Emp-hypothermia and Frostbite

December 2003Volume 5, Number 12

Authors

Luke Hermann, MDAssistant Professor, Department of EmergencyMedicine, Mount Sinai School of Medicine, NewYork, NY.

Scott Weingart, MDChief Resident, Mount Sinai School of Medicine,Department of Emergency Medicine, New York, NY.

Peer Reviewers

Wyatt W. Decker, MD, FACEPChair, Department of Emergency Medicine, MayoClinic and Mayo Medical School, Rochester, MN.

Scott Gallagher, MD, FACEPAspen Valley Hospital, Aspen, CO.

Charles Stewart, MD, FACEPColorado Springs, CO.

CME Objectives

Upon completing this article, you should be able to:1. describe common environmental conditions

and physical conditions that predispose a patientto hypothermia;

2. describe the diagnosis and managementof frostbite;

3. discuss the prehospital management of cold-related emergencies;

4. discuss salient points in the history and physicalexamination that can help identify conditionsthat can precipitate and/or complicatehypothermia; and

5. list indications and contraindications ofrewarming techniques for hypothermia.

Date of original release: December 1, 2003.Date of most recent review: November 10, 2003.See “Physician CME Information” on back page.

Associate Editor

Andy Jagoda, MD, FACEP, Vice-Chair of Academic Affairs,Department of EmergencyMedicine; Residency ProgramDirector; Director, InternationalStudies Program, Mount SinaiSchool of Medicine, New York, NY.

Editorial Board

Judith C. Brillman, MD, ResidencyDirector, Associate Professor,Department of EmergencyMedicine, The University ofNew Mexico Health SciencesCenter School of Medicine,Albuquerque, NM.

W. Richard Bukata, MD, ClinicalProfessor, Emergency Medicine,Los Angeles County/USC MedicalCenter, Los Angeles, CA; Medical

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 andChair, Department of EmergencyMedicine, University of Turin, Italy.

Michael J. Gerardi, MD, FAAP, FACEP,Clinical Assistant Professor,Medicine, University of Medicineand Dentistry of New Jersey;Director, Pediatric EmergencyMedicine, Children’s MedicalCenter, Atlantic Health System;Department of EmergencyMedicine, Morristown MemorialHospital.

Michael A. Gibbs, MD, FACEP, Chief,Department of EmergencyMedicine, Maine Medical Center,Portland, ME.

Gregory L. Henry, MD, FACEP,CEO, Medical Practice RiskAssessment, Inc., Ann Arbor,MI; Clinical Professor, Departmentof Emergency Medicine,University of Michigan MedicalSchool, Ann Arbor, MI; President,American Physicians AssuranceSociety, Ltd., Bridgetown,Barbados, West Indies; PastPresident, ACEP.

Jerome R. Hoffman, MA, MD, FACEP,Professor of Medicine/EmergencyMedicine, UCLA School ofMedicine; Attending Physician,UCLA Emergency Medicine Center;Co-Director, The DoctoringProgram, UCLA School of Medicine,Los Angeles, CA.

Francis P. Kohrs, MD, MSPH, LifelongMedical Care, Berkeley, CA.

Michael S. Radeos, MD, MPH,Attending Physician, Departmentof Emergency Medicine, LincolnMedical and Mental Health Center,Bronx, NY; Assistant Professor inEmergency Medicine, Weill Collegeof Medicine, Cornell University,New York, NY.

Steven G. Rothrock, MD, FACEP,FAAP, Associate Professorof Emergency Medicine,University of Florida; OrlandoRegional Medical Center; MedicalDirector of Orange CountyEmergency Medical Service,Orlando, FL.

Alfred Sacchetti, MD, FACEP,Research Director, Our Lady ofLourdes Medical Center, Camden,NJ; Assistant Clinical Professor

of Emergency Medicine,Thomas Jefferson University,Philadelphia, PA.

Corey M. Slovis, MD, FACP, FACEP,Professor of Emergency Medicineand Chairman, Department ofEmergency Medicine, VanderbiltUniversity Medical Center; MedicalDirector, Metro Nashville EMS,Nashville, TN.

Mark Smith, MD, Chairman,Department of EmergencyMedicine, Washington HospitalCenter, Washington, DC.

Charles Stewart, MD, FACEP, ColoradoSprings, CO.

Thomas E. Terndrup, MD, Professorand Chair, Department ofEmergency Medicine, Universityof Alabama at Birmingham,Birmingham, AL.

EMERGENCY MEDICINE PRACTICEA N E V I D E N C E - B A S E D A P P R O A C H T O E M E R G E N C Y M E D I C I N E

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Hypothermia And OtherCold-Related EmergenciesThe young woman is wheeled through the door at nearly midnight on New Year’s Eve.The paramedic gives the report: “Apparently she has a psych history. Family says she’sdepressed—left the house a few hours ago and might have taken an overdose. The policefound her in a snow bank. Thought she was dead at first, but we got some kind ofrhythm on the monitor and I think I felt a pulse.” Looking at the gurney, you see noobvious signs of life. As she’s transferred onto the hospital bed, the monitor beginsalarming—her rhythm has just converted to ventricular fibrillation.

HYPOTHERMIA develops when more heat is lost than the body cangenerate. While typically considered a wintertime condition, hypoth-

ermia can occur in any weather, and its cause is not limited solely toenvironmental exposure. Hypothermia can both complicate and even beprecipitated by many patient conditions, such as metabolic or circulatorydisorders, substance abuse, trauma, age, or even medication use. Rapididentification, careful selection of rewarming strategies, and attention to co-morbid illness are required for optimal care of the hypothermic patient.Furthermore, the ED treatment of other cold-related disorders, such asfrostbite, plays an important role in long-term outcomes.

This issue of Emergency Medicine Practice reviews the evidenceregarding the assessment and treatment of hypothermia and other cold-related disorders.

Critical Appraisal Of The Literature

There are few randomized, controlled trials to guide the clinician on thetreatment of hypothermia and cold-related disorders. Hypothermia isdifficult to study in a rigorous, prospective manner outside of the labora-tory. Most of our knowledge of accidental hypothermia comes from casereports and retrospective analysis, often giving variable results. Many of thestudies that elucidated the pathophysiology of hypothermia were per-formed decades ago and have not been repeated. Human studies are limitedto mild hypothermia because of ethical concerns. Animal models havecertainly furthered our understanding of the condition, but the results must

Emergency Medicine Practice 2 www.empractice.net • December 2003

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Table 1. Physiologic Responses To CoreTemperature Changes.

Normothermia 37ºC 98.6ºF

Mild hypothermia 35ºC 95ºF

Ataxia, confusion 33ºC 91.4ºF

Shivering ceases 31ºC 87.8

Severe hypothermia 30ºC 86ºF

Ventricular fibrillation risk 28ºC 82.4ºF

No response to pain 26ºC 78.8ºF

Cardiac output severely reduced 25ºC 77ºF

Loss of corneal reflexes; only 23ºC 73.4ºF isolated cases of survival below this level

be applied cautiously to humans as physiology differs.The most recent iteration of the American Heart

Association/International Liaison Committee on Resusci-tation (AHA/ILCOR) guidelines offers an evidence-based consensus opinion on the treatment of hypother-mia.1,2 While a good portion of the guidelines deals withthe treatment of cardiac arrest in the setting of hypother-mia, there are recommendations for the treatment ofvarious core temperatures. For instance, in mild hypoth-ermia (34ºC-36ºC), passive rewarming and active externalwarming are recommended. In moderate hypothermia(30ºC-34ºC), passive rewarming and active externalrewarming of the truncal areas only is recommended.(The latter recommendation is based on the suppositionthat rewarming only the trunk will decrease the possibil-ity of afterdrop.) For severe hypothermia (<30ºC), activeinternal rewarming is recommended. The strength ofevidence, and its limitations, supporting these consensusrecommendations is presented later in this review.

The state of Alaska has also released consensus-based guidelines, which are posted at http://www.hypothermia.org.3 These guidelines haverewarming protocols similar to the AHA/ILCORguidelines. It is interesting to note that the Alaskanprotocols also give strong warning regarding afterdropdespite disagreement among experts as to the clinicalrelevance of this phenomenon.

Epidemiology

Hypothermia is typically defined as a core body tempera-ture of 35ºC (95ºF) or less. While texts propose differentdefinitions, core temperatures of 30ºC-35ºC with aperfusing rhythm are generally defined as mild-to-moderate hypothermia. Symptoms include shivering,confusion and disorientation, memory loss, drowsiness,exhaustion, fumbling hands and poor coordination,slurred speech, and numbness. A core temperature of lessthan 30°C—defined as severe hypothermia—is oftenassociated with cardiac dysrhythmias. (Severe hypother-mia may also be defined as a core temperature of 30ºC-

35ºC with a non-perfusing rhythm.) Typical manifesta-tions of severe hypothermia include shallow breathing,weak pulse, a progressive decline in consciousness, and,ultimately, death. Although a few cases of extreme coldresuscitation have been reported, most patients whosecore temperature drops to less than 23°C will not survive.(See also Table 1.)

FrostbiteFrostbite is a disease of prolonged exposure to the cold.Military personnel, the homeless, participants in recre-ational winter activities, and those with outdoor occupa-tions are all at risk.4 Cofactors for risk of frostbite includeinadequate clothing, alcohol use, substance abuse, mentalillness, and contact with metal or moisture.5,6 Urban civilianstudies show a high incidence of alcohol intoxication andpsychiatric illness in frostbite cases.6,7 Individuals who areacclimated to cold environments may have more effectivedefenses against frostbite, possibly because they are moreaware of how to prepare for the cold.4

Pathophysiology

Accidental hypothermia can be classified as eitherprimary or secondary.

Primary hypothermia occurs when an otherwisehealthy subject is exposed to temperatures cold enough toovercome the body’s ability to appropriately thermoregu-late. While this type of hypothermia is frequently associatedwith prolonged activity in a cold environment, it is impor-tant to note that it can occur in any setting, even whenambient temperatures are relatively mild.8 Interestingly, inthe largest prospective study of accidental hypothermia todate, 69 of 428 cases occurred in Florida.5 Annual mortalitydue to primary hypothermia in the United States averagesslightly over 700 cases per year, with most occurring inurban settings.9 Primary hypothermia may be complicatedby drug and alcohol use, and/or concurrent homelessness,which may contribute to increased mortality in urbanat-risk populations.

Secondary hypothermia occurs in patients whoseunderlying medical conditions disrupt adequate ther-moregulatory mechanisms. As these patients are typicallyadmitted to the hospital with a primary diagnosis otherthan hypothermia (e.g., sepsis), the incidence of secondaryhypothermia may very well be grossly underreported.

ThermoregulationWhile exposure to an environment colder than bodytemperature is the common denominator to all forms ofhypothermia, an individual’s capacity to compensate forcold stress determines in part whether the patient willbecome hypothermic.

Body temperature is controlled by a balance betweenheat loss and heat production. Thermoregulation is acomplex process with overall control mediated by theanterior hypothalamus.10 When exposed to a cold environ-ment, peripheral receptors transmit stimuli through thespinal cord to the hypothalamus, initiating a number of

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Table 2. Thermoregulatory Risk FactorsFor Cold-Related Illnesses.

