Exertional Collapse and Sickle Cell Trait in a College Football Player
A 19-year-old college linebacker with known sickle cell trait (SCT) collapses during the first preseason practice in August (heat index 92°F, high humidity). He had been doing conditioning drills and complained of leg cramps and "feeling winded" before going down. He is conscious but in severe pain, with board-like bilateral thigh and low back pain, and is unable to stand. Temperature 99.8°F, HR 128, BP 118/70, respirations 30, SpO2 94% on room air. He is alert and oriented. He has no prior history of crisis. The team physician is on site; a sickle cell rapid test is not available, but his SCT status is documented in his records.
1. What is the leading diagnosis, and how do you distinguish it from heat stroke and from rhabdomyolysis alone?
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Leading diagnosis: exertional sickling (sickle cell trait–associated exertional collapse), with early rhabdomyolysis. The picture - SCT, high-intensity conditioning in heat, leg cramps progressing to severe pain and inability to continue, normal or near-normal temperature, and high respiratory rate - is the classic exertional sickling presentation. It is a medical emergency and a leading cause of death in athletes with SCT.
Versus heat stroke: core temperature here is normal (99.8°F). Heat stroke requires core temp >104°F with CNS dysfunction. This patient is oriented and afebrile, which argues strongly against heat stroke - though the two can coexist and cooling should not be withheld if there is doubt.
Versus rhabdomyolysis alone: rhabdomyolysis is almost certainly present (severe muscle pain, dark urine to check, CK will be high) and is part of the syndrome, but isolated exertional rhabdo does not fully explain the acute collapse with respiratory distress and the SCT substrate. Exertional sickling causes microvascular occlusion, muscle ischemia, and a compartment-syndrome-like picture, and can progress to acute chest syndrome and multiorgan failure.
Do not miss: compartment syndrome (check compartment pressures if pain is disproportionate, tense compartments, or pain with passive stretch), acute chest syndrome (hypoxia, chest pain, infiltrate), and cardiac events.
2. Outline the immediate management and the prevention plan for the rest of the season.
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Immediate management:
- Stop activity and remove from heat; do not let him "walk it off."
- High-flow oxygen (15 L/min by nonrebreather) - oxygen is a mainstay because it reduces sickling.
- Aggressive IV isotonic fluids (e.g., normal saline) to maintain perfusion and urine output; avoid hypotonic fluids and avoid overhydration.
- Monitor and treat for rhabdomyolysis/AKI: urinalysis, CK, creatinine, electrolytes; maintain urine output.
- Assess for compartment syndrome with serial exams and compartment pressures as indicated; surgical consultation if pressures are elevated.
- Transport to the ED for monitoring, serial labs, and evaluation for acute chest syndrome (chest imaging, pulse oximetry).
- Do not give antipyretics for fever unless there is a separate indication; there is no role for routine exchange transfusion in a mild episode, but severe acute chest syndrome or multiorgan failure warrants hematology involvement and consideration of transfusion/exchange.
Prevention for the season:
- Gradual acclimatization to heat and conditioning over 2–4 weeks; avoid timed "all-out" sprints and serial maximal efforts, especially early in preseason.
- Hydration and rest breaks; modify drills in high heat index.
- Education of the athlete, coaches, and athletic training staff about the warning signs (cramping, unusual breathlessness, pain) and the instruction to stop immediately.
- Do not restrict participation solely on the basis of SCT - with precautions, athletes with SCT can compete. Universal precautions (acclimatization, hydration, pacing) benefit all athletes.
- Ensure an emergency action plan and oxygen availability at all practices.