Recommendations for Routine Sickle Cell Trait Screening for NCAA Division I Athletes

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    The primary objectives of the preparticipation physical evalua-tioenSecmataking


    Effective PPE screening must, to the best of our abilities and

    PM&R 2011 by the American Academy of Physical Medicine and Rehabilitation193 74, February 2011

    Prin j.pmrj.2010.12.017

    164-1482/11/$36.00 Vol. 3, 168-1

    ted in U.S.A. DOI: 10.1016/

    8n (PPE) are screening for conditions that may be life threat-ing or disabling, or may predispose to injury or illness [1].ondary objectives include identifying personal health infor-tion that initiates discussion with the athlete, for example,ingknowledge gained, educating the athlete basedon screen-results, and applying precautions as warranted.The PPE, historically, has had little impact on the mortal-of athletes in sports. In our college athlete screening, wek, preeminently, to protect life. Success in screening, then,pends on identifying those conditions, diseases, or pro-ses that cause death in college athletes. Four commonses of nontraumatic death in an athlete in action arediac, asthma, exertional heat stroke, and exertional sick-g [2]. These same 4 causes are echoed in the 16 nontrau-tic National Collegiate Athletic Association (NCAA) Divi-n I football deaths since 2000. Of the 16 deaths, 4 werediac, one was asthma, and one was exertional heat stroke,d the inconvenient truth was that exertional sickling wasleading cause of death and accounted for 10 of the 16

    aths. A complication of a condition, sickle cell trait (SCT),sent in 3%-4% of NCAA Division I football players, ac-unted for 63% of the deaths.

    resources, identify those athletes with a condition, disease, orpredisposition to the 4 aforementioned causes of death. Sensi-tive and affordable testing for SCT in the PPE is available,beginning with a hemoglobin solubility test to detect hemoglo-binS and follow-up testing asnecessary to confirmSCT, excludeotherhemoglobin variants, andquantify hemoglobinS.The costof not testing must also be considered: athletes with SCT whocarry a risk of serious or fatal sickling crisis go undetected, theincalculable cost of a human life lost to exertional sickling, thefinancial fallout in gaining closure in death of an athlete [3], andthepotential impact upon careers [4]. A futuristic ideal is to havetrait status identified at birth, which will be charted, communi-cated, and follow the patient and/or athlete and offset futurerepetitive testing and expense.

    SCT status as a priority point of personal health informa-tion is evidenced by required natal hemoglobinopathy testingin all 50 states and the District of Columbia. However, resultsof a recent survey found that only 37% of families were toldof a positive newborn test for SCT [5]. In testing for SCT inour PPE at the University of Oklahoma, we identified 20football players with SCT. Only 3 knew their status, and, inone case, the parents were unaware. Screening for SCT isRecommendations for Routine SicTrait Screening for NCAA Division


    You are part of a panel determining recommendations foscreening for National Collegiate Athletic Association (NCAparticular, the panel would like your informed opinion whetshould be screened for sickle cell trait. The panel would likeanticipate screening will impact the morbidity and mortalityimpact on cost and time for appropriate administration ofmotion that NCAA Division I athletes should be screened fornderson, head athletic trainer for the University of Oklahoollege Athletic Trainers Society. Arguing against the motesting should not be part of the routine screening for Divisoperak, DO, fellowship director for the Primary Care Sporthe University of Pittsburgh, head team physician for Setoincent College, assistant team physician at Carnegie Mellonepresentative on the board of directors of the Big East Sport

    ott Anderson, ATC, RespondsCellhletes

    ine sickle cell traitvision I athletes. Inl Division I athletespinion on how youletes as well as theg. Arguing for thecell trait is Scott A.d president of the

    hat sickle cell traitAthletes, is Jeanneicine Fellowship atUniversity and St

    rsity, and physicianicine Society.