• Extremes of age (early childhood or age greater than 65)• Mental or physical disability• Psychiatric disorders (e.g., Alzheimer’s disease)• Dehydration• Factors that result in poor circulation (e.g., age, tight

clothing or boots, cramped positions, fatigue, certainmedications, smoking, alcohol, and diseases that affectthe blood vessels, such as diabetes)

• Factors that decrease the body’s 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, decreasedsubcutaneous fat, alcohol use)

• Factors that can contribute to loss of body thermoregula-tion (e.g., central nervous system pathology, trauma,stroke, Parkinson’s disease, neuropathies, spinal cordinjuries)

responses aimed at both heat production and conservation.The bulk of the body’s heat production is a result of

shivering, which raises the basal metabolic rate two to fivetimes.11 Inhibition of shivering in one controlled studycaused a 37% decrease in rewarming rates when comparedto shivering controls.12 Release of epinephrine and thyroidhormones during cold exposure, as well as other physi-ologic factors, act to increase nonshivering thermogenesis.13

Heat conservation is facilitated initially via periph-eral vasoconstriction, which redirects blood from the skininto the deeper tissues. Vasoconstriction is most pro-nounced in the extremities and can lead to a sixfoldincrease in insulating capacity.14 Additionally, behavioralresponses limit heat loss via mechanisms such as addinglayers of clothing and seeking shelter.

There are many predisposing factors for the develop-ment of hypothermia. (See also Table 2.) They can looselybe broken down into four categories: factors that impedecirculation, increase heat loss, decrease heat production,or cause impairment of thermoregulation. Significantoverlap between these categories exists.

Adequate circulation may be impaired by mechani-cal obstruction (such as tight-fitting clothing), certainmedications, smoking, or underlying disease processes(e.g., diabetes or peripheral vascular disease). Dehydra-tion can impede circulation by reducing overall volume.

Net heat loss occurs anytime environmental exposureovercomes the body’s ability to generate and conserve heat.Though this can occur in surprisingly temperate conditions,it is most dramatic in cold, windy environments andimmersion scenarios. Multiple medications and recreationaldrugs, particularly alcohol, can predispose to heat loss byimpairing vasoconstriction. Infants have a high surface-area-to-body-mass ratio, which speeds heat loss. All patientswith disruption of normal skin function are at risk forincreased heat loss. This predisposition is most dramatic inburn patients but is also present in any patient with anexfolialitive dermatitis.

Factors that predispose to inadequate heat productioninclude endocrinologic failure (hypothyroidism, hypoadren-alism), 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 ofcentral nervous system pathology (stroke, tumor, bleed),toxin exposure (particularly alcohol), or because ofinadequate peripheral sensory function (peripheralneuropathies, spinal cord transsection). Multiple drugscan impair central thermoregulation. Benzodiazapines,opioids, barbiturates, phenothiazines, atypicalantipsychotics, and tricyclic antidepressants all impaircentral thermoregulation and, via alpha blockade, inhibitvasoconstriction.15-17 Ethanol use predisposes to hypother-mia in multiple ways. It impairs judgment and thermalperception, which increases the risk of exposure, and italso causes peripheral vasodilation, impedes shivering,and predisposes to hypoglycemia.18 Additionally, it has adirect effect on the hypothalamus, which in turn resultsin a lowering of the thermoregulatory set point, resultingin a reduction of the core temperature.19

The elderly deserve special mention because of theirpredisposition to develop hypothermia. This is a reflec-tion of age-related impairment of many of the systemsthat allow appropriate thermoregulation. Heat produc-tion may be impaired because of a reduced shiveringresponse, decreased mobility, malnutrition, and dimin-ished lean body mass.20-22 The elderly are less able todiscriminate temperature changes and when exposed tocold environments are less able to vasoconstrict ad-equately.23 They may also be on multiple medications,particularly cardiac medications, that may increase theirrisk. Additionally, the elderly are more prone to coldexposure because of falls or illness. The importance ofinfection as a source of hypothermia in the elderly iswell-documented in the literature. Several studies havenoted that the incidence of sepsis in this group is ap-proximately 80%.24,25 Sepsis should be of particularconcern if the hypothermic patient was found indoors.26

Social factors such as living with inadequate heating dueto low income must also be considered.

Environmental Heat LossHeat loss occurs through four primary mechanisms:radiation, conduction, evaporation, and convection. Theratios by which these mechanisms produce heat loss varyin different exposure situations.27 The four environmentalconditions through which these mechanisms cause cold-related stress are low temperatures, high/cool winds,dampness, and cold water.

• Radiation is the transfer of particulate energythrough space. Radiation of heat occurs in allenvironments and is roughly proportional to thedifference between skin and ambient temperature.27

Loss of body heat through radiation occurs when theambient temperature is below 98.6ºF. Importantfactors in radiant heat loss are the surface area and


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Figure 1. The J wave.

The J wave (or Osborn wave) is associated with moderatehypothermia but has no prognostic significance.

the temperature gradient.28

• Conduction refers to heat transfer between twoobjects in direct contact. The most obvious exampleoccurs during immersion. Water conducts heat awayfrom the body 25 times faster than air because it hasa greater density (and therefore a greater heatcapacity).28 Survival times in ocean water immersionhave been estimated to be about 4.5 hours in 15ºCwater and less than two hours in 0ºC water.29 Patientswith a lower body mass (including children) and alower fat content are likely to cool down morerapidly.30 Wet clothes increase heat loss by five timesover dry clothes.28 The importance of other sub-stances’ thermal conductivity should not be over-looked; for instance, granite has four times theconductivity of water, a salient point in an elderlypatient who has spent several hours on a cold tilefloor after a fall.31

• Evaporation is heat loss that results from convertingwater from a liquid to a gas. In the hypothermicpatient, this occurs through insensible perspiration(the body sweats to maintain a humidity level ofabout 70% next to the skin; in cold, dry environ-ments, a great deal of moisture and heat can be lostthis way) and respiration (as water vapor duringexhalation). While evaporation can result in signifi-cant heat loss, another important effect is that theseprocesses reduce the overall circulating volume,which can lead to dehydration (which in turn makesthe body more susceptible to hypothermia and othercold-related illnesses).28

• Convection is heat transfer that is facilitated bymovement of air or liquid across an object. The rateof convective heat loss depends on the density of themoving substance (water convection occurs morequickly than air convection) and the velocity of themoving substance.28 When convection combines withevaporation (e.g., wet clothes on a cold, windy day),extreme heat loss can occur. Wind chill, a combina-tion of temperature and velocity, is a crucial factorto evaluate.

Systemic Effects Of HypothermiaCardiovascular SystemThe cardiovascular effects of hypothermia can be dividedinto two categories: electrical effects (conduction abnor-malities and arrhythmias) and hemodynamic effects. Theinitial cardiac response to cold stress is tachycardia,which is replaced by progressive bradycardia as tempera-tures decline. This is a result of both decreased spontane-ous depolarization and slowing of the conductionsystem. It is refractory to atropine.32 In one review of 22hypothermic patients, both bradycardia and the amountof QT interval prolongation were found to correlatesignificantly with declines in temperature.33 The observa-tion of a relative tachycardia in the hypothermic patientshould prompt the clinician to search for associatedconditions, such as occult traumatic bleeding, sepsis, ordrug ingestion. As heart rates decline, there is a progres-

sive reduction in cardiac output that mirrors the brady-cardia so that at 20ºC, cardiac output has declinedapproximately 80%.34 Interestingly, oxygen consumptionas a result of metabolism declines by approximately 6%per degree C, essentially matching the decline in cardiacoutput.35 This may explain why pulseless, profoundlyhypothermic patients have been resuscitated withoutevidence of ischemic injury to vital organs.

In addition to rate-related changes, one animalmodel study suggests both systolic and diastolic dysfunc-tion in severe hypothermia.36 In this study, eight dogswere cooled to 25ºC, resulting in a significant decline instroke volume and an increase in ventricular wallstiffness. Similarly, data from the surgical literature havenoted a decrease in ventricular contractility whenhypothermia is induced for surgical procedures.37

Peripheral resistance progressively increases as bodytemperature declines. One study of 11 dogs documented anincrease of 310% over normothermic controls at 20ºC.34 Thisincrease is likely multifactorial, related to increased bloodviscosity, hemoconcentration, and sympathetic tone.38-40

Osborn or J waves (see Figure 1) are one of the morewell-known ECG findings associated with hypothermiaand appear as an elevation at the junction of the QRS andST segments. They typically occur at core temperaturesless than 32ºC. In one prospective study of 43 hypother-mic patients, all patients whose temperature at presenta-tion was below 32.2ºC had J waves present, while 38% ofthose with temperatures above 32.2ºC did not.41 The exactetiology of the J wave is unknown but may be related toinjury current, delayed depolarization, or early repolar-ization that occurs in one area of the ventricle prior tocompletion of depolarization in another area.42,43 Al-though J waves are not pathognomonic for hypothermiaand have been reported in other disease states such assubarachnoid hemorrhage, normothermic normalpatients, and hypercalcemia, their presence is highlysuggestive of a significant decrease in core temperature.Aside from the observation that their size appearsinversely related to temperature, they do not appear tohave any prognostic value.44

Hypothermia is associated with a wide array of atrialand ventricular dysrhythmias. Atrial fibrillation, the mostcommonly cited hypothermic dysrhythmia, has beennoted in the surgical literature for decades. In patientsundergoing cardiac and neurosurgical procedures,hypothermia is often induced for protective benefit. Theincidence of atrial fibrillation in these patients increaseswith temperature drop and is frequently encountered at


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Ventricular fibrillation becomes more likely as tempera-tures decline below 28ºC, though its incidence may havebeen overestimated in the past.15,33 The potential forventricular fibrillation increases as core temperaturedeclines. This is partially due to a decrease in the fibrillationthreshold. There are multiple theories to explain thisobservation, related to acid-base disturbances, ischemia, andmyocardial temperature gradients.48,49

Traditional teaching is that induction of ventricularfibrillation can occur with rough handling, endotrachealintubation, or as a consequence of core afterdrop. There isno convincing evidence to substantiate the myth regardinginduction of ventricular fibrillation with moving or caring forthe hypothermic patient. Data from one multicenter studyof accidental hypothermia refute the claim that intuba-tion is likely to induce ventricular fibrillation.5

Once present, ventricular fibrillation is typicallyresistant to defibrillation until core temperatures areabove 28ºC. An isolated case report of successful defibril-lation at 25.6ºC does exist, supporting the currentrecommendation for an initial trial of defibrillation onceventricular fibrillation is identified.50

AfterdropCore temperature afterdrop refers to the observation thatas some patients are warmed, their core temperaturecontinues to decline. In the past, this continued drop ofcore temperature was believed to predispose the patientto the development of ventricular fibrillation, andrewarming strategies that were thought to minimizeafterdrop were encouraged. There is little evidence tosubstantiate these concerns, leading several experts toquestion the importance of afterdrop.51,52 There are twoexplanations for the phenomenon of afterdrop; one isbased on a conductive mechanism, and the other on aconvective mechanism.

The convective theory holds that the return of coolblood from peripheral circulation to the core leads toafterdrop. Historically, this has led many authors tocaution against active external rewarming for themoderately-to-severely hypothermic patient. As at leastone author has pointed out, this makes little intuitivesense given the extreme peripheral vasoconstriction thattypifies significant hypothermia.49 In fact, active externalrewarming has been shown in multiple studies to havelittle impact on afterdrop.53-61 In this group of studies, thelargest recorded afterdrop occurred in one of the passive

rewarming control arms, suggesting that convection islikely not the issue.59

Conductive heat transfer offers an alternative explana-tion for observed afterdrop. The hypothermic patient coolsfrom the outside in. Consequently, a heat gradient isestablished from the relatively warm core to the coolperiphery. This heat gradient does not reverse immediatelyupon initiation of rewarming. Until the gradient is reversed,further heat transfer occurs from the warmer core to coolerperipheral tissues. This mechanism is supported by theobservation that afterdrop has been demonstrated in afrozen leg of beef and a cooled bag of gelatin.62

Regardless of the mechanism, it is important to notethat afterdrop has not been shown to be of any clinicalimportance in rewarming the hypothermic patient.

