood
flow to the area. Platelet aggregation leads to thrombosis; red cell clumping and microvasculature collapse further complicate the picture. The result of vascular stasis is the late ischemic phase, in which injured areas, lacking blood flow, shift to irreversible damage. The pathophysiology of coldinduced skin injury bears many pathophysiological similarities to thermal burns; the same level of specialized care is required to achieve the best outcome.104
Frostnip
Frostnip is superficial ice crystal deposition on the skin and can be a warning sign for impending frostbite if exposure continues. Frostnip is generally a retrospective diagnosis, as it is defined by absence of tissue damage upon rewarming.
Chilblains
Chilblains (or pernio) is a non-freezing cold-related injury characterized by red, scaly lesions, often on the feet. They often occur in cold, humid environments. An association with sufferers of lupus has been seen. Treatment is supportive, though some European centers have tried calcium-channel blockers.9
Trench Foot
Trench foot is a process similar to chilblains. Trench foot results from prolonged exposure of the extremities to a cold, wet environment (or immersion), without actual freezing. It was common in trench warfare during World War I. It can occur at temperatures up to 60F if the feet are constantly wet.28 Continual exposure to cool, wet conditions causes peripheral circulation to the foot to decline. Symptoms of trench foot include a tingling and/or itching sensation, burning, pain, and swelling. The affected tissue generally dies and sloughs off. While severe cases may develop blisters and gangrene, massive tissue loss is rare and is dependent on the length of the exposure.105
Prehospital Care
In general, the priority in the prehospital care of the hypothermic patient is to stabilize the patient, minimize further heat loss, and provide rapid transport to a facility where definitive care can be provided. Distance and/or transport times to the healthcare facility, as well as institutional capabilities, often drive local protocols. (Wilderness medicine issues present several challenges that are beyond the scope of this article.) As hypothermia frequently causes significant hypoventilation, the presence of respirations and adequate airway patency should be carefully assessed. Supplemental oxygen should be supplied to all patients with ventilatory support as needed. If the patient is truly apneic, intubation should be performed. Cardiac electrical activity should be assessed as soon as is feasible. If an organized rhythm is present, pulses should be assessed. The severe vasoconstriction associated with hypothermia can make palpation of peripheral
pulses difficult. Carotid or femoral pulses should be palpated for 30-45 seconds (per American College of Cardiology guidelines) to confirm a pulseless state. If no pulses are present, CPR should be initiated. If initial cardiac monitoring demonstrates ventricular fibrillation, and attempt at defibrillation appears reasonable. Published guidelines recommend one series of defibrillation shocks (200J, 300J, 360J).1,106 If unsuccessful, further attempts at defibrillation should be withheld until rewarming can be accomplished, and CPR should be started. Fear of inducing ventricular fibrillation through handling or moving a patient are unwarranted and should never delay patient care. If the patient has a decreased level of consciousness, a fingerstick glucose should be obtained. If this is not possible, IV dextrose should be administered. Additionally, lethargic or comatose patients in whom opioid overdose is suspected should be given naloxone, as opioid overdose and hypothermia often occur in tandem. After assurance of the ABCs and treatment of coexisting injuries, the next priority is rapid transport and prevention of further heat loss. One controlled study that addressed prehospital rewarming found no difference in rewarming rates when subjects with mild hypothermia were randomized to either inhalation rewarming, active external rewarming, or passive rewarming.107 Given this fact and the fact that attempts at field rewarming can delay definitive care, passive rewarming is appropriate in the prehospital phase. Remove any wet or constricting clothing. Facilitate passive rewarming by wrapping the patient in dry blankets. Wrap any injured or frostbitten areas in sheets or blankets to prevent incidental trauma; splint and elevate all potential fractures. Though minimizing the time frozen is important for maximum tissue salvage in cases of frostbite, any potential for incomplete rewarming or refreezing make field rewarming a risky proposition.108 Dry heat should not be used as it can damage and dehydrate the already fragile tissue. Exposure to external sources of heat such as radiators or campfires should be avoided to prevent partial thawing. The erstwhile practice of massaging frostbitten areas with snow or warm hands only results in further mechanical trauma to the injured area. In cases of definite frostnip, rewarming can be done in the field. A nose can be warmed by blowing into hands cupped around it. Hands should be placed in the patients armpits.109
particularly important to determine whether contributing comorbid disease is present. Although a history is often difficult to obtain from a moderate or severely hypothermic patient, use witnesses, prehospital care providers, and family members to determine the following: Age Type and duration of exposure Preceding activity Alcohol or substance use Co-morbid illness, especially psychiatric disease, neurologic disease, diabetes, and hypothyroidism Current medications, especially sedative-hypnotics, antipsychotics, cardioactive medications, thyroid replacement, insulin, or oral hypoglycemic agents Usual level of functioning Review of systems: evidence of behavioral changes, impaired judgment, chest pain, etc. Medics should be questioned about the possibility of trauma as it frequently complicates hypothermia. Trauma may precede hypothermia, limiting a persons ability to seek shelter or warmth. In one retrospective study of 234 patients, injuries preceded hypothermia in 27% of cases.110 Trauma may also follow hypothermia, as a result of the confusion due to the decline in body temperature.
Physical Examination
Careful attention to determining the presence of respiration and circulation will guide initial therapy.
Airway
Determine whether the patient has a patent airway and is able to handle secretions. Indications for intubation of the hypothermic patient are identical to those in the normothermic patient with the caveat that pulse oximetry is not a reliable indicator of hypoxia. Although case reports have implicated intubation as a cause of ventricular fibrillation, several large series have disputed this.5,111,112 Most experts now agree that with preoxygenation, endotracheal intubation is unlikely to induce ventricular fibrillation.
Breathing
As body temperature falls, the respiratory rate slows. Progressive hypothermia slows metabolism; oxygen utilization and carbon dioxide production are decreased. From a practical standpoint, this means that a hypothermic patient who appears to be breathing too slow may in fact be breathing at a rate that is appropriate for his or her metabolic needs. This has led some experts to caution against overventilating the hypothermic patient.9,113 Overventilation can lead to significant respiratory alkalosis and may exacerbate myocardial irritability, which would increase the risk of ventricular fibrillation.114
Emergency Department Evaluation

As with all patients who present to the ED with serious illness, evaluation and stabilization should occur simultaneously. Remember that the presentation of the severely hypothermic patient can mimic death; careful assessment for signs of life may be required.
Circulation
Expect the severely hypothermic patient to be bradycardic. Determining the presence or absence of pulses can be problematic because of severe vasoconstriction and intravascular volume depletion. Spend 30-45
History
When confronted with the hypothermic patient, it is
seconds palpating for pulses in the carotid or femoral area. The use of a handheld Doppler may be helpful if pulses are difficult to detect. Remember that any pulse may provide perfusion adequate for the decreased metabolic demands that accompany severe hypothermia. If the patient is truly pulseless, current recommendations are to begin CPR. However, CPR should only be started if the physician is convinced pulses are absent.73 The effectiveness of bretylium for prophylaxis and treatment of hypothermic ventricular fibrillation has not been clearly established. Conflicting data from use in experimental dog models exist.115-117 Most recently, a randomized, blinded study compared bretylium to amiodarone and placebo in the treatment of hypothermic ventricular fibrillation in 30 dogs.118 Neither drug was significantly better at inducing chemical defibrillation or improving the resuscitation rate compared to placebo.
more invasive rewarming techniques. Primary hypoglycemia can present with low body temperatures and altered mental status. Secondary hypoglycemia can be seen in chronic cold exposure (particularly in patients with inadequate reserves) and with depletion of glycogen stores that can accompany prolonged environmental exposure. Alternately, the hypothermic patient will frequently present with hyperglycemia of multifactorial origin.
Pulse Oximetry
The peripheral vasoconstriction that accompanies hypothermia limits accurate pulse oximetry. In one prospective study of mildly hypothermic patients, oximetry functioned properly in only 77% of patients with a core temperature of 35.5C but increased to 92% at temperatures above 36C.120 These data suggest that pulse oximetry becomes less effective as temperatures decline and is unlikely to function appropriately even in mild hypothermia. To accurately determine oxygen saturation, an arterial blood gas should be obtained.
Disability
Assess the patients mental status. Hypothermia causes progressive alteration of cognitive functioning, culminating in electrocerebral silence and coma. Deep tendon reflexes and pupillary light response may be diminished and muscle tone increased. Examine the patient head to toe looking for clues to secondary disease processes. Look for evidence of trauma, including bruising and extremity deformity. Check the skin for track marks suggestive of opiate overdose. Look for bullae over pressure points, which can be seen in overdose. The hypothyroid patient may present with absence of the lateral third of the eyebrow, sparse pubic or axillary hair, a goiter, or waxy swelling of the skin and subcutaneous tissues. Patients with primary adrenal insufficiency may demonstrate hyperpigmentation.
Electrocardiography
Hypothermia causes a progressive slowing of electrical conduction that can be visualized on the ECG. Sinus bradycardia and prolonged QT intervals are to be expected as temperatures decline.121 Below 32C atrial fibrillation becomes common. At temperatures less than 28C, ventricular fibrillation and asystole are of greatest concern.
Complete Blood Count

