DTIC ADA529041: American College of Sports Medicine Roundtable on Exertional Heat Stroke - Return to Duty/Return to Play: Conference Proceedings

0.2 MB·English

by  Defense Technical Information Center

SPECIAL COMMUNICATION
American College of Sports Medicine Roundtable on
V
Exertional Heat Stroke Return to Duty/Return
to Play: Conference Proceedings
Francis G. O’Connor1, Douglas J.Casa2, Michael F. Bergeron3, Robert Carter III4, Patricia Deuster1,
Yuval Heled5, John Kark6, Lisa Leon4, Brendon MCDermott7, Karen O’Brien8, William O. Roberts9,
and Michael Sawka4
1Military and Emergency Medicine, Consortium for Health and Military Performance, Uniformed Services
University,Bethesda,MD; 2KoreyStringerInstitute,NeagSchoolof Education,Universityof Connecticut,Storrs,
CT;3SanfordSchoolofMedicineoftheUniversityofSouthDakota,SiouxFalls,SD;4U.S.ArmyResearchInstitute
of Environmental Medicine Thermal and Mountain Medicine Division, Natick, MA; 5Heller Institute of Medical
Research, Sheba Medical Center, Tel-Hashomer, Israel; 6Department of Hematology, Thomas Jefferson
University, Philadelphia, PA; 7Department of Health and Human Performance, University of Tennessee at
Chatanooga,Chattanooga,TN;8CommandSurgeon,U.S.ArmyTrainingandDoctrineCommand;9Department
of Family Medicine and Community Health, University of Minnesota, Minneapolis, MN
O’CONNOR,F.G.,D.J.CASA,M.F.BERGERON,R.CARTER,P.DEUSTER,Y.HELED,J.KARK,L.LEON,
B.MCDERMOTT,K.O’BRIEN,W.O.ROBERTS,andM.SAWKA.Americancollegeofsportsmedicineroundtable
onexertionalheatstrokeVreturntoduty/returntoplay:conferenceproceedings.Curr.SportsMed.Rep.,Vol.9,No.5,
pp.314Y321,2010.OnOctober22Y23,2008,anACSMRoundtablewasconvenedattheUniformedServicesUniversity(Bethesda,MD)
todiscussreturn-to-playorreturn-to-dutyforpeoplewhohaveexperiencedexertionalheatillness(EHI)andtodevelopconsensus-based
recommendations.TheconferenceassembledexpertsfromtheciviliansportsmedicinecommunityandtheDepartmentofDefenseto
discussrelevantEHIissues,suchaspotentiallong-termconsequences,theconceptofthermotolerance,andtheroleofthermaltolerance
testinginreturn-to-playdecisions.Althoughthegroupwasunabletomoveforwardwithnewconsensusrecommendations,theyclearly
documentedcriticalclinicalconcernsandscientificquestions,includingthefollowing:1)nouniformcoredefinitionsofEHI;2)limited
validatedcriteriatoassessrecoveryfromexertionalheatstroke(EHS);and3)inadequate abilitytopredictwhomaybepredisposed
toasubsequentheatinjuryafterEHS.Areasofpotentialfutureresearchareidentified.
INTRODUCTION tions that may include multisystem organ (liver, kidney,
muscle) and neurologic damage, as well as reduced exercise
Exertional heat illness (EHI), specifically exertional heat capacity and heat intolerance (12,52,57,69). Animal and
stroke (EHS), continues to be a significant problem con- human research suggest late or untreated EHS may result in
fronting athletes, coaches, and medical providers (12,47). In organ damage that continues for weeks to months and pos-
addition,EHIisamajorconcernforthemilitary,particularly sibly even after clinical symptoms or biomarkers have re-
during recruit training, and remains a common cause of pre- turned to normal (4,30,64). Whether this is true for rapidly
ventable nontraumatic exertion-related death (11,41,42). treated EHS is not known. In the military, studies have
Some individuals with EHS experience long-term complica- demonstrated that an initial EHI episode during basic train-
ingdoesnotpredictorimplyhospitalizationforanotherEHI
during subsequent military service. Importantly, occurrence
Address for correspondence: Francis G. O’Connor, M.D., M.P.H., FACSM, of EHI during basic training only has a small impact on sub-
Uniformed Services University, 4301 Jones Bridge Road, Bethesda, MD 20814 sequent militaryretention and hospitalization(44). Although
(E-mail: [email protected]). a recentepidemiological study ofmilitarycases suggested EHI
may increase long-term mortality from organ failure (kidney,
1537-890X/0905/314Y321 heart, liver), the timing and types of treatment for EHS were
CurrentSportsMedicineReports
Copyright*2010bytheAmericanCollegeofSportsMedicine not considered (64). This evidence emphasizes the need to
314
Copyright @ 2010 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited.
Report Documentation Page Form Approved
OMB No. 0704-0188
Public reporting burden for the collection of information is estimated to average 1 hour per response, including the time for reviewing instructions, searching existing data sources, gathering and
maintaining the data needed, and completing and reviewing the collection of information. Send comments regarding this burden estimate or any other aspect of this collection of information,
including suggestions for reducing this burden, to Washington Headquarters Services, Directorate for Information Operations and Reports, 1215 Jefferson Davis Highway, Suite 1204, Arlington
VA 22202-4302. Respondents should be aware that notwithstanding any other provision of law, no person shall be subject to a penalty for failing to comply with a collection of information if it

does not display a currently valid OMB control number.