    Scott A. Anderson, ATCHead Athletic Trainer, University ofOklahoma, Norman, OK; Co-Chair, Inter-Association Task Force on Sickle Cell Traitand the Athlete; President, College AthleticTrainers SocietyDisclosure: nothing to disclose

    Jeanne Doperak, DOUniversity of Pittsburgh Physicians;Department of Orthopaedic Surgery,University of Pittsburgh Medical CenterSports Medicine, Pittsburgh, PADisclosure: nothing to disclose

    Feature Editor:

    Gary P. Chimes, MD, PhDUniversity of Pittsburgh Medical Center,Pittsburgh, PA.Address correspondence toG.C.; e-mail: garypchimes@gmail.comDisclosure: nothing to discloseDisclosure Key can be found on the Table ofContents and at

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    169PM&R Vol. 3, Iss. 2, 2011ly established in the PPE monograph: Do you or some-e in your family have sickle cell trait or disease? Theestion within the question is should we have a laboratoryt to confirm that we know what we know, recognizingt accuracy of answers in PPE medical history forms ishly suspect [6]. The NCAAs screening requirement invision I institutions provides provision of documentedults of prior tests in lieu of PPE testing, but natal testults that do not track with the patient-athlete, along withinability to readily access past medical records renders, inst cases, a repeated test in the PPE as the sole source ofgnosis for the collegiate athlete.SCT status confirmation from the PPE leads to discussionhealth-related topics. Thus, targeted education, based on asitive SCT test, becomes the second pillar in an expandedrgin of safety for the collegiate athlete with SCT. Theletic trainer and team physician inform the athlete thatT is a condition, not a disease, and is consistent with armal, healthy life span. They discuss associated potentialmplications; genetic considerations with respect to familynning; any medical history relative to sickling events;ns, symptoms, and settings of exertional sickling; andcautions for the athlete with SCT. The college athlete whots positive is virtually assured of follow-up counseling,ereas some primary care physicians may feel ill preparedcounsel and/or reticent to refer for counseling [7].Tailored precautions for athletes with SCT offer the bestmise of preventing exertional sickling. The insult thatates the injury that is exertional sickling collapse is inten-y. Intensitymaymanifest in, inclusive of but not limited tobient heat stress, newness to altitude, acute illness, sus-ned intensity, heroic effort, or a relentless coach. Precau-n, among other points, entails modifying the work:restio in consideration of sports specificity to mitigate, if notolly offset, exertional sickling.Knowledge of SCT status facilitates a differential diagnosisthe field. Exertional sickling often presents with muscularmping and appearance of fatigue. In the absence of trait-tus awareness, exertional sickling that proved fatal hasen mistaken for exertional heat illness [8]. Symptoms ofkling in the athlete with SCT should always be assumedd managed as exertional sickling.We emphasize that SCT is no contraindication to partici-tion in sports [9,10]. A common criticism of screening ist athletes with SCT will be denied participation in sports.e risk of death for an athlete with SCT was established in74 when Polie Portier died of exertional sickling at theiversity of Colorado [11]. Despite 17 similar sicklingaths in college athletes since Polie Portier, no evidenceists that any athlete with SCT has been denied participationsports. Subsequent to Portiers death, the NCAA, in 1975,ommended screening for SCT, then rescinded the recom-

    ndation a few years later. Nonetheless, testing has oc-rred in NCAA institutions, at a variable rate, for 35 years.35 years of testing, there is no known case of any athleteing denied participation due to testing positive for SCT. In06, Clarke et al [12] published a survey of Division Ititutions from which one could estimate that 50% of thetitutions were testing for SCT in their PPE; yet, again, thereo evidence that any athlete has been denied an opportu-y to participate in sports. Undeniably, past discriminationsed on SCT status in societies other than sports is real, but,sports, it is a baseless fear.Another approach is universal precautions. Instead ofeening for SCT, apply precautions equally to all athletes.e U.S. Army proffered and popularized the concept thatertional heat illness is a trigger to sickling and that prevent-exertional heat illness will prevent SCT deaths. Despiteir universal precautions without screening, exertionalaths continue to occur in U.S. Army recruits with SCT, 6m 1992 to 2001, and at least one in 2008 and one in 2009.niversal precautions have not eliminated sickling deathsthe U.S. Army, nor will they in collegiate athletics.Death grabs the headlines, whereas, athletes who experi-ce nonfatal exertional sickling fly under the radar. Exer-nal sickling may cause severe ischemic rhabdomyolysis,ich results in compartment syndromes, myonecrosis, andte renal failure [13,14]. Splenic infarction occurs in ath-es with SCT newly exposed to elevation in altitude [15].ilure to consider sickling and its sequelae in a differentialgnosis and management has delayed proper care of SCTletes, and some have permanent consequences from whatould have been a reversible sickling complication.Given that athletes with SCT are participating in sports,orts medicine practitioners need to be armed to recognized manage exertional sickling as it presents. Knowledge,geted education, and tailored precaution become 3 pillarsan expanded margin of safety for the athlete with SCT inorts. Testing begets knowledge, knowledge begets targeteducation, education begets tailored precaution, and precau-n begets an expanded margin of safety in sports for thelete with SCT.

