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Pearls and Pitfalls

2010; Lippincott Williams & Wilkins; Volume: 9; Issue: 1 Linguagem: Inglês

10.1249/jsr.0b013e3181caa9fa

1537-8918

E. Randy Eichner,

Injury Epidemiology and Prevention

INTRODUCTION Exertional sickling was recently in the news, with NFL Pittsburgh Steelers safety Ryan Clark, who has sickle cell trait (SCT), told by his coach to skip the game against the Broncos in the mile-high altitude of Denver. When Clark played in Denver in 2005, he was diagnosed with a "splenic contusion." When he played in Denver in 2007, he experienced a sickling splenic infarct, developed a bacterial abscess in the necrotic spleen, had a splenectomy (and later a cholecystectomy), and lost the rest of that football season. Clark's dilemma - whether to play football again in Denver - has spurred discussion and debate among sports medicine physicians. SCT is rightly in the news because exertional sickling, which can cause fulminant ischemic rhabdomyolysis, is the leading killer in NCAA football conditioning/training, likely accounting for 8 of 20 NCAA football conditioning/training deaths this decade. This article examines SCT pearls and pitfalls. PEARL: EXERTIONAL SICKLING COLLAPSE IS AN INTENSITY SYNDROME Army research found that SCT increased the risk of sudden exercise-related death approximately 30-fold in military recruits. Later Army research identified the major syndrome as fatal rhabdomyolysis, the risk of which was increased approximately 200-fold in recruits with SCT (4,5). It was hypothesized that the trigger for the sickling event was exertional heat illness (EHI), but an analysis of 30 such cases suggests that many had only the physiologic hyperthermia of their exercise (1). Also, Army efforts to prevent recruit sickling deaths by precautions to prevent EHI brought mixed results: no sickling deaths were seen during the decade-long study (never published), but deaths began to occur again after the study ended. The setting and clinical features of exertional sickling collapse in athletes suggest that EHI per se is not the trigger. These collapses occur year round, in diverse climates and settings, including cool days in the mountains. Often, the athlete is out of an air-conditioned building only briefly, on the first day of football conditioning, for example, running only 800-1600 m before the collapse (1,3). The forces that cause exertional sickling - hypoxemia, lactic acidosis, muscle hyperthermia, and red-cell dehydration - come from intensity. Exertional sickling is an intensity syndrome, not an EHI. Heat/dehydration is no more the trigger than is thin mountain air, uncontrolled asthma, or a relentless coach. PITFALL: SICKLE TRAIT DOES NOT INCREASE THE RISK OF HEAT STROKE Contrary to common belief, SCT is not a risk factor for exertional heat stroke (EHS). In a 14-yr study of African-American recruits at Parris Island, 1500 with SCT versus 36,325 without SCT, the rate of EHI was identical in both groups, that is, 1 in 200 (5). The same researchers also examined emergency department visits and hospitalizations and found no evidence that SCT increased the risk of EHI in recruits. No good reason supports the belief that SCT increases the risk of EHS. So when, for example, an African-American football player with SCT collapses while running repeat sprints uphill and is transported fairly quickly to an emergency department, where his rectal temperature is 102.4°F, it is not accurate for the medical examiner to classify the death as caused by complications of EHS and list SCT as a risk factor for that EHS. It is far more likely that the death was caused by metabolic complications of exertional sickling, and the body temperature was physiologic - the temperature one would expect when a 300-lb football player runs repeat uphill sprints on a warm day. PEARL: EXERTIONAL SICKLING HAS A BROAD SCOPE Exertional sickling has killed many military recruits and football players in college, high school, and younger. It has killed basketball players in training, a boxer in a bout, and a man swimming in the ocean. It has killed firefighter and police recruits in training, National Guard and military men doing annual fitness or middle-distance runs, a juvenile-boot-camp adolescent doing an induction run, men running from police, and a Naval Academy midshipman doing a 1.5-mile timed run. It caused the collapse with major complications of a Homeland Security officer in a team competition at altitude, as well as similar collapses in cadets at the Air Force Academy. Recently, exertional sickling killed a college student forced to exercise in fraternity hazing. Non-fatal sickling collapses have occurred in college football and basketball and in middle-distance racing. Surely many cases go unreported. The scope of exertional sickling is broad (8,9). PITFALL: EXERTIONAL SICKLING IS UNDERDIAGNOSED Fatal exertional sickling is underdiagnosed. Why? Because too often a sickling death is misdiagnosed as a death from EHS or hypertrophic cardiomyopathy (HCM). In fact, HCM is likely overdiagnosed as a cause of death in African-American male football and basketball players. For example, in an often-cited study of 134 "cardiovascular deaths" in young competitive athletes, most deaths were in football and basketball, and the most common cause of death was HCM. Nearly half of the African-American male athletes died from "HCM" versus only one quarter of the white male athletes - this despite HCM being equal in incidence at birth in both populations. Only one death was attributed to exertional sickling (7). A similar study of 136 athletic deaths - likely including many of the same athletes as the often-cited study - attributed 7 (5%) of the 136 deaths to exertional sickling (10). Why the sharp racial discrepancy in HCM deaths in the often-cited study? Likely answer: HCM was overdiagnosed in African-American male athletes who had athlete's heart but died of exertional sickling. Seek not, find not. Studies suggest that in African-American male athletes, compared with white counterparts, hearts are normally larger, with thicker walls (2,6). It seems that exertional sickling deaths in African-American men are too often misdiagnosed as HCM. PEARL: EXERTIONAL SICKLING DEATHS ARE PREVENTABLE We can prevent exertional sickling collapses and deaths in athletes. Elsewhere, I have outlined simple precautions that enable athletes with SCT to thrive (3). To end these tragic deaths, we need to 1) confirm newborn SCT status or screen athletes for SCT, 2) modify training so that athletes with SCT can achieve their best safely, and 3) educate!