Case Presentation:
A 30‐year‐old man African American with sickle cell trait presented to the ED with a complaint of lower back muscle spasms that began near the end of a basketball game earlier that day. Exam revealed an afebrile well‐developed man with bilateral paraspinal muscle tenderness. Labs showed an elevated CPK at 1871 units/Liter, a normal serum K and Phos, and a Cr of 1.3 mg/dL. Urine dipstick demonstrated large heme and urine microscopy showed few RBCs. He was given intravenous fluid and then discharged from the ED with diazepam and oxycodone acetaminophen for presumed muscle spasms resulting in mild rhabdomyolysis. He returned 2 days later with increasing back pain, difficulty staying hydratec due to nausea, and new onset of tea‐colored urine. Repeat CPK was 50,522 units/Liter and Cr was 1.1 mg/dL. He was admitted for continuous intravenous hydration, pain control, and monitoring of his renal function. He developed fevers 2 days into his stay and continued to have severe back pain. An MRI of the lumbar spine showed findings consistent with rhabdomyolysis versus myositis. A muscle biopsy showed acule muscle degeneration without evidence of infection. His fevers subsided over the next few days as did his pain. His CPK dropped below 5000 units/L 9 days after his initial presentation.
Discussion:
Sickle cell trait (SCT) is a risk factor for acute exertional rhabdomyolysis (AER). Traditionally, individuals with sickle cell trait were thought to have minimal attributable clinical manifestations. However, a growing number of case reports of exercise induced rhabdomyolysis in patients with SCT demonstrate the increasing awareness of the associated morbidity. lt is likely that patients with SCT are susceptible to erythrocyte sickling and the resullanl microvascular occlusions when under severe hypoxic stress brought on by vigorous exercise and volume depletion. Treatment is supportive with intensive intravenous fluid to maintain high urine output, supplemental oxygen in the acute setting, monitoring of electrolytes and minerals, and pain control. Other causes of exercise related rhabdomyolysis should be considered including metabolic myopathies (example: carnitine palmitoyltransferase deficiency), hypokalemia or hypophosphatemia, and compartment syndrome. Risk factors for AER include high ambient temperatures, training at altitude, deconditioned individuals, and volume depletion. Although AER is uncommon, patients with known sickle cell trait should be warned of its possibility and recurrence and be advised to stay well hydrated during their time of exercise and stop exercising if severe muscle pains occur.
Conclusions:
Physicians caring for African American patients with exercise induced rhabdomyolysis should have a high suspicion of SCT associated AER and appropriately advise these patients on methods of future risk reduction.
Author Disclosure:
J. Dick III, none.