Femoroacetabular Impingement and Associated Labral Tears
Femoroacetabular impingement syndrome (FAIS) refers to pathologic abutment between the femoral head-neck junction and the acetabular rim. This generally occurs due to a combination of structural, soft tissue, and activity-related factors. Two main forms of FAIS include cam morphology and pincer morphology, and many people have both. Cam morphology refers to an abnormally shaped femoral head and neck junction that causes either a convexity at this location or a flattening at this location on the bone ( Fig. 11.1 ). This effectively causes a mismatch between the shape of the acetabulum and the femoral head, and the cam lesion impinges on the acetabular rim and labrum, and as it moves farther into the joint with flexion, it impinges on the cartilage as well. Pincer morphology refers to an abnormality of the acetabulum in which the socket is deep and covering too far over the femoral head ( Fig. 11.2 ). This causes the edge of the acetabulum and labrum to impinge upon the femoral neck with hip flexion. Many people have a combination of both these abnormalities. FAIS can cause labral tears from the chronic impingement of the labrum between the bones. , Additionally, impingement between a prominent anterior inferior iliac spine (AIIS) and the femoral head-neck junction, also called subspine impingement, can occur. Although all three types of FAIS are noted in female athletes, pincer morphology is more common in females, while males generally have larger cam lesions. FAIS is most often seen in active adolescents and adults and in athletes, as the demand on the hip is higher than that in sedentary people. All types of female athletes can develop FAIS; however, it is commonly seen in soccer, lacrosse, dance, and gymnastics.
Clinical Symptoms, Examination, Radiology, and Diagnosis
Most commonly, FAIS is described as a slow progression of pain over time rather than an acute injury. Classically, pain is in the groin or anterior hip and is described in a C-shaped location over the anterior and lateral groin crease, which is termed a “c-sign”. However, female patients may have pain patterns that are more laterally or even posteriorly based. Generally, pain is described as activity related, particularly with running or squatting, but it can also be associated with sitting for prolonged periods. Mechanical symptoms due to labral tears or cartilage injury in the hip may be present; however, most often a complaint of popping will be due to an associated internal or external snapping hip. Pain in certain muscle groups such as hip flexors, glutes, and short external rotators is commonly associated and should be considered as a source of pain, in addition to FAIS. ,
Physical examination related to possible FAIS should include a gait assessment, palpation of periarticular muscles, range-of-motion testing, and strength testing to determine if an intra- or extra-articular source of pain is present. , Classically, FAIS will cause pain with flexion, adduction, and internal rotation (FADIR) ( Fig. 11.3 ). This places the most contact between the femur and acetabulum and places the most pressure on the labrum. However, the combination of flexion, abduction, and external rotation (FABER) can cause pain if a labral tear or the position of impingement is more posteriorly based in some cases ( Fig. 11.4 ). Pain with flexion past 90 degrees may be associated with AIIS impingement.
Radiographs including an anteroposterior (AP) pelvis view, lateral hip view, and often a false profile view are taken for assessment of femoroacetabular impingement (FAI) morphology including cam lesion, pincer lesion, and prominent AIIS. The lateral center edge angle (LCEA) and the Tonnis angle are measured on an AP pelvis radiograph to evaluate the amount of coverage of the acetabulum and the slope of the acetabular roof, respectively ( Fig. 11.5A and B ). An LCEA between 25 and 40 degrees and a Tonnis angle between 0 and 10 degrees are considered normal. , The alpha angle is measured on a lateral view of the femur and measurements above 50–55 degrees indicate cam morphology. ( Fig. 11.5C ) The AIIS should have approximately 1 cm of space between its base and the edge of the acetabulum. , A thorough assessment of any concomitant acetabular dysplasia should be performed, as this is more common in females than males. Magnetic resonance imaging (MRI) is useful to determine the presence and extent of labral pathology, cartilage injury, and possible associated psoas or rectus tendonitis ( Fig. 11.6 ). Computed tomographic (CT) scan is helpful to understand the three-dimensional anatomy of the cam or pincer lesion and evaluate the femoral torsion for any femoral retroversion that could be exacerbating the FAIS.