    FERENCES. Bernhardt DT, Roberts WO, eds. PPE Preparticipation Physical Evalu-ation. 4th ed. Elk Grove Village, IL: American Academy of Pediatrics;2010.

    . Van Camp SP, Bloor CM, Mueller FO, Cantu RC, Olson HG. Nontrau-matic sports death in high school and college athletes. Med Sci SportsExerc 1995;27:641-647.

    . Day C. ONeal lawsuit settled for $2 million, athletic scholarshipplanned. Columbia Missourian March 12, 2009.

    . Witt G. Wheeler Brown dismissed as A&T athletics director. News &Record October 15, 2010.

    . Kavanaugh PL, Wang CJ, Therrell BL, Sprinz PG. Communication ofpositive newborn screening results for sickle cell disease and sickle celltrait: variations across states. AJM Genet C Semin Med Genet 2008;148C:15-22.

    . Carek PF, Futrell M, Hueston WJ. The preparticipation physical exam-

    ination history: who has the correct answers? Clin J Sport Med 1999;9:124-128.

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    Although the death of any young person is tragic, I believeit ithird leading cause of death in athletes means and how thiscompares with other causes of mortality. The overall greatestrisk of death in athletes is cardiovascular conditions, whichareparecpecargreyea10vehres




    plied to an athlete, especially one who has achieved great

    sport. The feared scenario is that an otherwise healthy youngman is passed over for a National Football League (NFL) orNational Basketball Association (NBA) draft pick because ateaSCrisThRylonteapla

    170 Anderson et al SICKLE CELL TRAIT SCREENING FOR DIVISION I ATHLETESthought to account for 0.46 deaths per 100,000 partici-nts [4]. Although there are no direct comparisons for SCT,ognize that, in the above cohort in which 7 athletesrished due to SCT, 100 were reported to have had fataldiac events [2]. Even more astonishing is that, by far, theatest risk of death in children from newborn through 19rs of age is unintentional events at a rate of 14.1 per0,000 [5], which includes occurrences such as motor

    icle and firearm accidents. We invest a large amount ofources and concern on the issues of screening when the

    chdem may not want to make any accommodations for hisT. There is evidence that high altitude and low oxygen arek factors for adverse events in an individual with SCT.ere have been professional athletes, such as Steelers safetyan Clark, who, after such an adverse event, opts to noger play in Denver. In opposition, Mr Clarks formermmate Santonio Holmes, who is also SCT positive, hasyed in Denver without any issues for years and at lasts important to gain some depth perception on what the success and may have the talent to make a career of his or her. Kemper AR, Uren RL, Moseley KL, Clark SJ. Primary care physiciansattitudes regarding follow-up care for children with positive newbornscreening results. Pediatrics 2006;118:1836-1841.

    . Gardner JW, Kark JA. Fatal rhabdomyolysis presenting as mild heatillness in military training. Mil Med 1994;159:160-163.

    . Diggs LW, Flowers E. High school athletes with the sickle cell trait (HbA/S). J Natl Med Assoc 1976;68:492-493.