1. REPORT DATE 3. DATES COVERED
2010 2. REPORT TYPE 00-00-2010 to 00-00-2010
4. TITLE AND SUBTITLE 5a. CONTRACT NUMBER
American College of Sports Medicine Roundtable on Exertional Heat
5b. GRANT NUMBER
Stroke - Return to Duty/Return to Play: Conference Proceedings
5c. PROGRAM ELEMENT NUMBER
6. AUTHOR(S) 5d. PROJECT NUMBER
5e. TASK NUMBER
5f. WORK UNIT NUMBER
7. PERFORMING ORGANIZATION NAME(S) AND ADDRESS(ES) 8. PERFORMING ORGANIZATION
Uniformed Services University,Military and Emergency Medicine, REPORT NUMBER
Consortium for Health and Military Performance,4301 Jones Bridge
Road,Bethesda,MD,20814
9. SPONSORING/MONITORING AGENCY NAME(S) AND ADDRESS(ES) 10. SPONSOR/MONITOR’S ACRONYM(S)
11. SPONSOR/MONITOR’S REPORT
NUMBER(S)
12. DISTRIBUTION/AVAILABILITY STATEMENT
Approved for public release; distribution unlimited
13. SUPPLEMENTARY NOTES
14. ABSTRACT

15. SUBJECT TERMS
16. SECURITY CLASSIFICATION OF: 17. LIMITATION OF 18. NUMBER 19a. NAME OF
ABSTRACT OF PAGES RESPONSIBLE PERSON
a. REPORT b. ABSTRACT c. THIS PAGE Same as 8
unclassified unclassified unclassified Report (SAR)
Standard Form 298 (Rev. 8-98)
Prescribed by ANSI Std Z39-18
better characterize treatment protocols in all future studies of seven 1-h topic blocks: definition and basic epidemiology,
EHS episodes to accurately determine recovery and the effect pathophysiology,recognitionandtreatment,thermaltolerance
ofsubsequentexercise-heatstressonvulnerabletissues.Inad- testing in recovery and return-to-play/duty, genetic and bio-
dition, future studies must address long-term risks from other marker testing in recovery and return-to-play/duty, the role
concomitant EHI insults, such as ischemia, oxidative, or of sickle cell trait (SCT) in EHI, prevention of an ensuing
nitrosativestress. incidentofEHS, and current civilian and military guidelines
Because of the potentially damaging effects of EHS, one for return-to-play/duty. At the conference conclusion, all
lingering question relates to return-to-play/duty. Current ci- speakers, discussants, and invited experts participated in a
vilian and military return-to-play/duty guidelines largely are jointsessiontodiscussareasofconsensusandcontroversyand
based on ‘‘best guess’’ estimates and clinical anecdotes, rather identify a potential ‘‘way ahead.’’ The speakers subsequently
thanvalidbiomarkersofrecoveryanddefinitivescientificevi- were asked to prepare a summary statement for each topic
dence (1,12,43). Most organizations recommend return-to- area to identify: what we know, what we do not know, and
play/duty after resolution of any abnormal clinical symptoms finally, where to go from here.
andagradualincreaseinphysicalactivityandexposuretoheat
stress (35). Although current American College of Sports
Medicine (ACSM) recommendations suggest EHS casualties
FINDINGSANDCONCLUSIONS
may return to practice and competition when the individual
has demonstrated ‘‘heat tolerance,’’ defining heat tolerance
DefinitionandEpidemiologyofEHS
andintoleranceisanareaofscientificcontroversy.TheIsraeli
DefenseForce(IDF)hasemployedaheattolerancetest(HTT)
Whatweknow
to evaluate fitness for return-to-duty for more than 30 yr;
1. EHS is defined as a multisystem illness characterized by
however, this approach was controversial among Roundtable
central nervous system (encephalopathy), organ (e.g.,
panelmembers.Theinabilitytoaccuratelydeterminecomplete
liver,renal),andtissue(e.g.,gut,muscle)dysfunctionor
recovery after EHI/EHS negatively impacts both athletes and
injuryassociatedwithhighbodytemperatures,generally
military force readiness. This article reports and discusses the
9104-F(40-C)attimeofinsult,fromstrenuousexercise
conference proceedings from an ACSM Roundtable held to
and/orenvironmental heatexposure(1,7,69).
discuss the topic of EHI/EHS: return-to-play and return-to-
2. The U.S. Army observed a fivefold increase in EHS
duty. The specific purpose of this Roundtable was to outline hospitalization rates from 1.8I100,000j1 in 1980 to
anddiscusstherelevantissues,potentialresearch,andcurrent 14.5I100,000j1 in 2001. Gender, race/ethnicity, and
consensusrecommendations.
geographichome oforigin canexplain much ofthe dif-
ferences in EHS hospitalization rates in military pop-
ulations (11,62), but approximately 50% of military
METHODS/APPROACH
EHS cases in basic training do not share these demo-
graphicsandshould,therefore,beconsideredmoderate-
OnOctober 22Y23,2008, anACSMRoundtablewascon-
tolow-riskindividuals(21).
venedattheUniformedServicesUniversity(USU,Bethesda,
3. SoldiershospitalizedforEHSsubsequentlyhadincreased
MD) to discuss the issue of when to return individuals (ath-
mortality (30 yr later) from cardiovascular, liver, renal,
letes and war fighters) who have experienced EHI to either
and gastrointestinal diseases compared with soldiers hos-
playordutyandtodevelopconsensus-basedrecommendations
pitalized for appendectomies (64). However, we do not
(Table 1). The conference assembled experts from both the
know if, when, or how the individuals with EHS were
civilian sports medicine community and the Department of
treatedwhenEHSwasrecognized.
Defense and in collaboration with the American Medical
Society of Sports Medicine (AMSSM) and the National
AthleticTrainersAssociation(NATA).Itwasstructuredinto Whatwedonotknow
1. Do differences in EHS definition change reported inci-
dencerates?
TABLE1. Roundtableeducationalobjectives. 2. What underlying factors account for the observed in-
creases in EHS hospitalization rates among military and
1.Reviewthedefinition,epidemiology,andpathophysiologyofheatstroke
possiblycivilianpopulations?
2.Reviewthediagnosisandmanagementofexertionalheatstroke 3. Doenvironmentalfactors,suchasinfection,andfatigue,
3.Describecurrentcivilianandmilitaryguidelinesthatdiscuss compromisemolecular protectionandincreaserisk?
return-to-duty/playaspertainingtoheatstroke 4. Does the use of selected categories of nutritional sup-
plements VstimulantsandthermogenicsV contribute
4.Discusstherolesofthermaltolerancetestingandgeneticandbiomarker
evaluationinreturn-to-duty/playaspertainingtoheatstroke toincreasedincidenceofEHS?
