Continuing Education Activity

Greater trochanteric pain syndrome (GTPS) presents a complex challenge in orthopedic and sports medicine, significantly impacting individuals, especially women, due to distinctive pelvic biomechanics and hormonal influences. This complex condition is influenced by interactions among various tissues under mechanical stresses and compasses conditions like greater trochanteric bursitis, abductor tendinopathy, and external snapping hip syndrome, leading to a broad spectrum of clinical presentations. Patients often report intermittent, debilitating pain across the lateral thigh and buttock, which can be aggravated by daily activities such as sitting, stair climbing, or engaging in high-impact exercises. Carefully assessing the patient's history, examination, and focused diagnostic imaging are essential for an accurate diagnosis.

This educational course discusses the complexities of GTPS and multifaceted nature—from clinical presentation, marked by pain and tenderness at the lateral aspect of the hip, to comprehensive management strategies. This activity equips healthcare professionals with an extensive toolkit covering conservative treatments, including physiotherapy and pharmacotherapy, alongside innovative interventions like platelet-rich plasma injections and discussing surgical options for cases that persist despite conventional therapies. Emphasizing an interprofessional team approach, the course highlights the importance of collaboration among healthcare professionals, from physicians to physical therapists, in developing effective patient care plans.

Objectives:

• Identify the etiology of greater trochanteric pain syndrome.
• Evaluate the common physical exam findings associated with greater trochanteric syndrome.
• Select the appropriate management options for greater trochanteric pain syndrome.
• Implement interprofessional team strategies for improving care coordination to improve patient outcomes.

Introduction

Patients diagnosed with lateral hip pain are commonly treated for trochanteric bursitis using non-steroidal anti-inflammatory drugs (NSAIDs), corticosteroid injections, and physical therapy.[1][2] While effective for many, this approach still leaves many patients with ongoing discomfort and limited functionality. Recent advancements in understanding have led to the recognition of greater trochanteric pain syndrome (GTPS) as a more accurate descriptor of this condition.[3] GTPS encompasses trochanteric bursitis, external coxa saltans (snapping hip), and abductor tendinopathy.[4][5]

Trochanteric bursitis, the predominant cause of GTPS, involves inflammation of the greater trochanteric bursa, which is located between the greater trochanter and the iliotibial band. This inflammation is commonly triggered by repetitive stress and trauma.[6] The condition manifests as pain in the lateral thigh, often aggravated by prolonged sitting, stair climbing, or engaging in high-impact exercises. The hip joint, bearing loads of 6 to 8 times the body weight during everyday activities, is particularly vulnerable to wear and tear.[6]

The diagnosis of GTPS is primarily clinical, with imaging used to differentiate it from other potential causes. A deep understanding of the relevant anatomy, clinical examination findings, and imaging results is essential in managing cases resistant to conservative treatment.[2][5] The standard treatment includes NSAIDs, physical therapy, and stretching exercises. Surgical intervention, both open and endoscopic, is reserved for cases where conservative methods are ineffective.[6]

Involved Anatomical Structures

Dysfunction at any anatomical junction can manifest as greater trochanteric pain syndrome.[7] The peritrochanteric space contains important anatomical structures that enable hip motion and stability.[2] A key structure is the subgluteus maximus bursa, also called the trochanteric bursa, which cushions movements of the overlying gluteus tendons, iliotibial band, and tensor fascia lata. The peritrochanteric space is superficially covered by a fibromuscular sheath comprising the gluteus maximus, tensor fascia lata, and iliotibial band.[2][4] Underneath lie the hip abductor and stabilizer muscles.[7] The gluteus minimus stabilizes the femoral head, originating from the pelvis and inserting at the greater trochanter.[8] The larger gluteus medius also inserts at the greater trochanter, initiates hip abduction, and stabilizes the femoral head. Finally, the tensor fascia lata forms the prime hip abductor. Proper functioning of these muscular and connective tissue structures enables painless motion and transfers weight laterally from the hip during gait.[7] 

Table

Table. Anatomical Structures Involved in Greater Trochanteric Pain Syndrome.

Etiology

Accurate diagnosis of the underlying condition is crucial for the effective treatment of GTPS, which encompasses bursitis, gluteal tears, and external snapping hip.[6] However, many patients have multiple concurrent diagnoses.[3][9] Historically, the primary source of lateral hip pain was attributed to inflammation of the peritrochanteric bursae.[4] This inflammation was thought to result from repetitive microtrauma and mechanical overload between the greater trochanter and the iliotibial band, stemming from overuse, trauma, or altered gait patterns. However, recent imaging studies more frequently identify abductor muscle tears, tendinosis, and thickening of the iliotibial band, rather than bursitis, as the primary sources of pain.[6]

Advancements in magnetic resonance imaging (MRI) and endoscopic techniques have led to an increased diagnosis of tears in the gluteus medius and minimus muscles.[10] These muscles' injury and degeneration pattern is similar to that observed in rotator cuff injuries, where abductor tears can vary from partial to full-thickness due to altered cellular healing response and diminished healing capability. Clinically, complete tears of the gluteus medius muscle are evidenced by abduction weakness during physical examination or a Trendelenburg gait.[11]

External coxa saltans, or snapping hip, is characterized by the iliotibial band "snapping" over the greater trochanter as the hip flexes from extension, often producing audible and painful sensations.[12] This repetitive motion can lead to thickening of the iliotibial band and subsequent bursal inflammation. While snapping may be asymptomatic, particularly in athletes, it can sometimes contribute to discomfort.[4] 