    . NATAConsensus Statement: sickle cell trait and the athlete, June 2007.Available at

    . Ewing PC. Death of an athlete with sickle cell trait. Med World News1974;15:44.

    anne Doperak, DO, Responds

    rly in any medical career, every clinician is taught to askeral questions regarding any test or procedure being or-red. First, what is the purpose of this test? Second, what do Iect the results to show? Third, what is the risk to the patient?ally, fourth and probably most important, how will theults of this test influence how I will care for this patient?In the case of sickle cell trait (SCT) testing, the answer to thet question is simple. The blood test is ordered to identify amoglobin abnormality. This variant has been linked to splenicarction, renalmedullary carcinoma, and,most importantly inr debate, exertional rhabdomyolysis [1].The foundation for this debate is that, among 136 well-died, sudden nontraumatic deaths in high school andllege athletics over a decade, the third-most common causedeath was found to be sickling-associated rhabdomyolysis. Under rare and extreme circumstances, usually in a lowygen environment, the red blood cell will classically de-m and is believed to clog the vessels and lead to rapid andminant muscle breakdown and eventually to multiorganlure and death. However, it is important to note that incumented cases of death related to SCT, the relationship isrely coincidental and not causative, because there is anbility to discern histologically artifactual postmortemkling from antemortem sickling, and there is no directdence that links the pathogenesis of these deaths to micro-cular obstruction by rigid erythrocytes [3].. Clarke CE, Paul S, Stilson M, Senf J. Sickle cell trait preparticipationscreening practices of collegiate physicians. Clin J Sport Med 2006;16:440.

    . Hale MH, Clugston JR, Prine BR, Pass AN, Gupta A. Severe low back painin a football player. Poster presentation for American Medical Society forSports Medicine 17th Annual Meeting. Las Vegas, NV. March 2008.

    . Schnebel B, Eichner ER, Anderson S, Watson C. Sickle cell trait andlumbar myonecrosis as a cause of low back pain in athletes [abstract].Med Sci Sports Exerc 2008;40(Suppl):537.

    . Ortega JO. Nausea, vomiting, and abdominal pain in a collegiatebasketball player. Clin J Sport Med 2006;16:443-444.

    mbers show that focusing our attention on seat belts andarm safety would save dozens more lives.Moving on to the second question in our algorithm, whichses the question, what do we expect the results to show?is is a simple data-driven answer that the majority of thoseted will be negative. The SCT genetic fingerprint evolvedAfrica. This heritable variation is protective against ma-ia. Darwinism in practice now shows that the generalpulation carries the SCT, with an expected black predom-nce. In fact, 8% of African Americans, 0.5% of Hispanics,d 0.2% of whites make up the approximately 2 millionriers that are affected in the United States [6]. This wouldan that a Division 1 screening program would most likelyntify 400-500 carriers each year, the majority of whomll be African American. Consistent with this expectation,7 of the deaths reported in the reference study above wereletes of African American descent [2].This quickly takes us to our third question, which in-lves looking at the risk of the test to the patient. The answerthis question is probably much greater than the averageder would anticipate. The tangible risk is low, very low. Aple venipuncture will sometimes cause bleeding, bruising,in at the site, and, rarely, infection.The intangible risk ismuchher. What does this label mean to a young athlete? How doprotect the patients privacy? Who pays for the test?Discrimination becomes a concern once any label is ap-eck will continue to do so as long as the league allows. Thisbate may be one that a professional organization will just

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    171PM&R Vol. 3, Iss. 2, 2011ite frankly not want to undertake; so, an equally talentedyer will be signed who is not SCT positive. For those whonk this would not or could not occur, we have seen ailar bias in the past. In 1970, the U.S. Air Force Academy

    rred individuals with SCT from enlisting, and some airlinesused to then hire them as pilots and flight attendants.uld our testing inadvertently cheat a young African Amer-n man out of his dream of being a professional athlete?Opponents to the above theory would say that HIPAAealth Insurance Portability and Accountability Act) and con-entiality laws should protect the athlete from this scenario.wever, that leads to our second point in the risk debate,ich is, how do we protect the test results? As you will reader in this article, one of the only interventions for SCT isdification of the athletes workouts. Given this, the entireching staff, including the strength and conditioning coaches,ll need to be aware of the players status. As if this were notough, should an adverse event occur, prompt managementd knowledge of the carrier state, in theory, should help withathletes care. Therefore, the entiremedical staff that cares forathlete, from the physician to the athletic trainers, and, evensome cases the athletic training students, will need to haveowledge of an athletes status. The U.S. Navy goes so far tontify each recruit with a neck tag and red belt for trainingrcises. I have no knowledge of a Division I program withual identificationon thefield, but,withwidedisseminationoformation, the concept of confidentiality becomes difficult, ift impossible.Is cost a risk? Yes, when it may exclude athletes fromrticipating if they cannot afford the testing. The averagest of a basic sickle cell test is variable across the country.r institution in Pittsburgh is charged $12.50 per test. Mostvision I schools will have approximately 150 incomingshman each year, with a total cost of approximately $1875.hough all programs are on economic contracture theseys, I believe that the majority of Division I schools wouldable to find this amount in their budgets. Where it be-mes more burdensome is down the road. Typical policyrts at the professional and/or Division 1 level and trickleswn through the collegiate pyramid to high schools. I canagine that one, not so far off, daymany ofmy less-fortunateh school athletes may not have the extra money to coverblood test and as a result may be unable to participate.This brings us to the final and, in my opinion, the mostportant question: how will the results affect treatment?e answer to this question I believe is the strongest reasony we should not be testing all Division I athletes at therrent time. As mentioned previously, the risk of a cata-ophic event from SCT rises in extreme environments thatses low oxygen and undue stress on the body. Specifi-ly, these include the following: dehydration, illness,orly controlled asthma, extreme fatigue, and altitude.