Rewarming ShockRewarming shock refers to cardiovascular collapse that canoccur as the patient is warmed. It is attributed to theincreases in the metabolic rate of peripheral tissue and theperipheral vasodilation that accompany external rewarm-ing.63 Cardiac output from the cool heart is unable to matchtissue demand, and a clinically apparent shock state ensues.Clinical experience with successful rewarming of severelyhypothermic patients using primarily external rewarmingtechniques has refuted this observation.64-66

Neurologic SystemThe neurologic manifestations of hypothermia are well-described in the literature. As with most of hypothermia,the bulk of our knowledge comes from case reports; nocontrolled studies exist. In the largest study specificallyaddressing the neurologic manifestations of accidentalhypothermia, several findings were observed to correlatesignificantly with reduction in core temperature.67 Thisreview of 97 patients found that as the patient’s tempera-tures decreased, the level of consciousness declined,pupillary light response and deep tendon reflexesdiminished, and muscular tone increased. In severehypothermia, this frequently resulted in patients whowere unresponsive to noxious stimuli and were areflexicwith fixed pupils and stiff bodies—a clinical picture thatcould easily be misinterpreted as death.

These observations are consistent with other reportsand align with the pathophysiologic changes of nerve tissuethat accompany hypothermia. Animal studies havedemonstrated that peripheral nerve conduction progres-sively decreases as temperatures decline.68 Additionally,muscle contraction has been shown to be temperaturedependent, as is synaptic delay time, which may partiallyexplain the dysarthria commonly observed in the hypother-mic patient.69,70 Electroencephalograms performed onpatients with induced hypothermia for surgical proceduresdemonstrate a progressive decrease in the frequency andamplitude of electrical activity, with electrocerebral silenceoccurring in the range of 13.5ºC-21.5ºC.71,72

Hematologic SystemHypothermia causes a multitude of hematologic changes,


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decline in temperature, there is a progressive hemocon-centration, resulting in an increase of the hematocrit byapproximately 2% for each 1ºC drop.73 This is likelysecondary to an increase in vascular permeability withresultant third spacing of fluids as well as free water lossvia cold-induced diuresis.74 Animal studies suggest thatsplenic contraction may play a role as well.75 As bloodcools, there is a concomitant increase in blood viscositythat can lead to microinfarction.74

Hypothermia affects coagulation and hemostasis inseveral ways. Lowering blood temperatures inhibitsenzymatic reactions of the clotting cascade, leading to aprogressive coagulopathy. If a tube of blood is cooled to28ºC, prothrombin times and partial thromboplastin timesincrease an average of 5 and 20 seconds, respectively.76 Asblood specimens are typically warmed to 37ºC in the lab,this coagulopathy will not be apparent in recorded pro-thrombin times or partial thromboplastin times.

Impaired hemostasis may be encountered because ofthrombocytopenia or a decrease in platelet activity.Thrombocytopenia can reflect splenic or hepatic seques-tration, marrow depression, or disseminated intravascu-lar coagulopathy.77,78 Platelet inhibition is believed to berelated to a temperature-mediated decline in thrombox-ane B2.79 Alternately, impaired synthesis of prostacyclinat low temperatures can lead to platelet aggregation andthrombosis, another catalyst for the development ofdisseminated intravascular coagulopathy.80 Disseminatedintravascular coagulopathy in the hypothermic patient isalso believed to be related to a release of thromboplastinfrom poorly perfused tissue.81

Respiratory SystemEarly tachypnea is followed by progressive slowing of therespiratory rate as temperatures decline.15 The decline inrespiratory rate correlates to decreasing core temperatureswith cessation of spontaneous respirations occurring indogs at 24ºC.82 The hypoventilation associated withhypothermia is likely related to two mechanisms. First, astemperature declines, metabolism slows, which results in a50% reduction of oxygen consumption and carbon dioxideproduction at 30ºC.74 Second, cooling of the respiratorycenters depresses ventilatory drive, with a response to pCO2

stimulation progressively attenuated below 34ºC.83

Protective airway mechanisms are impaired becauseof decreased ciliary motility, bronchorrhea, and cold-related thickening of respiratory tract secretions.84

Oxygenation may be further compromised by thedevelopment of noncardiac pulmonary edema.14

Renal SystemAs core temperature declines, a progressive diuresis occurs.Initially, this reflects an increase in renal blood flow second-ary to peripheral vasoconstriction.85 As temperaturescontinue to drop, the kidneys are unable to appropriatelyconcentrate the urine because of tubular dysfunction.86,87

This leads to a progressively dilute urine and continueddiuresis.87 Tubular dysfunction also limits renal clearance of

glucose and hydrogen ions, contributing to the hyperglyce-mia and acidosis associated with hypothermia.88

Gastrointestinal SystemHepatic dysfunction can occur with hypothermia and isgenerally attributed to decreased perfusion.74 Clearance oflactate is impaired, contributing to metabolic acidosis.74

Additionally, the liver’s ability to detoxify toxins is reduced,which complicates overdoses.89 Pancreatitis is noted atautopsy in 20%-30% of hypothermia-related deaths, withasymptomatic elevations of serum amylase levels occurringeven more frequently.90,91 The cause is not known, though itmay be related to thrombotic-related microinfarcts.92

Endocrine SystemIn hypothermia of abrupt onset in a healthy host,hyperglycemia should be expected. There are multiplecontributing mechanisms, including cold-related inhibi-tion of insulin secretion and increases in sympathetictone and glucagon levels that lead to an increase inglycogenolysis and gluconeogenesis.93,94 As core tempera-tures decline, insulin secretion by the pancreas decreasesand insulin resistance of target cells increases, leading toserum hyperglycemia.95 Insulin resistance makes its useineffective until temperatures are above 32ºC.14 Attemptsto lower the blood sugar of the hypothermic patient canresult in significant iatrogenic hypoglycemia oncerewarming occurs.9 If the patient remains hyperglycemicafter rewarming, diabetic ketoacidosis, hyperosmolarsyndrome, and pancreatitis should all be considered. Ifhypothermia has developed over a longer period of timeand in debilitated patients, hypoglycemia may bepresent. Increased metabolism associated with shiveringcan deplete glycogen stores, predisposing to the develop-ment of hypoglycemia.14

Thyroid, adrenal, and pituitary function is generallybelieved to be normal in simple exposure hypothermiabut may impair thermogenesis in patients with preexist-ing deficiencies. If the patient is resistant to rewarming,empiric administration of hydrocortisone or thyroidhormone should be considered.

Other Cold-Related InjuriesFrostbiteFrostbite occurs when the skin tissue actually freezes.Although frostbite typically occurs at temperatures below30°F (-1°C), wind chill effects can cause frostbite at above-freezing temperatures. Absolute air temperature is not asrelevant as the combination of ambient temperature,wind chill, and the presence or absence of precipitation.96

Initial effects of frostbite include uncomfortablesensations of coldness; a tingling, stinging, or achingfeeling of the exposed area is followed by numbness.Ears, fingers, toes, cheeks, and noses are primarilyaffected. Superficial frostbite involves just the skin; theexterior will be white and frozen but the tissue below thesurface is soft and resilient before rewarming. Deepfrostbite injuries involve underlying structures tissues(muscles, tendons, etc.).97 Before rewarming, the injured


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Any factors that decrease blood flow to a tissue areaof the body can contribute to frostbite. The body’sresponse to the extremes of temperature is to protect thecore. The peripheral vasoconstriction that occurs as aresult can be localized (e.g., as when one touches coldmetal) or generalized (e.g., a cold wind blows across yourscalp and the vessels in your hand constrict). Theresulting decreased blood flow to the skin can lower thetemperature of the tissues and predispose to injury. Sincewater conducts temperature far better than air, moisturewill also dramatically increase the chances of cold-relatedskin injury.

Fractures and muscular skeletal injuries pose furtherrisk of frostbite, as edema can also mechanically obstructblood flow. The body’s natural vasoconstrictive response todehydration increases the chances of frostbite. Smokingfurther exacerbates vasoconstriction in cold exposures.98

The pathogenesis of frostbite is classically divided intofour phases.9 In the prefreeze phase, skin temperature fallsuntil maximal vasoconstriction occurs at approximately15ºC. At 10ºC, to counter the deleterious effects of thisshunting of blood from the acral areas of the body (ears,nose, fingers, toes), the body allows intermittent blood flowthrough cold-induced vasodilation, also known as the“hunting response.” First described in 1830, cold-inducedvasodilation is a cycle of constriction and dilation of thevessels that allows warm blood to intermittently flow todistal areas and prevent freezing.99,100 People who are oftenexposed to a cold environment develop an enhanced cold-induced vasodilation response.100,101 Many other factorsaffect cold-induced vasodilation, such as diet, alcoholconsumption, altitude, race, age, and stress.100 Unfortu-nately, cold-induced vasodilation can be blunted bydehydration, hypoxia, altitude, or Raynaud’s phenomenon.Cold-induced vasodilation keeps a minimal level of bloodflow to the distal areas. If the temperature drops further, thecore will start to be cooled by the returning blood, and thehunting response will cease.97 At this point, the tissue in thedistal areas progresses to the next phase of damage.

When the skin temperature decreases to -4ºC orlower, the freeze phase begins with the formation ofextracellular ice crystals. This causes relative extracellulardehydration, resulting in the flow of cellular water out tothe interstitial space; eventually, cells will crenate andlyse. Intracellular ice crystal formation will also destroycells by direct mechanical damage. (Touching cold metal,certain chemicals like nitrous oxide, or certain super-cooled liquids, such as gasoline or “white gas” used incamping, can result in instant frostbite. In this type offlash freezing, intra- and extracellular ice crystals formsimultaneously, resulting in the rapid destruction of largeamounts of tissue.9)

The vascular stasis phase is accompanied by risingconcentrations of the breakdown products of dead cellsand the buildup of inflammatory mediators.102 Prostag-landins, histamine, thromboxane, and bradykinin all playa role in progressive tissue ischemia.103 Stasis causesinflammatory edema that further compromises blood

flow to the area. Platelet aggregation leads to thrombosis;red cell clumping and microvasculature collapse furthercomplicate the picture.

The result of vascular stasis is the late ischemicphase, in which injured areas, lacking blood flow, shift toirreversible damage. The pathophysiology of cold-induced skin injury bears many pathophysiologicalsimilarities to thermal burns; the same level of special-ized care is required to achieve the best outcome.104

FrostnipFrostnip is superficial ice crystal deposition on the skinand can be a warning sign for impending frostbite ifexposure continues. Frostnip is generally a retrospectivediagnosis, as it is defined by absence of tissue damageupon rewarming.

ChilblainsChilblains (or pernio) is a non-freezing cold-relatedinjury characterized by red, scaly lesions, often on thefeet. They often occur in cold, humid environments. Anassociation with sufferers of lupus has been seen.Treatment is supportive, though some European centershave tried calcium-channel blockers.9

Trench FootTrench foot is a process similar to chilblains. Trench footresults from prolonged exposure of the extremities to a cold,wet environment (or immersion), without actual freezing. Itwas common in trench warfare during World War I. It canoccur at temperatures up to 60ºF if the feet are constantlywet.28 Continual exposure to cool, wet conditions causesperipheral circulation to the foot to decline. Symptoms oftrench foot include a tingling and/or itching sensation,burning, pain, and swelling. The affected tissue generallydies and sloughs off. While severe cases may developblisters and gangrene, massive tissue loss is rare and isdependent on the length of the exposure.105

Prehospital Care

In general, the priority in the prehospital care of thehypothermic patient is to stabilize the patient, minimizefurther heat loss, and provide rapid transport to a facilitywhere definitive care can be provided. Distance and/ortransport times to the healthcare facility, as well asinstitutional capabilities, often drive local protocols.(Wilderness medicine issues present several challengesthat are beyond the scope of this article.)

