Femoral Head Contusion Without Hip Dislocation
Low-Energy Trauma in a Female Basketball Player
Sean T. Bryan, MD; John M. McShane, MD; Mark E. Schweitzer, MD
THE PHYSICIAN AND SPORTSMEDICINE - VOL 30 - NO. 11 - NOVEMBER 2021
In Brief: Femoral head contusions can occur concurrently with knee ligament injuries, patellar dislocations, or traumatic hip dislocations. Posterior hip subluxation is a possible mechanism in the absence of hip dislocation. Clinicians should have a high index of suspicion when evaluating an athlete who has significant hip or groin symptoms, despite having experienced seemingly minor or relatively low-energy trauma. Most patients should respond well to a period of non-weight bearing and a gradual return to exercise, but they may need to be monitored for future avascular necrosis and osteoarthritis in the affected hip.
Bone contusions (bone bruises) are traumatic lesions resulting in edema, hemorrhage, and microfracture of subchondral trabecular bone.1 These injuries frequently occur in conjunction with knee ligament injuries or patellar dislocations2-4 but have also been reported with traumatic hip dislocation.5 Bone contusions are radiographically occult, and their appearance on magnetic resonance imaging (MRI) has been well described. To our knowledge, this is the first reported case of femoral head contusion occurring without hip dislocation.
History. A 19-year-old college basketball player came to our office with pain in her left groin area after sustaining an injury 4 days earlier during a game. She had made a sudden turn to the right while reaching to contest a shot. Her left foot, however, remained planted on the floor. She immediately felt a painful popping in her left groin. Her entire left lower extremity momentarily went numb, then pain radiated from her left groin to her left foot. She did not fall but was unable to continue playing. She had not had any left hip trauma or groin pain prior to this injury.
She had been diagnosed as having right lower-lumbar facet irritation 4 months earlier. Her preparticipation exam noted significant pain with a combination of back extension and lateral bending to the right. Subsequent diagnostic evaluation of her lumbar spine included plain radiographs (they were normal) and a bone scan with single-photon emission computed tomography that revealed no evidence of spondylolysis or abnormal uptake in the left hip. Her back pain resolved after a course of physical therapy.
Four weeks before her left groin injury, she was experiencing left lower-leg and foot numbness. She was diagnosed as having left lower-extremity radiculitis. MRI of her lumbar spine demonstrated an annulus fibrosis tear at L5-S1, with a small central disk bulge. She responded well to a tapering dose of prednisone and physical therapy. Her symptoms had completely resolved 3 days before her left groin injury occurred. She reported no other medical problems, previous surgery, or drug allergy.
Physical exam. She appeared well developed and well nourished. No obvious deformity or swelling of the left hip was detected. Left hip range of motion was full without snapping, clicking, or clunking. Internal rotation caused significant pain. Anterior palpation over the left hip joint also was painful. Muscle strength testing of the left hip flexors, knee extensors, and hip adductors revealed no weakness or pain. Lumbar spine range of motion was full and painless. Bilateral patellar and Achilles deep tendon reflexes were normal and symmetric. Motor and sensory examination of both lower extremities was normal. Dural tension signs were negative.
Diagnosis. Because of clinical suspicion for a hip labrum tear or osteochondral fracture, a magnetic resonance arthrogram of the left hip was ordered. A region of marrow edema in the superior central femoral head consistent with a bone bruise (figure 1) and a possible posterior labrum tear (figure 2) were detected. No evidence of cortical fracture, avascular necrosis, capsular injury, osteochondral defect, or loose body was seen.
Treatment. The patient was given crutches and instructed to refrain from weight bearing for 2 weeks, after which she reported 75% improvement in her symptoms. She then was able to walk without pain, and hip examination revealed only minimal pain with full internal rotation. She was allowed to ride a stationary bicycle, use a stair climber, and shoot baskets, but was restricted from running for 2 more weeks. At 5 weeks postinjury she was asymptomatic, her hip examination was normal, and she was cleared to participate in sports without restriction.
