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Keywords

Clinical Practice in Athletic Training

Abstract

Background: Sickle cell trait (SCT) is associated with an increase in muscle breakdown after strenuous exercise due to improper blood flow to active muscles. Evidence suggests that individuals with SCT can increase muscle breakdown during exercise by as much as 54%. This case outlines a 21-year-old African collegiate sprinter with SCT who reported feeling a “pop” in her right hamstring that caused her to stop running mid-race. She reported that no pain was associated with the “pop” but was scared by the sensation. Evaluations of strength and range of motion were all unremarkable and there were no palpable deformities. She continued in her sport for 3 months until she suffered a similar injury on the left hamstring, again with an unremarkable evaluation. Because of a history of hamstring strains, she was referred to the team physician, where inflammation and a hardened nodule on the earlier-injured right hamstring led to ordering of bilateral magnetic resonance imaging (MRI). Differential Diagnosis: Hamstring strain, avulsion injury, hamstring tendinitis, adductor strain, and myositis ossificans were suspected. Treatment: The MRI revealed bilateral Grade 2 hamstring strains with evidence of prior ruptures in the mid-belly of the right hamstring, along with myositis ossificans (MO) and hematoma. The hematoma was aspirated, and the athlete began a rehabilitation protocol to get her back to running activity. However, after 2 months, the athlete was referred for a 2nd MRI due to an inability to sprint at full speed without pain. This MRI revealed that the MO and strain were still present, warranting a platelet-rich-plasma (PRP) injection to improve healing. Following the injection, the athlete returned to running for 3 months; however, she was unable to fully sprint without pain. A subsequent ultrasound showed that the MO had grown, and the decision was made to surgically remove the MO, followed by a rehabilitation program centered around restrengthening the hamstring. After 4 months of this program and running with the athletic trainer, she returned to practicing with the team. A month following the athlete’s return to sport, she felt a “pop” in her right quadricep while performing a reverse lunge. She was referred to the team physician, where a 3rd MRI scan was ordered. This scan revealed a Grade 2 strain in her rectus femoris with the presence of MO. This 2nd incidence of MO led to a consideration by her team athletic trainer that SCT might be a contributing factor to its development. Taking this into account, a PRP injection was administered to the quadriceps with the intent that the calcium deposits would resorb. The athlete began restrengthening exercises and a running progression that involved the use of an Alter-G treadmill, coupled with ample rest and hydration periods to combat a potential sickling event. Within 3 months from the PRP, she was able to fully compete. Uniqueness: There is scant research on myositis ossificans for athletes with SCT. The athlete in this case had repetitive tissue damage and the presence of MO, which may be related to muscle breakdown as a result of harboring SCT. Furthermore, this athlete did not initially present with common symptoms of a hamstring strain such as immediate pain, swelling, tenderness, palpable defect, and loss of function. The subsequent calcification that occurred in the rectus femoris created a potential link for MO and SCT given the 2nd incidence in a short time. Conclusion: This case describes a 21-year-old African sprinter with SCT, and multiple incidences of MO. Establishing if a link exists between MO and SCT could help provide better care for athletes harboring the SCT gene.

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