As hypothermia frequently causes significanthypoventilation, the presence of respirations andadequate airway patency should be carefully assessed.Supplemental oxygen should be supplied to all patientswith ventilatory support as needed. If the patient is trulyapneic, intubation should be performed.

Cardiac electrical activity should be assessed as soonas is feasible. If an organized rhythm is present, pulsesshould be assessed. The severe vasoconstriction associ-ated with hypothermia can make palpation of peripheral


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LLC pulses difficult. Carotid or femoral pulses should be

palpated for 30-45 seconds (per American College ofCardiology guidelines) to confirm a pulseless state. If nopulses are present, CPR should be initiated.

If initial cardiac monitoring demonstrates ventricularfibrillation, and attempt at defibrillation appears reason-able. Published guidelines recommend one series ofdefibrillation shocks (200J, 300J, 360J).1,106 If unsuccessful,further attempts at defibrillation should be withheld untilrewarming can be accomplished, and CPR should bestarted. Fear of inducing ventricular fibrillation throughhandling or moving a patient are unwarranted andshould never delay patient care.

If the patient has a decreased level of consciousness,a fingerstick glucose should be obtained. If this is notpossible, IV dextrose should be administered. Addition-ally, lethargic or comatose patients in whom opioidoverdose is suspected should be given naloxone, asopioid overdose and hypothermia often occur in tandem.

After assurance of the ABCs and treatment ofcoexisting injuries, the next priority is rapid transportand prevention of further heat loss. One controlled studythat addressed prehospital rewarming found no differ-ence in rewarming rates when subjects with mildhypothermia were randomized to either inhalationrewarming, active external rewarming, or passiverewarming.107 Given this fact and the fact that attempts atfield rewarming can delay definitive care, passiverewarming is appropriate in the prehospital phase.

Remove any wet or constricting clothing. Facilitatepassive rewarming by wrapping the patient in dryblankets. Wrap any injured or frostbitten areas in sheetsor blankets to prevent incidental trauma; splint andelevate all potential fractures. Though minimizing thetime frozen is important for maximum tissue salvage incases of frostbite, any potential for incomplete rewarmingor refreezing make field rewarming a risky proposition.108

Dry heat should not be used as it can damage anddehydrate the already fragile tissue. Exposure to externalsources of heat such as radiators or campfires should beavoided to prevent partial thawing. The erstwhilepractice of massaging frostbitten areas with snow orwarm hands only results in further mechanical trauma tothe injured area.

In cases of definite frostnip, rewarming can be donein the field. A nose can be warmed by blowing into handscupped around it. Hands should be placed in thepatient’s armpits.109

Emergency Department Evaluation

As with all patients who present to the ED with seriousillness, evaluation and stabilization should occur simulta-neously. Remember that the presentation of the severelyhypothermic patient can mimic death; careful assessmentfor signs of life may be required.

HistoryWhen confronted with the hypothermic patient, it is

particularly important to determine whether contributingcomorbid disease is present. Although a history is oftendifficult to obtain from a moderate or severely hypother-mic 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, thyroidreplacement, 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 oftrauma as it frequently complicates hypothermia. Traumamay precede hypothermia, limiting a person’s ability toseek shelter or warmth. In one retrospective study of 234patients, injuries preceded hypothermia in 27% ofcases.110 Trauma may also follow hypothermia, as a resultof the confusion due to the decline in body temperature.

Physical ExaminationCareful attention to determining the presence of respira-tion and circulation will guide initial therapy.

AirwayDetermine whether the patient has a patent airway and isable to handle secretions. Indications for intubation of thehypothermic patient are identical to those in the normother-mic patient with the caveat that pulse oximetry is not areliable indicator of hypoxia. Although case reports haveimplicated intubation as a cause of ventricular fibrillation,several large series have disputed this.5,111,112 Most expertsnow agree that with preoxygenation, endotracheal intuba-tion is unlikely to induce ventricular fibrillation.

BreathingAs body temperature falls, the respiratory rate slows.Progressive hypothermia slows metabolism; oxygenutilization and carbon dioxide production are decreased.From a practical standpoint, this means that a hypother-mic patient who appears to be breathing too slow may infact be breathing at a rate that is appropriate for his orher metabolic needs. This has led some experts to cautionagainst overventilating the hypothermic patient.9,113

Overventilation can lead to significant respiratoryalkalosis and may exacerbate myocardial irritability,which would increase the risk of ventricular fibrillation.114

CirculationExpect the severely hypothermic patient to bebradycardic. Determining the presence or absence ofpulses can be problematic because of severe vasoconstric-tion and intravascular volume depletion. Spend 30-45


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Continued on page 11

seconds palpating for pulses in the carotid or femoralarea. The use of a handheld Doppler may be helpful ifpulses are difficult to detect. Remember that any pulsemay provide perfusion adequate for the decreasedmetabolic demands that accompany severe hypothermia.If the patient is truly pulseless, current recommendationsare to begin CPR. However, CPR should only be started ifthe physician is convinced pulses are absent.73

The effectiveness of bretylium for prophylaxis andtreatment of hypothermic ventricular fibrillation has notbeen clearly established. Conflicting data from use inexperimental dog models exist.115-117 Most recently, arandomized, blinded study compared bretylium toamiodarone and placebo in the treatment of hypothermicventricular fibrillation in 30 dogs.118 Neither drug wassignificantly better at inducing chemical defibrillation orimproving the resuscitation rate compared to placebo.

DisabilityAssess the patient’s mental status. Hypothermia causesprogressive alteration of cognitive functioning, culminat-ing in electrocerebral silence and coma. Deep tendonreflexes and pupillary light response may be diminishedand muscle tone increased.

Examine the patient head to toe looking for clues tosecondary disease processes. Look for evidence of trauma,including bruising and extremity deformity. Check the skinfor track marks suggestive of opiate overdose. Look forbullae over pressure points, which can be seen in overdose.The hypothyroid patient may present with absence of thelateral third of the eyebrow, sparse pubic or axillary hair, agoiter, or waxy swelling of the skin and subcutaneoustissues. Patients with primary adrenal insufficiency maydemonstrate hyperpigmentation.

Frostbite And FrostnipAssess the severity of the frostbite injury prior to re-warming. Frostnip or superficial frostbite involves justthe skin; the exterior will be white and frozen but thetissue below the surface is soft and resilient beforerewarming. Deep frostbite injuries involve underlyingstructures.97 Before rewarming, the injured part will feelhard and solid, often compared to wood.

It is quite difficult to judge the severity of frostbiteprior to thawing and nearly impossible to predict theextent of injury directly after rewarming. The line ofdemarcation between tissue that will recover andpermanently injured areas can take weeks to becomefully established.119 Good prognostic signs after rewarm-ing are the early appearance of clear blebs across theentire extent of the injured area, early return of sensation,and soft subcutaneous tissue.9

Diagnostic Studies

GlucoseA bedside fingerstick glucose is fast, easy, and cheap.Correcting hypoglycemia can occur in tandem withrewarming the patient and may prevent the need for the

more invasive rewarming techniques. Primary hypoglyce-mia can present with low body temperatures and alteredmental status. Secondary hypoglycemia can be seen inchronic cold exposure (particularly in patients with inad-equate reserves) and with depletion of glycogen stores thatcan accompany prolonged environmental exposure.Alternately, the hypothermic patient will frequently presentwith hyperglycemia of multifactorial origin.

Pulse OximetryThe peripheral vasoconstriction that accompanieshypothermia limits accurate pulse oximetry. In oneprospective study of mildly hypothermic patients,oximetry functioned properly in only 77% of patientswith a core temperature of 35.5ºC but increased to 92% attemperatures above 36ºC.120 These data suggest that pulseoximetry becomes less effective as temperatures declineand is unlikely to function appropriately even in mildhypothermia. To accurately determine oxygen saturation,an arterial blood gas should be obtained.

ElectrocardiographyHypothermia causes a progressive slowing of electricalconduction that can be visualized on the ECG. Sinusbradycardia and prolonged QT intervals are to be expectedas temperatures decline.121 Below 32ºC atrial fibrillationbecomes common. At temperatures less than 28ºC, ventricu-lar fibrillation and asystole are of greatest concern.

Complete Blood CountAs body temperatures decline, a progressive hemocon-centration occurs. Hypothermia is known to causeleukocyte depletion.122 Lack of an elevated white bloodcell count, therefore, does not imply that a significantunderlying infection is absent. Platelet counts tend todrop secondary to splenic and hepatic sequestration.

ElectrolytesHypokalemia is expected from a shift of potassium into thecells.123 Hyperkalemia is indicative of cellular acidosis and amarker of poor prognosis. Data from a Mt. Hood, Oregon,tragedy suggest that severely elevated potassium levels maygive prognostic information. In this review of 10 hypother-mic patients, those who died had potassium levels greaterthan 10 mEq/L, while survivors had levels less than 7 mEq/L.124 Other studies also show that hyperkalemia can be usedto distinguish hypothermic patients who can be resuscitatedform those who cannot.125

Serum sodium, calcium, and chloride concentrationsshould not change appreciably at temperatures above25ºC.126

Renal FunctionElevation of blood urea nitrogen and creatinine arefrequently encountered in hypothermia. One study foundthe incidence of acute renal failure in accidental hypoth-ermia was 40% for patients who required admission to anICU.26 (However, this study focused on the “indoor”


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LLC Clinical Pathway: Rewarming The Hypothermic Patient

The evidence for recommendations is graded using the following scale. For complete definitions, see back page. Class I: Definitelyrecommended. 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 dependingupon a patient’s 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 anyformat without written consent of EB Practice, LLC.

Measure core temperature

➤

NO

➤

Temperature greater than 32ºC? ➤YES Passive rewarming

(Class II)• cover with blankets• ensure adequate energy stores to allow for shivering (IV dextrose or oral

carbohydrates)

Expected rewarming rate: <1ºC/hour

Does the patient have a pulse?

➤

NO

➤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: 1-3ºC/hour

Temperature not increasing or declining

➤

➤Patient loses pulse or core temperature is not increasing

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: 9ºC/hour, 8ºC/hour, and 3ºC/hour, respectively

• Bretylium 5 mg/kg IV for ventricular tachycardia/ventricular fibrillation (Class indeterminate)

➤

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hypothermic; these findings may not be as applicable tooutdoor enthusiasts.) The etiology is thought to reflect apre-renal state secondary to decreased renal blood flowand so may benefit from fluid resuscitation.74,127

Endocrine StudiesPreexisting endocrine failure predisposes to the develop-ment of hypothermia. Thyroid studies (TSH and free T4)and serum cortisol levels should be sent on any patientwhose history or physical examination suggests hypothy-roidism or adrenal insufficiency.

Arterial Blood GasesManagement of acid-base status in the hypothermic patientis complex. Data from case series indicate that patients maypresent either acidotic or alkalotic, with no clear predilectionfor either state.111 Multiple contributors to acidosis arepresent in the hypothermic patient. These include but arenot limited to respiratory depression, lactate generationfrom shivering, impaired hepatic function, and decreasedtissue perfusion. The tendency toward acidosis is balancedagainst the fact that as blood cools, it becomes progressivelyalkalotic. For example, a tube of blood with a pH of 7.4 anda pCO2 of 40 mmHg at 37ºC will register a pH of 7.5 and apCO2 of 30 mmHg at 30ºC.