As body temperatures decline, a progressive hemoconcentration occurs. Hypothermia is known to cause leukocyte depletion.122 Lack of an elevated white blood cell count, therefore, does not imply that a significant underlying infection is absent. Platelet counts tend to drop secondary to splenic and hepatic sequestration.
Frostbite And Frostnip

Assess the severity of the frostbite injury prior to rewarming. Frostnip or superficial frostbite involves just the skin; the exterior will be white and frozen but the tissue below the surface is soft and resilient before rewarming. Deep frostbite injuries involve underlying structures.97 Before rewarming, the injured part will feel hard and solid, often compared to wood. It is quite difficult to judge the severity of frostbite prior to thawing and nearly impossible to predict the extent of injury directly after rewarming. The line of demarcation between tissue that will recover and permanently injured areas can take weeks to become fully established.119 Good prognostic signs after rewarming are the early appearance of clear blebs across the entire extent of the injured area, early return of sensation, and soft subcutaneous tissue.9
Electrolytes
Hypokalemia is expected from a shift of potassium into the cells.123 Hyperkalemia is indicative of cellular acidosis and a marker of poor prognosis. Data from a Mt. Hood, Oregon, tragedy suggest that severely elevated potassium levels may give prognostic information. In this review of 10 hypothermic patients, those who died had potassium levels greater than 10 mEq/L, while survivors had levels less than 7 mEq/ L.124 Other studies also show that hyperkalemia can be used to distinguish hypothermic patients who can be resuscitated form those who cannot.125 Serum sodium, calcium, and chloride concentrations should not change appreciably at temperatures above 25C.126
Diagnostic Studies
Glucose
A bedside fingerstick glucose is fast, easy, and cheap. Correcting hypoglycemia can occur in tandem with rewarming the patient and may prevent the need for the
Renal Function
Elevation of blood urea nitrogen and creatinine are frequently encountered in hypothermia. One study found the incidence of acute renal failure in accidental hypothermia was 40% for patients who required admission to an ICU.26 (However, this study focused on the indoor
Continued on page 11
Clinical Pathway: Rewarming The Hypothermic Patient

Measure core temperature
Temperature greater than 32C?
NO
Does the patient have a pulse?
NO
Begin CPR and core rewarming

Cardiopulmonary bypass if rapidly available (Class II) or Left thoracotomy with mediastinal irrigation (Class II) or Pleural irrigation (Class II) Expected rewarming rates: 9C/hour, 8C/hour, and 3C/hour, respectively Bretylium 5 mg/kg IV for ventricular tachycardia/ventricular fibrillation (Class indeterminate)
The evidence for recommendations is graded using the following scale. For complete definitions, see back page. Class I: Definitely recommended. Definitive, excellent evidence provides support. Class II: Acceptable and useful. Good evidence provides support. Class III: May be acceptable, possibly useful. Fair-to-good evidence provides support. Indeterminate: Continuing area of research.
This clinical pathway is intended to supplement, rather than substitute for, professional judgment and may be changed depending upon a patients individual needs. Failure to comply with this pathway does not represent a breach of the standard of care.
Copyright 2003 EB Practice, LLC. 1-800-249-5770. No part of this publication may be reproduced in any format without written consent of EB Practice, LLC. Emergency Medicine Practice 10 www.empractice.net December 2003
YES
Passive rewarming
(Class II) cover with blankets ensure adequate energy stores to allow for shivering (IV dextrose or oral carbohydrates) Expected rewarming rate: <1C/hour
Temperature not increasing or declining
YES
Active external rewarming

forced air rewarming (Class II) or resistive heating (Class II) Combined with: airway rewarming (Class II) warmed IV fluids (Class III) Expected rewarming rate: 1-3C/hour
Patient loses pulse or core temperature is not increasing
Continued from page 9
hypothermic; these findings may not be as applicable to outdoor enthusiasts.) The etiology is thought to reflect a pre-renal state secondary to decreased renal blood flow and so may benefit from fluid resuscitation.74,127
(See Table 3.) The state of the literature does not allow for guidelines that are strongly evidence-based. There are very few randomized, controlled trials that have assessed the efficacy of the various rewarming techniques. Those that
Endocrine Studies
Preexisting endocrine failure predisposes to the development of hypothermia. Thyroid studies (TSH and free T4) and serum cortisol levels should be sent on any patient whose history or physical examination suggests hypothyroidism or adrenal insufficiency.
Table 3. Rewarming Techniques In Hypothermia.

Passive rewarming
Best for: Mildly hypothermic, healthy patients with an intact shivering response Pros: Effective and noninvasive Cons: Ineffective when core temperatures drop below the shivering threshold of 28C-30C; requires adequate glycogen stores Methods: Relies on intrinsic thermogenerative mechanisms of the patient, including shivering, and passive insulation techniques, such as using a cotton blanket; adequate energy substrate should be ensured either by provision of food or IV dextrose, provided the patient is not hyperglycemic on presentation
Arterial Blood Gases

Management of acid-base status in the hypothermic patient is complex. Data from case series indicate that patients may present either acidotic or alkalotic, with no clear predilection for either state.111 Multiple contributors to acidosis are present in the hypothermic patient. These include but are not limited to respiratory depression, lactate generation from shivering, impaired hepatic function, and decreased tissue perfusion. The tendency toward acidosis is balanced against the fact that as blood cools, it becomes progressively alkalotic. For example, a tube of blood with a pH of 7.4 and a pCO of 40 mmHg at 37C will register a pH of 7.5 and a pCO of 30 mmHg at 30C. Historically, two acid-base management strategies exist for the hypothermic patient: the pH-stat and alpha stat methods. The pH-stat method attempts to maintain an arterial pH of 7.4 when recorded values are adjusted to the patients actual temperature. This technique may paradoxically increase regional ischemia by diverting blood away from regions that are dependent on collateral perfusion.128 The alpha stat method attempts to keep pH at 7.4 when measured at 37C. In other words, no correction is made for the patients temperature and concomitant baseline alkalosis. Advantages of this technique revolve around improved cardiac performance. In one study of 181 cardiac bypass patients undergoing induced hypothermia, ventricular fibrillation occurred in 40% of patients managed with the pH-stat method but only 20% of patients managed with alpha stat.129 Most experts now recommend the alpha stat method for acid-base management.
2 2
Active external rewarming

Best for: Mild-to-moderate hypothermia Pros: Effective, noninvasive Methods: Forced air rewarming: Likely the most readily accessible delivery system for external rewarming; effective, noninvasive Resistive heating methods (i.e., electric blankets): Comparable efficacy to forced air rewarming Hot water baths: Generally not recommended; limits monitoring
Active core rewarming

Best for: Severe hypothermia (<30C) Pros: Quickest return to normothermia Cons: Increased risk of complications, especially as the degree of invasiveness increases Methods: Airway rewarming: Minimally invasive, practical Heated infusions: Simple, but clinical effect appears to be minor Gastrointestinal irrigation: Rewarming rates estimated at 1.5C per hour Peritoneal irrigation: Rewarming rates estimated at 1C2C per hour; placement of the peritoneal catheter requires expertise Pleural irrigation: Rewarming rates estimated at 3C per hour, plus direct warming of the heart; possibility of iatrogenic injury, requires large volumes of liquids Left-sided thoracotomy with internal cardiac massage and mediastinal irrigation: Indicated for severe hypothermia with cardiac arrest only; rapid rewarming rate (estimated at 8C per hour), allows for open cardiac massage; extremely invasive, potential for iatrogenic and infectious complications Cardiopulmonary bypass: Indicated for severe hypothermia with cardiac arrest only; extremely rapid rewarming rates (estimated at 9C per hour); requires significant technical expertise, availability is institutiondependent
Trauma Series
As trauma and hypothermia are frequently encountered together, a high index of suspicion must be maintained for occult traumatic injury. If traumatic injury is suspected, trauma protocols should be followed in tandem with resuscitation of hypothermia. Consider a head CT in patients with a suspicion of trauma or lack of neurologic improvement with rewarming.
Management
Rewarming Techniques In Hypothermia
Multiple techniques are available for rewarming the hypothermic patient. Each falls into one of three categoriespassive, active external, or active core rewarming.
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exist were comprised of healthy volunteers cooled to a mildly hypothermic temperature in a laboratory setting.51 Extrapolation of these data to the severely hypothermic patient with comorbidities should be done cautiously. In addition, when critically assessing the literature on rewarming, it is important to consider the implications of the outcome measure reportedthat is, does the rate of change of core temperature correlate with clinical outcome? Rate of rewarmingthe most frequent measure of efficacy reported in hypothermia trialshas not been convincingly tied to outcome. Though it would appear that the more invasive rewarming techniques will increase rewarming rates, this information is meaningless unless it translates into lower mortality. Other considerations when choosing a rewarming method include patient temperature at presentation, presence of a pulse, and institutional capabilities (i.e., access to cardiopulmonary bypass). The majority of hypothermic patients can be effectively rewarmed without having to resort to invasive techniques. If, however, core temperatures fail to increase or begin to decline, or the patients clinical status is deteriorating, invasive core rewarming should be aggressively pursued. Also, in cases of cardiac arrest in which return of a perfusing rhythm is temperaturedependent, rapid rewarming appears logical. This suggests an advantage to invasive rewarming techniques in this situation. Accurate determination and continual monitoring of the patients core temperature is important in formulating a rewarming strategy. Note that not all thermometers are suited to measuring low temperatures. In particular, tympanic and axillary temperature measurement should be avoided in suspected hypothermia.130 Oral temperature measurement may be sufficiently accurate but may interfere with airway management. On the whole, rectal temperature measurement is best suited for patients who do not require invasive rewarming, and bladder probes or pulmonary artery temperature measurement are best suited for patients who require invasive rewarming.130
Passive Rewarming
Passive rewarming allows the patient to warm by endogenous heat production alone. Adequate heat production is contingent on shivering, making passive rewarming ineffective when core temperatures drop below the shivering threshold of 28C-30C.14 Additionally, shivering requires adequate glycogen stores, making it less effective in elderly or debilitated patients and diabetics with too much insulin. Passive rewarming requires the patient to be wellinsulated. Wet clothing should be removed and the patient should be wrapped in blankets or sleeping bags. Conventional wisdom holds that blankets should be prewarmed to minimize further conductive heat loss.131 Since the heat capacity of a blanket is very small, warmed blankets have not been shown to significantly affect heat loss in clinical settings.132 The insulating ability of the cover is related to the layer of air trapped between the skin and the covers, not the material itself.133 This explains the observation that rewarming rates do not differ significantly with the use of aluminum space blankets or cloth blankets.134 Under ideal conditions, insulating a patient would reduce cutaneous heat loss to zero, which would allow for a rewarming rate of approximately 1C per hour.133 However, lower rewarming rates are observed clinically with passive rewarming, typically reducing heat loss by less than 50%.132,135 In rewarming studies in which passive rewarming was used as the placebo therapy, rewarming rates typically varied between 0.2C and 0.85C per hour.51 Passive rewarming appears to be most appropriate for healthy patients with an intact shivering response. In this group, adequate energy substrate should be ensured either by provision of food or IV dextrose, provided the patient is not hyperglycemic on presentation.
Active External Rewarming

