| || |Figure 1:
Proton density fat-saturated coronal MRI positive for osseous edema (double arrow) in proximal right femoral shaft with low-level periosteal reaction 13 cm below the level of the hip joint. No fracture line is visible. Findings are consistent with a stress reaction or early stress fracture.
Stress fractures were first reported by Briethaupt1 in 1885 when he described fifth metatarsal stress fractures in Prussian Army recruits. Devas2 and Devas and Sweetnam3 first described this condition in athletes in 1956 and 1958. Stress fractures occur from repetitive stress on dynamic bone with a maladaptation in which osteoclastic activity overpowers osteoblastic activity, leading to fatigue failure injuries. The stress injury is a result of excessive strain, recurring microdamage, and the inability to repair, or depressed bony remodeling in response to a normal strain.4 A stress reaction precedes a stress fracture and is defined as bone microfailure without cortical disruption.5 In a review of 320 stress fractures, Matheson et al6 reported a distribution of 49.1% located in the tibia, 25.3% in the tarsals, and 8.8% in the metatarsals. Johnson et al7 found that the stress fracture rate in collegiate male athletes was highest in track and field (9.7%), followed by lacrosse (4.3%), crew (2.4%), and football (1.1%). There is a great deal of literature regarding treatment of the more common stress injuries; however, the literature is sparse in regard to treatment of proximal femoral shaft stress reactions. To our knowledge, there are no previously reported studies in the literature regarding a proximal femoral shaft stress reaction/fracture in a professional football player, including imaging findings and treatment options.
A professional defensive back presented 1 week after noting mild soreness in the right proximal thigh during practices prior to a regular season game. He described the pain as a dull ache that was worse with running, especially during kickoff coverage plays. Despite the mild ache, he played without any adverse effects to his playing ability. The player felt as if his symptoms were similar to those of a muscle strain. Physical exam revealed pain to palpation deep in the anterior, distal groin region that was worse with resisted hip flexion. He also had pain when flexing the hip and extending the knee in the prone position. There was no pain with resisted sit-up or resisted hip adduction. Neurovascular exam was normal. The clinical diagnosis was a hip flexor strain, and a more thorough imaging work-up was performed for a definitive diagnosis.
Plain radiographs were negative. Magnetic resonance imaging (MRI) was positive for osseous edema in the proximal right femoral shaft with low-level periosteal reaction 13 cm below the level of the hip joint (Figure 1). No fracture line was visible. Findings were consistent with a stress reaction or early stress fracture. A Tc-99m-HDP 3-phase bone scan showed focal abnormal uptake along the medial proximal cortex of the right femoral shaft at the same level (Figure 2). This result corresponded to the abnormality seen on the MRI consistent with a stress reaction/fracture. A computed tomography (CT) scan without contrast with reformatted images revealed a benign periosteal reaction and a small cortical lucency consistent with a stress reaction or early stress fracture (Figure 3).
| |Figure 2:
Tc-99m-HDP 3-phase bone scan showing focal abnormal uptake along the medial proximal cortex of the right femoral shaft at the same level.
The player was instructed to use crutches and remain nonweight bearing on the right lower extremity. A bone stimulator was initiated, and the patient was withheld from lower extremity impact exercises, including football. At 1 week, he had no pain, and the nonweight-bearing status was discontinued. The bone stimulator was continued for a total of 3 weeks. He began to ride a stationary bike 10 days from diagnosis. He remained asymptomatic. Treadmill running was initiated at 2 weeks. Seventeen days postdiagnosis, a functional field progression was begun. The player remained asymptomatic and was slowly progressed to functional activities during practice over the next week. He participated in a game 4 weeks postinjury without recurrent symptoms.
A repeat MRI was completed 5 weeks from presentation (4 days following his first game) and showed no significant change in appearance of the proximal right femoral stress reaction (Figure 4). These imaging findings persisted despite the player remaining symptom free for the remainder of the season. A follow-up MRI was ordered 2 months from the original MRI that showed significant interval decrease in the amount of subperiosteal edema (Figure 5). There was also central resolution of the endosteal edema at the site of the fracture on the prior studies.
Stress fractures are common injuries in athletes, accounting for as much as 10% of all injuries seen by sports medicine physicians.6 Although this may be an underestimate, femoral shaft stress fractures are uncommon and may account for approximately 3.5% of all stress fractures.8,9 Femoral shaft stress fractures occur more commonly in athletes competing in long-distance running, ballet, and jumping.10,11 To our knowledge, there have been no case reports of femoral stress fractures in professional football players. Three main issues are important to review in this case: early diagnosis is the key to the treatment and early return to play; imaging studies lag behind clinical symptoms; and the treatment regimen should consist of a period of rest and be tailored to the individual.
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| Figure 3: CT scan without contrast showing a benign-appearing periosteal reaction and a small cortical lucency consistent with early stress fracture. Figure 4: STIR coronal MRI showing no significant change in appearance of periosteal reaction and bony edema from 5 weeks previous. Figure 5: STIR coronal MRI showing significant interval decrease in the amount of subperiosteal edema. |
We feel the most important lesson learned was the early detection of the stress reaction when only mild symptoms were present. Magnetic resonance imaging confirmed our clinical diagnosis of a hip flexor strain. A bone scan and CT scan were ordered for correlation. We were surprised to find the imaging abnormalities and would suggest ordering early MRI for such symptoms in professional football players. We believe the early detection in the stress reaction phase, before any sign of fracture, afforded accelerated rehabilitation. An early diagnosis is also key to preventing a complete displaced fracture, which has been reported in athletes in the literature.12,13 Forces transmitted to the femur from the activity of the vastus medialis and adductor brevis may increase the risk of fractures in the proximal femoral shaft area. This area is also subject to a high amount of compression strain.11 Therefore, it is easy to see how this injury can be mistaken for a hip flexor or adductor injury and early MRI imaging may be warranted.