    ese factors simply can be addressed by universal precau-ns. We should be protecting all of our athletes as if theyd SCT by keeping them well hydrated and by followingAA guidelines for acclimatization. Every players asthmaould be well controlled, and anyone who is febrile shouldheld from play. Most schools that are currently testingve variable provisions, and many do not make any partic-r accommodations for athletes who are SCT positive.hough there is a policy for testing, there is no set guidelineth what to do with the positive results. This leaves manyth the impression the test is done for medical-legal impli-ions rather than the well being of the athlete.The other point that remains unclear is if the knowledge ofositive test prevents deaths. The NCAA has collected data8 university deaths from SCT over the past decade. Ofse 8 athletes, 4 were known to be SCT positive beforeccumbing [7]. This statement alone raises doubt that thetem we have currently in place is a best-practice model.In athletics, we often refer to military data, because the 2ups tend to bemade up of young, healthy individuals whotinely engage in rigorous physical activity in environmen-extremes. Each branch of the military has developed itsn policy regarding sickle cell testing. The U.S. Navy, asntioned above, screens and labels individuals with a redlt during training. The U.S. Air Force screens and offers thetion of discharge to those individuals who test positive.e U.S. Marines screen but do not alter the routine of thoseo are positive. Finally, the U.S. Army, in 1996, ceasedeening and just use across-the-board precautions [3].Perhaps our best resource for planning the future is byking at the past. In 1970, under the leadership of Presidentxon, the country implemented a nationwide sickle celleening program. The policy was not well planned out, andny of the same issues that have been raised above led to antcry of discrimination and lack of provisions for positive testults. Since that time, these programs have either been discon-ued or heavilymodified [8]. Although a screening program ine form, not just including Division I athletics, but for the

    erall increasingly active population at large,may be beneficial,eeds to be more carefully constructed. The goal should be tovide the maximum benefit targeted to the highest risk pop-tion. There must not only be policies in place for screeningt also clear establishment of how to address the positiveultswhile assuringpatient privacy. In addition, there needs toa greater commitment of research time and money to thisease process to make more evidence-based practices. In 1973,w England Journal of Medicine ran an editorial [9] on sickle cellting that stated thepolicywas introducedbefore evidence that apulsoryprogram isneeded,desiredor in thebest interest of thected community. In 2010, I could not have said it any better.

    FERENCESEichner ER. Sickle cell trait. J Sport Rehab 2007;16:197-203.Van Camp SP, Bloor CM, Mueller FO, Cantu RC, Olson HG. Nontrau-

    matic sports death in high school and college athletes. Med Sci SportsExerc 1995;27:641-647.

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    scadesimspthe NFL and the NBA test for SCT. Ryan Clarks case does notmake him a poster child for discrimination. Rather, ClarkscasstawhtrepliReact





    REFERENCES1. Mitchell BL. Sickle cell trait and sudden deathbringing it home. J Nat




    172 Anderson et al SICKLE CELL TRAIT SCREENING FOR DIVISION I ATHLETESe evidences the outcome ignorance breeds as SCTtus is unknown and unknowing caregivers languishile the athlete-patient suffers, undiagnosed and un-ated, through what should be a readily recognized com-cation of SCT: splenic infarct with elevation in altitude.turn to play for Clark, and others, becomes an electiveion based on knowledge.