With external rewarming, heat is applied directly to the surface of the body. Multiple techniques are described in the literature, including hot water bottles, hot bath
Cost- And Time-Effective Strategies For Cold-Related Emergencies

1. Employ the least invasive rewarming measures possible. The vast majority of hypothermic patients do not require invasive rewarming techniques. In mild hypothermia, removal of wet clothing, covering with a blanket, and ensuring adequate energy stores to allow for shivering is usually sufficient. In moderate or severe hypothermia, as long as the patient has a pulse, active external rewarming is typically sufficient. Save invasive techniques for pulseless patients and those who do not respond to the preceding measures. 2. Check the bedside glucose. A bedside glucose measurement is a fast, easy, and inexpensive test that can help pinpoint hypoglycemia, which can contribute to or be precipitated by hypothermia. Correcting the hypoglycemia is an important adjunct to rewarming the patient and may prevent the need for more invasive rewarming techniques. 3. Question witnesses. Co-morbid illness, medications, and other factors can precipitate and/or alter the management of hypothermia. Witnesses, prehospital care providers, and family members can help determine crucial factors such as the patients medical background, social circumstances, and possible occult trauma. v
12
immersion, forced air rewarming, circulating water mattresses or plumbed garments, and, most recently, resistive heating. External rewarming techniques accomplish heat gain via two mechanismsconduction and convection. Conductive heat transfer occurs from the skin into the underlying tissue and is a relatively inefficient means of core rewarming. Convective heat transfer occurs as blood warmed in peripheral tissues is carried to the core. Despite some theoretic concerns, active external rewarming has been demonstrated to be safe and effective across the range of hypothermic patients and realistically represents the cornerstone of management of hypothermia. It also has been shown to be more effective in infants and children compared to adults because of their larger surface-area-to-body-mass index.136 In most hospital settings, forced air rewarming is likely to be the most readily accessible delivery system for external rewarming. Commercial devices are frequently used to rewarm patients in the surgical setting. Units typically consist of a heating device that directs warm air through a plastic blanket and across the patients body via slits cut into the underside of the blanket. In a randomized study of patients with moderate hypothermia (mean temperature, 29C), forced air rewarming was shown to rewarm significantly quicker than passive rewarming combined with inhalation rewarming.137 The rewarming rate with forced air rewarming was 2.4C per hour, and no difference in afterdrop was noted between the two groups. Other controlled studies in mildly hypothermic patients have not demonstrated a significant increase in afterdrop with forced air rewarming compared to passive rewarming. Rewarming rates have varied from 0.9C-3.3C per hour.54,56 Although controlled trials of forced air rewarming to treat severe hypothermia do not exist, several case series indicate it to be an effective modality in this setting. In a review of 36 patients who presented over a 10-year period, Roggla et al found forced air rewarming combined with inhalation and warmed infusion therapy to be an effective and noninvasive method of rewarming.65 Median patient temperature was 25.8C, rewarming took an average of 9.5 hours at a rate of 1.1C per hour, and it was successful in 92% of cases. Patients who arrested prior to hospital arrival were excluded. In another review of 15 patients with a mean temperature less than 27C, all were effectively rewarmed to above 35C using forced air rewarming.64 Resistive heating methods (electric blankets) have shown comparable efficacy to forced air rewarming in minimizing heat loss during operative procedures.138 Additionally, they have been shown to be significantly more effective than passive rewarming in one randomized, controlled trial.134 Because of their portability and minimal electrical requirements, resistive heating may represent a viable rewarming mechanism for prehospital care providers. The use of hot water baths is generally not recommended because of the limitations it imposes on monitoring. The use of hot water containers placed in high blood
flow areas such as the axilla and groin has also been described as a rewarming method. Given the small surface areas involved, this technique is unlikely to be efficacious.133 Additionally, animal models have shown that even at fluid temperatures of 45C, thermal burns are likely to occur.133 In fact, a review by the American Society of Anesthesiologists found that hot water bottles were the most common cause of perioperative thermal injury.139
Active Core Rewarming