Historically, two acid-base management strategies existfor the hypothermic patient: the pH-stat and alpha statmethods. The pH-stat method attempts to maintain anarterial pH of 7.4 when recorded values are adjusted to thepatient’s actual temperature. This technique may paradoxi-cally increase regional ischemia by diverting blood awayfrom regions that are dependent on collateral perfusion.128

The alpha stat method attempts to keep pH at 7.4 whenmeasured at 37ºC. In other words, no correction is made forthe patient’s temperature and concomitant baselinealkalosis. Advantages of this technique revolve aroundimproved cardiac performance. In one study of 181 cardiacbypass patients undergoing induced hypothermia, ventricu-lar fibrillation occurred in 40% of patients managed with thepH-stat method but only 20% of patients managed withalpha stat.129 Most experts now recommend the alpha statmethod for acid-base management.

Trauma SeriesAs trauma and hypothermia are frequently encounteredtogether, a high index of suspicion must be maintainedfor occult traumatic injury. If traumatic injury is sus-pected, trauma protocols should be followed in tandemwith resuscitation of hypothermia. Consider a head CT inpatients with a suspicion of trauma or lack of neurologicimprovement with rewarming.

Management

Rewarming Techniques In HypothermiaMultiple techniques are available for rewarming thehypothermic patient. Each falls into one of three catego-ries—passive, active external, or active core rewarming.

Table 3. Rewarming Techniques InHypothermia.

Passive rewarmingBest for: Mildly hypothermic, healthy patients with an intact

shivering responsePros: Effective and noninvasiveCons: Ineffective when core temperatures drop below the

shivering threshold of 28ºC-30ºC; requires adequateglycogen stores

Methods: Relies on intrinsic thermogenerative mechanismsof the patient, including shivering, and passive insulationtechniques, such as using a cotton blanket; adequateenergy substrate should be ensured either by provisionof food or IV dextrose, provided the patient is nothyperglycemic on presentation

Active external rewarmingBest for: Mild-to-moderate hypothermiaPros: Effective, noninvasiveMethods:

• Forced air rewarming: Likely the most readily accessibledelivery 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; limitsmonitoring

Active core rewarmingBest for: Severe hypothermia (<30ºC)Pros: Quickest return to normothermiaCons: Increased risk of complications, especially as the

degree of invasiveness increasesMethods:

• Airway rewarming: Minimally invasive, practical• Heated infusions: Simple, but clinical effect appears to

be minor• Gastrointestinal irrigation: Rewarming rates estimated

at 1.5ºC per hour• Peritoneal irrigation: Rewarming rates estimated at 1ºC-

2ºC per hour; placement of the peritoneal catheterrequires expertise

• Pleural irrigation: Rewarming rates estimated at 3ºC perhour, plus direct warming of the heart; possibility ofiatrogenic injury, requires large volumes of liquids

• Left-sided thoracotomy with internal cardiac massageand mediastinal irrigation: Indicated for severehypothermia with cardiac arrest only; rapid rewarmingrate (estimated at 8ºC per hour), allows for open cardiacmassage; extremely invasive, potential for iatrogenicand infectious complications

• Cardiopulmonary bypass: Indicated for severe hypoth-ermia with cardiac arrest only; extremely rapid rewarm-ing rates (estimated at ≥ 9ºC per hour); requiressignificant technical expertise, availability is institution-dependent

(See Table 3.)The state of the literature does not allow for guide-

lines that are strongly evidence-based. There are very fewrandomized, controlled trials that have assessed theefficacy of the various rewarming techniques. Those that


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LLC exist were comprised of healthy volunteers cooled to a

mildly hypothermic temperature in a laboratory setting.51

Extrapolation of these data to the severely hypothermicpatient with comorbidities should be done cautiously.

In addition, when critically assessing the literatureon rewarming, it is important to consider the implica-tions of the outcome measure reported—that is, does therate of change of core temperature correlate with clinicaloutcome? Rate of rewarming—the most frequent measureof efficacy reported in hypothermia trials—has not beenconvincingly tied to outcome. Though it would appearthat the more invasive rewarming techniques willincrease rewarming rates, this information is meaninglessunless it translates into lower mortality. Other consider-ations when choosing a rewarming method includepatient temperature at presentation, presence of a pulse,and institutional capabilities (i.e., access to cardiopulmo-nary bypass).

The majority of hypothermic patients can be effec-tively rewarmed without having to resort to invasivetechniques. If, however, core temperatures fail to increaseor begin to decline, or the patient’s clinical status isdeteriorating, invasive core rewarming should beaggressively pursued. Also, in cases of cardiac arrest inwhich return of a perfusing rhythm is temperature-dependent, rapid rewarming appears logical. Thissuggests an advantage to invasive rewarming techniquesin this situation.

Accurate determination and continual monitoring ofthe patient’s core temperature is important in formulat-ing a rewarming strategy. Note that not all thermometersare suited to measuring low temperatures. In particular,tympanic and axillary temperature measurement shouldbe avoided in suspected hypothermia.130 Oral tempera-ture measurement may be sufficiently accurate but mayinterfere with airway management. On the whole, rectaltemperature measurement is best suited for patients whodo not require invasive rewarming, and bladder probesor pulmonary artery temperature measurement are bestsuited for patients who require invasive rewarming.130

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 requireinvasive rewarming techniques. In mild hypothermia, removal ofwet clothing, covering with a blanket, and ensuring adequateenergy stores to allow for shivering is usually sufficient. Inmoderate or severe hypothermia, as long as the patient has apulse, active external rewarming is typically sufficient. Saveinvasive techniques for pulseless patients and those who do notrespond 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 contributeto or be precipitated by hypothermia. Correcting thehypoglycemia is an important adjunct to rewarming the patientand may prevent the need for more invasive rewarmingtechniques.

3. Question witnesses.Co-morbid illness, medications, and other factors can precipitateand/or alter the management of hypothermia. Witnesses,prehospital care providers, and family members can helpdetermine crucial factors such as the patient’s medicalbackground, social circumstances, and possible occult trauma. ▲

Passive RewarmingPassive rewarming allows the patient to warm byendogenous heat production alone. Adequate heatproduction is contingent on shivering, making passiverewarming ineffective when core temperatures dropbelow the shivering threshold of 28ºC-30ºC.14 Addition-ally, shivering requires adequate glycogen stores, makingit less effective in elderly or debilitated patients anddiabetics with too much insulin.

Passive rewarming requires the patient to be well-insulated. Wet clothing should be removed and thepatient should be wrapped in blankets or sleeping bags.Conventional wisdom holds that blankets should beprewarmed to minimize further conductive heat loss.131

Since the heat capacity of a blanket is very small, warmedblankets have not been shown to significantly affect heatloss in clinical settings.132 The insulating ability of thecover is related to the layer of air trapped between theskin and the covers, not the material itself.133 Thisexplains the observation that rewarming rates do notdiffer significantly with the use of aluminum spaceblankets or cloth blankets.134 Under ideal conditions,insulating a patient would reduce cutaneous heat loss tozero, which would allow for a rewarming rate of approxi-mately 1ºC per hour.133 However, lower rewarming ratesare observed clinically with passive rewarming, typicallyreducing heat loss by less than 50%.132,135 In rewarmingstudies in which passive rewarming was used as the“placebo” therapy, rewarming rates typically variedbetween 0.2ºC and 0.85ºC per hour.51

Passive rewarming appears to be most appropriatefor healthy patients with an intact shivering response. Inthis group, adequate energy substrate should be ensuredeither by provision of food or IV dextrose, provided thepatient is not hyperglycemic on presentation.

Active External RewarmingWith external rewarming, heat is applied directly to thesurface of the body. Multiple techniques are described inthe literature, including hot water bottles, hot bath


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External rewarming techniques accomplish heat gainvia two mechanisms—conduction and convection.Conductive heat transfer occurs from the skin into theunderlying tissue and is a relatively inefficient means ofcore rewarming. Convective heat transfer occurs as bloodwarmed in peripheral tissues is carried to the core.

Despite some theoretic concerns, active externalrewarming has been demonstrated to be safe andeffective across the range of hypothermic patients andrealistically represents the cornerstone of management ofhypothermia. It also has been shown to be more effectivein infants and children compared to adults because oftheir larger surface-area-to-body-mass index.136

In most hospital settings, forced air rewarming is likelyto be the most readily accessible delivery system for externalrewarming. Commercial devices are frequently used torewarm patients in the surgical setting. Units typicallyconsist of a heating device that directs warm air through aplastic blanket and across the patient’s body via slits cut intothe underside of the blanket.

In a randomized study of patients with moderatehypothermia (mean temperature, 29ºC), forced air rewarm-ing was shown to rewarm significantly quicker than passiverewarming combined with inhalation rewarming.137 Therewarming rate with forced air rewarming was 2.4ºC perhour, and no difference in afterdrop was noted between thetwo groups. Other controlled studies in mildly hypothermicpatients have not demonstrated a significant increase inafterdrop with forced air rewarming compared to passiverewarming. Rewarming rates have varied from 0.9ºC-3.3ºCper hour.54,56

Although controlled trials of forced air rewarming totreat severe hypothermia do not exist, several case seriesindicate it to be an effective modality in this setting. In areview of 36 patients who presented over a 10-year period,Roggla et al found forced air rewarming combined withinhalation and warmed infusion therapy to be an effectiveand noninvasive method of rewarming.65 Median patienttemperature was 25.8ºC, rewarming took an average of 9.5hours at a rate of 1.1ºC per hour, and it was successful in92% of cases. Patients who arrested prior to hospital arrivalwere excluded. In another review of 15 patients with a meantemperature less than 27ºC, all were effectively rewarmed toabove 35ºC using forced air rewarming.64

Resistive heating methods (electric blankets) haveshown comparable efficacy to forced air rewarming inminimizing heat loss during operative procedures.138

Additionally, they have been shown to be significantlymore effective than passive rewarming in one random-ized, controlled trial.134 Because of their portability andminimal electrical requirements, resistive heating mayrepresent a viable rewarming mechanism for prehospitalcare providers.

The use of hot water baths is generally not recom-mended because of the limitations it imposes on monitor-ing. The use of hot water containers placed in high blood

flow areas such as the axilla and groin has also beendescribed as a rewarming method. Given the small surfaceareas involved, this technique is unlikely to be efficacious.133

Additionally, animal models have shown that even at fluidtemperatures of 45ºC, thermal burns are likely to occur.133 Infact, a review by the American Society of Anesthesiologistsfound that hot water bottles were the most common causeof perioperative thermal injury.139

Active Core RewarmingCore rewarming refers to techniques that warm thepatient from the inside out. There are several theoreticbenefits to this approach. The core organs are responsiblefor over 50% of heat production in basal metabolism atnormothermia.52 This percentage is even higher inhypothermia because peripheral tissue is colder and lessmetabolically active than the core. Metabolism increaseswith rewarming, leading to an increase in heat produc-tion. By concentrating rewarming efforts on the mostmetabolically active tissues, the body’s own capacity toproduce heat is exploited to maximal effect. The phenom-enon of afterdrop is believed to be avoided with corerewarming, though the importance of this observation isdebated. Additionally, rewarming shock is presumablyless likely with core rewarming.

Different techniques for core rewarming include heatedinfusions, airway rewarming, heated lavage (gastric,bladder, colonic, peritoneal, thoracic, mediastinal), andextracorporeal blood rewarming. From a practical perspec-tive, core rewarming provides the quickest return tonormothermia but is associated with increased risk,especially as the degree of invasiveness increases.

Airway RewarmingAirway rewarming represents a minimally invasive,practical method for core rewarming. Its primary benefitappears to be a reduction in the amount of heat lost throughexhalation, with a possible small amount of heat gain.140

Estimates of the amount of heat lost via respirationvary between 10% and 30%.141 In induced hypothermiafor surgical procedures, the calculated percentage was10% in one study.142 As hypothermia typically causes aslowing of respiration, the expected amount of heat lossvia the respiratory tract might be expected to be lowerthan in the normothermic patient.

The amount of heat gain provided by airwayrewarming is difficult to assess given a lack of controlledtrials; however, its use has been shown to contribute torewarming.111 The increase in rewarming rates appears tobe modest, varying between 0.05ºC and 0.1ºC per hourwith face mask or an increase of 0.5ºC per hour whenprovided via endotracheal tube.143

Airway rewarming has been shown to reducemortality.144 Given the modest expected gains in rewarm-ing rates, it should be used as an adjunct to othertherapies. Airway rewarming at temperatures up to 46ºCappears safe. One report of thermal injury to the lungsoccurred in a patient treated with oxygen heated to 80ºCfor 11 hours.140


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The use of heated infusions offers a simple method forrewarming, although the clinical effect appears to beminor. The calculated amount of heat gain to a 70 kg manby 1 liter of fluid preheated to 42ºC is 0.33ºC.11 Whilegains may be negligible, warmed fluids may be valuableby limiting further cooling of the patient. The hazard oflarge volume resuscitation with room air temperaturefluids has been repeatedly noted in the trauma literature.

Various commercially available warmers allowinfusion of fluids at rates up to 500 cc/min at 35ºC. If afluid warmer is not available, a microwave oven can beused to heat the fluid. Recommendations based onprevious studies indicate that heating of 1 liter ofcrystalloid fluid at the high setting for two minutes issafe and effective.145-148 Given the higher power outputcommon among newer microwaves, calibration prior toheating is recommended. In a recent study, one liter bagsof fluid were heated on high power for two minutes in16 different microwave ovens.149 Nine of 16 microwavesheated the fluid to a temperature greater than 42ºC,the generally accepted maximum temperature forfluid resuscitation.

Even if fluid is appropriately heated, conductive heatloss prior to infusion is unavoidable. This can be mini-mized by insulating the preheated fluid bag and keepingtube lengths as short as possible.150

Cavity LavagePlacement of warmed fluid into body cavities has beenused as a rewarming method for several decades.Techniques range from minimally invasive (gastricirrigation) to very invasive (thoracotomy with mediasti-nal irrigation). Rewarming rates vary significantlybetween techniques.

Gastrointestinal IrrigationGastrointestinal irrigation is accomplished by infusion ofwarmed fluids via a tube placed in either the colon orstomach. Most published data focuses on gastric irrigation.Typical techniques involve delivery of warmed fluid (40ºC)into the stomach in aliquots of 200-300 cc. After a briefperiod (10-15 minutes), the fluid is then removed either bysuction or gravity drainage, and the cycle is continued.

There are several proposed advantages to gastricirrigation. It is quick and easy to set up; it may preferen-tially warm the liver, speeding metabolism of drugs andlactate; and, by virtue of its location, it may selectivelywarm the heart.151 On the other hand, it increases the riskof aspiration (patients should undergo tracheal intuba-tion prior to irrigation if there is any question regardingtheir ability to handle secretions); serum electrolyte levelsfluctuate with large-volume irrigation; lavage should bestopped during CPR; and there is the potential forinitiation of ventricular fibrillation during placement ofthe gastric tube.9 Finally, there are concerns that therelatively small surface area of the stomach is unlikely toprovide large amounts of heat transfer. In animal studies,rewarming rates are reported in the range of 3ºC per

hour, and the procedure appears to be without significantmorbidity.152,153 Data from the largest prospective hypoth-ermia study found less dramatic rewarming rates, withthe average over the first two hours of rewarmingapproximately 1.5ºC per hour.5

Peritoneal IrrigationPeritoneal irrigation uses the large surface area of theperitoneum and gut to accomplish heat transfer fromwarmed fluids. Fluid (typically normal saline or lactatedRinger’s solution) is warmed to 40ºC-45ºC and theninfused through a peritoneal catheter. Fluid is typicallyleft in place for 20-30 minutes and then is aspirated.Placement of the catheter can be performed by eitheropen or percutaneous (Seldinger) technique. Prior toinsertion, the bladder and stomach should be emptied. Tospeed rewarming, a second catheter can be placed fordrainage. Some practitioners recommend using fourcatheters, placing one in each quadrant and using two forinfusion and two for drainage.

Advantages of peritoneal irrigation include preferen-tial rewarming of the liver, its ability to be performed intandem with CPR, and its potential to dialyze off drugsand toxins. Disadvantages include the relatively invasivenature of the procedure. Placement of the peritonealcatheter requires expertise, as iatrogenic intraabdominalinjury can occur. In animal studies, rewarming rates withperitoneal irrigation vary between 3ºC and 6ºC perhour.152,154 Data from human reports suggest rates of 1ºC-2ºC per hour.5

Pleural IrrigationIrrigation of one or both hemithoraces with warmed fluidhas been demonstrated to be an effective method ofrewarming.153-155 Pleural irrigation requires placement oftwo thoracostomy tubes (36-40 F). The anterior (infusion)tube should be placed in the second or third intercostalspace in the midclavicular line. The posterior (drainage)tube should be placed in the fifth or sixth intercostalspace in the posterior axillary line. Warmed normal saline(40ºC-42ºC) is then infused through the anterior tube anddrained via the posterior tube. Flow rates described inthe literature vary between 180-850 cc per minute.153-155

Perhaps the most important advantage offered bypleural irrigation is its warming of the heart. Addition-ally, it is a technique that is well within the scope of mostemergency physicians’ technical skills. Disadvantagesinclude the possibility of iatrogenic injury to lungs,vasculature, and heart during tube placement; thepossible development of a tension hydrothorax ifadequate drainage is not ensured; and the large volumeof warmed fluid required (11-33 liters per hour). Animalstudies indicate rewarming rates in the 5ºC-6ºC per hourrange.154,155 Data from case reports suggest rates closer to3ºC per hour.156,157

Thoracotomy With Internal Cardiac MassageAnd Mediastinal IrrigationLeft-sided thoracotomy with internal cardiac massage


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Ten Pitfalls To Avoid

1. “I didn’t have a thermometer for the rewarming bath—sowhat if it took 90 minutes to rewarm her hand?”

The rewarming bath must be tightly maintained between37ºC and 41ºC to maximize tissue salvage. A standard oralor rectal patient thermometer can be used to monitor thewater temperature.

2. “His frostbitten leg didn’t look all that bad, so I sent himhome.”

Frostbite injuries can look far worse hours to days afterinitial evaluation. Frostbite patients require admission fortherapy and monitoring.

3. “The hospital was about 40 minutes away, so we just puthim in the ambulance with his foot up against the heatingvents. We rewarmed his extremity much sooner thanwaiting to get to the ED.”

Field rewarming is difficult to monitor, and the riskof refreezing usually far outweighs the benefits ofearlier thawing. Consider field rewarming only whentransport time will be severely extended. Even then,rewarming must still be done with a water bath at37ºC-41ºC.

4. “How was I supposed to know the patient was thathypothermic? The thermometer read 34ºC.”

Since most standard hospital thermometers only read aslow as 34ºC, a high index of suspicion is mandatory toquickly recognize moderate-to-severe hypothermia.

5. “It’s not my fault she died. I quickly initiated rewarmingtherapy and sent her to the floor.”

This octogenarian died of septic shock the day after shewas admitted. A conversation with the medics or familywould have identified the fact that she was found indoorsand alerted you to the possibility of sepsis. Remember thatin the elderly, a high percentage of hypothermia issecondary to another disease process. These etiologies,especially sepsis, need to be pursued.

6. “Of course I started an insulin drip—the patient’s bloodsugar was over 500.”

Below 32ºC, the body is insulin-resistant and the drug is notwell-metabolized. When this patient was rewarmed, thecombination produced such profound hypoglycemia thathe nearly died.

7. “How was I supposed to know the patient had a severe GIbleed? His hematocrit was only slightly low, and his heartrate was normal.”

Remember that hypothermia produces a progressivebradycardia and hemoconcentration. A relative tachycardiaor normal hematocrit should prompt you to consider thepossibility of a GI bleed and guaiac the stool.

8. “It was an open-and-shut case. The patient was rigid, withfixed pupils and asystole on the monitor.”

If you had talked to the medics, you would have realizedthat the patient was found down in a snow bank. Severehypothermia can mimic death, and multiple case reports ofmiraculous saves exist. Rewarming to 32ºC with concurrentCPR should at least be attempted prior to calling the code.

9. “How was I supposed to know she had a subdural? Shewas found down, and her degree of hypothermia wasconsistent with her neuro exam.”

Detecting traumatic injury in the hypothermic patient canbe problematic. A complete secondary survey is imperativeand may give clues to occult injury. Mental status shouldimprove with rewarming, which mandates the need forrepeat examinations as the patient warms.

10. “He was hypothermic on presentation, so I immediatelybegan rewarming. What’s the problem?”

The patient’s glucose on routine labs came back at 12. Afingerstick glucose on all hypothermic patients is quick,easy, and rules out one reversible cause of secondaryhypothermia. While hypoglycemic patients still requirerewarming, raising the blood sugar is also necessary. ▲

and mediastinal irrigation represents the most invasivecore rewarming technique. This method has beenadvocated for use in the setting of severe hypothermiawith cardiac arrest because of its rapid rewarming rateand because it allows for open cardiac massage.

Although rate of rewarming has not been shown tocorrelate with outcome, in cases of cardiac arrest it seemsintuitive that definitive rewarming should be accom-plished as quickly as possible. Below 28ºC, attempts atdefibrillation are unlikely to be successful, and organperfusion is dependent on CPR.9 Several studies haveindicated that open cardiac massage is a more effectivemeans of providing adequate perfusion than standardCPR.158,159 It should be noted that in severe hypothermia,stiffening of the heart may preclude effective opencardiac massage, though this appears to be a rare

observation and was not noted in a recent review ofseven patients.160

Published rewarming rates with mediastinalirrigation are approximately 8ºC per hour. Multiple casereports attest to its efficacy as a rewarming method.63,161,163

In one review of seven patients who received an EDthoracotomy for hypothermic cardiac arrest, the survivalrate was 71%.63

The major disadvantage of this technique is itsdegree of invasiveness and potential for iatrogenicvascular injury and infectious complications. However,studies have shown a relatively low rate of infection withED thoracotomy.164,165

Extracorporeal Blood RewarmingCore rewarming by cardiopulmonary bypass has been


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Table 4. One Protocol For Treating FrostbiteInjuries.

1.On arrival, rapidly rewarm the affected areas in warmwater at 37ºC-41ºC for 15-30 minutes or until thawing iscomplete.

2.On completion of rewarming, treat the affected parts asfollows: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 40ºC.

3.For documentation, obtain photographic records onadmission, at 24 hours, and serially every 2-3 days untildischarge.

4.Prohibit smoking.

Adapted from: McCauley RL, Hing DN, Robson MC, et al. Frostbiteinjuries: a rational approach based on the pathophysiology. J Trauma1983 Feb;23(2):143-147.

shown to be an extremely rapid way to rewarm hypoth-ermic patients, with rates in excess of 9ºC per hour.166

Intuitively, rapid rewarming becomes most important incases of cardiac arrest in which restoration of an orga-nized rhythm is temperature-dependent. In this situation,cardiopulmonary bypass gives the added advantage ofimmediate restoration of adequate organ perfusion,which presumably imparts a better outcome. For hypoth-ermic patients in cardiac arrest treated with cardiopulmo-nary bypass, published survival rates vary between 13%and 60%.167-170 Other methods of extracorporeal bloodrewarming include continuous arteriovenous andvenovenous rewarming and hemodialysis (which alsohas the advantage of removing toxins from the blood).Commercial arteriovenous rewarming kits are availableand require only cannulation of a central (femoral) arteryand vein. They rely on arterial pressure as a pump andare not useful in an arrest situation. Several studies haveshown them to be an effective method of rapid rewarm-ing, with rates of over 4ºC per hour.171-173

Frostbite/FrostnipRewarmingOptimal rewarming is performed in a water bath at 37ºC-41ºC.174-176 (See also Table 4.) The water bath temperatureshould be strictly regulated using a thermometer, asvariations above the recommended range can cause burnsand those below will rewarm too slowly. The rewarminggenerally takes 15-30 minutes. Have the patient move thefrostbitten body part during rewarming, if possible. Signs ofsuccessful rewarming are increased pliability of the injuredarea as well as erythema and hyperemia.

Oral or intravenous hydration should be administeredto any frostbite patient who appears dehydrated, as this will

augment blood flow. As the rewarming process can beintensely painful, parenteral analgesics are necessary.

Aloe VeraTopical aloe vera (Dermaide aloe), applied to the entirefrostbitten area (especially to both intact and debridedblisters) improves tissue salvage.102 Aloe vera, when usedin conjunction with an oral antithromboxane agent, limitstissue loss after frostbite injury.103 Aloe has antioxidant,antithromboxane, as well as antibacterial effects.

NSAIDsAntiprostaglandins have had proven benefit in animalexperiments and human studies for the treatment offrostbite 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 standardtherapy in a treatment group of 38 patients with moder-ate-to-severe frostbite, there was no significant tissueloss.103 However, ibuprofen is now the agent of choice asit blocks thromboxane without inhibiting prostaglandins,which may bolster healing.4,103,119 In a study 154 patientstreated with ibuprofen (12 mg/kg PO per day) combinedwith aloe vera and antibiotics, morbidity and hospitalstay were reduced when compared to a control group.175

At least one center is using intravenous ketorolac forfrostbite injuries brought in prethaw.109

Two types of blisters may form after rewarming:hemorrhagic and clear. The hemorrhagic blisters are asign of deep injury; they should not be debrided as thiswill lead to desiccation of the underlying structures.Though controversial, most sources recommend aspira-tion or debridement of clear blisters. The rationale forthis action is to remove the blister fluid, which is high inthromboxane. Thromboxane is a known destructivemediator in thermal burn injuries.177 The hypothesis thatthe clear blisters of frostbite were also high in thrombox-ane was proven by the aspiration of 10 frostbite patients’blisters.178 Removal of the blister fluid therefore limitsexposure of the tissue to thromboxane.

Other MedicationsThe skin breakdown and post-thaw edema of frostbiteinjuries decrease the natural antistreptococcal propertiesof the skin. Most advocate waiting for signs of infectionbefore administering antibiotics. Frostbite injuries aretetanus-prone wounds.179 Tetanus prophylaxis must begiven to any patient whose status is unknown or lapsed.

Cutting Edge / Controversies

Two studies have explored the use of hyperthermic fluidinfusion as a rewarming method. Both studies wereperformed on dogs cooled to 30ºC and then rewarmedwith intravenous fluids heated to 65ºC.180,181 Rewarmingrates averaged 3.6ºC per hour, and no complicationsrelated to the hyperthermic fluids were noted. The use ofhyperthermic fluids has not been reported in humans.

The use of a device that applies negative pressure


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E, LLCand heat to the forearm and hand of hypothermicpatients has demonstrated mixed rewarming results.Theoretically, the negative pressure overcomes ther-moregulatory vasoconstriction, allowing more effectivetransfer of heat from the periphery to the core. Resultsfrom an initial trial showed a tenfold increase in rewarm-ing rates when compared to controls.182 In subsequentstudies, however, rewarming rates in the negativepressure device groups have not been significantly fasterthan those in the passive rewarming groups.183,184

Finally, the use of amino acid infusions has beendemonstrated to induce thermogenesis and reducehypothermia in surgical patients.185,186 The use of thistechnique has yet to be reported accidental hypothermia.

Disposition

HypothermiaMaintain a low threshold for admitting patients withhypothermia. Hypothermia is often a complex, multifac-torial disease that requires admission for appropriatetreatment, particularly in the very young and the elderly.

Patients with mild-to-moderate hypothermia whoadequately rewarm in the ED and are otherwise healthymay be discharged if the circumstances of their hypother-mia have been adequately resolved. For homelesspersons, this may entail provision of warm, well-fittingclothing (in particular, hats, gloves, and footwear),187 anda social work evaluation for placement in a shelter. Forpatients who live alone, this may entail evaluation of thehome environment, including assessment of heating andfood. For patients who present intoxicated, this mayentail referral to detoxification centers.

Frostbite/FrostnipPatients with frostbite require admission or close outpatientfollow-up, as the injury can look far worse 12-24 hoursfollowing initial ED presentation. The conventionalaphorism when discussing the surgical treatment offrostbite has been, “Frostbite in January, surgery in July.”119

This referred to the fact that the line of demarcation of injurycould take days to weeks to fully establish. However, theadvent of two imaging techniques has allowed earlydemarcation and surgical intervention. Technetium-99scanning has been used in a number of studies with goodcorrelation between the early images and eventual line ofdemarcation.188,189 The newer modality in frostbite injuries ismagnetic resonance imaging, which shows promise forrapid assessment of injuries.190

Admitted patients should receive daily hydro-therapy, limb elevation, and continued NSAIDs andtopical aloe vera. Depending on the extent of the injury,further debridement, escharotomy, or operative interven-tion may be required.

Summary

Hypothermia is a condition that can occur because ofisolated cold exposure alone, in combination with

precipitating factors such as alcohol use or trauma, or asa result of another disease process. While everyone issusceptible to hypothermia, those at the extremes of ageas well as those with impaired thermoprotective behav-iors due to trauma, intoxication, infection, or neurologicor psychiatric disease carry a higher risk of hypothermiawhen exposed to cold stress. Treatment strategies forhypothermia should emphasize rapid invasive rewarm-ing for patients with severe hypothermia and activenoninvasive rewarming for patients with mild-to-moderate hypothermia. ▲

References

Evidence-based medicine requires a critical appraisal ofthe literature based upon study methodology andnumber of subjects. Not all references are equally robust.The findings of a large, prospective, randomized, andblinded trial should carry more weight than a case report.

To help the reader judge the strength of eachreference, pertinent information about the study, such asthe 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 informativereferences cited in the paper, as determined by theauthors, will be noted by an asterisk (*) next to thenumber of the reference.

1. Cummins RO. ACLS for Experienced Providers. Dallas:American Heart Association; 2003. (Textbook)

2. Cummins RO. Guidelines 2000 for Cardiopulmonary Resuscita-tion and Emergency Cardiovascular Care. Dallas: AmericanHeart 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 inmanagement of hypothermia and frostbite injury. Surg ClinNorth Am 1991 Apr;71(2):345-370. (Review)

5.* Danzl DF, Pozos RS, Auerbach PS, et al. Multicenterhypothermia survey. Ann Emerg Med 1987 Sep;16(9):1042-1055. (Multicenter; 428 patients)

6. Knize DM, Weatherley-White RC, Paton BC, et al. Prognos-tic factors in the management of frostbite. J Trauma 1969Sep;9(9):749-759.

7. Pinzur MS, Weaver FM. Is urban frostbite a psychiatricdisorder? Orthopedics 1997 Jan;20(1):43-45. (Retrospective;20 patients)

8. Sim MM, Kuo YC. Accidental hypothermia in the subtrop-ics. 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: quantita-tive aspects of therapy. JACEP 1979 Dec;8(12):523-527.(Review, case report)

12. Giesbrecht GG, Goheen MS, Johnston CE, et al. Inhibitionof shivering increases core temperature afterdrop andattenuates rewarming in hypothermic humans. J ApplPhysiol 1997 Nov;83(5):1630-1634. (Controlled clinical trial;8 patients)

13. Fregly M. Activity of the hypothalamic-pituitary-thyroid


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and Biochemistry. New York: Pergamon Press; 1990.(Textbook chapter)

14. Granberg PO. Human physiology under cold exposure.Arctic Med Res 1991;50 Suppl 6:23-27. (Review)

15. Wong KC. Physiology and pharmacology of hypothermia.West J Med 1983 Feb;138(2):227-232. (Review)

16. Frank SM, Raja SN, Wu PK, et al. Alpha-adrenergicmechanisms of thermoregulation in humans. Ann N Y AcadSci 1997 Mar 15;813:101-110. (Prospective; 19 patients)

17. Brevik A, Farver D. Atypical antipsychotic induced mildhypothermia. S D J Med 2003 Feb;56(2):67-70. (Case report)

18. Lomax P, Bajorek JG, Bajorek TA, et al. Thermoregulatorymechanisms and ethanol hypothermia. Eur J Pharmacol 1981May 22;71(4):483-487. (Animal study)

19. Kalant H, Le AD. Effects of ethanol on thermoregulation.Pharmacol Ther 1983;23(3):313-364. (Review)

20. Collins KJ, Dore C, Exton-Smith AN, et al. Accidentalhypothermia and impaired temperature homoeostasis inthe elderly. Br Med J 1977 Feb 5;1(6057):353-356. (Longitudi-nal; 47 patients)

21. Vassilieff N, Rosencher N, Sessler DI, et al. Shiveringthreshold during spinal anesthesia is reduced in elderlypatients. Anesthesiology 1995 Dec;83(6):1162-1166. (Prospec-tive; 28 patients)

22. Smolander J. Effect of cold exposure on older humans. Int JSports Med 2002 Feb;23(2):86-92. (Review)

23. Collins KJ, Exton-Smith AN, Dore C. Urban hypothermia:preferred temperature and thermal perception in old age.Br Med J (Clin Res Ed) 1981 Jan 17;282(6259):175-177.(Comparative; 30 patients)

24. Kramer MR, Vandijk J, Rosin AJ. Mortality in elderlypatients with thermoregulatory failure. Arch Intern Med1989 Jul;149(7):1521-1523. (Retrospective; 54 patients)

25. Darowski A, Najim Z, Weinberg JR, et al. Hypothermia andinfection in elderly patients admitted to hospital. AgeAgeing 1991 Mar;20(2):100-106. (Follow-up study; 25patients)

26. Megarbane B, Axler O, Chary I, et al. Hypothermia withindoor occurrence is associated with a worse outcome.Intensive Care Med 2000 Dec;26(12):1843-1849. (Retrospec-tive; 81 patients)

27. Brengelmann GL. Body temperature regulation. In: PattonHD, et al, eds. Textbook of Physiology: Circulation, Respiration,Body Fluids, Metabolism, and Endocrinology. 21st ed.Philadelphia: W.B. Saunders; 1989. (Textbook chapter)

28. Curtis R. Outdoor Action Guide to Hypothermia and ColdWeather Injuries. 1995 Outdoor Action Program, PrincetonUniversity. http://www.cdc.gov/nasd/docs/d001201-d001300/d001216/d001216.html.

29. Hayward JS, Eckerson JD, Collis ML. Thermal balance andsurvival time prediction of man in cold water. Can J PhysiolPharmacol 1975 Feb;53(1):21-32. (Volunteer study)

30. Glickman-Weiss EL, Hearon CM, Prisby R, et al. Theperceptual and physiological responses of high and low fatwomen exposed to 5 degrees C air for 120 minutes.Wilderness Environ Med 1998 Winter;9(4):204-210. (Com-parative; 8 patients)

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181. Wiley D, Sheaff C, Nagy K, et al. Hyperthermic resuscitationis safe and effective after hemorrhagic shock in dogs. J Trauma2000;48:1052-1056. (Animal, prospective; 14 subjects)

182. Grahn D. Recovery from mild hypothermia can be acceleratedby mechanically distending blood vessels in the hand. J ApplPhysiol 1998;85:1643-1648. (Prospective; 10 patients)

183. Taguchi A, Arkilic CF, Ahluwalia A, et al. Negativepressure rewarming vs. forced air rewarming in hypother-mic postanesthetic volunteers. Anesth Analg 2001;92:261-266. (Prospective; 7 patients)

184. Smith CE, Parand A, Pinchak AC, et al. The failure of negativepressure rewarming (Thermostat™) to accelerate recoveryfrom mild hypothermia in postoperative surgical patients.Anesth Analg 1999;89:1541-1545. (Prospective; 60 patients)

185. Sellden E, Lindahl SGE. Amino acid-induced thermogen-esis reduces hypothermia during anesthesia and shortenshospital stay. Anesth Analg 1999;89:1551-1556. (Prospec-tive; 75 patients)

186. Widman J, Hammarqvist F, Sellden E. Amino acid infusioninduces thermogenesis and reduces blood loss during hiparthroplasty under spinal anesthesia. Anesth Analg2002;95:1757-1762. (Prospective; 46 patients)

187. John Abeysekera, The use of personal protective clothingand devices in the cold environment, Coldtech PreliminaryStudy Report Division of Industrial Ergonomics Department ofHuman Work Sciences Luleå University, Sweden.

188. Salimi Z, Vas W, Tang-Barton P, et al. Assessment of tissueviability 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 tissueviability with triple-phase bone scanning. Radiology 1989Feb;170(2):511-514. (Prospective; 7 patients)

190. Barker JR, Haws MJ, Brown RE, et al. Magnetic resonanceimaging of severe frostbite injuries. Ann Plast Surg 1997Mar;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 toovercome the body’s ability to appropriatelythermoregulate.

b. only occurs in extremely cold weather.c. occurs in patients whose underlying medical

conditions disrupt adequate thermoregulatorymechanisms.

d. occurs only in pediatric or elderly patients .

82. Secondary hypothermia:a. occurs in patients whose underlying medical

conditions disrupt adequate thermoregulatorymechanisms.

b. may be underreported because patients tend tobe admitted to the hospital with a primarydiagnosis other than hypothermia.

c. is caused by conditions that impedecirculation, increase heat loss, decreaseheat production, or cause impairment ofthermoregulation.

d. all of the above.

83. The bulk of the body’s heat production is aresult 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 con-

trolled 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 useare examples of:a. factors that result in poor circulation.b. factors that decrease the body’s 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 inthe hypothermic patient.a. Trueb. False


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Topics:immune thrombocytopenic purpura • occupational exposures •

low back pain • pediatric growth plate injuries • acute asthma •

tuberculosis • pulmonary embolism • community-acquired pneu-

monia • difficult airway management • acute chest syndrome in

sickle cell disease • cocaine-associated chest pain • oral agents

for type 2 diabetes mellitus • heat stroke • high-altitude illness •

illness after international travel • gastric decontamination • major

radiation exposure • cervical spine injury in blunt trauma • knee

injuries • preventing medical errors

87. The elderly are at increased risk for hypothermiabecause of:a. age-related impairment of thermoregulatory

systems.b. their reduced shivering response, decreased

mobility, malnutrition, and diminished leanbody mass.

c. reduced vasoconstriction.d. multiple medication use, particularly cardiac

medications.e. all of the above.

88. Expected neurologic findings in the severelyhypothermic patient include all of the followingexcept:a. unresponsive to noxious stimuli.b. fixed pupils.c. hyperreflexia.d. increased muscular tone.

89. The observation of a relative tachycardia in thehypothermic patient:a. is normal in the later stages of hypothermia.b. should prompt the clinician to search for

associated conditions, such as occult traumaticbleeding, 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 inmultiple studies to have little impact on afterdrop.a. Trueb. False

92. Which of the following is a poor prognostic sign incases of frostbite?a. The early appearance of clear blebs across the

entire extent of the injured areab. Early return of sensationc. Hemorrhagic blistersd. Soft subcutaneous tissue

93. Which of the following rewarming techniques isleast appropriate for patients with mild-to-moder-ate hypothermia and an intact shivering response?a. Passive rewarmingb. Forced air rewarmingc. Resistive heating methods (e.g., electric

blankets)d. Peritoneal irrigation

94. In the severely hypothermic patient, intubationshould be avoided if possible because it is likely toinduce ventricular fibrillation.a. Trueb. False

95. Which of the following is not recommended in themanagement of frostbite?a. Rewarming in a water bath upon arrivalb. Parenteral analgesics during rewarmingc. Debridement of hemorrhagic blistersd. Tetanus prophylaxis


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Emergency Medicine Practice is not affiliated with any pharmaceutical firm or medical device manufacturer.

Direct all editorial or subscription-related questions to EB Practice, LLC: 1-800-249-5770 • Fax: 1-770-500-1316 • Non-U.S. subscribers, call: 1-678-366-7933

EB Practice, LLC • 305 Windlake Court • Alpharetta, GA 30022E-mail: [email protected] • Web Site: http://www.empractice.net

Emergency Medicine Practice (ISSN 1524-1971) is published monthly (12 times per year) by EB Practice, LLC, 305 Windlake Court, Alpharetta, GA 30022. Opinions expressed are not necessarilythose of this publication. Mention of products or services does not constitute endorsement. This publication is intended as a general guide and is intended to supplement, rather thansubstitute, professional judgment. It covers a highly technical and complex subject and should not be used for making specific medical decisions. The materials contained herein are notintended to establish policy, procedure, or standard of care. Emergency Medicine Practice is a trademark of EB Practice, LLC. Copyright 2003 EB Practice, LLC. All rights reserved. No part of thispublication may be reproduced in any format without written consent of EB Practice, LLC. Subscription price: $299, U.S. funds. (Call for international shipping prices.)

President and CEO: Robert Williford. Publisher: Heidi Frost. Research Editors: Ben Abella, MD, University of Chicago; Richard Kwun, MD, Mount Sinai School of Medicine.

Physician CME InformationThis CME enduring material is sponsored by Mount Sinai School of Medicine andhas been planned and implemented in accordance with the Essentials andStandards of the Accreditation Council for Continuing Medical Education. Creditmay be obtained by reading each issue and completing the printed post-testsadministered in December and June or online single-issue post-testsadministered at www.empractice.net.

Target Audience: This enduring material is designed for emergency medicinephysicians.

Needs Assessment: The need for this educational activity was determined by asurvey of medical staff, including the editorial board of this publication; reviewof morbidity and mortality data from the CDC, AHA, NCHS, and ACEP; andevaluation of prior activities for emergency physicians.

Date of Original Release: This issue of Emergency Medicine Practice was publishedDecember 1, 2003. This activity is eligible for CME credit through December1, 2006. The latest review of this material was November 10, 2003.

Discussion of Investigational Information: As part of the newsletter, faculty maybe presenting investigational information about pharmaceutical products thatis outside Food and Drug Administration approved labeling. Informationpresented as part of this activity is intended solely as continuing medicaleducation and is not intended to promote off-label use of any pharmaceuticalproduct. Disclosure of Off-Label Usage: This issue of Emergency Medicine Practicediscusses no off-label use of any pharmaceutical product.

Faculty Disclosure: In compliance with all ACCME Essentials, Standards, andGuidelines, all faculty for this CME activity were asked to complete a fulldisclosure statement. The information received is as follows: Dr. Hermann, Dr.Weingart, Dr. Decker, Dr. Gallagher, and Dr. Stewart report no significant financialinterest or other relationship with the manufacturer(s) of any commercialproduct(s) discussed in this educational presentation.

Accreditation: Mount Sinai School of Medicine is accredited by the AccreditationCouncil for Continuing Medical Education to sponsor continuing medicaleducation for physicians.

Credit Designation: Mount Sinai School of Medicine designates this educationalactivity for up to 4 hours of Category 1 credit toward the AMA Physician’sRecognition Award. Each physician should claim only those hours of creditactually spent in the educational activity. Emergency Medicine Practice is approvedby the American College of Emergency Physicians for 48 hours of ACEP Category1 credit (per annual subscription). Emergency Medicine Practice has been reviewedand is acceptable for up to 48 Prescribed credit hours by the American Academyof Family Physicians. Emergency Medicine Practice has been approved for 48Category 2-B credit hours by the American Osteopathic Association.

Earning Credit: Two Convenient Methods

• Print Subscription Semester Program: Paid subscribers with current andvalid licenses in the United States who read all CME articles during eachEmergency Medicine Practice six-month testing period, complete the post-test and the CME Evaluation Form distributed with the December and Juneissues, and return it according to the published instructions are eligible forup to 4 hours of Category 1 credit toward the AMA Physician’s RecognitionAward (PRA) for each issue. You must complete both the post-test and CMEEvaluation Form to receive credit. Results will be kept confidential. CMEcertificates will be delivered to each participant scoring higher than 70%.

• Online Single-Issue Program: Paid subscribers with current and validlicenses in the United States who read this Emergency Medicine Practice CMEarticle and complete the online post-test and CME Evaluation Form atwww.empractice.net are eligible for up to 4 hours of Category 1 credittoward the AMA Physician’s Recognition Award (PRA). You must completeboth the post-test and CME Evaluation Form to receive credit. Results willbe kept confidential. CME certificates may be printed directly from the Website to each participant scoring higher than 70%.

Class I• Always acceptable, safe• Definitely useful• Proven in both efficacy and

effectiveness

Level of Evidence:• One or more large prospective

studies are present (withrare exceptions)

• High-quality meta-analyses• Study results consistently

positive and compelling

Class II• Safe, acceptable• Probably useful

Level of Evidence:• Generally higher levels

of evidence• Non-randomized or retrospec-

tive studies: historic, cohort, orcase-control studies

• Less robust RCTs• Results consistently positive

Class III• May be acceptable• Possibly useful• Considered optional or

alternative treatments

Level of Evidence:• Generally lower or intermediate

levels of evidence

• Case series, animal studies,consensus panels

• Occasionally positive results

Indeterminate• Continuing area of research• No recommendations until

further research

Level of Evidence:• Evidence not available• Higher studies in progress• Results inconsistent,

contradictory• Results not compelling

Significantly modified from: TheEmergency Cardiovascular CareCommittees of the American HeartAssociation and representativesfrom the resuscitation councils ofILCOR: How to Develop Evidence-Based Guidelines for EmergencyCardiac Care: Quality of Evidenceand Classes of Recommendations;also: Anonymous. Guidelines forcardiopulmonary resuscitation andemergency cardiac care. EmergencyCardiac Care Committee andSubcommittees, American HeartAssociation. Part IX. Ensuringeffectiveness of community-wideemergency cardiac care. JAMA1992;268(16):2289-2295.

Class Of Evidence Definitions

Each action in the clinical pathways section of Emergency Medicine Practicereceives an alpha-numerical score based on the following definitions.

96. Which of the following rewarming techniquesprovides the most rapid increase in coretemperature?a. Passive rewarmingb. Cardiopulmonary bypassc. Forced air rewarmingd. Heated infusions

This test concludes the July through December 2003semester testing period of Emergency Medicine Practice. Theanswer form for this semester and a return envelope havebeen included with this issue. Please refer to the instruc-tions printed on the answer form. All paid subscribers areeligible to take this test.

Monthly online CME testing is available for subscribersat no extra charge at http://www.empractice.net.

Emp-hypothermia and Frostbite

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