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

Abstract and Introduction


We report the athletic, the clinical, and the pathological details of a case of fatal rhabdomyolysis during training in a college football player with sickle cell trait (SCT) who collapsed minutes after running 16 successive sprints of 100 yd each. The player, 19 yr old, African American, was apparently healthy when he took the field for the conditioning run. No exertional heat illness was present. After collapsing on-field, the player soon went into coma and developed fulminant rhabdomyolysis, profound lactic acidosis, acute myoglobinuric renal failure, refractory hyperkalemia, and disseminated intravascular coagulation. Despite intensive care in the hospital, he died about 15 h after admission, likely from a hyperkalemic cardiac arrhythmia; the terminal rhythm was pulseless electrical activity. The forensic autopsy confirmed that the cause of death was acute exertional rhabdomyolysis associated with SCT. Counting this case, at least 15 college football players with SCT have died from complications of exertional sickling, as have younger football players and other athletes. In SCT, maximal, sustained exercise evokes four forces that can foster sickling: hypoxemia, acidosis, hyperthermia, and red cell dehydration. The setting, the clinical and laboratory features, and the clinicopathological correlation here suggest that the fulminant rhabdomyolysis and its fatal sequelae were from exertional sickling. These data suggest that screening and simple precautions for SCT may be warranted to prevent tragedies like this and enable all athletes with SCT to thrive in their sports.


Sickle cell trait (SCT) is common and generally benign. More than 3 million Americans have SCT-about 1 in 12 blacks and between 1 in 2000 and 1 in 10,000 whites-and almost all live normal, healthy lives. However, for some carriers, SCT can pose clinical problems. As they grow older, many SCT carriers lose the ability to concentrate fully the urine; this usually is harmless. Two other clinical complications in SCT-splenic infarction at altitude and intermittent gross hematuria-are not life threatening and are covered elsewhere.[6] Some athletes with SCT, however, develop a syndrome that can be grave or even rapidly fatal: fulminant exertional rhabdomyolysis.

Fulminant rhabdomyolysis is an underrecognized and misdiagnosed cause of sudden collapse in sports. Among 136 well-studied, sudden, nontraumatic sports deaths in high school and college athletes over a decade, the third most common cause of death, behind cardiovascular conditions and heatstroke, accounting for 5% of the deaths, was sickling-associated rhabdomyolysis.[20]

Sudden death in SCT was first reported in 1970 in four recruits undergoing Army basic combat training at an altitude of 4060 ft.[10] One recruit died of what seemed to be an acute coronary event, but in three recruits, profound metabolic acidosis and early hyperkalemia (plus peaked T waves on electrocardiogram [EKG] in one) suggested that fulminant, sickling-associated rhabdomyolysis played a role in the deaths. Four similar cases were soon reported from the US Air Force, two recruits in basic training (not at altitude) and two cadets at the Air Force Academy (7200 ft). Three survived. All four had exertional rhabdomyolysis, hyperkalemia, disseminated intravascular coagulation (DIC), and acute myoglobinuric renal failure requiring dialysis.[13] All seven of these recruits or cadets with SCT were exercising vigorously when they collapsed, but none had heatstroke. Rectal temperatures were normal or mildly elevated; the highest being 102°F.[10,13] The four men in the second report were the only ones hospitalized for rhabdomyolysis and renal failure, among thousands of trainees subjected to the same physical and environmental stresses, leading the authors to conclude that major exertional rhabdomyolysis may be more likely to occur in trainees with SCT.[13]

Exertional sickling without major heat stress seems also a likely cause of collapse from fulminant rhabdomyolysis in some athletes with SCT. Counting this case, at least 15 college football players have died from complications associated with SCT, as have younger football players and other athletes.[4,5,7] The typical SCT syndrome is demonstrated by this case of a college football player in training.


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