Core rewarming refers to techniques that warm the patient from the inside out. There are several theoretic benefits to this approach. The core organs are responsible for over 50% of heat production in basal metabolism at normothermia.52 This percentage is even higher in hypothermia because peripheral tissue is colder and less metabolically active than the core. Metabolism increases with rewarming, leading to an increase in heat production. By concentrating rewarming efforts on the most metabolically active tissues, the bodys own capacity to produce heat is exploited to maximal effect. The phenomenon of afterdrop is believed to be avoided with core rewarming, though the importance of this observation is debated. Additionally, rewarming shock is presumably less likely with core rewarming. Different techniques for core rewarming include heated infusions, airway rewarming, heated lavage (gastric, bladder, colonic, peritoneal, thoracic, mediastinal), and extracorporeal blood rewarming. From a practical perspective, core rewarming provides the quickest return to normothermia but is associated with increased risk, especially as the degree of invasiveness increases.
Airway Rewarming
Airway rewarming represents a minimally invasive, practical method for core rewarming. Its primary benefit appears to be a reduction in the amount of heat lost through exhalation, with a possible small amount of heat gain.140 Estimates of the amount of heat lost via respiration vary between 10% and 30%.141 In induced hypothermia for surgical procedures, the calculated percentage was 10% in one study.142 As hypothermia typically causes a slowing of respiration, the expected amount of heat loss via the respiratory tract might be expected to be lower than in the normothermic patient. The amount of heat gain provided by airway rewarming is difficult to assess given a lack of controlled trials; however, its use has been shown to contribute to rewarming.111 The increase in rewarming rates appears to be modest, varying between 0.05C and 0.1C per hour with face mask or an increase of 0.5C per hour when provided via endotracheal tube.143 Airway rewarming has been shown to reduce mortality.144 Given the modest expected gains in rewarming rates, it should be used as an adjunct to other therapies. Airway rewarming at temperatures up to 46C appears safe. One report of thermal injury to the lungs occurred in a patient treated with oxygen heated to 80C for 11 hours.140
13
Heated Infusions
The use of heated infusions offers a simple method for rewarming, although the clinical effect appears to be minor. The calculated amount of heat gain to a 70 kg man by 1 liter of fluid preheated to 42C is 0.33C.11 While gains may be negligible, warmed fluids may be valuable by limiting further cooling of the patient. The hazard of large volume resuscitation with room air temperature fluids has been repeatedly noted in the trauma literature. Various commercially available warmers allow infusion of fluids at rates up to 500 cc/min at 35C. If a fluid warmer is not available, a microwave oven can be used to heat the fluid. Recommendations based on previous studies indicate that heating of 1 liter of crystalloid fluid at the high setting for two minutes is safe and effective.145-148 Given the higher power output common among newer microwaves, calibration prior to heating is recommended. In a recent study, one liter bags of fluid were heated on high power for two minutes in 16 different microwave ovens.149 Nine of 16 microwaves heated the fluid to a temperature greater than 42C, the generally accepted maximum temperature for fluid resuscitation. Even if fluid is appropriately heated, conductive heat loss prior to infusion is unavoidable. This can be minimized by insulating the preheated fluid bag and keeping tube lengths as short as possible.150
hour, and the procedure appears to be without significant morbidity.152,153 Data from the largest prospective hypothermia study found less dramatic rewarming rates, with the average over the first two hours of rewarming approximately 1.5C per hour.5
Peritoneal Irrigation
Peritoneal irrigation uses the large surface area of the peritoneum and gut to accomplish heat transfer from warmed fluids. Fluid (typically normal saline or lactated Ringers solution) is warmed to 40C-45C and then infused through a peritoneal catheter. Fluid is typically left in place for 20-30 minutes and then is aspirated. Placement of the catheter can be performed by either open or percutaneous (Seldinger) technique. Prior to insertion, the bladder and stomach should be emptied. To speed rewarming, a second catheter can be placed for drainage. Some practitioners recommend using four catheters, placing one in each quadrant and using two for infusion and two for drainage. Advantages of peritoneal irrigation include preferential rewarming of the liver, its ability to be performed in tandem with CPR, and its potential to dialyze off drugs and toxins. Disadvantages include the relatively invasive nature of the procedure. Placement of the peritoneal catheter requires expertise, as iatrogenic intraabdominal injury can occur. In animal studies, rewarming rates with peritoneal irrigation vary between 3C and 6C per hour.152,154 Data from human reports suggest rates of 1C2C per hour.5
Cavity Lavage
Placement of warmed fluid into body cavities has been used as a rewarming method for several decades. Techniques range from minimally invasive (gastric irrigation) to very invasive (thoracotomy with mediastinal irrigation). Rewarming rates vary significantly between techniques.
Pleural Irrigation
Irrigation of one or both hemithoraces with warmed fluid has been demonstrated to be an effective method of rewarming.153-155 Pleural irrigation requires placement of two thoracostomy tubes (36-40 F). The anterior (infusion) tube should be placed in the second or third intercostal space in the midclavicular line. The posterior (drainage) tube should be placed in the fifth or sixth intercostal space in the posterior axillary line. Warmed normal saline (40C-42C) is then infused through the anterior tube and drained via the posterior tube. Flow rates described in the literature vary between 180-850 cc per minute.153-155 Perhaps the most important advantage offered by pleural irrigation is its warming of the heart. Additionally, it is a technique that is well within the scope of most emergency physicians technical skills. Disadvantages include the possibility of iatrogenic injury to lungs, vasculature, and heart during tube placement; the possible development of a tension hydrothorax if adequate drainage is not ensured; and the large volume of warmed fluid required (11-33 liters per hour). Animal studies indicate rewarming rates in the 5C-6C per hour range.154,155 Data from case reports suggest rates closer to 3C per hour.156,157
Gastrointestinal Irrigation
Gastrointestinal irrigation is accomplished by infusion of warmed fluids via a tube placed in either the colon or stomach. Most published data focuses on gastric irrigation. Typical techniques involve delivery of warmed fluid (40C) into the stomach in aliquots of 200-300 cc. After a brief period (10-15 minutes), the fluid is then removed either by suction or gravity drainage, and the cycle is continued. There are several proposed advantages to gastric irrigation. It is quick and easy to set up; it may preferentially warm the liver, speeding metabolism of drugs and lactate; and, by virtue of its location, it may selectively warm the heart.151 On the other hand, it increases the risk of aspiration (patients should undergo tracheal intubation prior to irrigation if there is any question regarding their ability to handle secretions); serum electrolyte levels fluctuate with large-volume irrigation; lavage should be stopped during CPR; and there is the potential for initiation of ventricular fibrillation during placement of the gastric tube.9 Finally, there are concerns that the relatively small surface area of the stomach is unlikely to provide large amounts of heat transfer. In animal studies, rewarming rates are reported in the range of 3C per
Thoracotomy With Internal Cardiac Massage And Mediastinal Irrigation

Left-sided thoracotomy with internal cardiac massage
14
and mediastinal irrigation represents the most invasive core rewarming technique. This method has been advocated for use in the setting of severe hypothermia with cardiac arrest because of its rapid rewarming rate and because it allows for open cardiac massage. Although rate of rewarming has not been shown to correlate with outcome, in cases of cardiac arrest it seems intuitive that definitive rewarming should be accomplished as quickly as possible. Below 28C, attempts at defibrillation are unlikely to be successful, and organ perfusion is dependent on CPR.9 Several studies have indicated that open cardiac massage is a more effective means of providing adequate perfusion than standard CPR.158,159 It should be noted that in severe hypothermia, stiffening of the heart may preclude effective open cardiac massage, though this appears to be a rare
observation and was not noted in a recent review of seven patients.160 Published rewarming rates with mediastinal irrigation are approximately 8C per hour. Multiple case reports attest to its efficacy as a rewarming method.63,161,163 In one review of seven patients who received an ED thoracotomy for hypothermic cardiac arrest, the survival rate was 71%.63 The major disadvantage of this technique is its degree of invasiveness and potential for iatrogenic vascular injury and infectious complications. However, studies have shown a relatively low rate of infection with ED thoracotomy.164,165
Extracorporeal Blood Rewarming

Core rewarming by cardiopulmonary bypass has been
Ten Pitfalls To Avoid

1. I didnt have a thermometer for the rewarming bathso what if it took 90 minutes to rewarm her hand? The rewarming bath must be tightly maintained between 37C and 41C to maximize tissue salvage. A standard oral or rectal patient thermometer can be used to monitor the water temperature. 2. His frostbitten leg didnt look all that bad, so I sent him home. Frostbite injuries can look far worse hours to days after initial evaluation. Frostbite patients require admission for therapy and monitoring. 3. The hospital was about 40 minutes away, so we just put him in the ambulance with his foot up against the heating vents. We rewarmed his extremity much sooner than waiting to get to the ED. Field rewarming is difficult to monitor, and the risk of refreezing usually far outweighs the benefits of earlier thawing. Consider field rewarming only when transport time will be severely extended. Even then, rewarming must still be done with a water bath at 37C-41C. 4. How was I supposed to know the patient was that hypothermic? The thermometer read 34C. Since most standard hospital thermometers only read as low as 34C, a high index of suspicion is mandatory to quickly recognize moderate-to-severe hypothermia. 5. Its not my fault she died. I quickly initiated rewarming therapy and sent her to the floor. This octogenarian died of septic shock the day after she was admitted. A conversation with the medics or family would have identified the fact that she was found indoors and alerted you to the possibility of sepsis. Remember that in the elderly, a high percentage of hypothermia is secondary to another disease process. These etiologies, especially sepsis, need to be pursued. 6. Of course I started an insulin dripthe patients blood sugar was over 500. Below 32C, the body is insulin-resistant and the drug is not well-metabolized. When this patient was rewarmed, the combination produced such profound hypoglycemia that he nearly died. 7. How was I supposed to know the patient had a severe GI bleed? His hematocrit was only slightly low, and his heart rate was normal. Remember that hypothermia produces a progressive bradycardia and hemoconcentration. A relative tachycardia or normal hematocrit should prompt you to consider the possibility of a GI bleed and guaiac the stool. 8. It was an open-and-shut case. The patient was rigid, with fixed pupils and asystole on the monitor. If you had talked to the medics, you would have realized that the patient was found down in a snow bank. Severe hypothermia can mimic death, and multiple case reports of miraculous saves exist. Rewarming to 32C with concurrent CPR should at least be attempted prior to calling the code. 9. How was I supposed to know she had a subdural? She was found down, and her degree of hypothermia was consistent with her neuro exam. Detecting traumatic injury in the hypothermic patient can be problematic. A complete secondary survey is imperative and may give clues to occult injury. Mental status should improve with rewarming, which mandates the need for repeat examinations as the patient warms. 10. He was hypothermic on presentation, so I immediately began rewarming. Whats the problem? The patients glucose on routine labs came back at 12. A fingerstick glucose on all hypothermic patients is quick, easy, and rules out one reversible cause of secondary hypothermia. While hypoglycemic patients still require rewarming, raising the blood sugar is also necessary. v
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shown to be an extremely rapid way to rewarm hypothermic patients, with rates in excess of 9C per hour.166 Intuitively, rapid rewarming becomes most important in cases of cardiac arrest in which restoration of an organized rhythm is temperature-dependent. In this situation, cardiopulmonary bypass gives the added advantage of immediate restoration of adequate organ perfusion, which presumably imparts a better outcome. For hypothermic patients in cardiac arrest treated with cardiopulmonary bypass, published survival rates vary between 13% and 60%.167-170 Other methods of extracorporeal blood rewarming include continuous arteriovenous and venovenous rewarming and hemodialysis (which also has the advantage of removing toxins from the blood). Commercial arteriovenous rewarming kits are available and require only cannulation of a central (femoral) artery and vein. They rely on arterial pressure as a pump and are not useful in an arrest situation. Several studies have shown them to be an effective method of rapid rewarming, with rates of over 4C per hour.171-173
augment blood flow. As the rewarming process can be intensely painful, parenteral analgesics are necessary.
Aloe Vera
Topical aloe vera (Dermaide aloe), applied to the entire frostbitten area (especially to both intact and debrided blisters) improves tissue salvage.102 Aloe vera, when used in conjunction with an oral antithromboxane agent, limits tissue loss after frostbite injury.103 Aloe has antioxidant, antithromboxane, as well as antibacterial effects.
NSAIDs
Antiprostaglandins have had proven benefit in animal experiments and human studies for the treatment of frostbite due to their antithromboxane activity.102 Initially, aspirin (325 mg PO per day) was the agent of choice. When aspirin in this dosage was added to standard therapy in a treatment group of 38 patients with moderate-to-severe frostbite, there was no significant tissue loss.103 However, ibuprofen is now the agent of choice as it blocks thromboxane without inhibiting prostaglandins, which may bolster healing.4,103,119 In a study 154 patients treated with ibuprofen (12 mg/kg PO per day) combined with aloe vera and antibiotics, morbidity and hospital stay were reduced when compared to a control group.175 At least one center is using intravenous ketorolac for frostbite injuries brought in prethaw.109 Two types of blisters may form after rewarming: hemorrhagic and clear. The hemorrhagic blisters are a sign of deep injury; they should not be debrided as this will lead to desiccation of the underlying structures. Though controversial, most sources recommend aspiration or debridement of clear blisters. The rationale for this action is to remove the blister fluid, which is high in thromboxane. Thromboxane is a known destructive mediator in thermal burn injuries.177 The hypothesis that the clear blisters of frostbite were also high in thromboxane was proven by the aspiration of 10 frostbite patients blisters.178 Removal of the blister fluid therefore limits exposure of the tissue to thromboxane.
Frostbite/Frostnip Rewarming
Optimal rewarming is performed in a water bath at 37C41C.174-176 (See also Table 4.) The water bath temperature should be strictly regulated using a thermometer, as variations above the recommended range can cause burns and those below will rewarm too slowly. The rewarming generally takes 15-30 minutes. Have the patient move the frostbitten body part during rewarming, if possible. Signs of successful rewarming are increased pliability of the injured area as well as erythema and hyperemia. Oral or intravenous hydration should be administered to any frostbite patient who appears dehydrated, as this will
Table 4. One Protocol For Treating Frostbite Injuries.