Magnetic resonance imaging is an excellent imaging modality for stress reactions/fractures given its high sensitivity, specificity, and ability to image surrounding soft tissues. Short tau inversion recovery and fat-suppressed images are best for seeing early osseous edema.9,14 In our player, the STIR and fat-suppressed images were positive early and allowed early detection and prompt treatment. Stress fractures show resolution of abnormality on STIR images within 6 months in 90% of cases.9 Furthermore, in this referenced study, 7 of 10 asymptomatic patients had normal MRIs by 3 months.9 Our player’s MRI still showed an increased signal on the STIR images at 5 weeks despite no symptoms, but at 2 months was completely resolved. The normalization of the MRI was quick and could be due to the early detection. Repeat MRI is not necessary as treatment should be guided more by patient symptoms.
We were unable to find a standardized treatment protocol to follow in the literature for this injury in professional football players. Ivkovic et al15 presented a treatment algorithm for femoral stress fractures in runners. They discussed a 4-phase treatment plan, with each phase lasting 3 weeks. The athletes were progressed from rest to nonweight-bearing exercises to cross training and then to gradual return to running. Their athletes returned to unrestricted running between 12 and 18 weeks. We believe we were able to be more aggressive in our treatment plan because we diagnosed the stress reaction very early. We found it is important to tailor the treatment protocol to the individual. A period of rest allows bone repair to predominate over resorption.11 The term rest is undefined in the literature. We chose a period of nonweight bearing until the patient was asymptomatic, even on physical examination. This period lasted 1 week for our patient. A structured functional progression was begun under supervision over the next 3 weeks as long as the patient remained asymptomatic. We were prepared to decrease his activity at any sign of return of symptoms. The cross training also allowed some relative rest time and further healing to occur, while maintaining cardiovascular endurance. Other treatment modalities to consider include hormonal or dietary supplements and the use of a bone stimulator. We do not have documented evidence of the utility of a bone stimulator for these acute fractures. O’Brien et al16 discussed the use of a stimulator for treatment of a refractory pelvis stress fracture. In summary, our treatment was not based on a defined time table, but was tailored to the individual and progressed based on symptomatology.
- Breithaupt MD. Zur pathologie des menschlichen fusses. Med Zeitung. 1855; 24:169.
- Devas MB. Stress fractures of the tibia in athletes or shin soreness. J Bone Joint Surg Br. 1958; 40(2):227-239.
- Devas MB, Sweetnam R. Stress fractures of the fibula. J Bone Joint Surg Br. 1956; 38(4):818-829.
- Boden BP, Osbahr DC. High risk stress fractures: evaluation and treatment. J Am Acad Orthop Surg. 2000; 8(6):344-353.
- Diehl JJ, Best TM, Kaeding CC. Classification and return-to-play considerations for stress fractures. Clin Sports Med. 2006; 25(1):17-28.
- Matheson GO, Clement DB, McKenzie DC, Taunton JE, Lloyd-Smith DR, MacIntyre JG. Stress fractures in athletes: a study of 320 cases. Am J Sports Med. 1987; 15(1):46-58.
- Johnson AW, Weiss CB Jr, Wheeler DL. Stress fractures of the femoral shaft in athletes—more common than expected. A new clinical test. Am J Sports Med. 1994; 22(2):248-256.
- Stanitski CL, McMaster JH, Scranton PE. On the nature of stress fractures. Am J Sports Med. 1978; 6(6):391-396.
- Theodorou SJ, Theodorou DJ, Resnick D. Imaging findings in symptomatic patients with femoral diaphyseal stress injuries. Acta Radiol. 2006; 47(4):377-384.
- Arendt E, Agel J, Heikes C. Stress injuries to bone in college athletes: a retrospective review of experience at a single institution. Am J Sports Med. 2003; 31(6):959-968.
- DeFranco MJ, Recht M, Schils J, Parker RD. Stress fractures of the femur in athletes. Clin Sports Med. 2006; 25(1):89-103.
- Farkas TA, Zane RD. Comminuted femur fracture secondary to stress during the Boston marathon. J Emerg Med. 2006; 31(1):79-82.
- Finestone AS, Glatstein M, Novack V, Rath E, Milgrom C. The completely asymptomatic displaced femoral stress fracture: a case report and review of the literature. Mil Med. 2006; 171(1):37-39.
- Datir AP. Stress-related bone injuries with emphasis on MRI. Clinical Radiol. 2007; 62(9):828-836.
- Ivkovic A, Bojanic I, Pecina M. Stress fractures of the femoral shaft in athletes: a new treatment algorithm. Br J Sports Med. 2006; 40(6):518-520.
- O’Brien T, Wilcox N, Kersch T. Refractory pelvic stress fracture in a female-long distance runner. Am J Orthop. 1995; 24(9):710-713.
Drs Webb and Rettig and Ms Hunker are from Methodist Sports Medicine/The Orthopedic Specialists, Indianapolis, Indiana.
Drs Webb and Rettig and Ms Hunker have no relevant financial relationships to disclose.
Correspondence should be addressed to: Patti J. Hunker, MS, Methodist Sports Medicine/The Orthopedic Specialists, 201 Pennsylvania Pkwy, Ste 325, Indianapolis, IN 46280.