The hip is the specialized structure connecting the hemipelvis to the femur. The interaction of the femoral head, neck, and trochanters to the acetabulum and pelvis involves a complex array of tissue. Abnormalities of the bony morphology or soft tissues can lead to overload. It has been proposed that 5% to 6% of sports injuries of the hip occur at the hip and pelvis. Overuse is the most prevalent etiologic cause of such injuries. Certain activities can lead to a “conflict” between the acetabulum and femur, resulting in injury. In the absence of direct impact of tissue, endurance sports can result in a hip overuse injury as a result of a mismatch between the active and recovery phases of training. Regardless of the sport or activity, classification by level of involvement—osteochondral, inert soft tissue, contractile muscle, or neural—is helpful in establishing a diagnosis and treatment plan. The chapter outlines hip overuse injuries using the previously described schema.
This chapter also provides a framework to evaluate and treat overuse injuries of the hip. To organize and provide a framework for this chapter, a layered approach characterized by the senior author (B.T.K.) is used. The layered understanding of potential etiologic contributors to hip pain is useful ( Table 85-1 ). The first layer, the osteochondral layer, which comprises the bone architecture of the hip and pelvis, determines many of the kinetic/kinematic forces that contribute to hip overuse injury. Surrounding the osteochondral layer is the inert layer—primarily the labrum and the hip joint capsule. Biomechanical forces act on the labrum and capsule, which are susceptible to mechanical impingement and failure under asymmetric biomechanical forces. The next layer is the contractile or dynamic layer, including the muscles that cross the hip joint. The contractile layer is best organized by region: anterior, lateral, posterior, and medial. Lastly, the neural layer must be considered when developing a differential of pain relating to overuse of the hip.
|Osteochondral||Bony structure of hip and pelvis/femoroacetabular articulation|
|Inert||Static stabilizing structures including the hip capsule, ligaments, and labrum|
|Contractile/dynamic||Muscles that cross the hip joint|
|Neural||Sensory and motor nerves in the hip region|
A thorough history, physical examination, and knowledge of hip anatomy and function are fundamental to making an accurate diagnosis. The differential diagnosis of hip and groin pain in athletes is broad and determined by factors such as age and activity type. Before establishing a musculoskeletal diagnosis, causes of referred hip pain must be considered. These causes may include intraabdominal disorders, genitourinary abnormalities, or gynecological abnormalities. Lumbar spine pathology also may cause hip or pelvis pain. Extraarticular versus intraarticular pathology can be accurately distinguished with a meticulous history, physical examination, and workup. Stress fractures in women of relevant age should prompt assessment for amenorrhea, eating disorders, and osteoporosis.
Evaluation of gait, biomechanics, and alignment should be performed in addition to focal evaluation of the area of injury. Complete examination of the hip should include inspection, palpation, range of motion testing, strength testing, sensory examination, neurovascular examination, and special tests, with comparison between the injured and uninjured limb. Braly et al. presented an 11-point physical evaluation tool including systematic evaluation in the standing, seated, supine, lateral, and prone positions.
Irregularities of the femoroacetabular articulation are a possible source of hip pain in athletes. Morphologic femoroacetabular abnormalities can cause labral and chondral damage. Most patients with labral tears also have bony abnormalities such as hip dysplasia and femoroacetabular impingement (FAI). In patients with FAI, morphopathology of the femur or acetabulum damages the chondrolabral structures during normal joint motion. The most common type of morphopathology is the mixed cam and pincer lesion, which occurs along the anterior femoral neck and the anterior-superior acetabular rim. The accepted mechanism of flexion and internal rotation produces abutment and impingement of the labrum and cartilage. Such repetitive microtrauma results in joint degeneration.
Biomechanically, cam lesions result from a decrease in femoral head-neck offset, resulting in additional bone overgrowth. Cam lesions are most commonly seen on the anterior and anterosuperior aspect of the femoral neck and are seen in people with FAI. Pincer impingement is bony change in the acetabulum itself and is observed in 42% of people with FAI. Structured pincer lesions manifest as either a deep acetabulum or retroverted acetabulum, which leads to an apparent deeper anterior acetabular wall. FAI can result in pathology including primary labral tears, chondropathy, and hip osteoarthritis when the hip joint is placed into a position of impingement in a repetitive fashion during sporting activities.