1.On arrival, rapidly rewarm the affected areas in warm water at 37C-41C for 15-30 minutes or until thawing is complete. 2.On completion of rewarming, treat the affected parts as follows: a. Debride white blisters and institute topical treatment with aloe vera (Dermaide aloe) every six hours. b.Leave hemorrhagic blisters intact and institute topical aloe vera (Dermaide aloe) every six hours. c. Elevate the affected part(s) with splinting as indicated. d.Administer tetanus prophylaxis (toxoid or Ig). e.Analgesia: opiate, intramuscularly or intravenously as indicated. f. Administer ibuprofen 400 mg orally every 12 hours. g.Perform daily hydrotherapy for 30-45 minutes at 40C. 3.For documentation, obtain photographic records on admission, at 24 hours, and serially every 2-3 days until discharge. 4.Prohibit smoking.
Adapted from: McCauley RL, Hing DN, Robson MC, et al. Frostbite injuries: a rational approach based on the pathophysiology. J Trauma 1983 Feb;23(2):143-147.
Other Medications
The skin breakdown and post-thaw edema of frostbite injuries decrease the natural antistreptococcal properties of the skin. Most advocate waiting for signs of infection before administering antibiotics. Frostbite injuries are tetanus-prone wounds.179 Tetanus prophylaxis must be given to any patient whose status is unknown or lapsed.
Cutting Edge / Controversies