5.Describetheprocessofrehabilitation,clearance,andpreventionin
return-to-duty/playaspertainingtoheatstroke
Wherewegofromhere
6.Constructagroupconsensusdocumentthatidentifiescurrentconcepts 1. Conduct a survey in sports medicine and athletic train-
withregardstoreturn-to-duty/playaspertainingtoheatstrokeand
ingcommunities regarding theknowledge ofEHI toin-
outlinesrequiredareasforfurtherresearch
clude‘‘How doyoudefineEHS?’’
Volume9c Number5c September/October2010 SpecialCommunication 315
Copyright @ 2010 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited.
2. Conduct epidemiological studies to determine the in- 4. Doespriorinfectionproduceproinflammatorycytokines
trinsic and extrinsic factors contributing to recent in- that deactivate the cells’ ability to protect against heat
creases inEHSinathleteandmilitarypopulations. shockbynegatingATT?
3. Monitor prospectively long-term organ damage in 5. How long does the organ pathology and vulnerability
EHS patients based on the timing and type of cooling persist after EHS, with and without immediate, rapid
intervention. cooling?
6. Whatmolecularbiomarkers canbeused toindicate full
recoveryafteranepisodeofEHI/EHS?
7. What pharmacological interventions can be used to
Pathophysiology reduce morbidity and mortality from EHI/EHS and
facilitateresetofATT?
Whatweknow
1. Heatstrokeoftenisclassifiedas‘‘classic’’or‘‘exertional,’’
with the former primarily observed in sick and compro-
Wherewegofromhere
mised populations during heat waves and the latter pri-
1. Develop in vivo animal models of EHS (‘‘classic’’ and
marily observed in apparently healthy and physically fit
‘‘exertional’’)toevaluatepharmacologicalinterventions
populations when engaged in physical exertion in vary-
andreturn-to-activityguidelines.
ingenvironments(69).
2. Develop and evaluate pharmacological treatments in
2. Untreated EHS, compared with ‘‘classic’’ heatstroke, in-
humans for EHS to reduce morbidity and mortality and
duces greater morbidity and mortality and more likely is
acceleratereturn-to-activity.
associatedwithrhabdomyolysis,renalfailure,liverdamage,
3. Develop novel approaches to induce ATT and quantify
hyperkalemia,hypercalcemia,andhypoglycemia(69).
molecularbiomarkersofATTinductionanddeactivation.
3. Environmental and exercise heat stress produce cardio-
vascularchallengesasbloodflowisdivertedfromviscera
to skin and vital organs. Reduced perfusion of the in-
RecognitionandTreatment
testine can result in ischemia and endotoxemia; this
exposes organs to oxidative-nitrosative stress, hypoper-
Whatweknow
fusion, ischemia, and hyperthermia. A systemic inflam-
1. Promptly recognized and rapidly cooled EHS patients
matory response syndrome (SIRS) can be initiated and
demonstrate both markedly improved survival and
leadtomultiorgandysfunction(7,69).
reducedcomplications(2,6,10,16,46,48).Unrecognized,
4. Current theories regarding EHS include the ‘‘multiple
untreated EHS often is fatal (46). Early season heat-
hit’’ hypothesis, which identifies rapid hyperthermia
related high-school football deaths occur most often in
(possibly mediated via the vagus nerve through endo-
the first 1Y4 d of practice, which emphasizes a need for
toxinreleaseandotherfactors)inducedbycompromised
acclimatizationandon-sitemedicalcaretopreventfatal
molecular protective mechanism in tissues and possibly
EHS(47).
mediated by prior viral exposure and other factors
2. The risk of EHI in susceptible individuals increases as
(60,61).Inaddition,endotoxinreleaseisthoughttolead
wetbulbglobetemperature(WBGT)rises(17,45,50).
to production of pyrogenic cytokines, which may com-
3. Although EHS most commonly occurs in hot envi-
promisefurthernormalthermoregulation(7).
ronments,italsocanoccurinrelativelycoolconditions
5. Histological evidence of profound damage to liver, kid-
(G10-CWBGT)(48,49).
neys, intestine, spleen, and brain has been reported
4. Protective equipment worn by football players and
consistently in those who have not been treated in a
military personnel reduces the ability to dissipate heat
timely manner. Brain injury appears to be most con-
fromthebodyandlowersthetolerableWBGTlevelthat
centrated in the cerebellum, with evidence of Purkinje
issafeforfullactivity(28).
layer involvement (34). Other hyperthermia-induced
5. Rectal temperature is the only consistently reliable
brain dysfunctions likely include blood brain barrier
and valid way to measure core temperature in the field
breakdown, blood-cerebral spinal fluid barrier break-
(3,9,15,17,53). However, cooling never should be de-
down, serum protein leakage, and exacerbated drug-
layed in an individual suspected of EHS where rectal
inducedtoxicity(27,34,58).
temperaturemonitoringisnotpossible.
6. Whole-body, cold-water immersion with the water ag-
gressively stirred will induce the fastest cooling rates for
Whatwedonotknow treating EHI/EHS (6). Whole-body cold-water accom-
1. Doinfection,muscleinjuryand/orotherunknownfactors panied by ice massage of major muscle groups also is
prime the acute phase response and augment the hyper- successful,althoughcoolingratesarenotashighaswith
thermiaofexercise? cold-waterimmersion(35).
2. Do any of these factors uncouple molecular protective
mechanismstoinduceunexpectedEHS?
3. What are the molecular mechanism(s) of acquired ther- Whatwedonotknow
maltolerance(ATT)andhowmighttheybemanipulated 1. What are the earliest signs and symptoms that are har-
toimprovetissueprotection? bingersofimpendingEHS?
316 CurrentSportsMedicineReports www.acsm-csmr.org
Copyright @ 2010 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited.
2. Howlongisthe‘‘goldenhour’’inEHSrecognitionand 2. Altering what (if any) inherent mechanisms (and how)
treatment? can facilitate recovery beyond immediate treatment of
3. What is the optimum body cooling end point for treat- thepatient?
ingEHS?
4. HowarecoolingratesofEHSpatientsinfluencedbythe
Wherewegofromhere
specificanthropometriccharacteristicsoftheindividual?
1. Research biologic markers and/or testing protocols of
recovery in a wide range of EHI and EHS patients with
the goal being able to identify primary indicator(s) to
Wherewegofromhere
assistinclinicaldecision-makingfollowingEHS.