Initial treatment for FAIS includes conservative care including activity modification, physical therapy, and antiinflammatory medications. Therapy should focus on core strength, stability, and balancing of muscle groups including anterior and posterior chains. Selective injections may be helpful in confirming a diagnosis of FAIS when a possible extra-articular source of pain is in question, such as psoas or rectus tendonitis. Female athletes have a higher incidence of psoas snapping and tendonitis than males, and this may be difficult to differentiate from FAIS. , Intra-articular injections may also be used as part of conservative treatment. A single injection may be an effective aide in pain relief and may facilitate a course of physical therapy or allow further athletic participation. There is evidence, however, that 2–3 months should pass between the injection of corticosteroid and surgical intervention to prevent an increase in perioperative infection rate.
If nonoperative treatment fails to improve pain and mechanical symptoms, surgical intervention most commonly includes hip arthroscopy to perform labral repair (or reconstruction with a graft), femoroplasty and/or acetabuloplasty, and possible AIIS decompression. If a concomitant diagnosis of acetabular dysplasia is present, the surgeon should consider whether a periacetabular osteotomy for correction of dysplasia is necessary. Patients should be counseled that an associated snapping psoas or iliotibial band (ITB) may not be immediately corrected with hip arthroscopy. Rather, their soft tissues will benefit from a course of postoperative physical therapy after the underlying anatomic abnormalities have been addressed.
Outcomes of hip arthroscopy for FAIS show good improvement in functional scores and return to athletic participation in 50%–95% of female patients. Some studies show that overall improvement is lower in females than males. Older females, especially, tend to show less improvement in functional scores and worse outcomes than their younger female counterparts. , There is evidence that arthroscopy in patients with combined borderline acetabular dysplasia and FAI can be successful, but arthroscopy for isolated dysplasia with a labral tear is not indicated.
Hip Dysplasia and Associated Labral Tears
Acetabular dysplasia refers to an increasingly wide spectrum of pathologies that affect the acetabular and proximal femoral morphology. , The dysplastic acetabulum is typically shallow and low in volume, creating an abnormal articulation between it and the femoral head ( Fig. 11.7 ). This mismatch can create intra-articular damage due to excessive stress on the labrum and cartilage and extra-articular stress on muscles and tendons, which are overloaded due to the abnormal hip joint. Dysplasia is now recognized as a cause of primary osteoarthritis (OA) of the hip. Various patterns of dysplasia can occur, and some can be subtle on radiographic examination. The undercoverage of the femoral head can be global, or it can be focal in the anterior, lateral, or even posterior acetabulum in cases of acetabular retroversion. , Each of these may cause a different location of labral or chondral injury, as well as a different pattern of symptoms. The concept of microinstability in the setting of dysplasia refers to the mismatch and undercoverage of the femoral head causing some laxity of the joint, which is sensed by the body. The periarticular muscles such as gluteal muscles or hip flexors are then overloaded and can become a source of discomfort. It is common to see a combination of ligamentous laxity and dysplasia in females. This combination can exacerbate the microinstability due to the increased range of motion these athletes will have, in addition to increased capsular volume or incompetence. ,
Clinical Symptoms, Examination, Radiology, and Diagnosis
Many female athletes presenting with symptoms from acetabular dysplasia will note an insidious onset of pain that is often activity related. If groin pain or a c-sign is a main complaint, intra-articular pathology or hip flexor tendonitis should be considered. If the pain is mainly laterally based, often a large component of pain is due to gluteal overload. If posterior pain is present, posterior undercoverage should be considered. , Anterior pain may be exacerbated with activities involving hip flexion and significant external rotation, as they place stress on the labrum and anterior capsule, respectively. Additionally, symptoms of psoas snapping may be a sign of anterior instability, as the psoas acts as a secondary stabilizer. Long periods of weight-bearing activity such as walking or running also place stress on the gluteal musculature and may exacerbate lateral pain.