No gold standard exists for diagnosing FAI, and not all persons with FAI experience hip pathology. Signs associated with FAI include reduced hip internal rotation with hip flexion and a positive flexion, adduction, and internal rotation (FADIR). Positive FADIR testing is common in persons with FAI and may warrant radiographic examination. Therapeutic intervention involves decreasing frequency and duration of positional impingement. Flexion, internal rotation, and adduction should be limited.
Femoral Neck Stress Fractures
The mechanical loading and arthrokinematics of femoroacetabular morphology interact with gravity to produce injury. Together, bony architecture and the muscles in the hip and pelvis play a role in the development of stress injuries. The muscles in the hip and pelvis are important in balancing torque forces such as those at the femoral neck. If the muscles become fatigued with activity and, particularly in areas of baseline weakness, the ability of the muscles to absorb gravitational forces is lost, these forces are transmitted to a greater degree to the bone. Additionally, these forces can be transmitted asymmetrically through the hip joint, resulting in a stress injury in the setting of morphologic abnormality.
A compression-side femoral neck stress fracture is defined as sclerosis or localization of injury to the compression side of the femoral neck on the basis of imaging studies, with subdivisions based on the presence of a fatigue line ( Fig. 85-1 ). The three subtypes consist of no fatigue line, a fatigue line greater than 50%, and a fatigue line less than 50% of the femoral neck. Stage 1 is characterized by normal radiographs and abnormal uptake on a bone scan, or magnetic resonance imaging (MRI) signal intensity on T2-weighted or short tau inversion recovery images. Stage 2 is notable for endosteal or periosteal callous without overt fracture, and stage 3 is notable for evidence of a cortical crack without displacement. In tension-side fractures, a callus or disruption of the cortical surface on the tension side (superior) of the femoral neck is observed. In the case of tension-side stress fractures, surgical management is required to stabilize the fracture to avoid the complications of a femoral neck fracture.
Pelvic and Sacral Stress Fractures
A pelvic stress fracture is defined by damage to the inferior pubic rami, likely from shear force between the medial adductor muscle group and the lateral hamstring attachment, causing repetitive overload and increasing the likelihood of a stress fracture. Sacral stress fractures are rare and occur as a result of vertical force transmission through the spinal column to the sacrum and ilium. Sacral stress fractures occur unilaterally, primarily at the sacral ala ( Fig. 85-2 ).
Acetabular Labral Tears
Acetabular labral tears are common causes of hip pain in athletes. Functionally, the labrum deepens the acetabulum, contributing to the hip dynamic stability by maintaining femoral head contact within the acetabulum. Negative intraarticular pressure of the joint is maintained by the acetabular labrum. Causes of acetabular labral tears are multifactorial. They are associated with tearing as a result of direct trauma, Legg-Calvé-Perthes disease, osteoarthritis, classic hip dysplasia, microinstability, and FAI. Wenger et al . reported that 87% of 31 patients with labral tears were found to have at least one structural abnormality, including retroverted acetabulum, abnormal femoral head-neck offset, and coxa valga. Repetitive microtrauma is also a potential mechanism of injury in these patients.
Plain radiographs are useful in localizing structural bony abnormalities but not soft tissue injury. As many as two thirds of labral tears occur in the anterosuperior labrum, possibly because of poor vascular supply and exposure to higher forces or stresses as a result of anterosuperior impingement in FAI. Repetitive twisting, hyperextension, hyperflexion, hyperabduction, and/or frequent external rotation of the hip may result in labral tears.
The mechanism of injury for labral tears is repetitive high impact within the joint, resulting in anteromedial groin pain and limited hip range of motion.
In summary, labral tears are commonly seen as a result of overuse injuries. FAI and developmental hip dysplasia increase the risk of labral tears. Conservative management should always precede surgical intervention. Improving hip joint neuromotor control should be a goal in physical therapy by activating deep stabilizing muscles. Gait retraining should aim to reduce excessive hip extension and loading of anterior hip structures.
Structural risk factors for labral tears include static overload, dynamic impingement, and dynamic instability. Static overload includes lateral or anterior undercoverage, femoral anteversion, or femoral valgus. Dynamic impingement would include FAI, femoral retroversion, and femoral varus. Finally, dynamic instability can occur when functional range is greater than the morphologic constraints. An example would be posterior subluxation from an anterior cam, levering the hip in excessive flexion.
Hip pain from overuse is often linked to muscle imbalances, with muscle strains tending to be the most common type of injuries. Muscles that cross two joints and fast-twitch type 2 fibers are most often involved, especially during activities requiring eccentric contraction. When injury does occur, it is commonly at the myotendinous junction where biomechanical shear forces are most focal. Ultrasound can be used to assess tendon degradation and muscle tear. MRI can provide high-resolution multiplanar visualization of the tissues involved. Classification of muscle strain based on MRI findings is possible as follows: first degree (stretch injury), second degree (partial tear), and third degree (complete rupture). Modifiable risk factors include muscle imbalance between agonists and antagonists, fatigue, lack of flexibility, and poor trunk coordination. Overuse can involve the anterior, lateral, medial, and/or posterior hip musculature.
The iliopsoas is the main flexor of the hip joint. From its origin off the anterior bodies and transverse processes of the lumbar vertebrae, the muscle courses across the pelvic brim to its insertion on the lesser trochanter of the femur. The most common causes for iliopsoas tendonitis/bursitis are rheumatoid arthritis, acute trauma, and overuse. The iliopsoas bursa is the largest bursa in the hip, positioned between iliopsoas and the pelvic brim. Iliopsoas bursitis is most common in young female athletes who may present with a combination of anterior hip pain and a palpable audible snap ( Fig. 85-3 ).
It is postulated that repetitive hip flexion and extension is the primary biomechanical mode of injury, which is often seen in high-risk sports such as rowing and running. In rowers, excessive hip flexion during the stroke can irritate the iliopsoas bursa via internal snapping of the hip. Paluska has highlighted the role of sprinting and hill climbing in causing friction of the iliopsoas tendon on the iliopectineal eminence, anterior femoral head, and anterior hip capsules, effectively causing iliopsoas bursitis. Additional evidence is now available that implicates the iliopsoas in hip impingement. Patient presentation includes a positive FADIR test, painful resisted hip flexion, and tenderness over the iliopsoas on palpation. Radiographic findings show normal head-neck offset, but a labral tear is seen on imaging and intraoperatively.
Coxa Saltans Syndrome (Snapping Hip)
Snapping hip syndrome—coxa saltans—is characterized by an audible snap or catch of the hip. External coxa saltans defines lateral symptoms, and internal coxa saltans describes medial symptoms. Mechanistically, snapping of the iliopsoas over the iliopectineal eminence, anterior femoral head, or anterior hip results in audible internal snapping. Other mechanical hypotheses for internal snapping include accessory iliopsoas tendinous slips, stenosing tenosynovitis of the iliopsoas insertion, iliopsoas tendon snapping over a bony ridge at its insertion at the lesser trochanter, snapping of the iliofemoral ligament over the anterior femoral head, and subluxation of the long head of the biceps femoris at the ischium (snapping bottom). More recent ultrasound investigation has demonstrated snapping over the iliacus muscle. Persons at risk include those who perform movements with high flexion angles (associated with internal and external rotation) or repetitive hip flexion maneuvers.
The snapping of the iliotibial band across the greater trochanter results in visible external (lateral) snapping. Mechanistically, the iliotibial band glides over the trochanter when moving from extension to flexion, as in biking and running. External snapping hip is more common than internal snapping hip. Palpable snapping of these tendons during examination confirms diagnosis. Although the utility of imaging is limited, dynamic ultrasound analysis has been suggested to be useful in differentiating the diagnosis. Repetitive snapping in both cases may lead to iliopsoas bursitis or tendonitis.
Rectus Femoris Injury/Overuse
The rectus femoris (straight and reflected head) and the sartorius are also hip flexors. Strains in these muscles generally occur at the myotendinous junction ( Fig. 85-4, A ). In addition, muscles that cross two joints are at higher risk for strains. Both have also been implicated in apophyseal avulsion injuries in skeletally immature patients. Although this issue predominantly affects adolescents, a case report demonstrated a proximal avulsion in two National Football League kickers, soon followed by a larger National Football League survey. Investigators surmise that these injuries occur in kickers who go from a hip-extended/knee-flexed starting point to a hip-flexed/knee-extended position. These injuries can be managed conservatively. One complication has been extraarticular impingement, specifically subspine impingement in patients with rectus femoris avulsions. Subspine impingement is characterized by pain in straight flexion, causing the inferior portion of the femoral neck to abut the overhanging anterior inferior iliac spine ( Fig. 85-4, B ).
Hip Abductor Overuse
Muscle imbalance and overuse of the hip abductors is a major cause of hip abductor injury ( Fig. 85-5 ). The wider female pelvis has been postulated to increase the likelihood of injury in women. Morphologic abnormalities such as hip dysplasia can cause biomechanical overload of the abductor group.