1. Maintaintreatmentlogswithtemperaturemeasuresand
2. Evaluate nutritional, medical, and physiological strat-
resolution of central nervous system dysfunction during
egies to facilitate recovery and potentially shorten the
EHS treatment; this will allow for better understanding
amount of time lost in military training and/or athletic
ofthetimesequenceandprognosisinthosewhosurvive
competition.
andthosewhodonot.
3. Determinewhetherbiologicmarkersofsystemicdamage
2. Investigate the utility of cooling to lower temperatures
indicatefunctionaldeficitsthathinderreturn-to-activity
than currently recommended (38.3-Y38.9-C), i.e., ther- and the significance of delayed markers in evaluating
apeuticmildhypothermiaasatreatmentendpoint.
immediatedamage.
PhysiologicalRecovery ThermalToleranceTesting
Whatweknow Whatweknow
1. Severityofandpresumably recoveryfrom EHSdepends 1. The IDF currently uses a HTT for assessing heat in-
uponproper,acutetreatmentforeachbodyorgansystem tolerance post EHS and guiding return-to-duty deci-
ortissueaffected. sions(39,40).
2. Morbidity and mortality are a direct result of ischemia, 2. TheIDFHTTisbasedupontheassertionthattolerance
oxidative, and nitrosative stress. The prognosis is worse toheatstressvaries among individuals.Individualswho
incaseswhenTcoreremainsabovethecriticalthreshold are unable to tolerate a specific heat challenge, as indi-
of 40.5-Y41.0-C (105-Y106-F) for any period of time cated by someone whose body temperature rises earlier
andearlyinterventionisdelayed(13,23,38). and at a higher rate than others, under the same envi-
3. Cardiovascular function, if impaired, usually recovers ronmental and exercise conditions, aredefined as‘‘heat
within hours following EHS (15,26,54Y56). How- intolerant’’(39).
ever,depending on the treatment, EHI may increase 3. Many factors underlying heat intolerance are acquired
long-term mortality from organ failure, including the and can permanently or temporarily affect the thermo-
heart (64). regulatoryresponseasdemonstratedduringtheHTT(18).
4. Hepatic tissue biomarkers may show hepatic stress for 4. SomeevidenceindicatesEHSpatientsmaybeathigher
24Y48hpriortoreturningtonormalvalues(4,46,59).In riskforanotherEHSevent(19,24,51,59).
the absence of appropriate treatment and cooling, he- 5. Although the IDF has safely used the HTT to return
patic tissue injury may persist for weeks to months after soldiers to duty for over 30 yr, some in the Roundtable
traditional biomarkers have returned to normal (4). panel questioned the validity of this test for return-to-
WhetherthisistrueforrapidlytreatedEHSisnotknown. dutyclearance.
Also,renalfailureiscommonwithEHSandmayrequire
weeksforrecovery(7).Aspreviouslydescribed,EHImay
Whatwedonotknow
increase long-term morbidity from organ failure, to in-
1. Doesthelevelofheatintolerance,asdefinedbytheHTT,
clude the liver and kidney, in the absence of adequate
predictwhowillexperienceasubsequentEHI/EHS?
rapidcooling(64).
2. Does EHS induce an altered ability to thermoregulate,
5. Systemic biomarkers of musculoskeletal damage with
andifso,forhowlong?
associated rhabdomyolysis (creatine kinase [CK], myo-
3. Howcandeficitswithinthethermoregulatorysystembe
globin) may increase for 24Y96 h prior to returning to
quantified?
normalvalues(25,33,36).
4. Is heat intolerance following EHS and demonstrated
6. Central nervous system function generally recovers rap-
by HTT a reflection of a prior EHS or preexisting
idly in most survivors who are immediately cooled;
susceptibility?
however, additional evidence suggests severe EHS can
5. Can the results of an HTT in a recent EHS patient
result in significant, and often permanent, neurologic
dictate/predictappropriatephysicalactivityprogressions
complications(33,36,52).
duringtherehabilitationprocess?
Whatwedonotknow Wherewegofromhere
1. Can systemic biologic markers or a HTT identify re- 1. Determine mechanisms altering thermoregulation, as
coveryorfutureriskfollowingEHS? measuredbyHTTafterEHS.
Volume9c Number5c September/October2010 SpecialCommunication 317
Copyright @ 2010 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited.
2. Improveunderstandingoftheetiologyofheatintolerance. 6. Thepotentialofcommonover-the-countermedications,
3. Developavalid,safe,andsimplefieldtesttopredictheat such as nonsteroidal antiinflammatory drugs (NSAID),
tolerance and potentially a risk profile for susceptibility to compromise hypothalamic and liver function, exac-
toanotherEHS. erbate tissue injury, and/or impede tissue recovery must
bestudied.
GeneticTestingandBiomarkers
SickleCellTrait
Whatweknow
1. Thermoregulatory responses during EHS recovery con- Whatweknow
sist of hypothermia and/or recurrent fever in both 1. Sickle cell trait (SCT) is characterized by the inheri-
humanandanimalmodels(32,34).AlthoughtheseT tance of a normal hemoglobin gene (HbA) from one
core
responsesarethoughttoreflectbraininjury,orinfluence parent and an abnormal, mutated B1-globin sickle he-
the hypothalamus, which may lead to thermoregulatory moglobingene(HbS)fromtheotherparent.
‘‘instability,’’ actual damage to the hypothalamus has 2. The prevalence of SCT in the United States is estim-
beenundetectablein125fatalcasesofheatstroke(34). ated at approximately 8% in African-American people
2. Thermoregulatory profiles of heat-stroked mice during and0.05%inCaucasianpeople(63).
recoveryindicatehypothermiaisaregulatedresponseto 3. The literature has documented numerous cases of exer-
protectagainst tissueinjury(32,68). tionalsuddendeathinAfrican-Americansoldiersinbasic
3. Cytokines are likely key mediators of heat-induced training and athletes with SCT. Contributing factors
SIRS (7,29). High circulating levels of pro- and appeartoincludedehydration,exertionintheheat,high-
antiinflammatory cytokines correlate with morbidity/ intensity exercise, and exertion-related acidosis, any of
mortality in EHS patients and animal models of heat which could lead to polymerization of HbS, as well as
stroke(5,7,8,14,22,31). immune and vascular responses, to result in subsequent
4. Cytokine knockout mice show enhanced heat stroke vascularocclusionandrelatedconsequences(63).
mortality(30). 4. Fewer exercise-related deaths have been reported for
5. High interferon-inducible gene expression suggests that soldiersparticipatinginadvancedspecialtytrainingafter
prodromal (viral) illness may predispose to EHS suscep- graduationthanfromrecruittraining;thissuggeststhose
tibility(61). who are susceptible have either been eliminated from
the at-risk pool or have been placed in less susceptible
settings(20,21,44,66).