Epidemiology

GTPS, which includes trochanteric bursitis, abductor tendinopathy, and snapping hip (externa salta), affects individuals across a broad spectrum of ages and demonstrates notable prevalence rates, occurring in approximately 15% of women and 8% of men.[12] The conditions epidemiology unfolds intriguing patterns across sex, age, and geographical differences.[6][13][14]

Demographics 

Though affecting around 1.8 individuals per 1000 patients annually, GTPS is more prevalent in women. Studies across the globe, including the US, Korea, and Finland, report a 2- to 5-fold higher risk compared to men. This disparity points towards the influence of sex hormones, anatomical differences, and biomechanics.[6] Individuals between 40 and 60 years bear the brunt of GTPS, with a peak incidence ranging from around 40 to 50 years. This trend appears universal, as observed in US, Europe, and Asia studies. Interestingly, a potential second peak in younger active populations emerges, highlighting the interplay of age with other risk factors.[14][15]

Beyond Demographics: A Deeper Dive

Research consistently identifies a strong association between GTPS and higher body mass index (BMI). The increased mechanical stress on the hip joint in obese individuals likely plays a key role, with US studies reporting a 2.8-fold higher incidence rate in individuals with high BMI. Furthermore, repetitive tasks involving hip flexion and abduction (eg, running and stair climbing) can lead to overuse and inflammation and have been associated with GTPS development.[14]

Biomechanical imbalances also contribute to GTPS. Underlying issues like leg length discrepancies or weak pelvic floor muscles can alter normal stress distribution in the hip joint, potentially influencing GTPS risk. Additionally, conditions like diabetes or inflammatory arthritis might indirectly influence GTPS development through their systemic effects on inflammation and tissue health.[15]

Nuances within the Syndrome

Snapping hip exhibits similar epidemiological patterns to GTPS, with a prevalence favoring females and a potential association with increased BMI. This suggests shared risk factors and potential interconnectedness within the syndrome.[6] Additionally, individuals with femoroacetabular impingement (FAI) and bursitis, characterized by bony abnormalities in the hip joint, might have a higher risk of chronic bursitis, with a 7% prevalence observed in one study. This highlights the complex interplay of anatomical factors and their potential contribution to specific subcategories within GTPS.[5]

A Global Mosaic

Due to diverse diagnostic approaches and reporting practices, capturing an exact global picture of GTPS remains challenging.[6] Data suggests higher reported prevalence in developed nations, potentially reflecting factors like sedentary lifestyles, obesity rates, and healthcare access.[14] Limited access to healthcare and diverse lifestyles might mask the true extent of GTPS in developing nations, necessitating further research and awareness efforts.[15]

Pathophysiology

GTPS involves more than the historically implicated bursal inflammation besides the greater trochanter; GTPS is a complex condition influenced by interactions among various tissues under mechanical stress.[12][14] Although some patients with GTPS exhibit bursitis, bursal inflammation is often a secondary complication resulting from repetitive friction between the greater trochanter and the iliotibial band (ITB), commonly due to activities (eg, running or stair climbing). This repetitive motion is thought to cause microtrauma, where the gluteal tendons, mainly the gluteus medius and minimus, attach to the greater trochanter.[5][16]

This microtrauma can incite changes within the tendons, beginning with local inflammation and the release of inflammatory mediators.[2] This process can lead to a vicious cycle of tissue degradation and attempted repair. With ongoing stress, the pathology evolves into a disorganized state of collagen within the tendons.[12] Research indicates a decrease in the tendon's primary structural component, type 1 collagen, and an increase in type 3 collagen, which is mechanically inferior, leading to weakened tendons and continued microtrauma.[9][16] Moreover, chronic stress may cause hypercellularity and an excessive increase in cell numbers, which, despite being a reparative response, may further disrupt tissue organization and compromise tendon integrity. Proteoglycan content and new blood vessel formation also increase, potentially changing the tendon's biomechanical properties and contributing to pain.[9][14][16]

History and Physical

Clinical History

Conducting a comprehensive history and physical is key for diagnosing lateral hip pain.[12][14][17] Practitioners should understand the primary nature of the complaint, the onset, and duration of symptoms, how symptoms have progressed over time, factors that aggravate or alleviate the pain, and any prior treatments attempted, including nonsurgical interventions such as activity modifications, physical therapy, and medication.[1][6] Additionally, clinicians should inquire about any history of trauma, the mechanism of injury, specific characteristics of the pain, and the patient's medical and surgical history, encompassing conditions like hypertension, diabetes mellitus, rheumatologic illnesses, and cancer.[14]

Key clinical manifestations of greater trochanteric pain syndrome (GTPS) typically include lateral hip tenderness, discomfort during hip rotation, abduction, adduction, resistance to hip abduction, and positive outcomes on Patrick-FABER testing.[12] Patients often describe posterolateral thigh or back pain radiating down the leg, paresthesias, and difficulty lying on the affected side, with symptoms sometimes persisting from weeks to years before treatment.[18][19]

Aggravating factors include side-bending, sleeping on the painful side, and prolonged sitting.[12] Concurrent back and hip pain with neural symptoms like weakness or numbness may indicate spinal pathology. Mechanical symptoms, including snapping and popping, may signify specific structural abnormalities. Many patients attempt various treatments before presentation; therefore, documenting their history of physical therapy, medications, injections, and any previous hip surgeries is essential, particularly if they've had a trochanteric osteotomy or surgery involving the abductors.[14][20]

Physical Exam A summary of the GTPS physical exam is presented in the following table, followed by a detailed hip evaluation.[17]

Table

Table. Greater Trochanteric Pain Syndrome Clinical Examination.

Systemic Hip Examination

A careful assessment of the patient's history, examination, and systematic diagnostic evaluation are essential for an accurate diagnosis. Physical examination should begin with documentation of vital signs.[5] Febrile patients with hip pain must be evaluated for possible septic hip arthritis. Attention should be paid to the position in which the patient keeps the hip while at rest.[19][21] Patients with synovitis or a hip effusion often keep the hip in a flexed, abducted, and externally rotated position, placing the hip capsule at its largest potential volume. The following comprehensive hip exam should be performed to determine if findings most indicative of GTPS pathology are present:[12][17]

Standing hip exam

The examination includes general body habitus (eg, BMI and alignment), gait stability/alignment, and leg stance. Clinical observation of abnormal gait patterns, such as antalgic gait, abductor-deficient gait (ie, Trendelenburg gait), pelvic wink, excessive internal or external rotation, short leg limp, and abnormal foot progression, must be evaluated.[19] An antalgic gait will have a shortened stance phase, indicative of hip, pelvic, or lower back pain. A Trendelenburg gait is characteristic of abductor weakness. During the evaluation, the pelvis will drop on the contralateral side during the stance phase of gait. The gluteus medius and minimus are not strong enough to keep the pelvis level; as this weakness progresses, a compensatory weight shift toward the affected side may occur.[19] The single-leg stance phase stance is similar to the Trendelenburg test and helps identify a patient with weakened abductor muscles. Single-leg stance evaluates the mechanics of the hip abductor musculature and proprioception.[17] While standing, the patient lifts the unaffected leg forward to 45-degree hip flexion and 45-degree knee flexion while holding this position for 6 seconds. A positive test is a pelvic shift or a decrease of >2 cm. 

Seated hip exam

The seated exam evaluates motor function, sensation, and circulation. Motor functions include assessing muscles supplied by various nerves, including the femoral, obturator, superior gluteal, and sciatic nerves.

Supine hip exam

While the patient is supine, evaluate the hip range of motion with a specific concentration on flexion, extension, adduction, and abduction. The internal rotation at the hip evaluates the stability of the pelvis with flexion at 90 degrees with a neutral abduction angle.[17] There are specific provocative maneuvers that can enhance the physical examination: 

• FADDIR: Performed by flexion, adduction, and internal thigh rotation at 90 degrees. A positive test results when there is anterior or anteromedial pain. This occurs due to the impingement of the anterior and anterolateral part of the femoral neck against the superior and anterior acetabular rim.
• Superiorolateral impingement test: This is performed with passive movement of the thigh into flexion and external rotation. A positive test results when there is the recreation of anterolateral pain. This indicates the impingement of the superior and superolateral part of the head-neck junction against the superior or acetabular rim. 
• DEXRIT/DIRI: The dynamic external rotatory impingement test and dynamic internal rotatory impingement test consist of flexing the contralateral leg while bringing the affected hip to a 90-degree flexion. In the DEXRIT test, the hip is passively ranged through a wide arc of abduction and external rotation. In the DIRI, the hip passively ranges through a wide arc of adduction and internal rotation. For both maneuvers, the reproduction of a patient's pain in a specific position will correlate with the site of bony impingement in a clockwise fashion. 
• FABER: This test involves flexion, abduction, and external hip rotation. The FABER test facilitates the differentiation of hip pain in the abducted position and is conducted by palpating the greater trochanter with resisted hip abduction and external derotation.
• Posterior rim impingement: The patient is positioned at the bed's edge, legs hanging freely. The patient draws up both legs toward the chest, eliminating lumbar lordosis. The affected leg is then extended off the table while abducting and externally rotating the hip into full extension. This allows the evaluation of the congruence of the posterolateral part of the femoral neck against the posterior acetabular rim. A positive test is noted when posterior pain is recreated at this position; if anterior pain is recreated, the patient may be diagnosed with hip instability. 

Prone hip exam

The prone position is optimal for identifying the precise location of pain related to the sacroiliac (SI) joint region and assessing femoral anteversion. Craig's test is performed by flexing the knee to 90 degrees, and while using the leg as a lever, the hip is internally rotated until the greater trochanter is felt to be most prominent. Femoral anteversion, normally between 8 and 15 degrees, or retroversion, is measured by the angle between the tibia and an imaginary vertical line. If there is a significant difference in IR in the extended and seated flexed position, the examiner should differentiate between osseous and ligamentous causes.

Focused Exam for Greater Trochanteric Pain Syndrome 

Greater trochanteric bursitis

Patients often report unilateral lateral hip pain that can be localized to a specific area directly over the greater trochanter of the proximal femur. This discomfort is typically reproduced by palpating the greater trochanter, indicating inflammation of the bursa.[19] Additionally, patients may exhibit an antalgic gait or a Trendelenburg gait. The pain usually develops gradually, but the patient can still ambulate. Patients can typically perform a straight leg raise without pain, and the execution of a log roll, which involves the internal and external rotation of the leg at the hip joint with the hip flexed to 90°, should not elicit hip joint pain. This discomfort frequently intensifies with prolonged activity or movements that require pelvic stabilization, such as standing on one leg. The skin typically appears normal upon examination, with no signs of erythema or increased warmth. Pain is often induced by femur adduction and alleviated by abduction, as these movements create and relieve tension on the overlying iliotibial band (ITB).[17]

External snapping hip (coxa saltans)

External snapping hip syndrome, or coxa saltans, is characterized by an audible or palpable snap in the hip joint. This snapping or sensation of subluxation of the hip (ie, pseudosubluxation) can often be directly visualized or palpated under the patient's skin and confirmed by palpating the greater trochanter as the hip is flexed. Applying pressure will likely stop the snapping, confirming the diagnosis.[17]

The area over the greater trochanteric region may be painful due to concomitant greater trochanter bursitis, abductor tendon pathology, or inflammation of the iliotibial band. The patient is placed in a lateral position to test for external snapping hip, and the Ober test is performed to assess for iliotibial band tightness. While the patient is in this same position, the knee and hip can be cycled through flexion, abduction, and external rotation to extension, adduction, and internal rotation to provoke the snapping. The Ober test can also be performed with the hip in extension, neutral, and flexion when assessing for contractures of the ITB.[21]

 Abductor Tendonitis

Patients with abductor tendinopathy typically present with lateral proximal hip pain that is chronic and progresses gradually over time. The pain often worsens with lying on the affected side or activities like walking and stair climbing that load the abductors.[19] Examination reveals exquisite tenderness to palpation along the anterior greater trochanter and pain and weakness with resisted hip abduction testing.[17]

Additional hallmark examination findings for abductor tendinopathy and GTPS include a positive Trendelenburg sign and pain with resisted external hip rotation. The Trendelenburg sign indicates proximal abductor weakness when the patient's torso leans over the affected hip due to the inability of the gluteals to stabilize the pelvis. Resisted rotation testing helps distinguish cases of GTPS from intra-articular hip pathologies. Clinicians can also assess single-leg standing and perform" a "jump "sign" by directly palpating the greater trochanter to differentiate GTPS from other lateral hip pain etiologies.[21]

Evaluation

Diagnostic Imaging Studies

The primary imaging techniques utilized for GTPS diagnosis include plain x-rays, ultrasound, and magnetic resonance imaging (MRI).[22]

X-rays

Initial plain films help evaluate lateral hip pain by excluding intraarticular pathologies, including osteoarthritis, femoroacetabular impingement, and dysplasia.[23] This allows the identification of alternate symptom etiologies before instituting greater trochanteric pain syndrome (GTPS) treatment. Diagnostic anesthetic-corticosteroid injections also distinguish intraarticular versus extrinsic lateral hip pain generators while potentially alleviating symptoms. Plain films are often normal in GTPS, though may reveal intrabursal calcifications, abductor tendinosis, or enthesophytes. However, these signs demonstrate low sensitivity and specificity. Plain films lack distinct findings but remain valuable for ruling out competing diagnoses so appropriate GTPS therapy can be initiated without unnecessary advanced imaging. A diagnostic injection assesses the hip joint while providing therapeutic confirmation if lateral symptoms resolve.[24]

Magnetic resonance imaging

Magnetic resonance imaging (MRI) represents the diagnostic cornerstone for GTPS, excellently delineating intra- and extra-articular hip structures.[23] MRI visualizes inflammation surrounding the greater trochanter, consistent with trochanteric bursitis. Characteristic MRI findings of gluteus medius tendinosis include tendon thickening and increased T2 signal, while partial and complete tear morphologies are well delineated. Multiple analyses validate MRI accuracy against operative inspection, proving high sensitivity and specificity for abductor tears. Studies also reveal patients with torn gluteus medius frequently exhibit ipsilateral tensor fascia lata hypertrophy, plausibly compensating for weakened abductors.[22]

Ultrasonography

Ultrasound is a rapid, accessible adjuvant to MRI, enabling dynamic visualization ideal for external snapping hip where the trochanter moves against the iliotibial band.[23] Targeted palpation and diagnostic injections can precisely pinpoint pain generators. Tendinosis appears as tendon thickening with lost fibrillar pattern and hypoechoic fluid. Bursitis manifests as anechoic fluid distending the subgluteus maximus or medius bursae. Reviews demonstrate ultrasound boasts high sensitivity and positive predictive value for abductor abnormalities. A specific analysis of hip ultrasounds in GTPS patients revealed prevalent gluteal tendinosis and iliotibial band thickening, while bursitis proved less common.[22]

Treatment / Management

Nonsurgical ManagementNonsurgical management of GTPS typically begins with conservative interventions like activity modification and physical therapy, which include exercises aimed at strengthening and stretching the muscles around the hip.[12][5] Weight management is also advised when relevant. Pharmaceutical treatments often involve NSAIDs for their anti-inflammatory effects, although they must be used cautiously in patients with certain health risks.[19] Corticosteroid injections are another common treatment, providing targeted relief. Advanced therapies, including platelet-rich plasma (PRP) injections and extracorporeal shock wave therapy (ESWT), have been explored for cases resistant to these measures, with ESWT showing particular promise when combined with exercise regimens.[21] The success rate of these conservative measures is high, with most patients experiencing resolution of symptoms.[5]

Pharmacologic therapy

Oral NSAIDs are crucial for inhibiting the inflammatory cascade and providing symptomatic pain relief for trochanteric bursitis symptoms. However, before initiating NSAIDs, it is essential to confirm that patients have no contraindications. Individuals currently taking blood thinners or at high risk of gastrointestinal (GI) bleeding should avoid NSAID therapy.[5][25]

Physical therapy

Physical therapy focused on quadriceps strengthening and ITB stretching is important for addressing the underlying pathology.[12] In addition, hip abduction exercises should be incorporated to enhance the stretching and strengthening of the gluteus medius and gluteus minimus muscles.[12][13] Instructing adolescent athletes on proper running and jumping techniques is crucial to preserving hip mobility and flexibility during trochanteric bursitis treatment.[3][26][25]

• Quadriceps strengthening and iliotibial band (ITB) stretching address muscle imbalances and tightness that can contribute to GTPS.[25]
• Hip abduction exercises further enhance the strengthening of the gluteal muscles.
• Educating young athletes on proper running and jumping techniques helps prevent future recurrences and maintain hip mobility during treatment.
• Eccentric exercise (EE) is recognized as a superior approach when compared to a generic exercise regimen. Research has shown that the gradual introduction of eccentric training results in significant strength improvements in older adults without concomitant adverse changes in clinical markers of muscle damage (serum creatine kinase, tumor necrosis factor).[27]

Corticosteroid injections

Trochanteric bursitis can be effectively managed with steroid injections.[12][25] These injections administer a localized dose of cortisone, frequently combined with a local anesthetic (eg, lidocaine). This treatment offers relief and directly targets local inflammation; orthopedic surgeons and primary care clinicians can administer it. These are minor outpatient procedures conducted using standard sterile techniques. Long-term outcomes are comparable between individuals who receive corticosteroid injections and those who undergo physical therapy.[14][25]

Corticosteroid injections have been widely studied, with symptom duration varying greatly among patients and improvements from treatment ranging significantly. No substantial difference was found between standard and ultrasound-guided injections, though the latter may benefit individuals with larger physiques.[19]

Platelet-rich plasma injections

The application of platelet-rich plasma (PRP) injections continues to be a subject of ongoing discussion within orthopedics and sports medicine.[15][28] A recent level I systematic review, which examined 3 randomized clinical trials (RCTs) and 2 case series from the literature, demonstrated patient improvement at 3- and 12-month follow-ups.[29] However, the review's authors recognized the limited availability of high-quality evidence conclusively favoring PRP injections over the nonoperative approaches mentioned earlier.[16] As a result, PRP is not considered the standard of care for greater trochanteric bursitis.[3][13][20]

Extracorporeal shock wave therapy

Extracorporeal shock wave therapy (ESWT) is an effective treatment for GTPS, especially in cases where high signals are evident on MRI.[19] Furia et al found ESWT to be more effective than corticosteroid injections or home exercises in treating the condition.[30] Combining ESWT with a specific exercise regimen has demonstrated a success rate of 86.8% in just 2 months after therapy, proving its safety and effectiveness in addressing GTPS.[28]

Surgical Management

Surgical intervention for GTPS should be reserved for patients with symptoms exceeding 6 to 12 months who haven't responded to conservative treatment. The chosen technique depends on the pain's etiology, and both open and endoscopic approaches are available.[5]

Trochanteric bursitis

Surgical management of recalcitrant greater trochanteric bursitis has an extensive track record spanning decades. Open techniques combining iliotibial band (ITB) release with trochanteric bursectomy were first popularized by Brooker in 1979. While the technique has evolved, both open and arthroscopic approaches incorporate sharp debridement and excision of inflamed bursal tissue.[31] Key technical aspects emphasized by experienced surgeons include adequately removing the subgluteal bursa, reducing greater trochanter prominence, and performing an ITB release over the trochanter's anterior facet.[17][28][31]

Multiple small case series demonstrate good outcomes after open ITB release and bursectomy. A study of 12 bursitis patients undergoing trochanteric osteotomy noted 11 patients reporting great or very great improvement at average 2-year follow-up despite 5 patients having already failed prior open procedures.[32] Isolated arthroscopic bursectomy also shows favorable results. Two series detail significant improvement in functional scores and pain with few recurrences or revisions needed.[33][34]

External snapping hip

Multiple surgical techniques effectively treat the external snapping hip, which arises from the posterior iliotibial band (ITB) thickening and repeatedly snapping over the greater trochanter during hip motion. Open and arthroscopic approaches to ITB release have reduced pain and snapping.[35] The open release includes an ITB Z-plasty combined with a greater trochanteric bursectomy.[36] These procedures demonstrate high rates of symptom relief with minimal need for revision. Arthroscopic techniques also show efficacy using a diamond-shaped ITB fenestration over the greater trochanter. Despite increased cost and time, the arthroscopic approach results in a faster recovery. While high-quality comparative effectiveness data is lacking across multiple case series, open and arthroscopic ITB releases provide reliable refractory external snapping hip options.[35][36]

Hip abductor tears

Treatment decisions for torn hip abductors now mirror the progression once seen for rotator cuff repairs. Both open and arthroscopic techniques successfully treat partial and full-thickness tears. For irreparable tears, transfers or allograft augmentation have been utilized. 

Full-thickness gluteus medius tears are increasingly recognized, with multiple case series reporting a prevalence between 20% and 25% during arthroplasty.[37] Open repairs employ suture anchors or transosseous trochanteric drilling.[38] A series of 72 open repairs showed 95% of patients exhibiting decreased pain and improved function at 1 year. Another group developed a tear classification scheme, finding significant gains in Harris hip scores comparable to arthroplasty outcomes.[39] However, those with massive tears fared poorly. Though no comparative effectiveness trials exist, most authors advise open techniques for more giant chronic tears.

Endoscopic abductor repair has also been described and demonstrates similar favorable outcomes.[39][40] Reports describe combined arthroscopic treatment of intra-articular hip disease alongside gluteus medius repair via separate peritrochanteric portals. At minimum 2-year follow-up, patients exhibit decreased pain and improved strength.[40]

Differential Diagnosis

The following conditions are some of the differential diagnoses of lateral hip pain that should be considered as GTPS can be challenging, even for the most experienced clinicians:

 Table. Differential Diagnoses for Greater Trochanteric Pain Syndrome

Table

Associated Etiology Involved Joint

DDX references.[1][12]

Prognosis

Preexisting conditions, therapeutic decisions, and individual patient responses significantly affect the progression of GTPS.[12][19] Although outcomes are typically favorable, the course of GTPS can be complicated, with a notable recurrence rate following initial, temporary pain relief from medications.[5] Lievense et al reported that patients with concurrent osteoarthritis are 4.8 times more likely to experience persistent symptoms 1 year after treatment.[5] Additionally, corticosteroid treatments, while effective, are associated with a 2.7-fold increase in the likelihood of symptom recurrence within a 5-year timeframe.[5]

The impact of trochanteric bursitis transcends clinical symptoms, affecting both work and leisure activities. Approximately 34% of affected individuals report significant occupational impairment, and 25% have missed work due to the condition.[25][41] Moreover, sleep disturbances afflict 40% of sufferers, and more than half report a substantial decline in sports performance, highlighting the widespread effects of the condition. Conservative management has proven effective, with Schapira et al observing rapid and enduring pain relief after local corticosteroid and anesthetic injections in 90.3% of patients.[42] Some studies have suggested that topical NSAIDs are as beneficial as oral NSAIDs in managing symptoms of GTPS.[9]

Complications

GTPS significantly impairs daily functioning beyond the primary symptomatology of hip pain.[5] The syndrome seldom presents direct complications; however, its chronic pain and resultant functional deficits profoundly diminish the quality of life. GTPS patients frequently encounter difficulties with routine ambulation, stair navigation, and bed transfers, resulting in the following:

• Diminished physical activity: Anticipatory pain avoidance and mobility restrictions commonly precipitate a decline in physical activity, detrimentally affecting health and fitness parameters.
• Occupational interference: Functional impairments may compromise occupational performance, catalyzing absenteeism and diminished work efficacy.
• Social withdrawal: Pain-related activity limitations can induce isolation and reduce participation in social and recreational endeavors, adversely affecting psychosocial health.

The therapeutic modalities for GTPS, while alleviating symptoms, present potential adverse effects. NSAIDs, for instance, pose risks of gastric mucosal damage and hemorrhage, with heightened risk profiles in patients with comorbidities or concurrent anticoagulant therapy.[9] Anemia awareness is vital due to the possibility of covert gastrointestinal bleeding. Corticosteroid injections offer analgesia but are not devoid of risks, including hyperglycemia, particularly in diabetics, and postinjection site complications.[21]

Deterrence and Patient Education

Effective management of GTPS hinges on clear communication and setting realistic patient expectations.[19] Clinicians should help patients comprehend that conservative approaches such as physical therapy and activity modifications may require 3 months or more to alleviate symptoms fully. Stressing adherence to these treatment regimens is critical to achieving optimal outcomes. Additionally, patients should be informed of the potential long-term risks, including tendon weakening associated with corticosteroid injections, to make informed treatment decisions.[21]

Preventative strategies, including appropriate stretching and training, are advantageous for young athletes, yet many GTPS cases stem from trauma or indeterminate origins.[19] In these instances, highlighting the generally favorable prognosis and effectiveness of conservative management is crucial. The early use of anti-inflammatory medications, possibly in conjunction with corticosteroid injections, and reassuring patient communication often results in symptom resolution and high patient satisfaction. In cases where conservative treatments fail, surgical options may be explored for chronic or recurrent GTPS. Patients must be apprised of the variable success rates and possible complications of surgical interventions. Open dialogue and well-grounded expectations are instrumental in equipping patients to manage their condition effectively.

Pearls and Other Issues

Key facts to bear in mind regarding GTPS include:

• Conservative treatment is the gold standard for GTPS, with a success rate of over 90%.
• Greater trochanteric pain syndrome is often underdiagnosed. 
• GTPS can take 3 months or longer to resolve, and educating the patient about this timeline is essential.
• Physical therapy and activity modifications need to be encouraged.
• Corticoid steroid injections may potentially weaken the tendon structure in the long term.

Enhancing Healthcare Team Outcomes

An evidence-based, standardized protocol for GTPS management remains elusive; however, outcomes are notably improved with an interprofessional healthcare team approach. Such teams generally comprise medical professionals, including physicians, osteopathic doctors, nurse practitioners, physician assistants, orthopedic specialists, chiropractors, physical therapists, and nursing staff. Essential to this interprofessional strategy is maintaining open communication and meticulous documentation of patient encounters, treatment interventions, and progress. Such practices are critical to ensuring precise diagnoses and efficacious treatment plans, ultimately contributing to superior patient outcomes.[21]

Primary care clinicians often serve as the first point of contact. They are pivotal in diagnosing and managing trochanteric bursitis, which can significantly reduce healthcare expenditures by averting unnecessary specialist referrals. While a majority of patients report favorable outcomes, clinicians should recognize that the recovery period can span several weeks and, in some cases, may necessitate a referral to an orthopedic surgeon for potential surgical intervention.[35]

Review Questions

• Access free multiple choice questions on this topic.
• Comment on this article.

References

1.

Livingston JI, Deprey SM, Hensley CP. DIFFERENTIAL DIAGNOSTIC PROCESS AND CLINICAL DECISION MAKING IN A YOUNG ADULT FEMALE WITH LATERAL HIP PAIN: A CASE REPORT. Int J Sports Phys Ther. 2015 Oct;10(5):712-22. [PMC free article: PMC4595924] [PubMed: 26491621]

2.

Williams BS, Cohen SP. Greater trochanteric pain syndrome: a review of anatomy, diagnosis and treatment. Anesth Analg. 2009 May;108(5):1662-70. [PubMed: 19372352]

3.

Fearon A, Stephens S, Cook J, Smith P, Neeman T, Cormick W, Scarvell J. The relationship of femoral neck shaft angle and adiposity to greater trochanteric pain syndrome in women. A case control morphology and anthropometric study. Br J Sports Med. 2012 Sep;46(12):888-92. [PMC free article: PMC3597182] [PubMed: 22547561]

4.

Strauss EJ, Nho SJ, Kelly BT. Greater trochanteric pain syndrome. Sports Med Arthrosc Rev. 2010 Jun;18(2):113-9. [PubMed: 20473130]

5.

Lievense A, Bierma-Zeinstra S, Schouten B, Bohnen A, Verhaar J, Koes B. Prognosis of trochanteric pain in primary care. Br J Gen Pract. 2005 Mar;55(512):199-204. [PMC free article: PMC1463090] [PubMed: 15808035]

6.

Segal NA, Felson DT, Torner JC, Zhu Y, Curtis JR, Niu J, Nevitt MC., Multicenter Osteoarthritis Study Group. Greater trochanteric pain syndrome: epidemiology and associated factors. Arch Phys Med Rehabil. 2007 Aug;88(8):988-92. [PMC free article: PMC2907104] [PubMed: 17678660]

7.

Robertson WJ, Gardner MJ, Barker JU, Boraiah S, Lorich DG, Kelly BT. Anatomy and dimensions of the gluteus medius tendon insertion. Arthroscopy. 2008 Feb;24(2):130-6. [PubMed: 18237695]

8.

Tsutsumi M, Nimura A, Akita K. The Gluteus Medius Tendon and Its Insertion Sites: An Anatomical Study with Possible Implications for Gluteus Medius Tears. J Bone Joint Surg Am. 2019 Jan 16;101(2):177-184. [PubMed: 30653048]

9.

Reid D. The management of greater trochanteric pain syndrome: A systematic literature review. J Orthop. 2016 Mar;13(1):15-28. [PMC free article: PMC4761624] [PubMed: 26955229]

10.

Pfirrmann CW, Chung CB, Theumann NH, Trudell DJ, Resnick D. Greater trochanter of the hip: attachment of the abductor mechanism and a complex of three bursae--MR imaging and MR bursography in cadavers and MR imaging in asymptomatic volunteers. Radiology. 2001 Nov;221(2):469-77. [PubMed: 11687692]

11.

Tibor LM, Sekiya JK. Differential diagnosis of pain around the hip joint. Arthroscopy. 2008 Dec;24(12):1407-21. [PubMed: 19038713]

12.

Redmond JM, Chen AW, Domb BG. Greater Trochanteric Pain Syndrome. J Am Acad Orthop Surg. 2016 Apr;24(4):231-40. [PubMed: 26990713]

13.

Stephens G, O'Neill S, Mottershead C, Hawthorn C, Yeowell G, Littlewood C. "It's just like a needle going into my hip, basically all of the time". The experiences and perceptions of patients with Greater Trochanteric Pain syndrome in the UK National Health Service. Musculoskelet Sci Pract. 2020 Jun;47:102175. [PubMed: 32452392]

14.

Speers CJ, Bhogal GS. Greater trochanteric pain syndrome: a review of diagnosis and management in general practice. Br J Gen Pract. 2017 Oct;67(663):479-480. [PMC free article: PMC5604828] [PubMed: 28963433]

15.

Bicket L, Cooke J, Knott I, Fearon A. The natural history of greater trochanteric pain syndrome: an 11-year follow-up study. BMC Musculoskelet Disord. 2021 Dec 20;22(1):1048. [PMC free article: PMC8691027] [PubMed: 34930192]

16.

Silva F, Adams T, Feinstein J, Arroyo RA. Trochanteric bursitis: refuting the myth of inflammation. J Clin Rheumatol. 2008 Apr;14(2):82-6. [PubMed: 18391676]

17.

Bird PA, Oakley SP, Shnier R, Kirkham BW. Prospective evaluation of magnetic resonance imaging and physical examination findings in patients with greater trochanteric pain syndrome. Arthritis Rheum. 2001 Sep;44(9):2138-45. [PubMed: 11592379]

18.

Poultsides LA, Bedi A, Kelly BT. An algorithmic approach to mechanical hip pain. HSS J. 2012 Oct;8(3):213-24. [PMC free article: PMC3470663] [PubMed: 24082863]

19.