Two studies have explored the use of hyperthermic fluid infusion as a rewarming method. Both studies were performed on dogs cooled to 30C and then rewarmed with intravenous fluids heated to 65C.180,181 Rewarming rates averaged 3.6C per hour, and no complications related to the hyperthermic fluids were noted. The use of hyperthermic fluids has not been reported in humans. The use of a device that applies negative pressure
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and heat to the forearm and hand of hypothermic patients has demonstrated mixed rewarming results. Theoretically, the negative pressure overcomes thermoregulatory vasoconstriction, allowing more effective transfer of heat from the periphery to the core. Results from an initial trial showed a tenfold increase in rewarming rates when compared to controls.182 In subsequent studies, however, rewarming rates in the negative pressure device groups have not been significantly faster than those in the passive rewarming groups.183,184 Finally, the use of amino acid infusions has been demonstrated to induce thermogenesis and reduce hypothermia in surgical patients.185,186 The use of this technique has yet to be reported accidental hypothermia.
precipitating factors such as alcohol use or trauma, or as a result of another disease process. While everyone is susceptible to hypothermia, those at the extremes of age as well as those with impaired thermoprotective behaviors due to trauma, intoxication, infection, or neurologic or psychiatric disease carry a higher risk of hypothermia when exposed to cold stress. Treatment strategies for hypothermia should emphasize rapid invasive rewarming for patients with severe hypothermia and active noninvasive rewarming for patients with mild-tomoderate hypothermia. v
References
Evidence-based medicine requires a critical appraisal of the literature based upon study methodology and number of subjects. Not all references are equally robust. The findings of a large, prospective, randomized, and blinded trial should carry more weight than a case report. To help the reader judge the strength of each reference, pertinent information about the study, such as the type of study and the number of patients in the study, will be included in bold type following the reference, where available. In addition, the most informative references cited in the paper, as determined by the authors, will be noted by an asterisk (*) next to the number of the reference.
1. Cummins RO. ACLS for Experienced Providers. Dallas: American Heart Association; 2003. (Textbook) 2. Cummins RO. Guidelines 2000 for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Dallas: American Heart Association; 2000. (Textbook) 3. Hypothermia prevention, recognition and treatment. http:/ /www.hypothermia.org/protocol.htm. (State protocol) 4. Britt LD, Dascombe WH, Rodriguez A. New horizons in management of hypothermia and frostbite injury. Surg Clin North Am 1991 Apr;71(2):345-370. (Review) 5.* Danzl DF, Pozos RS, Auerbach PS, et al. Multicenter hypothermia survey. Ann Emerg Med 1987 Sep;16(9):10421055. (Multicenter; 428 patients) 6. Knize DM, Weatherley-White RC, Paton BC, et al. Prognostic factors in the management of frostbite. J Trauma 1969 Sep;9(9):749-759. 7. Pinzur MS, Weaver FM. Is urban frostbite a psychiatric disorder? Orthopedics 1997 Jan;20(1):43-45. (Retrospective; 20 patients) 8. Sim MM, Kuo YC. Accidental hypothermia in the subtropics. Am J Emerg Med 2000 May;18(3):357-358. (Letter) 9. Auerbach PS. Wilderness Emergency Medicine. 3rd ed. St. Louis, MO: Mosby; 2001. (Textbook) 10. Hammel HT. Regulation of internal body temperature. Annu Rev Physiol 1968;30:641-710. (Review) 11. Myers RA, Britten JS, Cowley RA. Hypothermia: quantitative aspects of therapy. JACEP 1979 Dec;8(12):523-527. (Review, case report) 12. Giesbrecht GG, Goheen MS, Johnston CE, et al. Inhibition of shivering increases core temperature afterdrop and attenuates rewarming in hypothermic humans. J Appl Physiol 1997 Nov;83(5):1630-1634. (Controlled clinical trial; 8 patients) 13. Fregly M. Activity of the hypothalamic-pituitary-thyroid
Disposition
Hypothermia
Maintain a low threshold for admitting patients with hypothermia. Hypothermia is often a complex, multifactorial disease that requires admission for appropriate treatment, particularly in the very young and the elderly. Patients with mild-to-moderate hypothermia who adequately rewarm in the ED and are otherwise healthy may be discharged if the circumstances of their hypothermia have been adequately resolved. For homeless persons, this may entail provision of warm, well-fitting clothing (in particular, hats, gloves, and footwear),187 and a social work evaluation for placement in a shelter. For patients who live alone, this may entail evaluation of the home environment, including assessment of heating and food. For patients who present intoxicated, this may entail referral to detoxification centers.
Frostbite/Frostnip
Patients with frostbite require admission or close outpatient follow-up, as the injury can look far worse 12-24 hours following initial ED presentation. The conventional aphorism when discussing the surgical treatment of frostbite has been, Frostbite in January, surgery in July.119 This referred to the fact that the line of demarcation of injury could take days to weeks to fully establish. However, the advent of two imaging techniques has allowed early demarcation and surgical intervention. Technetium-99 scanning has been used in a number of studies with good correlation between the early images and eventual line of demarcation.188,189 The newer modality in frostbite injuries is magnetic resonance imaging, which shows promise for rapid assessment of injuries.190 Admitted patients should receive daily hydrotherapy, limb elevation, and continued NSAIDs and topical aloe vera. Depending on the extent of the injury, further debridement, escharotomy, or operative intervention may be required.
Summary
Hypothermia is a condition that can occur because of isolated cold exposure alone, in combination with
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acute pancreatitis. Br Med J 1974 Mar 30;1(908):614. (Case report) Maclean D, Griffiths PD, Browning MC, et al. Metabolic aspects of spontaneous rewarming in accidental hypothermia and hypothermic myxoedema. Q J Med 1974 Jul;43(171):371-387. (Prospective; 88 patients) Stoner HB, Frayn KN, Little RA, et al. Metabolic aspects of hypothermia in the elderly. Clin Sci (Lond) 1980 Jul;59(1):1927. (Retrospective; 43 patients) Curry DL, Curry KP. Hypothermia and insulin secretion. Endocrinology 1970 Oct;87(4):750-755. (Animal study) Wilson O, Goldman RF. Role of air temperature and wind in the time necessary for a finger to freeze. J Appl Physiol 1970 Nov;29(5):658-664. (Prospective; 72 experiments) Purdue GF, Hunt JL. Cold injury: a collective review. J Burn Care Rehabil 1986 Jul-Aug;7(4):331-342. (Review) Kyosola K. Clinical experiences in the management of cold injuries: a study of 110 cases. J Trauma 1974 Jan;14(1):32-36. (Retrospective; 110 patients) Lewis T. Observations upon the reactions of the human skin to cold. Heart 1930;15:177-181. (Prospective; 34 patients) Daanen HA. Finger cold-induced vasodilation: a review. Eur J Appl Physiol 2003 Jun;89(5):411-426. (Review) Greenfield ADM. Cold vasoconstriction and vasodilation. Irish J Med Sci 1951;309:415. (Review) Raine TJ. Antiprostaglandins and antithromboxanes for treatment of frostbite. Surg Forum 1980;31:557-559. (Animal study; 20 subjects) McCauley RL, Hing DN, Robson MC, et al. Frostbite injuries: a rational approach based on the pathophysiology. J Trauma 1983 Feb;23(2):143-147. (Prospective; 38 patients) Vogel JE, Dellon AL. Frostbite injuries of the hand. Clin Plast Surg 1989 Jul;16(3):565-576. (Review) Ungley CC, Channell GD, Richards RL. The immersion foot syndrome. 1946. Wilderness Environ Med 2003 Summer;14(2):135-141; discussion 134. (Review) Kerber RE, Ornato JP, Brown D, et al. Guidelines for cardiopulmonary resuscitation and emergency care. Emergency Cardiac Care Committee and Subcommittees, American Heart Association Part IV. Special resuscitation situations. JAMA 1992 Oct 28;268(16):2242-2250. Sterba JA. Efficacy and safety of prehospital rewarming techniques to treat accidental hypothermia. Ann Emerg Med 1991 Aug;20(8):896-901. (Randomized, controlled trial; 8 patients) Minor TM, Shumacker HB Jr. An evaluation of tissue loss following single and repeated frostbite injuries. Surgery 1967 Apr;61(4):562-563. (Animal study) Hackett P. Frostbite and cold injuries. Audiodigest Emergency Medicine 2002;19(2). (Review) Locher T, Walpoth B, Pfluger D, et al. Accidental hypothermia in Switzerland (1980-1987)case reports and prognostic factors. Schweiz Med 1991;121(27-28):1020-1028. Miller JW, Danzl DF, Thomas DM. Urban accidental hypothermia: 135 cases. Ann Emerg Med 1980 Sep;9(9):456461. (Retrospective; 135 presentations in 114 patients) Ledingham IM, Mone JG. Treatment of accidental hypothermia: a prospective clinical study. Br Med J 1980 Apr 26;280(6222):1102-1105. (Prospective; 44 patients) Giesbrecht GG. Emergency treatment of hypothermia. Emerg Med 2001;13:9-16. (Review) Brown EB, Miller FA. Ventricular fibrillation following a rapid fall in carbon dioxide concentration. Am J Physiol 1952;169:56-60. (Animal study; 17 subjects)
115. Murphy K, Nowak RM, Tomlanovich MC. Use of bretylium tosylate as prophylaxis and treatment in hypothermic ventricular fibrillation in the canine model. Ann Emerg Med 1986 Oct;15(10):1160-1166. (Animal study) 116. Elenbaas RM, Mattson K, Cole H, et al. Bretylium in hypothermia-induced ventricular fibrillation in dogs. Ann Emerg Med 1984 Nov;13(11):994-999. (Animal study) 117. Bjornstad H, Mortensen E, Sager G, et al. Effect of bretylium tosylate on ventricular fibrillation threshold during hypothermia in dogs. Am J Emerg Med 1994 Jul;12(4):407-412. (Animal study) 118.* Stoner J, Martin G, OMara K, et al. Amiodarone and bretylium in the treatment of hypothermic ventricular fibrillation in a canine model. Acad Emerg Med 2003 Mar;10(3):187-191. (Animal study) 119. Murphy JV, Banwell PE, Roberts AH, et al. Frostbite: pathogenesis and treatment. J Trauma 2000 Jan;48(1):171178. (Review) 120. Kober A, Scheck T, Lieba F, et al. The influence of active warming on signal quality of pulse oximetry in prehospital trauma care. Anesth Analg 2002 Oct;95(4):961-966. (Randomized, controlled trial; 24 patients) 121. Gould L, Gopalaswamy C, Kim BS, et al. The Osborn wave in hypothermia. Angiology 1985 Feb;36(2):125-129. (Case report) 122. Shenaq SA, Yawn DH, Saleem A, et al. Effect of profound hypothermia on leukocytes and platelets. Ann Clin Lab Sci 1986 Mar-Apr;16(2):130-133. (17 patients) 123. Koht A, Cane R, Cerullo LJ. Serum potassium levels during prolonged hypothermia. Intensive Care Med 1983;9(5):275277. (Observational; 6 patients) 124. Hauty MG, Esrig BC, Hill JG, et al. Prognostic factors in severe accidental hypothermia: experience from the Mt. Hood tragedy. J Trauma 1987 Oct;27(10):1107-1112. (Retrospective; 10 patients) 125. Olsen DH, Gothgen IH. Treatment of accidental hypothermia. Ugeskr Laeger 2000 Sep 4;162(36):4790-4794. [Danish] (Review) 126. Fisher B, Russ C, Fedor EJ, et al. Experimental evaluation of prolonged hypothermia. AMA Arch Surg 1955 Sep;71(3):431-448. (Animal study; 20 subjects) 127. McKean WI, Dixon SR, Gwynne JF, et al. Renal failure after accidental hypothermia. Br Med J 1970 May 23;2(707):463464. (Case report) 128. Kofstad J. Blood gases and hypothermia: some theoretical and practical considerations. Scand J Clin Lab Invest Suppl 1996;224:21-26. (Review) 129 Kroncke GM, Nichols RD, Mendenhall JT, et al. Ectothermic philosophy of acid-base balance to prevent fibrillation during hypothermia. Arch Surg 1986 Mar;121(3):303-304. (Observational; 181 patients) 130. Robinson JL, Seal RF, Spady DW, et al. Comparison of esophageal, rectal, axillary, bladder, tympanic, and pulmonary artery temperatures in children. J Pediatr 1998 Oct;133(4):553-556. (Comparative) 131. Cohen S, Hayes JS, Tordella T, et al. Thermal efficiency of prewarmed cotton, reflective, and forced-warm-air inflatable blankets in trauma patients. Int J Trauma Nurs 2002 Jan-Mar;8(1):4-8. (Comparative; 298 patients) 132. Sessler DI, Schroeder M. Heat loss in humans covered with cotton hospital blankets. Anesth Analg 1993 Jul;77(1):73-77. (Comparative; 6 patients) 133. Sessler DI. Complications and treatment of mild hypothermia. Anesthesiology 2001 Aug;95(2):531-543. (Review) 134. Greif R, Rajek A, Laciny S, et al. Resistive heating is more effective than metallic-foil insulation in an experimental
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135.
136.
137.
138.
139.
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141.
142. 143. 144.
145.
146.
147.
148.
149.
150.
151. 152.
153.
model of accidental hypothermia: A randomized controlled trial. Ann Emerg Med 2000 Apr;35(4):337-345. (Randomized, controlled trial; 8 patients) Sessler DI, McGuire J, Sessler AM. Perioperative thermal insulation. Anesthesiology 1991 May;74(5):875-879. (Comparative) Szmuk P, Rabb MF, Baumgartner JE, et al. Body morphology and the speed of cutaneous rewarming. Anesthesiology 2001 Jul;95(1):18-21. (Comparative) Steele MT, Nelson MJ, Sessler DI, et al. Forced air speeds rewarming in accidental hypothermia. Ann Emerg Med 1996 Apr;27(4):479-484. (Randomized, controlled trial; 16 patients) Negishi C, Hasegawa K, Mukai S, et al. Resistive-heating and forced-air warming are comparably effective. Anesth Analg 2003 Jun;96(6):1683-1687. (Randomized, controlled trial; 24 patients) Cheney FW, Posner KL, Caplan RA, et al. Burns from warming devices in anesthesia. A closed claims analysis. Anesthesiology 1994 Apr;80(4):806-810. (Retrospective; 3000 total claims included 54 burns, of which 28 resulted from materials or devices used to warm patients) Weinberg AD. The role of inhalation rewarming in the early management of hypothermia. Resuscitation 1998 Feb;36(2):101-104. (Review) Brandson RD, Chatburn RL. Humidification of inspired gases during mechanical ventilation. Respir Care 1993;38:461. (Editorial) Sessler DI. Mild perioperative hypothermia. N Engl J Med 1997 Jun 12;336(24):1730-1737. (Review) Shanks CA. Heat gain in the treatment of accidental hypothermia. Med J Aust 1975 Aug 30;2(9):346-349. (Case report) Lloyd EE. Airway rewarming in the treatment of accidental hypothermia: A review. J Wilderness Med 1990;1:65-78. (Review) Leaman PL, Martyak GG. Microwave warming of resuscitation fluids Ann Emerg Med 1985 Sep;14(9):876-879. (Prospective) Werwath DL, Schwab CW, Scholten JR, et al. Warming nondextrose crystalloid in a microwave oven. Ann Emerg Med 1986 Feb;15(2):228-230. (Prospective) Anshus JS, Endahl GL, Mottley JL. Microwave heating of intravenous fluids. Am J Emerg Med 1985 Jul;3(4):316-319. (Prospective) Aldrete JA. Preventing hypothermia in trauma patients by microwave warming of i.v. fluids. J Emerg Med 1985;3(6):435-442. (Prospective) Delaney A. Reliability of modern microwave ovens to safely heat intravenous fluids for resuscitation. Emerg Med (Fremantle) 2001 Jun;13(2):181-185. (Prospective; 16 units tested) Faries G, Johnston C, Pruitt KM, et al. Temperature relationship to distance and flow rate of warmed i.v. fluids. Ann Emerg Med 1991 Nov;20(11):1198-1200. (Prospective) Jolly BT, Ghezzi KT. Accidental hypothermia. Emerg Med Clin 1992;10 (2):311. Levitt MA, Kane V, Henderson J, et al. A comparative rewarming trial of gastric versus peritoneal lavage in a hypothermic model. Am J Emerg Med 1990 Jul;8(4):285-288. (Comparative; 11 patients) Brunette DD, Sterner S, Robinson EP, et al. Comparison of gastric lavage and thoracic cavity lavage in the treatment of severe hypothermia in dogs. Ann Emerg Med 1987 Nov;16(11):1222-1227. (Animal study)
154. Otto RJ, Metzler MH. Rewarming from experimental hypothermia: comparison of heated aerosol inhalation, peritoneal lavage, and pleural lavage. Crit Care Med 1988 Sep;16(9):869-875. (Animal study) 155. Barr GL, Halvorsen LO, Donovan AJ. Correction of hypothermia by continuous pleural perfusion. Surgery 1988 May;103(5):553-557. (Animal study) 156. Walters DT. Closed thoracic cavity lavage for hypothermia with cardiac arrest. Ann Emerg Med 1991 Apr;20(4):439-440. (Letter) 157. Winegard C. Successful treatment of severe hypothermia and prolonged cardiac arrest with closed thoracic cavity lavage. J Emerg Med 1997 Sep-Oct;15(5):629-632. (Case report) 158. Gazmuri RJ, Becker J. Cardiac resuscitation. The search for hemodynamically more effective methods. Chest 1997 Mar;111(3):712-723. (Review) 159. Boczar ME, Howard MA, Rivers EP, et al. A technique revisited: hemodynamic comparison of closed- and openchest cardiac massage during human cardiopulmonary resuscitation. Crit Care Med 1995 Mar;23(3):498-503. (Prospective, comparative; 10 patients) 160.*Brunette DD, McVaney K. Hypothermic cardiac arrest: an 11 year review of ED management and outcome. Am J Emerg Med 2000 Jul;18(4):418-422. (Retrospective; 7 patients received an ED thoracotomy) 161. Kangas E, Niemela H, Kojo N. Treatment of hypothermic circulatory arrest with thoracotomy and pleural lavage. Ann Chir Gynaecol 1994;83(3):258-260. (Case report) 162. Althaus U, Aeberhard P, Schupbach P, et al. Management of profound accidental hypothermia with cardiorespiratory arrest. Ann Surg 1982 Apr;195(4):492-495. (Case report) 163. Coughlin F. Heart-warming procedure. N Engl J Med 1973 Feb 8;288(6):326. (Letter) 164. Altermeir WA, Todd J. Studies on the incidence of infection following open chest cardiac massage for cardiac arrest. Ann Surg 1963;158:596-607. (Retrospective; 43 patients) 165. Tavares S, Hankins JR, Moulton AL, et al. Management of penetrating cardiac injuries: the role of emergency room thoracotomy. Ann Thorac Surg 1984 Sep;38(3):183-187. (64 patients) 166. Splittgerber FH, Talbert JG, Sweezer WP, et al. Partial cardiopulmonary bypass for core rewarming in profound accidental hypothermia. Am Surg 1986 Aug;52(8):407-412. (Review, case report) 167. Farstad M, Andersen KS, Koller ME, et al. Rewarming from accidental hypothermia by extracorporeal circulation. A retrospective study. Eur J Cardiothorac Surg 2001 Jul;20(1):58-64. (Retrospective; 26 patients) 168. Walpoth BH, Walpoth-Aslan BN, Mattle HP, et al. Outcome of survivors of accidental deep hypothermia and circulatory arrest treated with extracorporeal blood warming. N Engl J Med 1997 Nov 20;337(21):1500-1505. (Multicenter, retrospective; 46 patients) 169.*Kornberger E, Mair P. Important aspects in the treatment of severe accidental hypothermia: the Innsbruck experience. J Neurosurg Anesthesiol 1996 Jan;8(1):83-87. (Retrospective; 55 patients) 170. Vretenar DF, Urschel JD, Parrott JC, et al. Cardiopulmonary bypass resuscitation for accidental hypothermia. Ann Thorac Surg 1994 Sep;58(3):895-898. (Review) 171. Gentilello LM, Cobean RA, Offner PJ, et al. Continuous arteriovenous rewarming: rapid reversal of hypothermia in critically ill patients. J Trauma 1992 Mar;32(3):316-325. (Prospective; 34 patients)
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172. Gentilello LM, Cortes V, Moujaes S, et al. Continuous arteriovenous rewarming: experimental results and thermodynamic model simulation of treatment for hypothermia. J Trauma 1990 Dec; 30(12):1436-1449. (Prospective, animal; 8 subjects) 173. Knight DA, Manifold CA, Blue J, et al. A randomized, controlled trial comparing arteriovenous to venovenous rewarming of severe hypothermia in a porcine model. J Trauma 2003 Oct; 55(4): 741-746. (Animal study) 174. Crimson JM. Studies on gangrene following cold injury VI. J Clin Invest 1947;26:468-475. (Animal study) 175. Heggers JP, Robson MC, Manavalen K, et al. Experimental and clinical observations on frostbite. Ann Emerg Med 1987 Sep;16(9):1056-1062. (Prospective; 154 patients) 176. Malhotra MS, Mathew L. Effect of rewarming at various water bath temperatures in experimental frostbite. Aviat Space Environ Med 1978 Jul;49(7):874-876. (Animal study) 177. Robson MC, DelBeccaro EJ, Heggers JP, et al. Increasing dermal perfusion after burning by decreasing thromboxane production. J Trauma 1980 Sep;20(9):722-725. (Animal study) 178. Robson MC, Heggers JP. Evaluation of hand frostbite blister fluid as a clue to pathogenesis. J Hand Surg [Am] 1981 Jan;6(1):43-47. (Prospective; 10 patients) 179. Didlake RH. Tetanus following frostbite injury. Contemp Orthop 1985;4:784. (Review) 180. Sheaff CM, Fildes JJ, Keogh P, et al. Safety of 65 degrees C intravenous fluid for the treatment of hypothermia. Am J Surg 1996;172:52-55. (Animal, prospective; 10 subjects) 181. Wiley D, Sheaff C, Nagy K, et al. Hyperthermic resuscitation is safe and effective after hemorrhagic shock in dogs. J Trauma 2000;48:1052-1056. (Animal, prospective; 14 subjects) 182. Grahn D. Recovery from mild hypothermia can be accelerated by mechanically distending blood vessels in the hand. J Appl Physiol 1998;85:1643-1648. (Prospective; 10 patients) 183. Taguchi A, Arkilic CF, Ahluwalia A, et al. Negative pressure rewarming vs. forced air rewarming in hypothermic postanesthetic volunteers. Anesth Analg 2001;92:261266. (Prospective; 7 patients) 184. Smith CE, Parand A, Pinchak AC, et al. The failure of negative pressure rewarming (Thermostat) to accelerate recovery from mild hypothermia in postoperative surgical patients. Anesth Analg 1999;89:1541-1545. (Prospective; 60 patients) 185. Sellden E, Lindahl SGE. Amino acid-induced thermogenesis reduces hypothermia during anesthesia and shortens hospital stay. Anesth Analg 1999;89:1551-1556. (Prospective; 75 patients) 186. Widman J, Hammarqvist F, Sellden E. Amino acid infusion induces thermogenesis and reduces blood loss during hip arthroplasty under spinal anesthesia. Anesth Analg 2002;95:1757-1762. (Prospective; 46 patients) 187. John Abeysekera, The use of personal protective clothing and devices in the cold environment, Coldtech Preliminary Study Report Division of Industrial Ergonomics Department of Human Work Sciences Lule University, Sweden. 188. Salimi Z, Vas W, Tang-Barton P, et al. Assessment of tissue viability in frostbite by 99mTc pertechnetate scintigraphy. AJR Am J Roentgenol 1984 Feb;142(2):415-419. (Prospective; 7 patients) 189. Mehta RC, Wilson MA. Frostbite injury: prediction of tissue viability with triple-phase bone scanning. Radiology 1989 Feb;170(2):511-514. (Prospective; 7 patients) 190. Barker JR, Haws MJ, Brown RE, et al. Magnetic resonance imaging of severe frostbite injuries. Ann Plast Surg 1997 Mar;38(3):275-279. (Case report; 2 patients)
Physician CME Questions