Whatwedonotknow
1. How accurately do gene and protein expression profiles
measured in the circulation reflect injury at the tissue Whatwedonotknow
level? 1. What portion ofEHS-relateddeaths inmilitaryrecruits
2. Are circulating proteins (e.g., cytokines) appropriate bio- isindependentlyaresultofSCT?
markersoftissueinjuryandrecoveryoftissuefunction? 2. Does the risk of serious complications from EHI among
3. Do monokines released by skeletal muscle during exer- recruitswithSCTpositivelycorrelatewiththedegreeof
ciseservearoleinEHS? hyposthenuria?
4. Whatisthetimecourseoftissueinjuryandcellularreset/ 3. Are SCT or EHS deaths inadvertently attributed to
recoveryafterEHS? unrecognizedcardiacabnormalitiesorviceversa?
5. Doesrestorationoforganfunctiontoahomeostaticlevel 4. DoesSCTpredisposetoEHIorEHS?
reflect the ability of that organ to respond to a subse-
quentheat-related event?
Wherewegofromhere
1. Examine the relationship of exercise duration and in-
Wherewegofromhere tensity under unique environmental conditions to de-
1. Animal models are needed to study the time course of velop field profile responses for the SCT and normal
thermoregulatory, cardiovascular, liver, kidney, and hemoglobin populations. This will assist in understand-
othertissueinjurychangesduringrecoveryfromEHS. ingtherelationshipofexerciseintensityanddurationto
2. Thecontributionofskeletalmuscletothecytokinemilieu potentialphysiologicalresponsesandrisk.
needstobefurtherdelineatedwithrespecttoEHS. 2. Utilize risk profiles from prior heat exposures to modify
3. TheefficacyoftherapeutictreatmentsforEHSrecovery exercise intensity and duration for military personnel,
needstobeevaluatedinconsciousanimalmodels. regardless ofhemoglobintype.
4. The relationship between circulating biomarkers and 3. Determine the effectiveness of reducing the daily exer-
changes in specific cell populations at the tissue level cise load based on the prior day’s temperature (24-C or
(e.g.,Kupffercells,hepatocytes,splenocytes)needstobe some other temperature) or a combination of consec-
delineated during EHS recovery to advance targeted utivedayheatexposures.
therapeutics. 4. Investigate the role of other single-nucleotide poly-
5. The protective function of heat-induced hyperthermia morphisms (SNP) in exercise-related sudden death and
and/orfeverrequireselucidation. SCT in recruit populations to test whether other gene
318 CurrentSportsMedicineReports www.acsm-csmr.org
Copyright @ 2010 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited.
variants are associated with risk of death in those who 2. Most guidelines are ‘‘common sense’’ recommendations
have experienced life-threatening EHI. Particular atten- that require return to an asymptomatic state, return to
tion should focus on genes associated with anesthesia- normal laboratory parameters, and a cautious reintro-
relatedmalignanthyperthermiaand/orothergenesrelated ductiontophysicalactivitytoensureacclimatization(35).
topotentialmechanismsofEHI. 3. The current recommendations from the ACSM for re-
5. Perform more accurate population studies to define the turninganathletetotrainingandcompetitionare(1):
risk of exercise-related sudden cardiac arrest events and a.‘‘Refrainfromexerciseforatleast7dfollowingrelease
deaths with and without SCT for military populations frommedicalcare;
atdifferent stagesoftheircareer. b.Follow up about 1 wk postincident for physical ex-
6. Investigate the association between urine-specific grav- amination, and lab testing or diagnostic imaging of
ityandSCTasafunctionofEHI. affected organs based upon the clinical course of the
heatstrokeincident;
c.Whenclearedforreturn-to-activity,beginexercisein
PreventionofEHS a cool environment and gradually increase the dura-
tion, intensity, and heat exposure over 2 wk to dem-
Whatweknow onstrateheattoleranceandtoinitiateacclimatization;
1. Individual risk factors for EHS include age 940 yr, med- d.If return to vigorous activity is not accomplished over
ications (anticholinergics, antihistamines, stimulants to 4wk,consideralaboratoryexercise-heattolerancetest;
include medication for attention deficit/hyperactivity dis- e. Clear the athlete for full competition if heat tolerant
order, angiotensin-converting enzyme [ACE] inhibitors, after2to4wkoffulltraining.’’
anddiuretics),skindisease(eczema,poisonivy,skingraft,
burns),acuteillness,chronicmedicalconditionsthatcause
Whatwedonotknow
autonomicdysfunction,dehydration,pooracclimatization,
1. How should we quantify the magnitude and persistence
highbodymassindex,useofselecteddietarysupplements,
oforganinjuryfromEHS?
and/orpoorconditioning(21).
2. Whatarethelong-term healthimplicationsofEHS?
2. Heatstraininresponsetoheatstressiscumulative(65).
3. Whatclinicalaidscanaphysicianusetoassessrecovery
3. Coaches, trainers, and leaders can mitigate EHS risk by
fromEHS?
alteringclothing,intensity,anddurationofactivity,rest
4. How can we ascertain that an athlete/soldier has fully
periods,and/orenvironmental heatload(20).
recoveredfromanEHI?
4. Adherencetowork-restcycles,acclimatizationprotocols,
andhydrationguidelinesimprovesheattolerance(37,67).
Wherewegofromhere
1. Ascertain the time course of clinical and physiologic
Whatwedonotknow
recoveryfromEHS.