Follow-up. She resumed playing basketball and did well until 11 weeks postinjury, when she came to the training room reporting an achy, throbbing pain in the left groin that increased with running, riding a stationary bike, and inclement weather. Physical examination of the left hip revealed full range of motion, mild pain with internal rotation, moderate tenderness over the anterior aspect of the joint, and a palpable painless anterior snap with flexion, but no clunk. Our concern for avascular necrosis prompted a repeat MRI scan (without intra-articular contrast) 3 months postinjury that demonstrated no evidence of avascular necrosis, osteochondral defect, osteoarthritis, or iliopsoas bursitis. The femoral head marrow edema had resolved completely. Based on this result, we continued conservative treatment, and her symptoms gradually improved over the next month.
We discussed possible increased risk of future hip osteoarthritis and avascular necrosis with the patient and her mother. The patient made an informed decision that she wanted to continue to play sports. We felt it was reasonable for her to do so, provided her symptoms continued to improve, she had no functional limitations, and her symptoms did not acutely worsen. We discussed that hip arthroscopy may be indicated if her symptoms persisted or worsened, or if she developed any mechanical symptoms, because her initial magnetic resonance arthrogram raised concern for a possible labrum tear. At 4 months postinjury, she reported only occasional mild discomfort and no limitations to physical activity.
Finding the Cause
Occasionally, significant trauma to the femoral head and acetabulum can occur without hip dislocation. Four such cases have been reported. Two cases, like ours, involved relatively low-energy trauma. Mody and Wainwright6 reported two cases in women, ages 57 and 53, who had femoral head fractures without dislocation that resulted from tripping and falling.
The other two cases involved high-energy trauma. Van der Werken and Blankensteijn7 described a case of femoral head fracture without dislocation in a 25-year-old man who was struck by a car while riding a moped. Allard et al8 reported a case of acetabular bone contusion, seen on MRI and confirmed by biopsy, in a 65-year-old woman who was in a car accident and experienced recurrent symptoms 4 months later. A repeat MRI performed 7 months posttrauma revealed avascular necrosis of the femoral head. This case raised concern that our patient's femoral head contusion might also lead to avascular necrosis.
Mechanism of injury. Several hypotheses might explain our patient's femoral head contusion. Injury to the femoral head is possible if high forces are transmitted through the long axis of the femur while the femoral head is reduced. However, our patient's left foot never left the ground; therefore, it is extremely unlikely that the axial forces alone reached such a level. Falling directly on the greater trochanter could cause such an injury, but no fall occurred. Our patient's described mechanism likely involved a combination of axial loading and either internal or external rotation acting on her left hip. Simultaneous axial loading and internal rotation with the hip slightly flexed could cause posterior subluxation of the femoral head. In our patient, these forces could have been high enough to cause trabecular injury and possibly a labrum tear, but not high enough to cause cortical disruption or frank dislocation.
To better understand how posterior hip subluxation can cause femoral head contusion, we considered how a posterior hip dislocation could cause femoral head fracture. One possible mechanism is that the femoral head fractures on the way out as it strikes the posterior acetabular ridge. One report7 postulated that at 60° or less of hip flexion, the firm superior portion of the acetabular rim can resist posterior dislocation while causing significant injury to the femoral head. This mechanism probably applies to our patient.
She was standing at the time of injury, and her left foot was on the floor, so her left hip must have been flexed at less than 60°. A posterior hip subluxation also could explain both a posterior labral injury and a sciatic neurapraxia. The symptom distribution of sciatic neurapraxia corresponds to the location of radiating pain and paresthesia reported by our patient. Moreover, superior femoral head contusions have been observed in cases of posterior hip dislocation.5
Our patient's previous L5-S1 disk injury and resultant left lower-extremity radiculitis may have predisposed her to left hip injury. Although she progressed well through a course of physical therapy, she may have had some residual weakness of her left hip external rotator muscles, but we had not tested for that on the previous exam. Residual weakness would have made it easier for her femoral head to internally rotate and posteriorly sublux.
Given that posterior hip dislocation and subluxation are essentially the same mechanism, differing only in the magnitude of force involved, it is highly probable that posterior subluxation can cause femoral head contusions as well. The bone contusion findings in these cases,5 therefore, support our hypothesis of posterior subluxation as her mechanism of injury.
Alternate hypotheses. Conversely, one could postulate that her femoral head subluxated in the opposite direction. Her sudden turn to the right with her left foot planted on the floor could have forced her extended left hip into external rotation, resulting in an anterior subluxation. In this scenario, the femoral head injury could have occurred on reduction. It is unclear to us whether or not reduction forces following anterior hip subluxation are high enough to cause trabecular injury, let alone a posterior labral injury, but it seems unlikely.
Anterior hip subluxation could have placed traction on her femoral nerve. If so, one would expect the distribution of her pain and paresthesia to have included her anterior-medial thigh, not her lower leg and foot as she described. Based on these discrepancies, we contend that the anterior hip subluxation hypothesis is not adequately supported by our patient's history or study findings. Thus, we conclude that the most likely mechanism of injury was posterior hip subluxation.
The patient's injury could also have been complicated by a subtle articular cartilage fissure or flap overlying the bone bruise. Because she did not undergo hip arthroscopy, we cannot conclusively rule out this possibility, but we feel it is highly improbable. Two separate MRI scans were performed, and the first used intra-articular contrast to improve sensitivity for detecting osteochondral lesions. Neither scan demonstrated any evidence of articular cartilage damage; therefore, the existence of such an injury is extremely unlikely.
Theoretically, significant complications associated with bone contusions are possible. Two animal studies9,10 involving rabbits and dogs suggest that bone contusions can lead to osteoarthritis. Because insufficient human clinical data exist, treatment for bone contusions remains controversial. Both MRI scans of our patient failed to demonstrate any evidence of osteoarthritis, and her symptoms were improving. We therefore decided that hip radiographs would be of no added benefit at the time. Based on available data, she may be at increased risk for developing left hip osteoarthritis in the future.
As previously stated, avascular necrosis of the femoral head is a potential complication in our patient. Prednisone therapy for radiculitis may increase her risk of developing avascular necrosis. Given her recurrent symptoms and physical findings at 11 weeks postinjury, a repeat MRI was clearly indicated. This study demonstrated complete resolution of the femoral head marrow edema, confirming the initial diagnosis of a bone bruise. Her subsequent clinical improvement further ruled out the possibility that the initial arthrogram findings represented a variant of avascular necrosis. The question remains whether to just follow her symptoms or to perform a third scan at some designated point, possibly 4 months postinjury (based on the time to onset of avascular necrosis symptoms in the acetabular contusion case), to screen for early necrosis.
Clearly, more clinical data are necessary and would be helpful in making such a decision. For example, a future study might show that when avascular necrosis occurs after a femoral head contusion, it usually occurs at a particular interval. One could then perform a scan early in this period, even in the absence of symptoms, knowing that the less invasive interventions (eg, non-weight bearing, core decompression) tend to have better outcomes when performed early in the course.
Shooting From the Hip
Based on this case, we propose that posterior hip subluxation be considered as a possible mechanism when femoral head contusion is seen in the absence of hip dislocation. A high index of suspicion is needed when evaluating an athlete who reports significant hip or groin symptoms despite seemingly minor or relatively low-energy trauma. Further studies focusing on treatment and long-term outcomes of bone contusions are necessary to help guide clinicians faced with similar cases in the future.
Dr Bryan is an assistant professor of family medicine at the Medical College of Georgia in Augusta and Mercer University School of Medicine in Macon, Georgia, and the director of the sports medicine fellowship for Southwest Georgia Family Practice Residency at Phoebe Putney Memorial Hospital in Albany, Georgia. Dr McShane is a clinical assistant professor and director of sports medicine in the department of family medicine, and Dr Schweitzer is an associate professor of radiology, professor of orthopedic surgery, and director of musculoskeletal imaging in the department of radiology, at Jefferson Medical College at Thomas Jefferson University in Philadelphia. Address correspondence to Sean T. Bryan, MD, 2336 Dawson Rd, Suite 2200, Albany, GA 31707; e-mail to [email protected].
Disclosure information: Drs Bryan, McShane, and Schweitzer disclose no significant relationship with any manufacturer of any commercial product mentioned in this article. No drug is mentioned in this article for an unlabeled use.