    Dr Doperak cites the greatest risk of death in athletes isdiovascular, which echoesMaron. Maron et al [5] and Van

    5.Med Assoc 2007;99:300-305.Anzalone ML, Green VS, Buja M, et al. Sickle cell trait and fatal rhabdo-myolysis in football training: a case study. Med Sci Sports Exerc 2010;42:3-7.Wirthwein DP, Spotswood SD, Barnard JJ, Prahlow JA. Death due tomicrovascular occlusion in sickle-cell trait following physical exertion. JForensic Sci 2001;46:399-401.Murphy JR. Sickle cell hemoglobin (Hb AS) in black football players.JAMA 1973:225:981-982.ultaneously shows no contraindication to participation inorts at the highest levels for the athlete with SCT [4]. BothMitchell BL. Sickle cell trait and sudden deathbringing it home. J NatMed Assoc 2007;99:300-305.Maron BJ, Gohman TE, Aeppli D. Prevalence of sudden cardiac deathduring competitive sports activities in Minnesota high school athletes.J Am Coll Cardiol 1998;32:1881-1884.National MCH Center For Child Death Review. Available at: AccessedNovember 2010.Bonham VL, Dover GJ, Drody LC. Screening student athletes for sickle

    ott Anderson, ATC, Rebuts

    Doperak and Mitchell [1] are inarguably accurate withpect to no direct evidence links the pathogenesis of theseertional sickling] deaths to microvascular obstruction byid erythrocytes. Reality recognizes little likelihood thatre will ever be direct evidence, given that no institutionaliew board will grant permission for a study to establishect evidence due to the plausibility of a causal relationshipmorbidity and mortality in exertion with SCT.A causal relationship exists in antemortem sickling attopsy as evidenced by extensive sickling despite transfu-n of normal red blood cells; splenomegaly due to conges-n of sickled red cells occurs over time versus postmortem; extensive presence of sickled red blood cells in the braind cardiac conduction system [3]; and, major congestionntified behind the sickling, a strong suggestion that thell-beating heart was trying to pump blood through organsoked with sickling.Skeptics give grudging ground to rare and extreme cir-mstances of sickling-associated rhabdomyolysis that leadsdeath, but, with a curious exclusion of athletes. Theireats are that events occur in the untrained, the settings areited to extreme environmental heat, altitude, and/or de-dration. Sickling-associated rhabdomyolysis collapse andath in working athletes has occurred weeks into a trainingimen, at altitude and at sea level, in even moderate ambi-t conditions, and virtually year round.Discrimination discussion deserves reprise due to there in the scenario of a denied professional career. Inci-nce of SCT in NFL players denies discrimination as itcell traita social and clinical experiment. N Engl J Med 2010;363:997-999.Thomas K, Zarda B. In NCAA, question of bias over a test for a genetictrait. New York Times. April 11, 2010.Rutkow IM, Lipton JM. Some negative aspects of state health depart-ments policies related to screening for sickle cell anemia. Am J PublicHealth 1974;64:217-221.Whitten CF. Sickle cell programming - an imperiled promise. N EnglJ Med 1973;286:1129-1132.

    mp et al [6] read the same data and drew different conclu-ns on SCT deaths: Marons one death to Van Camps 7aths. Maron [7] subsequently revealed that his study de-n did not include a systematic analysis for SCT. A reason-le question is raised regarding hypertrophic cardiomyop-y (HCM) as being an over-called cause of death in blackle athletes versus exertional sickling as one acknowledges:incidence of HCM at birth is the same for black males andite males, yet HCM is a called cause of death at twice thee in black athletes versus white athletes, plus morpholog-l attributes of athletes heart and an NFL study showingckmale athletes with larger hearts and thicker walls [8], allcombination with exclusion of SCT as a potential cause ofath [9].Confidentiality concerns are another pseudoscare. Colle-te athletic medicine holds an obligation to HIPAA and themily Educational Rights and Privacy Act. The Family Ed-ational Rights and Privacy Act mandates stricter guidelinesrelease of information than does HIPAA. Athletic medi-e specialists are professionals who practice in safeguardingathlete per federal law.In 1992, the NCAA rescinded a recommendation for SCTting, not because of discrimination or program failuret for sociopolitical reasons, which triggered a descent intoorance regarding SCT and the athlete. In 2010, in the besterests of the athlete, NCAA Division I joined all 50 states,District of Columbia, the U.S. Marines, the U.S. Air Force,U.S. Navy, the NFL, and the NBA in testing for SCT . . .