1. Whatpreventionmitigationmeasuresaremosteffective
2. Determine the risk for subsequent EHI after one EHI
forEHS?
episode.
2. What are the best techniques to ‘‘microclimate’’ cool
3. Develop regional centers to assist in making difficult
athletesandsoldierse.g.,undergarmentcoolingvests?
clinicaldecisionsonathletes/soldierswhohavehadEHS.
3. WhatistheroleofautonomicinstabilityinEHS?
4. Develop and implement a strategy for clinical and
4. Does reestablishing autonomic stability improve EHS
physiologicresearchintheareaofenvironmentalillness
morbidityandmortality?
toimprovethecurrentevidencebase.
5. Developbetterclinicaltools,educationalprotocols,and
practice guidelines for returning EHS patients to the
Wherewegofromhere
fieldofplay/duty.
1. Develop individual cooling devices that can sustain
training and allow rapid rehabilitation when mild symp-
tomsofheatstressarenoted.
2. Compare and contrast the encephalopathy of EHS and CONCLUSION
concussiveinjury.
3. Determine whether medications that improve auto- The principal goal of the ACSM Roundtable discussion
nomic instability in the acute management of EHS was to develop a consensus document reflecting the best
improvelong-termoutcomes. guidance to return athletes and soldiers to activity follow-
ing EHI, in particular, EHS. Although the conference suc-
ceeded in discussing relevant issues, such as the potential
CurrentGuidelinesforReturn-to-Play long-term consequences of EHI, and current controversies,
such as the concept of thermotolerance and the role of ther-
Whatweknow mal tolerance testing in assisting in return-to-play decisions,
1. No comprehensive and validated guidelines or recom- the assembled attendees were unable to move forward with
mendations exist for returning athletes/soldiers to play/ new consensus recommendations. The conference proceed-
duty(35,43). ings, however, clearly documented critical clinical concerns
Volume9c Number5c September/October2010 SpecialCommunication 319
Copyright @ 2010 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited.
TABLE2. Armymedicaldepartmentexertionalheatillness Athletic Trainers association, the American Medical Society of Sports
definitionsforthepurposeofmedicalprofiling. Medicine,andHQInc.(CoreBodyTemperatureMonitoringSystems).
Theopinionsandassertionscontainedhereinaretheprivateviewsofthe
Heatexhaustion(HE)isdefinedasasyndromeofhyperthermia authorsandarenottobeconstruedasofficialorasreflectingtheviewsofthe
(coretemperatureattimeofeventusuallye40-Cor104-F)withphysical U.S.Army,theU.S.Navy,ortheDepartmentofDefense.
collapseordebilitationoccurringduringorimmediatelyfollowing
exertionintheheat,withnomorethanminorcentralnervoussystem
(CNS)dysfunction(e.g.,headache,dizziness).HEresolvesrapidlywith
References
minimalcoolingintervention
Heatinjury(HI)isdefinedasHEwithclinicalevidenceoforgan(e.g.,liver, 1. ArmstrongLE,CasaDJ,Millard-StaffordM,etal.AmericanCollegeof
renal,stomach)and/ormuscle(e.g.,rhabdomyolysis)damagewithout Sports Medicine position stand. Exertionalheat illness during training
sufficientneurologicalsymptomstobediagnosedasheatstroke andcompetition.Med.Sci.SportsExerc.2007;39:556Y72.
2. ArmstrongLE,CragoAE,AdamsR,etal.Whole-bodycoolingofhyper-
Heatstroke(HS)isdefinedasasyndromeofhyperthermia
thermicrunners:comparisonoftwofieldtherapies.Am.J.Emerg.Med.
(coretemperatureattimeofeventusuallyQ40-Cor104-F),physical 1996;14:355Y8.
collapseordebilitation,andencephalopathyasevidencedbydelirium, 3. Armstrong LE, Maresh CM, Crago AE, et al. Interpretation of aural
stupor,orcoma,occurringduringorimmediatelyfollowingexertionor temperatures duringexercise,hyperthermia, andcoolingtherapy. Med.
significantheatexposure.HScanbecomplicatedbyorganand/ortissue Exerc.NutHealth.1994;3:9Y16.
damage,systemicinflammatoryactivation,anddisseminatedintravascular 4. Bianchi L, Ohnacker H, Beck K, Zimmerli-Ning M. Liver damage in
coagulation heatstrokeanditsregression.Abiopsystudy.Hum.Pathol.1972;3:237Y48.
5. BouchamaA,al-SedairyS,SiddiquiS,etal.Elevatedpyrogeniccytokines
inheatstroke.Chest.1993;104:1498Y502.
and scientific questions that persist at this time. These ques- 6. BouchamaA,DehbiM,Chaves-CarballoE.Coolingandhemodynamic
managementinheatstroke:practicalrecommendations.Crit.Care.2007;
tions limit the development of grade A, scientific, evidence-
11:R54.
based guidelines for return-to-play/return-to-duty. Critical 7. Bouchama A, Knochel JP. Heat stroke. N. Engl. J. Med. 2002; 346:
concernsofRoundtablememberswerethefollowing: 1978Y88.
& 8. BouchamaA,RobertsG,AlMohannaF,etal.Inflammatory,hemostatic,
AlackofconsensusonthecoredefinitionsofEHI and clinical changes in a baboon experimental model for heatstroke.
&
Limited scientifically valid criteria to assess recovery J.Appl.Physiol.2005;98:697Y705.
fromEHS 9. Brengelman GL. The dilemma of body temperature measurement. In:
& ShirakiK,YousefMK,editors.ManinStressfulEnvironments:Thermaland
Inadequate scientifically valid criteria to predict who
WorkPhysiology.Springfield:Thomas;1987.
maybepredisposedtoasubsequentheatinjuryafterEHS
10. BrodeurVB,DennettSR,GriffinLS.Exertionalhyperthermia,icebaths,
andemergencycareatTheFalmouthRoadRace.J.Emerg.Nurs.1989;
As a direct result of this Roundtable, military attendees in
15:303Y12.
conjunctionwithcivilianexpertswereabletoholdfurtherdis-
11. CarterR3rd,CheuvrontSN,WilliamsJO,etal.Epidemiologyofhos-
cussions relative to the dilemmas and issues previously identi- pitalizations and deaths from heat illness in soldiers. Med. Sci. Sports
fied. The U.S. Army medical department, in June of 2009, Exerc.2005;37:1338Y44.
subsequently moved forward with new definitions (Table 2) 12. CasaD,ArmstrongLE,GanioME,YearginSW.Exertionalheatstroke
incompetitiveathletes.Curr.SportsMed.Rep.2005:309Y17.
and recommendations for soldiers who sustain an exertional
13. CasaDJ,McDermottBP,LeeEC,etal.Coldwaterimmersion:thegold
heatinjury(www.champ.usuhs.mil/chclinicaltools.html).These standardforexertionalheatstroketreatment.Exerc.SportSci.Rev.2007;
guidelines reflect the current best evidence and are based on 35:141Y9.