Physical examination of a patient with possible acetabular dysplasia should include evaluation of gait, palpation of periarticular muscles, range of motion, and strength to determine locations of pain and intra- versus extra-articular sources of pain. Examination maneuvers related to dysplasia include an anterior apprehension test in which the patient is placed in the position in Fig. 11.4 and the femur is forced into external rotation ( Fig. 11.8 ). Pain or apprehension anteriorly, which is improved with posteriorly directed force on the joint (similar to a shoulder apprehension test), can be a sign of anterior instability. FADIR or FABER test results may be positive for pain if there is a labral tear. Evaluation of abductor fatigue with the Trendelenburg sign or trochanteric region pain with abductor strength testing indicates lateral overload. Internal and external rotation in flexion gives an idea of femoral torsion. Increased internal rotation indicates femoral anteversion, and increased external rotation indicates femoral retroversion. Both are seen in the setting of dysplasia and have treatment implications. Ligamentous laxity should be evaluated, as this also has treatment implications. The Beighton criteria is the most common way to qualify the level of general ligamentous laxity. Laxity, specifically of the hip capsule, can be tested with a log roll test and a dial test, both of which evaluate the amount of rotation and the spring back the capsule has in a neutral position of extension.
Initial radiographic evaluation is similar to evaluation for FAIS with AP Pelvis, lateral, and false profile radiographs. An LCEA below 25 degrees indicates dysplasia. Evaluation for increased alpha angle and combined dysplasia and FAI is important for treatment. MRI may show a labral tear, and it is important to evaluate the quality of the labral tissue, as it can often appear degenerative. , CT scan with evaluation of femoral torsion also aides in the evaluation of the three-dimensional nature of the acetabular dysplasia and any contribution of femoral anteversion to an instability picture.
In most cases, treatment for dysplasia begins with conservative management. Activity modification, antiinflammatory medications, and physical therapy are first-line treatment options. Physical therapy will focus on core strength, abductor strength, and balancing of anterior and posterior chain muscle groups. If the athlete is a dancer or other flexibility sport athlete, a thorough evaluation of compensatory movements during sport should be performed.
If nonsurgical management fails, treatment of dysplasia often requires periacetabular osteotomy for correction of the acetabular anatomy. , The goal of this surgery is to reorient the acetabulum such that the weight-bearing dome of the acetabulum is centered over the femoral head. Often this is combined with a hip arthroscopy if a labral tear or cam lesion is also present.
Iliopsoas Tendonitis and Internal Snapping Hip Syndrome
The iliopsoas muscle has been seen to be a source of a spectrum of hip symptoms, from debilitating mechanical hip pain to asymptomatic snapping of the hip. Internal snapping hip, also known as coxa saltans interna, is defined as the iliopsoas musculotendinous junction snapping over the anterior pelvic structures deep to it, including the iliopectineal ridge, the iliopsoas bursa, the iliofemoral ligament, the superior pubic ramus, the anterior capsule, the femoral head, or the lesser trochanter of the femur, with the femoral head being the most common location. ,
The psoas muscle originates from the lumbar spine (T12-L4), joins with the iliacus muscle at the levels of L5-S2, and inserts on the lesser trochanter as the iliopsoas tendon acting as one of the body’s strongest hip flexors. , Additional movements of the iliopsoas muscle include abduction and external rotation of the femur, in addition to flexion. Philippon et al. report in their anatomic study of cadaveric iliopsoas tendons that the majority of hips examined had iliopsoas tendons composed of more than two tendons and that the largest tendon usually was the psoas major, which tends to lie more medially and may not be the first tendon encountered endoscopically.
Clinical Symptoms, Examination, Radiology, and Diagnosis
Symptoms range from audible, nonpainful snapping to debilitating pain preventing athletic participation. Usually, pain is located anteriorly and is worsened with activities involving hip flexion to extension or hip circumduction. , It is more commonly seen in women and girls than in men and boys. Other activities of daily life that may worsen the painful snapping of internal coxa saltans include rising from a chair or walking upstairs. Athletic activities commonly associated with internal snapping hip are ones that involve large hip range-of-motion movements and high hip flexion such as dance, soccer, football, running, and hockey.
Physical examination maneuvers to detect internal snapping hip typically involve the hip moving from flexion to extension. The snap can be palpated or heard as the patient moves from hip flexion to extension at around 30 degrees of flexion. Another method to detect internal coxa saltans is to begin with the patient supine with the involved hip flexed, abducted, and externally rotated (FABER) and to bring the patient’s leg into an extended, adducted, and internal rotated position in a circumduction motion ( Fig. 11.9 ). The author’s preferred technique is to perform a “bicycle maneuver” where the patient laying supine cycles his/her legs as if riding a bicycle, with the hips alternating from flexion to extension bilaterally and the ipsilateral knee of the flexed hip also flexed to 90 degrees ( Fig. 11.10 ). Finally, tenderness to palpation of the iliopsoas tendon anteriorly and pain with resisted hip flexion are signs of iliopsoas tendonitis/bursitis related to internal snapping hip syndrome.
While imaging is not always required to diagnose internal snapping hip, it is helpful in determining the likely location of iliopsoas contact with the anterior pelvic structures and can aid in management. , Additionally, imaging can identify concomitant pathology such as FAI and the sources of intra-articular snapping hip, such as chondromatosis and loose bodies. , Snapping psoas is commonly associated with hip dysplasia and ligamentous laxity. A standing anteroposterior radiograph of the pelvis and false profile view of the affected hip are the primary radiographic imaging views preferred by the senior author, as they allow for identification of bony abnormalities, such as exostoses or osteophytes, causing the symptomatic contact with the iliopsoas tendon, sites of impingement (including FAI), or evidence of dysplasia.
MRI has been thought of as a limited study in the past owing to the dynamic nature of the internal coxa saltans and the static nature of the imaging modality, but more recent studies describe the consistent ability of MRI to diagnose abnormalities associated with the iliopsoas tendon, anterior capsule, bursa, and the surrounding musculature that correspond to the patient’s complaints. Inflammation of the iliopsoas muscle and/or tendon can give indirect evidence of internal snapping hip syndrome. The key to utilize MRI is to compare the patient’s symptoms and examination findings, as some large abnormalities in the iliopsoas tendon and/or surrounding structures may be present in a patient without symptoms. Therefore MRI can be a useful adjunct to physical examination and ultrasound, but it should not be used in isolation.
Dynamic ultrasound is the most valuable imaging modality used in diagnosing internal snapping hip syndrome, especially because it is a dynamic phenomenon. , Winston et al. reviewed snapping hips in ballet dancers and found snapping in 29 of 46 hips (63%) utilizing ultrasound, with 27 being from the iliopsoas and 2 of 29 from the ITB. Pelsser et al. studied 40 hips in 20 patients with unilateral or bilateral symptoms and visualized snapping on ultrasound in 26 of 40 (65%) hips, with 2 of 26 being from ITB external snapping and the rest from the iliopsoas. An additional benefit of ultrasound is that it is noninvasive and of relatively low cost but does require a skilled ultrasonographer.
The large majority of patients with internal coxa saltans require nonoperative treatment alone. , Since internal snapping hip syndrome is usually from overuse, the mainstay of treatment is nonsurgical intervention focusing on activity modifications, including a significant rest period, ice, pain control with antiinflammatory agents, and physical therapy. , , Physical therapy targets muscle imbalances, especially anterior musculature tightness, through active and passive stretching regimens. , Stretching and conservative treatment should start making improvements within 2–4 weeks. If no improvement is noted after that time, rapid return to play and training remains an ultimate priority, or an athlete is unable or unwilling to avoid the exacerbating activity, therapeutic injections of local anesthetic and corticosteroid have shown clinical improvements. These improvements are maximized when combined with continued rest, avoidance of aggravating activities (e.g., hip flexion >90 degrees), stretching, use of modalities (e.g., cryotherapy, electric stimulation), and use of nonsteroidal antiinflammatory drugs (NSAIDs). Wahl et al. report their tendon sheath cocktail of choice as including 40 mg of triamcinolone acetonide (Kenalog), 0.5 mL of 1% lidocaine, and 0.5 mL of 0.5% bupivacaine. They report utilizing this injection with stretching, NSAIDs, and temporary avoidance of training and drills and have found athletes able to return to sport in as little as 1 week.
Consistent conservative treatment may take 6–12 months to regain normal hip function without evidence of snapping or pain. Despite this duration, continued postural and movement patterns and stretching activities are encouraged to prevent recurrence. Several authors agree that conservative treatment should continue for at least 3–4 months before considering surgical intervention. , , However, after that time, surgical treatment can be pursued especially if an athlete needs to return to sport and all other diagnoses have been excluded.
Surgical intervention is focused on functionally lengthening the iliopsoas tendon by either transection or fractional lengthening. Additionally, the location of lengthening has also varied in the literature but tends to be one of the following zones: central compartment (at the level of the femoral head and hip capsule and pelvic brim), peripheral compartment (at the level of the inferior hip capsule and superior to the lesser trochanter), and at the lesser trochanter. A level I randomized trial and a level IV comparative study found that the location of release at either the lesser trochanter or the central compartment yielded nonsignificant differences between the two and favorable results for both. , ,
Surgical intervention has been approached both open and arthroscopically, although arthroscopic treatments currently show less morbidity and improved results compared with an open approach. , A systematic review of open versus arthroscopic treatments of internal snapping hip syndrome found that an arthroscopic approach was associated with a decreased failure rate, lower complication rate, and decreased postoperative pain.
While overall outcomes seem to be good, the largest complication with open or arthroscopic approaches seems to be transient iliopsoas muscle weakness. This weakness seems to resolve by 3–6 months postoperatively, with no difference regarding the level of tendon release. Return to sports can be expected around 9 months postoperatively.
Iliotibial Band Tightness and External Snapping Hip Syndrome
External snapping hip syndrome, or external coxa saltans, is due to the posterior aspect of the ITB or the anterior aspect of the gluteus maximus muscle snapping across the greater trochanter at the lateral aspect of the hip. It is usually a visible, dynamic phenomenon and one that patients describe as catching, “giving way,” or even the sensation of hip dislocation. External snapping hip is more common than its internal counterpart, but is diagnosed and treated similarly.
The iliotibial tract is formed proximally from two muscles: the tensor fascia lata (TFL) anteriorly and the gluteus maximus posteriorly. The TFL originates along the lateral iliac crest between the anterior superior iliac spine and the tubercle of the iliac crest. It then inserts on to the ITB or iliotibial tract, which continues down the lateral thigh and inserts at Gerdy’s tubercle on the anterolateral aspect of the proximal tibia. The gluteus maximus, which can also attribute to external coxa saltans, also originates on the iliac crest, but only crosses the hip joint inserting on the posterior aspect of the ITB and the linea aspera distal to the greater trochanter via the gluteal sling. , Functionally, the ITB crosses both the hip and knee joints and acts to help stabilize the pelvis in one-legged stance with abduction of the TFL and helps stabilize the knee in extension. The ITB lies posterior to the greater trochanter in extension and mechanistically glides anteriorly over the greater trochanter when the hip moves to flexion. ,
Clinical Symptoms, Examination, Radiology, and Diagnosis
Due to the often visible nature of external snapping hip syndrome, coxa saltans externa is typically easier to diagnose than coxa saltans interna. Patients tend to locate pain and symptoms at the lateral aspect of the hip and may complain of dislocating their hip, snapping, catching, or giving way. , , The patient will frequently offer to demonstrate the snapping.
On physical examination, having the patient lie on his/her side with the affected hip up will allow for evaluation with the Ober test, bicycle test, and direct palpation. To perform the Ober test, the patient will first flex the unaffected and affected hips, and the affected hip will be extended and adducted by the examiner. If a snap is palpated as the hip is extended, this is positive for external snapping. If the affected leg cannot adduct past neutral, this test is positive for ITB tightness ( Fig. 11.11 ). The bicycle test is performed with the patient lying on the unaffected side and cycling the affected hip as if peddling a bicycle. The examiners hand rests on the greater trochanter to feel the snap.
Imaging is similar to the methods used in internal snapping hip syndrome, where dynamic ultrasound is usually the most valuable modality. Usually a thickened ITB and/or focal thickening of the anterior gluteus maximus is visualized snapping over the greater trochanter.
Similar to internal snapping hip, the treatment of choice for external snapping hip syndrome is conservative therapy. , Activity modification, rest, cryotherapy, antiinflammatory agents, and focused physical therapy are critical to symptomatic resolution. Commonly, an imbalance between gluteus maximus and TFL activation contributes to the pathology and can be an area of focus with biofeedback and neuromuscular retraining.
If conservative measures are not offering improvement for the athlete, and rapid return to sport remains a priority, then consideration of an ITB bursa injection with local anesthestic and corticosteroid is warranted.
Recalcitrant painful snapping after conservative treatments for 3–4 months is rare but can be escalated to surgical intervention. , , Goals of surgery for external snapping hip syndrome is to minimize the forces and tension the ITB undergoes when gliding across the greater trochanter. , This is usually achieved by lengthening the ITB and various methods have been visited in the literature, including a formal Z-lengthening, a Z-shaped release, a cross-shaped release, , and a release of the gluteus maximus tendon insertion to the femur. A formal Z-lengthening was originally described by Brignall and Stainsby where a 10-cm incision is made over the greater trochanter laterally, with two-thirds of the incision below the greater trochanter. An 8-cm longitudinal incision is made in the fascia lata and the proximal limb is made posterocaudally and the distal limb is made anteroproximally at 45 degrees to the longitudinal incision. The flaps are reoriented to gain more length to the ITB and sutured in place. Intraoperative Ober test and range of motion ensure no snapping of the ITB is visualized or palpated. Variations of the shape of ITB incision have been described. , Polesello et al. describe a newer technique of releasing the gluteus maximus insertion instead of the ITB in hopes of creating a more physiologic approach to decrease ITB tension. Many options exist, with no randomized controlled trials comparing the various methods. While participant numbers are low in most studies, overall outcomes appear good with the majority of patients returning to preinjury levels and painful snapping resolving.
Greater trochanteric bursitis is an inflammatory condition part of a larger entity called greater trochanteric pain syndrome (GTPS). GTPS also includes gluteus medius and minimus tendinopathy (see more details in the section Gluteal Tendonitis and Tears) and external coxa saltans (see the section Iliotibial Band Tightness and External Snapping Hip Syndrome). Several authors agree that greater trochanteric bursitis is largely a sequela of another inciting pathology that should be addressed to obtain full resolution of the greater trochanteric pain. ,
The peritrochanteric bursae have been described as three fluid-filled sacs to protect and decrease friction of the gluteal tendons, the ITB, and the TFL, with some anatomic variations having four in total. Each bursal sac is named with respect to the location under which tendon it resides: the subgluteus maximus bursa (aka trochanteric bursa), the subgluteus medius bursa, and the subgluteus maximus bursa. The first one is the largest and most commonly indicated in GTPS.
Clinical Symptoms, Examination, Radiology, and Diagnosis
Being aware of the associated hip diagnosis in the setting of greater trochanteric bursitis is critical in fully diagnosing and therefore appropriately treating the patient. Concomitant diagnoses including external coxa saltans, gluteus medius or minimus tendinopathy, and recalcitrant greater trochanteric bursitis are important to delineate when examining the patient. ,
Direct palpation over the greater trochanter can help discern the location of pathology and the associated cause. With the patient lying on the contralateral leg in a lateral position, tenderness to palpation over the anterior superior greater trochanter likely indicated gluteus minimus pathology, as this is the location of insertion on the greater trochanter. The gluteus medius inserts along the posterosuperior aspect of the greater trochanter, indicating tenderness along this region is more likely associated with the gluteus medius tendon. Tenderness to palpation along the central and distal portions of the greater trochanter aligns with the pathology focused at the trochanteric bursa, also known as the subgluteus maximus bursa. A tight ITB can also cause or worsen trochanteric bursal pain, so there will be indications of a tight ITB on examination, such as during the Ober test (described in further detail in the Section Iliotibial Band Tightness and External Snapping Hip Syndrome).
Treatment for greater trochanteric bursitis and GTPS is largely nonoperative with focus on rest, cryotherapy, stretching the ITB and gluteal musculature, and antiinflammatory agents. , Corticosteroid injections are commonly initiated once other more conservative measures fail.
Once extensive nonoperative modalities have been exhausted for 6–12 months, and the athlete is unable to return to training or competition, surgical intervention may be discussed. Surgical options include, open versus endoscopic bursectomy, proximal or distal Z-plasty of the ITB, longitudinal release of the ITB, trochanteric reduction osteotomy, and repair of gluteus medius and/or minimus tears.
Gluteal Tendonitis and Tears
Commonly described as “rotator cuff” disease of the hip, the spectrum of gluteal tendinitis, tendinopathy, and tears is an important cause of lateral greater trochanteric hip pain, particularly in female patients. Although the precise prevalence of gluteal tendinopathy in the overall population is unknown, increasing awareness of this diagnosis has led to the thought that the majority of lateral greater trochanteric pain is attributable not to bursitis, but to gluteal tendinopathy. Radiologic studies of patients with symptomatic greater trochanter pain have demonstrated that bursitis is rarely the primary underlying cause of pain, with one study demonstrating a rate of only 20% of trochanteric bursitis in 877 patients with lateral greater trochanteric hip pain. In addition, 49% of these patients were found to have abnormalities of the gluteus medius, gluteus minimus, or both.
Although gluteal tears and tendinosis are typically seen in patients in the fourth through sixth decades of life, recognition of this pathology will become increasingly important in the management of female athletes. The average age of road race participants was 40 years in the United States in 2011, and with both the overall aging population and the increased participation of females in triathlons and long-distance running, the incidence of symptomatic gluteal tears and tendinosis will likely increase. ,
The abductor complex of the hip includes the gluteus minimus, gluteus medius, and TFL. These muscles all originate on different portions of the iliac crest and have different sites of tendinous insertion. The TFL becomes contiguous with the ITB and inserts on Gerdy’s tubercle on the lateral condyle of tibia, whereas the gluteus medius and minimus tendons insert onto different portions of the greater trochanter. An anatomic cadaver study of the insertion site of the gluteus medius demonstrated that the posterior portion of the gluteus medius tendon was thicker and inserts on the superoposterior facet of the greater trochanter in a straight line, whereas the anterolateral tendon was thinner in substance and inserted on the lateral facet of the greater trochanter via a posteroinferior direction. This may have important implications in the surgical treatment of gluteus medius tears as well as provide some explanation for why tears of the anterior fibers are generally reported to be of greater frequency than those of posterior fibers. The gluteus minimus additionally has dual insertion at both the lateral facet of the greater trochanter as well as the hip capsule itself.
The posterior portion of the gluteus medius tendon as well as the gluteus minimus have been shown to be important dynamic femoral head stabilizers. , Although traditionally gluteus medius was thought to be the main hip abductor for single-leg stance and pelvic balance during walking, it is likely the force vector of the TFL that generates the most hip abduction power and contributes the greatest force to these activities.
The main function of gluteus medius and minimus is as pelvic and hip joint stabilizers. Weakness of the hip abductor complex can lead to overuse injuries, strains of the hip adductors, patellofemoral pain, and the Trendelenburg gait. Tears of the gluteus medius and minimus are usually degenerative akin to rotator cuff tendinopathy, but traumatic tears of the gluteus tendons have also been rarely reported.
Clinical Symptoms, Examination, Radiology, and Diagnosis
Typically, patients with gluteal tendinopathy present with an insidious onset of greater trochanteric hip pain and tenderness. Pain is often worse at night, exacerbated by direct pressure on the lateral aspect of their hip, and may be worse with activities such as walking or climbing stairs. Some patients will have a limp to varying degrees and will exhibit the Trendelenburg gait. , Rarely, a patient will give a history of an acute inciting injury just prior to the onset of symptoms.
Clinical examination of a patient presenting with GTPS will help aid in the diagnosis of the underlying condition. Assessing for other coexisting or unrelated pathology should be performed, including a thorough lumbar spine examination for spondylolisthesis, lysis, and lumbar stenosis.
Both active and passive hip range of motion should be evaluated to assess for underlying OA or, as can be particularly relevant in the case of female athletes, an occult stress fracture of the proximal femur. Superior gluteal nerve disease is generally rare but can be seen in conditions of diabetes mellitus. The provider should maintain a higher level suspicion of iatrogenic gluteal neuropathy in patients presenting with abduction weakness and muscle wasting in the setting of previous hip surgery.
Assessing for tenderness, examining for atrophy of peritrochanteric musculature, and testing muscle strength should all be performed. Physical examination should include the assessment of gait, specifically watching for any antalgic limping or the Trendelenburg sign. Single-leg stance can also be performed to identify abductor weakness. Pain within 30 s of a single-leg stance can be very predictive (98%) of gluteal tendinosis when combined with MRI abnormalities. Hip abduction strength should be tested in a side-lying position and has shown to be the most valid and reliable assessment of unilateral abduction strength. A single-leg squat is another test that may be utilized in athletes to assess for gluteal weakness. Patients with dysfunction of their hip abductors or weakness have been found to have both difficulty in performing a single-leg squat and delayed onset of gluteus medius activation during single-leg squat based on electromyographic findings.
Trochanteric bursitis can be present in the setting of gluteal tendinosis, or less commonly, in isolation. Many of the symptoms of gluteal tendinosis and trochanteric bursitis can be overlapping, but continued pain and residual abduction weakness after a corticosteroid injection into the bursa has been performed can be suggestive of gluteal tendon pathology.
Ultrasound is one imaging modality that can be utilized to further diagnose GTPS. Tendinosis is demonstrated on ultrasound by decreased echogenicity within the tendon. Partial- and full-thickness tears can also be seen on ultrasound as an anechoic defect disrupting the continuity of the tendon. One study correlated ultrasound and intraoperative findings and found that in 17 of 19 patients with gluteal tendinopathy, ultrasound correctly diagnosed the underlying condition. However, ultrasound demonstrated poor specificity when identifying gluteal tendinosis in five of the six patients with normal gluteal tendon anatomy. Another study with a small series of patients, published in 2010, demonstrated a positive predictive value of 1.0 for diagnosing gluteal tendon tears with ultrasound findings as described earlier.
Plain radiographs are useful in the setting of lateral trochanteric hip pain to evaluate for any underlying or concomitant hip OA. Specific radiographic findings of gluteal tendinosis can be seen on plain radiographs and can include sclerosis or osteophytes of the greater trochanter.
MRI has aided significantly in the diagnosis of gluteal tendinosis and tears ( Fig. 11.12 ). Previous MRI studies of this pathology have identified that gluteus medius tears are far more common than gluteus minimus tears. The diagnostic accuracy has been reported in a wide range with most studies showing good sensitivity and specificity for the identification of gluteal tendon tears. , MRI can also be utilized to quantify the percentage of fatty infiltration of the gluteus medius and minimus, which has been shown to influence outcomes following repair.