    t only if SCT status is absent from their personal healthMaronBJ,Shirani J,PoliacLC,et al. Suddendeath inyoungcompetitiveathletes:clinical, demographic, and pathologic profiles. JAMA 1996;276:199-204.

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    I fsonenurepwhdeAnwisudaanpaprReAnprBamatiotiofigdaassinfpricatesplaleague does not provide insight into the original questionof

    Mr Andersons second key point, that universal pre-cautions have not eliminated sickling deaths in the Armyis also without any scientific data to support this broadstadedetioTh



    tesresmotowo3 misshowever, that better data are needed before proceeding to

    more research and targeted testing.


    173PM&R Vol. 3, Iss. 2, 2011tement. It is true that there have been nontraumaticaths in the military linked to SCT over the past 2cades; however, there is no proof that universal precau-

    ns were being followed by those individuals affected.ese protective measures only work if they are used 2.FERENCESCBS Sports. Non-traumatic deaths in college football since 2000. Avail-able at: Ac-why we should test all Division I athletes. mass screening, with all of its potential for undesirable stig-matization [5]. I, too, oppose mass screenings and advocateVan Camp SP, Bloor CM, Mueller FO, Cantu RC, Olson HG. Nontrau-matic sports death in high school and college athletes. Med Sci SportsExerc 1995;27:641-647.Maron BJ. Sickle cell trait and sudden death in athletes [letter]. JAMA1996;276:1472.

    Doperak Rebuts

    pplaud my colleague for his compelling argument andee that athletes health and safety is our primary concern.wever, Mr Andersons 2 key points, namely the number ofaths since 2000 attributed to SCT and that universal pre-tions have not been successful in the military population,lacking only one very important thing: references!The number of nontraumatic deaths in NCAA Divisionootball has been reported frequently in popular mediaurces such as CBS Sports and USA Today. Many of thesewspaper and magazine articles cite similar but not exactmbers to those reported in our debate. CBS Sportsorts 10 Division I football deaths since 2000, 5 ofich were from SCT [1]. USA Today reports a total of 21aths 9 of which are linked to SST [2]; noting, that Mrderson reports 16 deaths, of which 10 were from SCTthout an identifiable source. The NCAA football injuryrveillance document published in 2007, which includesta though the 2004 season and discusses concussiond heat illness, does not even mention SCT in the 12-ge record [3]. Several literature searches for these dataoduce only an editorial from Current Sports Medicineports [4]. This article lists the same numbers as Mrderson but cites the sole source as a January 2010esentation given by . . . you guessed it . . . Mr Anderson!sed on these discrepancies, using this misleading data toke a sweeping policy change before NCAA confirma-n and publication is premature and impulsive. In addi-n, the numbers are only for Division I football, and theures are not broken down by gender or race. Because theta collection was limited to football, one would safelyume that the deaths were all men, and, based onormation obtained from another one of Mr Andersonsevious presentations, most if not all, were African Amer-n. These specifics, if true, do make a good case forting all African American NCAA Division I footballyers for SCT. However, the data provided by my col-Magalski A, Maron BJ, Main ML, et al. Relation of race to electrocardio-graphic patterns in elite American football players. J Am Coll Cardiol2008;51:2250-2255.Eichner ER. Sickle cell trait in sports. Curr Sports Med Rep 2010;9:347-351.

    propriately. One could compare a similar scenario ofiversal precautions for bloodborne pathogens in health-e. Despite strict Occupational Safety and Health Ad-nistration standards to protect both the provider andpatient against diseases such as human immunodefi-

    ncy virus and hepatitis, there are still a number oforted cases secondary to exposure each year. If thoseividuals infected did not wear gloves or use the appro-

    iate universal precautions when the exposure occurred,u cannot fault the system but rather the individual.ilarly, if a team or military unit is not following guide-

    es for hydration and a death occurs, then this is not alure of the structure but a human error in choosing toregard the system. Even the American Society of Hema-ogy in a September 2010 meeting reports the militaryperience suggests that prevention of complications inllege athletes should be possible by applying universalecautions without the need to single out affected indi-uals for specific treatment [5].The question of discrimination, although addressed byAnderson, is still more speculation than fact. Althoughdoes site references that state no discrimination haser occurred, I would challenge, how do they reallyow? These scenarios are often played out in a way thaten the athlete is not aware of being the victim. In anye, I introduced the issue as a possibility and one that Ilieve in reviewing the data unarguably and unfortu-tely still exists.In conclusion, I do believe that there is a place for SCTting in athletics. However, those creating policy needmoreearch and information to answer the question, what is thest effective application of these resources? Referring backthe American Society of Hematology, which concluded itsrkshop by stating, Given that SCT affects approximatelyillion individuals in the United States, this may be an

    ue of genuine public health concern. It is very clear,cessed November 2010.USA Today. Lawsuit prompts NCAA to screen athletes for sickle cell.

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    174 Anderson et al SICKLE CELL TRAIT SCREENING FOR DIVISION I ATHLETEStain conditions that have such a high degree of morbidityt they necessitate appropriate screening for the safety ofathlete or patient. For example, it obviously would not bee for a football player to play with an acutely torn anteriorciate ligament, so all reasonable injury monitoring pro-ms will monitor for anterior cruciate ligament tears. Onother side of the injury spectrum, although glaucoma is a

    ndition that would present an athlete with an increasede of morbidity, it is uncommon enough in young athletesthat glaucoma is not a condition that is regularly checkedinjury monitoring programs. The key question for thisint/Counterpoint, then, is whether SCT is more similar toL injuries or to glaucoma.One of the challenges in answering this question is inowing the actual numbers of athletes affected. Injury mon-ring for NCAA Division I football players is quite good, atst compared with other sports, but, even so, the crux of theagreement between our 2 discussants was largely based onispute on the actual injury rates. Another issue that needsd even deaths in athletes, yet is not routinely tested inletes. Similarly, obstructive sleep apnea may also be anue. So may some of the more mild forms of osteogenesisperfecta. Even if all of these conditions are reasonable toeck in isolation, the aggregate cost of testing for all of thesenditions may not be, either because of cost or because ofministrative burden.On some level, testing athletes is a zero sum game, be-se we do not have infinite resources for testing all condi-ns, so I would argue that there are 2 thresholds that need tocrossed before we justify testing. First, is there a prevent-le morbidity that could be reduced with testing? Second, iss the particular issue that we should be addressing or arere more pertinent issues that have a higher morbidity?Does SCT testing meet either of these thresholds? Scottderson makes a compelling case that it does, and Jeanneperak presents a compelling argument that it does not. Ins case it is left for you, the reader, to decide.Available at: November 2010.Randall D, Ferrara M, Agel J, et al. Descriptive epidemiology of collegiatemens football injuries: National Collegiate Athletic Association injurysurveillance system, 1988-1989 through 2003-2004. J Athl Train 2007;42:221-233.

    4. McGrew CA. NCAA football and conditioning drills. Curr Sports MedRep 2010;9:185-186.

    5. Framing the research agenda for sickle cell trait: NHLBI workshop focuses oncurrent scientific understanding of the health implications for individuals withSCT. Available at: Accessed November 2010.

    ary Chimes, MD, PhD Responds

    sting for SCT is a contentious issue among sports medicinenicians, and I thank Scott Anderson and Jeanne Doperakappropriately establishing the parameters for the discus-n. Both of them raise important issues that are relevant forth sports medicine clinicians and for clinicians at large;mely, what is the appropriate threshold for monitoring forondition with potential morbidity?I believe we would all be in agreement that there are

    consideration is the total cost of monitoring, not just for SCT,but for all conditions. For the sake of argument, let us assumethat we agree that SCT is something that should be moni-tored. However, there may be other conditions that havesimilar rates of morbidity but that have not yet been broughtto the public attention, because there have not been high-profile deaths. For example, it is likely that a bleeding disor-der such as von Willebrand disease has associated morbidity


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