‘‘commonsense’’recommendations:theyrequire‘‘returntoan 14. ChangDM.Theroleofcytokinesinheatstroke.Immunol.Invest.1993;
22:553Y61.
asymptomaticstate,’’normallabparametersforkeyendorgan
15. CostriniAM.Emergencytreatmentofexertionalheatstrokeandcom-
function, and cautious and graduated reintroduction to activ-
parisonofwholebodycoolingtechniques.Med.SciSportsExerc.1990;
ity to ensure acclimatization. The currently available science 22:15Y8.
cannotsupportahigh-level,evidence-based,consensusreturn- 16. Crouse B, Beattie K. Marathon medical services: strategies to reduce
to-playdocument,andmuchworkhasyettobeaccomplished. runnermorbidity.Med.Sci.SportsExerc.1996;28:1093Y6.
17. DeschampsA,LevyRD,CosioMG,etal.Tympanictemperatureshould
The panel strongly believes this document provides a strong
notbeusedtoassessexerciseinducedhyperthermia.Clin.J.SportsMed.
foundationforfutureclinicalandbenchresearchinthisvitally 1992;2:27Y32.
importantarea. 18. Epstein Y. Heat intolerance: predisposing factor or residual injury?
Med.Sci.SportsExerc.1990;22:29Y35.
19. EpsteinY,ShapiroY,BrillS.Roleofsurfacearea-to-massratioandwork
Acknowledgments efficiencyinheatintolerance.J.Appl.Physiol.1983;54:831Y6.
20. GardnerJW,GutmannFD,PotterRN,KarkJA.Nontraumaticexercise-
TheauthorsacknowledgethattheACSMRoundtableinvolvedmorethan50 related deaths in the U.S. military, 1996Y1999. Mil. Med. 2002; 167:
professionals including not only speakers, who comprised the writing group, 964Y70.
butdiscussantsandexperts,fromboththemilitaryandciviliansportsmedicine 21. GardnerJW,KarkJA,KarneiK,etal.Riskfactorspredictingexertional
communities.Wewouldspecificallyliketoacknowledgetheconferencedis- heatillnessinmaleMarineCorpsrecruits.Med.Sci.SportsExerc.1996;
cussantswhodeliveredpreparedremarks:Drs.JohnGardner,JohnCapacchione, 28:939Y44.
Thomas Hustead, Rodney Gonzalez, Scott Pyne, Steve Blivin, Jay Heaney, 22. Hammami MM, Bouchama A, Al-Sedairy S, et al. Concentrations of
Michael Ferrara, and Rebecca Lopez. A special thanks to invited speakers soluble tumor necrosis factor and interleukin-6 receptors in heatstroke
including LTG Frank Kearney, MG George Weightman, and Mr. James R. andheatstress.Crit.CareMed.1997;25:1314Y9.
Whitehead, ACSM Executive Vice President, as well as conference coor- 23. HeledY,Rav-AchaM,ShaniY,etal.The‘‘golden’’hourforheatstroke
dinatorsMs.JaneSenior,Ms.LynnWalters,andMs.JenniferDavis. treament.Mil.Med.2004;169:184Y6.
ThisACSMRoundtablewastheresultofeducationalsupportfromthe 24. HeledY,MoranDS,MendelL,etal.HumanACEI/Dpolymorphismis
ACSM and the USU Consortium for Health and Military Performance associatedwithindividualdifferencesinexerciseheattolerance.J.Appl.
(CHAMP). Additional financial support was obtained from the National Physiol.2004;97:72Y6.
320 CurrentSportsMedicineReports www.acsm-csmr.org
Copyright @ 2010 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited.
25. HsuYD,LeeWH,ChangMK,etal.Bloodlactatethresholdandtype 48. RobertsWO.Exertionalheatstrokeduringacoolweathermarathon:a
IIfibrepredominanceinpatientswithexertionalheatstroke.J.Neurol. casestudy.Med.Sci.SportsExerc.2006;38:1197Y203.
Neurosurg.Psych.1997;62:182Y7. 49. RobertsWO.Exertionalheatstrokeinthemarathon.SportsMed.2007;
26. Kew MC, Tucker RB, Bersohn I, Seftel HC. The heart in heatstroke. 37:440Y3.
Am.HeartJ.1969;77:324Y35. 50. Roberts WO. Managing heatstroke: on-site cooling. Phys. Sportsmed.
27. Kiyatkin EA. Physiological and pathological brain hyperthermia. Prog. 1992;17Y28.
BrainRes.2007;162:219Y43. 51. RobinsonS,WileySL,MyhreLG,etal.Temperatureregulationofmen
28. Kulka TJ, Kenney WL. Heat balance limits in football uniforms: how followingheatstroke.Isr.J.Med.Sci.1976;12:786Y95.
different uniform ensembles alter the equation. Phys Sportsmed. 2002; 52. RomeroJJ,ClementPF,BeldenC.Neuropsychologicalsequelaeofheat
30:29Y39. stroke:reportofthreecases.Mil.Med.2000;165:500Y3.
29. Lambert GP. Role of gastrointestinal permeability in exertional heat- 53. RonnebergK,RobertsWO,McBeanAD,CenterBA.Temporalartery
stroke.Exerc.SportSci.Rev.2004;32:185Y90. and rectal temperature measurements in collapsed marathon runners.
