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

Case Presentation

A 19-yr-old African American football player in Texas collapsed during training. His medical history included seasonal allergies and "fatigue and shortness of breath with exercise" at the age of 13 yr—which may have been exercise-induced asthma—when he started playing baseball. He did not use tobacco, drugs, or alcohol. An aunt had SCT, but neither he nor the university knew he had SCT.

The collapse occurred during a late September conditioning workout. The workout began at 4:00 p.m. with weight lifting indoors. At 4:30 p.m., the athletes went outdoors for sprints. The player was apparently healthy when he took the field for the conditioning run. The climate was mild; the turf temperature was 76°F with mild wind.

The player ran 16 sprints of 100 yd each. Rest breaks were 1 min between each of the first four sprints, 2 min between each of the next four sprints, and l min between each of the last eight sprints. The player may have struggled and lagged behind teammates (media report) in the final sprints. By about 4:55 p.m., he completed the sprints and complained of shortness of breath and lower extremity discomfort. He was alert at first, but over the next 10 min became lethargic, so the university emergency medical service (EMS) was called. The player was conscious and breathing rapidly. His legs were too weak to support his weight, so he was loaded onto a cart and driven to the training room, where his legs were elevated and he was given supplemental oxygen and ventilated via a bag-valve mask. At 5:12 p.m., the university EMS arrived, gave 100% oxygen via a bag-valve mask, started intravenous fluids, and called the Fire Department EMS.

At 5:28 p.m., the Fire Department EMS arrived. By then, he was unconscious and unresponsive to pain, with sluggish pupils, shallow respirations, not moving extremities, and a Glascow coma score of 3. His blood oxygen saturation by pulse oximetry on ambient air was 62% and on high-flow oxygen increased to 100% within 3 min. He was nasally intubated. EKG showed sinus tachycardia and peaked T waves in leads V2-V3. He was rushed to the hospital, arriving in the emergency room at 5:52 p.m., where initial blood pressure was 151/49 mm Hg, pulse 126 min,−1 respirations 30 min−1, and temperature 97°F (site not specified).

Initial laboratory work showed a profound lactic acidosis: arterial blood gas at 7 p.m. showed pH 7.05, PCO2 45 mm Hg, PO2 540 mm Hg, HCO3 13 mEq·L, lactic acid 33 mmol·L−1 (upper limit of normal (ULN) = 2.2 mmol·L−1), and serum bicarbonate 8 mEq·L−1 (lower limit of normal (LLN) = 24 mEq·L−1). There was evidence for acute rhabdomyolysis: elevated serum myoglobin 7485 ng·mL−1 (ULN = 72 ng·mL−1), serum creatine kinase 536 U·L−1 (ULN = 220 U·L−1), serum phosphorus 12.8 mg·dL−1 (ULN = 4.5 mg·dL−1), and serum potassium on the high side at 5.2 mEq·L−1 (ULN = 5.1 mEq·L−1). There was evidence for acute renal failure (serum creatinine elevated at 2.3 mg·dL−1) and DIC (prothrombin time 23 s, partial thromboplastin time 84 s, fibrinogen 87 mg·dL−1, and fibrin split products >20 μg·mL−1). Chest x-ray was normal; EKG showed peaked T waves. A serum drug screen was negative and cerebrospinal fluid was unremarkable. White blood cell count was 9700 mm−3, with a left shift in the differential count. Hemoglobin was 14.5 g·dL−1 (but hours later fell to a nadir of 4.3 g·dL−1), and platelet count was 149,000 mm−3.

Consultations included cardiology, who did bedside echocardiography and thought the primary problem was not cardiac; neurology, who did the lumbar puncture and an electroencephalogram that showed no epileptiform activity; neurosurgery, who thought no surgical intervention was needed; and infectious disease, who treated him with antibiotics for possible septicemia.

Through the evening and night, he remained unresponsive and bled copiously from the nose and venipuncture sites. His lower extremities were repeatedly described as "rigid" and "stiff" and "unable to bend." He was given intravenous fluids, started on renal dialysis by nephrology consultants, and transfused with 20 U of fresh frozen plasma, 10 U of red blood cells, and 4 U of platelets. Serum creatine kinase rose to >41,000 U·L−1 (the top level on their test scale) by 10:27 p.m., confirming fulminant rhabdomyolysis. Hyperkalemia was refractory, with serum potassium rising to 7.1 mEq·L−1 by 8:27 p.m. and to 9 mEq·L−1 2 h later. He died about 15 h after admission. It seems very likely that the proximate cause of death was a hyperkalemic cardiac arrhythmia. The terminal rhythm was pulseless electrical activity.


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