81. Primary hypothermia: a. occurs when an otherwise healthy subject is exposed to temperatures cold enough to overcome the bodys ability to appropriately thermoregulate. b. only occurs in extremely cold weather. c. occurs in patients whose underlying medical conditions disrupt adequate thermoregulatory mechanisms. d. occurs only in pediatric or elderly patients . 82. Secondary hypothermia: a. occurs in patients whose underlying medical conditions disrupt adequate thermoregulatory mechanisms. b. may be underreported because patients tend to be admitted to the hospital with a primary diagnosis other than hypothermia. c. is caused by conditions that impede circulation, increase heat loss, decrease heat production, or cause impairment of thermoregulation. d. all of the above. 83. The bulk of the bodys heat production is a result of: a. release of epinephrine. b. release of thyroid hormones. c. shivering. d. vasoconstriction. 84. In the severely hypothermic patient: a. hyperglycemia should be aggressively controlled with insulin. b. with atrial fibrillation, anticoagulation should be started. c. active external rewarming has been shown to be safe and effective. d. a normal or low hematocrit is expected because of fluid shifts. 85. Psoriasis, dermatitis, burns, dehydration, decreased subcutaneous fat, and alcohol use are examples of: a. factors that result in poor circulation. b. factors that decrease the bodys ability to produce heat. c. factors that can result in increased body heat loss. d. factors that can contribute to loss of body thermoregulation. 86. Pulse oximetry is a reliable indicator of hypoxia in the hypothermic patient. a. True b. False
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87. The elderly are at increased risk for hypothermia because of: a. age-related impairment of thermoregulatory systems. b. their reduced shivering response, decreased mobility, malnutrition, and diminished lean body mass. c. reduced vasoconstriction. d. multiple medication use, particularly cardiac medications. e. all of the above. 88. Expected neurologic findings in the severely hypothermic patient include all of the following except: a. unresponsive to noxious stimuli. b. fixed pupils. c. hyperreflexia. d. increased muscular tone. 89. The observation of a relative tachycardia in the hypothermic patient: a. is normal in the later stages of hypothermia. b. should prompt the clinician to search for associated conditions, such as occult traumatic bleeding, sepsis, or drug ingestion. c. is normal in children. d. is normal in the elderly. 90. Osborn or J waves: a. are a little-known ECG finding associated with hypothermia. b. have significant prognostic value. c. appear as an elevation at the junction of the QRS and ST segments. d. decrease in size as core temperature decreases. 91. Active external rewarming has been shown in multiple studies to have little impact on afterdrop. a. True b. False 92. Which of the following is a poor prognostic sign in cases of frostbite? a. The early appearance of clear blebs across the entire extent of the injured area b. Early return of sensation c. Hemorrhagic blisters d. Soft subcutaneous tissue 93. Which of the following rewarming techniques is least appropriate for patients with mild-to-moderate hypothermia and an intact shivering response? a. Passive rewarming b. Forced air rewarming c. Resistive heating methods (e.g., electric blankets) d. Peritoneal irrigation
94. In the severely hypothermic patient, intubation should be avoided if possible because it is likely to induce ventricular fibrillation. a. True b. False 95. Which of the following is not recommended in the management of frostbite? a. Rewarming in a water bath upon arrival b. Parenteral analgesics during rewarming c. Debridement of hemorrhagic blisters d. Tetanus prophylaxis
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96. Which of the following rewarming techniques provides the most rapid increase in core temperature? a. Passive rewarming b. Cardiopulmonary bypass c. Forced air rewarming d. Heated infusions This test concludes the July through December 2003 semester testing period of Emergency Medicine Practice. The answer form for this semester and a return envelope have been included with this issue. Please refer to the instructions printed on the answer form. All paid subscribers are eligible to take this test.
Physician CME Information