30. LeonL.Heatstrokeandcytokines.Prog.BrainRes.2007;162:481Y524. Med.Sci.SportsExerc.2008;40:1373Y5.
31. Leon LR, Blaha MD, DuBose DA. Time course of cytokine, cortico- 54. Rousseau JM, Villevieille T, Schiano P, et al. Reversible myocar-
sterone,andtissueinjuryresponsesinmiceduringheatstrainrecovery. dial dysfunction after exertional heat stroke. Int. Care Med. 2001; 27:
J.Appl.Physiol.2006;100:1400Y9. 328Y9.
32. LeonLR,DuBoseDA,MasonCW.Heatstressinducesabiphasicther- 55. RoyburtM,EpsteinY,SolomonZ,ShemerJ.Longtermpsychological
moregulatory response in mice. Am. J. Physiol. Regul. Integr. Comp. andphysiologicaleffectsofheatstroke.Phys.Behav.1993:265Y7.
Physiol.2005;288:R197Y204. 56. Shahid MS, Hatle L, Mansour H, Mimish L. Echocardiographic and
33. LewHL,LeeEH,DateES,MelnikI.Rehabilitationofapatientwith Doppler study of patients with heatstroke and heat exhaustion. Int. J.
heatstroke:acasereport.Am.J.Phys.Med.Rehabil.2002;81:629Y32. Card.Imaging.1999;15:279Y85.
34. MalamudN,HaymakerW,CusterRP.Heatstroke:aclinico-pathologic 57. Shapiro Y, MagazanikA, UdassinR, et al. Heat intolerance in former
studyof125fatalcases.Mil.Surg.1946;99:397Y449. heatstrokepatients.Ann.Intern.Med.1979;90:913Y6.
35. McDermott BP, Casa DJ, Yeargin SW, et al. Recovery and return to 58. SharmaHS. Methodsto producehyperthermia-inducedbraindysfunc-
activity following exertional heat stroke: considerations for the sports tion.Prog.BrainRes.2007;162:173Y99.
medicinestaff.J.SportRehabil.2007;16:163Y81. 59. ShiboletS,CollR,GilatT,SoharE.Heatstroke:itsclinicalpictureand
36. Mehta AC, Baker RN. Persistent neurological deficits in heat stroke. mechanismin36cases.Q.J.Med.1967;36:525Y48.
Neurology.1970:336Y40. 60. Sonna LA, Sawka MN, Lilly CM. Exertional heat illness and human
37. Montain SJ, Latzka WA, Sawka MN. Fluid replacement recommen- geneexpression.Prog.BrainRes.2007;162:321Y46.
dationsfortraininginhotweather.Mil.Med.1999;164:502Y8. 61. SonnaLA,WengerCB,FlinnS,etal.Exertionalheatinjuryandgene
38. MoranDS,Eli-BerchoerL,HeledY,etal.Heatintolerance:doesgene expression changes: a DNA microarray analysis study. J. Appl. Physiol.
transcriptioncontribute?J.Appl.Physiol.2006;100:1370Y6. 2004;96:1943Y53.
39. Moran DS, Erlich T, Epstein Y. The heat tolerance test: an efficient 62. StallonesRA,GauldRL,DodgeHJ,LammersTF.Anepidemiological
screeningtoolforevaluatingsusceptibilitytoheat.J.SportRehabil.2007; studyofheatinjuryinarmyrecruits.AMAArch.Ind.Health.1957;15:
16:215Y21. 455Y65.
40. MoranDS,HeledY,StillL,etal.Assessmentofheattoleranceforpost 63. TsarasG, Owusus-ansah A, Boateng FO, et al. Complications associated
exertionalheatstrokeindividuals.Med.Sci.Monit.2004;10:CR252Y7. withsicklecelltrait:abriefnarrativereview.Am.J.Med.2009;122:507Y12.
41. MSMR.Update:HeatInjuriesAmongU.S.MilitaryMembers,2007.In: 64. WallaceRF,KriebelD,PunnettL,etal.Priorheatillnesshospitalization
MedicalSurveillanceMonthlyReport.2008,p.2Y3. andriskofearlydeath.Environ.Res.2007;104:290Y5.
42. MSMR. Update: Heat Injuries, Active Component. U.S. Armed Forces, 65. WallaceRF,KriebelD,PunnettL,etal.Theeffectsofcontinuoushot
2009,2010;17:6Y8. weathertrainingonriskofexertionalheatillness.Med.Sci.SportsExerc.
43. O’ConnorFG,WilliamsAD,BlivinS,etal.Guidelinesforreturntoduty 2005;37:84Y90.
(play) after heat illness: a military perspective. J. Sport Rehabil. 2007; 66. WallaceRF,KriebelD,PunnettL,etal.Riskfactorsforrecruitexertional
16:227Y37. heat illness by gender and training period. Aviat. Space Environ. Med.
44. PhinneyLT,GardnerJW,KarkJA,WengerCB.Long-termfollow-up 2006;77:415Y21.
afterexertionalheatillnessduringrecruittraining.Med.Sci.SportsExerc. 67. Wenger HA, Bell GJ. The interactions of intensity, frequency and
2001;33:1443Y8. durationof exercise training in alteringcardiorespiratory fitness. Sports
45. RaeDE,KnobelGJ,MannT,etal.Heatstrokeduringenduranceexercise: Med.1986;3:346Y56.
isthereevidenceforexcessiveendothermy?Med.Sci.SportsExerc.2008; 68. Wilkinson DA, Burholt DR, Shrivastava PN. Hypothermia following
40:1193Y204. whole-body heating of mice: effect of heating time and temperature.
46. RobertsWO.Atwelveyearprofileofmedicalinjuryandillnessforthe Int.J.Hyperthermia.1988;4:171Y82.
TwinCitiesMarathon.Med.Sci.SportsExerc.2000;32:1549Y55. 69. Winkenwerder W, Sawka M. Disorders due to heat and cold. In:
47. RobertsWO.Deathintheheat:canfootballheatstrokebeprevented? Goldman L, editor. Cecil Medicine. Philadelphia: Saunders Elsevier;
Curr.SportsMedRep.2004;3:1Y3. 2008.
Volume9c Number5c September/October2010 SpecialCommunication 321
Copyright @ 2010 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited.