Sickle Cell Trait and Fatal Rhabdomyolysis in Football Training: A Case Study

Mary L. Anzalone; Valerie S. Green; Maximillian Buja; Luis A. Sanchez; Rajesh I. Harrykissoon; E. Randy Eichner


Med Sci Sports Exerc. 2010;42(1):3-7. 

In This Article


This college football player collapsed with fulminant rhabdomyolysis after running 16 successive sprints of 100 yd each in training at sea level in a mild climate. The setting, the clinical features, the laboratory profile, and the clinicopathological correlation strongly suggest that the fulminant rhabdomyolysis was ischemic, from exertional sickling. No exertional heat illness (EHI) was present, although the player's body may have encountered measurable heat strain. He rapidly developed profound lactic acidosis, hyperkalemia, acute myoglobinuric renal failure, and DIC. The player died 15 h after hospital admission, likely from cardiac arrhythmia from refractory hyperkalemia. No one knew he had SCT, and it seems likely that the treating physicians were initially unclear as to what may have caused his collapse.

This medical emergency, sudden collapse from fulminant rhabdomyolysis without EHI and coincident with apparent exertional sickling, is similar to the collapse syndrome first reported in seven vigorously exercising military recruits and cadets.[10,13] It is also similar to the fatal sickling collapses of at least 14 other college football players with SCT, the first in 1974.[4,5,7] Although some of these football players collapsed during or immediately after intense football drills (e.g., rapid tempo, multiple station, or "mat drills"), most of them, like the player herein, had been running serial sprints (some on day 1 of summer practice), collapsed after only 800-1600 m of sprinting, and had no evidence of EHI.[4,5,7,18]

Controversy exists on the role of EHI in exertional collapse for those with SCT. US Army researchers found that the risk of sudden unexplained death during basic training was 40 times more common for black recruits with SCT than for all other recruits.[11] In follow-up analyses, Gardner and Kark[8] and Kark and Ward[12] found that exercise-related death in black recruits with SCT was 30 times more common than in black recruits without SCT and concluded that EHI was a culprit in SCT deaths. They outlined 30 SCT exercise collapses (21 fatal) and concluded that EHI was present in 22. However, only 2 had temperatures as high as 105°F, 2 were at 103-104°F, 16 were at 102°F or lower (7 of these were 99°F or lower), and 10 had no temperature recorded.[12] Gardner and Kark[8] detailed the collapse and death of a soldier with SCT who marched 3 miles on a cool morning. The clinical course was classical for fulminant rhabdomyolysis, and rectal temperature on collapsing was only 98°F. Accordingly, the data do not support that collapse was prompted by EHI. Considering the study of the aforementioned 30 cases, although 102°F, for example, implies measurable heat strain, it seems likely that many of the SCT collapses analyzed were associated not really with EHI but only with the expected physiologic hyperthermia of strenuous exercise. These authors do note that most SCT deaths they studied were from acute rhabdomyolysis and that the risk of fatal exertional rhabdomyolysis is increased about 200-fold in SCT.[8,12]

Gardner and Kark[8] and Kark and Ward[12] went on to show that measures to prevent EHI could decrease SCT-related deaths. Preventive measures included decreasing exercise intensity and increasing rest cycles and hydration as ambient temperatures rose. It seems likely that these precautions decreased SCT-related deaths in basic training, not so much by preventing EHI but more by making the exercise easier-and so decreasing the forces that foster sickling-just as breathing supplemental oxygen when exercising at altitude would decrease SCT-related deaths. Recent data suggest the SCT death rate may be increasing again in the US Army.[19]

Strenuous exercise evokes four forces that in concert are proposed to foster sickling in SCT: 1) severe hypoxemia, 2) metabolic (lactic) acidosis, 3) hyperthermia in working muscles, and 4) red cell dehydration, as red cells lose water traversing the hyperosmotic milieu of the working muscle.[5] Exercise physiology research shows that in SCT, during intense exertion and hypoxemia, sickle cells can accumulate in the venous blood and that systemic dehydration increases heat strain and worsens exertional sickling.[1,17] These and other factors that contribute to exertional sickling collapse are detailed elsewhere.[4,5,7] Field studies in Africa suggest that SCT runners are limited not in single sprints but in middle distance or altitude running.[16] The pattern in American athletes seems similar.

This case study focuses on football because at least 15 college football players with SCT have died in training with apparent concomitant exertional sickling. Similar collapses have resulted in death in football players in high school and as young as 12 yr. Several nonfatal collapses with sickling in football training also exist.[2] Collapse with sickling but not EHI has also occurred in distance racing or running[3,9,14] and has resulted in hospitalization or death of college or high school basketball players (two were young women) in training,[4,5,7] typically during intense sprints on the court or while running laps on a track. In 2008, a Golden Gloves boxer with SCT died after a collapse (associated with sickling) evoked by a three-round bout. A near-fatal collapse associated with sickling was recently reported in a police academy cadet with SCT who tried to run 1.5 miles.[15] Evidence suggests that the harder and the faster these athletes go, the earlier and the greater the apparent sickling. Symptoms of suspected sickling can begin in only 2 to 3 min of sprinting or in any other all-out, sustained exertion, and analysis of collapses in SCT athletes suggests that sickling can quickly increase to grave levels if the stricken athlete struggles on or is urged on by the coach.[5,7]

In our opinion and field experience, screening and precautions can prevent sickling-associated collapse and death in sports. Precautions are detailed elsewhere,[7] but in general, the evidence suggests that the SCT athlete should build up slowly in training, tempo of drills should be slowed, and longer periods of rest given. The SCT athlete should run no timed serial sprints or miles and should avoid lengthy, sustained sprints or any all-out exertion beyond 2 to 3 min without a rest. Work/rest cycles should be adjusted for heat and altitude. The athlete should stay hydrated, and any asthma must be controlled. The emphasis with coaches should be that if SCT athletes can set their own pace, they seem to do fine; moreover, if any STC athlete begins to struggle in any drill, the drill should be stopped and medical attention should be prompt. It is critical for coaches and medical support staff to appreciate that prompt action can save a life. We suggest to have the athlete lie down, check vital signs, give supplemental oxygen by face mask, cool the athlete if necessary, and failing immediate improvement, call 911, attach an automated external defibrillator (AED), start an intravenous line with normal saline solution, get the athlete to the hospital quickly, and tell the emergency room doctors to expect fulminant rhabdomyolysis and its grave metabolic complications.[7]


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