This CME enduring material is sponsored by Mount Sinai School of Medicine and has been planned and implemented in accordance with the Essentials and Standards of the Accreditation Council for Continuing Medical Education. Credit may be obtained by reading each issue and completing the printed post-tests administered in December and June or online single-issue post-tests administered at www.empractice.net. Target Audience: This enduring material is designed for emergency medicine physicians. Needs Assessment: The need for this educational activity was determined by a survey of medical staff, including the editorial board of this publication; review of morbidity and mortality data from the CDC, AHA, NCHS, and ACEP; and evaluation of prior activities for emergency physicians. Date of Original Release: This issue of Emergency Medicine Practice was published December 1, 2003. This activity is eligible for CME credit through December 1, 2006. The latest review of this material was November 10, 2003. Discussion of Investigational Information: As part of the newsletter, faculty may be presenting investigational information about pharmaceutical products that is outside Food and Drug Administration approved labeling. Information presented as part of this activity is intended solely as continuing medical education and is not intended to promote off-label use of any pharmaceutical product. Disclosure of Off-Label Usage: This issue of Emergency Medicine Practice discusses no off-label use of any pharmaceutical product. Faculty Disclosure: In compliance with all ACCME Essentials, Standards, and Guidelines, all faculty for this CME activity were asked to complete a full disclosure statement. The information received is as follows: Dr. Hermann, Dr. Weingart, Dr. Decker, Dr. Gallagher, and Dr. Stewart report no significant financial interest or other relationship with the manufacturer(s) of any commercial product(s) discussed in this educational presentation. Accreditation: Mount Sinai School of Medicine is accredited by the Accreditation Council for Continuing Medical Education to sponsor continuing medical education for physicians. Credit Designation: Mount Sinai School of Medicine designates this educational activity for up to 4 hours of Category 1 credit toward the AMA Physicians Recognition Award. Each physician should claim only those hours of credit actually spent in the educational activity. Emergency Medicine Practice is approved by the American College of Emergency Physicians for 48 hours of ACEP Category 1 credit (per annual subscription). Emergency Medicine Practice has been reviewed and is acceptable for up to 48 Prescribed credit hours by the American Academy of Family Physicians. Emergency Medicine Practice has been approved for 48 Category 2-B credit hours by the American Osteopathic Association. Earning Credit: Two Convenient Methods
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Emp-Hypothermia and Frostbite

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EMERGENCY MEDICINE PRACTICE .

EMPRACTICE NET A N E V I D E N C E - B A S E D A P P ROAC H T O E M E RG E N C Y M E D I C I N E

Hypothermia And Other Cold-Related Emergencies

Critical Appraisal Of The Literature

Table 1. Physiologic Responses To Core Temperature Changes.

Emergency Medicine Practice

www.empractice.net December 2003

Table 2. Thermoregulatory Risk Factors For Cold-Related Illnesses.

Environmental Heat Loss

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Emergency Medicine Practice

Systemic Effects Of Hypothermia Cardiovascular System

Figure 1. The J wave.

Emergency Medicine Practice

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Emergency Medicine Practice

Other Cold-Related Injuries Frostbite

Emergency Medicine Practice

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Emergency Medicine Practice

Emergency Department Evaluation

Emergency Medicine Practice

www.empractice.net December 2003

Complete Blood Count

Frostbite And Frostnip

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Emergency Medicine Practice

Clinical Pathway: Rewarming The Hypothermic Patient

Temperature greater than 32C?

Does the patient have a pulse?

Begin CPR and core rewarming

Temperature not increasing or declining

Active external rewarming

Patient loses pulse or core temperature is not increasing

Continued from page 9

Table 3. Rewarming Techniques In Hypothermia.

Arterial Blood Gases

Active external rewarming

Active core rewarming

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Emergency Medicine Practice

Active External Rewarming

Cost- And Time-Effective Strategies For Cold-Related Emergencies

Emergency Medicine Practice

www.empractice.net December 2003

Active Core Rewarming

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Emergency Medicine Practice

Thoracotomy With Internal Cardiac Massage And Mediastinal Irrigation

Emergency Medicine Practice

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Extracorporeal Blood Rewarming

Ten Pitfalls To Avoid

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Emergency Medicine Practice

Table 4. One Protocol For Treating Frostbite Injuries.

Cutting Edge / Controversies

Emergency Medicine Practice

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