Pianka MA, Serino J, DeFroda SF, Bodendorfer BM. Greater trochanteric pain syndrome: Evaluation and management of a wide spectrum of pathology. SAGE Open Med. 2021;9:20503121211022582. [PMC free article: PMC8182177] [PubMed: 34158938]

20.

Sayegh F, Potoupnis M, Kapetanos G. Greater trochanter bursitis pain syndrome in females with chronic low back pain and sciatica. Acta Orthop Belg. 2004 Oct;70(5):423-8. [PubMed: 15587030]

21.

Ho GW, Howard TM. Greater trochanteric pain syndrome: more than bursitis and iliotibial tract friction. Curr Sports Med Rep. 2012 Sep-Oct;11(5):232-8. [PubMed: 22965345]

22.

Kong A, Van der Vliet A, Zadow S. MRI and US of gluteal tendinopathy in greater trochanteric pain syndrome. Eur Radiol. 2007 Jul;17(7):1772-83. [PubMed: 17149624]

23.

Westacott DJ, Minns JI, Foguet P. The diagnostic accuracy of magnetic resonance imaging and ultrasonography in gluteal tendon tears--a systematic review. Hip Int. 2011 Nov-Dec;21(6):637-45. [PubMed: 22038311]

24.

Hartigan DE, Perets I, Walsh JP, Domb BG. Imaging of Abductor Tears: Stepwise Technique for Accurate Diagnosis. Arthrosc Tech. 2017 Oct;6(5):e1523-e1527. [PMC free article: PMC5709972] [PubMed: 29354468]

25.

Lustenberger DP, Ng VY, Best TM, Ellis TJ. Efficacy of treatment of trochanteric bursitis: a systematic review. Clin J Sport Med. 2011 Sep;21(5):447-53. [PMC free article: PMC3689218] [PubMed: 21814140]

26.

Rowand M, Chambliss ML, Mackler L. Clinical inquiries. How should you treat trochanteric bursitis? J Fam Pract. 2009 Sep;58(9):494-500. [PubMed: 19744419]

27.

Harris-Love MO, Seamon BA, Gonzales TI, Hernandez HJ, Pennington D, Hoover BM. Eccentric Exercise Program Design: A Periodization Model for Rehabilitation Applications. Front Physiol. 2017;8:112. [PMC free article: PMC5322206] [PubMed: 28280471]

28.

Rompe JD, Segal NA, Cacchio A, Furia JP, Morral A, Maffulli N. Home training, local corticosteroid injection, or radial shock wave therapy for greater trochanter pain syndrome. Am J Sports Med. 2009 Oct;37(10):1981-90. [PubMed: 19439758]

29.

Mautner K, Colberg RE, Malanga G, Borg-Stein JP, Harmon KG, Dharamsi AS, Chu S, Homer P. Outcomes after ultrasound-guided platelet-rich plasma injections for chronic tendinopathy: a multicenter, retrospective review. PM R. 2013 Mar;5(3):169-75. [PubMed: 23399297]

30.

Furia JP, Rompe JD, Maffulli N. Low-energy extracorporeal shock wave therapy as a treatment for greater trochanteric pain syndrome. Am J Sports Med. 2009 Sep;37(9):1806-13. [PubMed: 19439756]

31.

Brooker AF. The surgical approach to refractory trochanteric bursitis. Johns Hopkins Med J. 1979 Sep;145(3):98-100. [PubMed: 470296]

32.

Govaert LH, van der Vis HM, Marti RK, Albers GH. Trochanteric reduction osteotomy as a treatment for refractory trochanteric bursitis. J Bone Joint Surg Br. 2003 Mar;85(2):199-203. [PubMed: 12678352]

33.

Fox JL. The role of arthroscopic bursectomy in the treatment of trochanteric bursitis. Arthroscopy. 2002 Sep;18(7):E34. [PubMed: 12209419]

34.

Baker CL, Massie RV, Hurt WG, Savory CG. Arthroscopic bursectomy for recalcitrant trochanteric bursitis. Arthroscopy. 2007 Aug;23(8):827-32. [PubMed: 17681203]

35.

Ilizaliturri VM, Martinez-Escalante FA, Chaidez PA, Camacho-Galindo J. Endoscopic iliotibial band release for external snapping hip syndrome. Arthroscopy. 2006 May;22(5):505-10. [PubMed: 16651159]

36.

Provencher MT, Hofmeister EP, Muldoon MP. The surgical treatment of external coxa saltans (the snapping hip) by Z-plasty of the iliotibial band. Am J Sports Med. 2004 Mar;32(2):470-6. [PubMed: 14977676]

37.

Howell GE, Biggs RE, Bourne RB. Prevalence of abductor mechanism tears of the hips in patients with osteoarthritis. J Arthroplasty. 2001 Jan;16(1):121-3. [PubMed: 11172282]

38.

Walsh MJ, Walton JR, Walsh NA. Surgical repair of the gluteal tendons: a report of 72 cases. J Arthroplasty. 2011 Dec;26(8):1514-9. [PubMed: 21798694]

39.

McCormick F, Alpaugh K, Nwachukwu BU, Yanke AB, Martin SD. Endoscopic repair of full-thickness abductor tendon tears: surgical technique and outcome at minimum of 1-year follow-up. Arthroscopy. 2013 Dec;29(12):1941-7. [PubMed: 24140139]

40.

Domb BG, Botser I, Giordano BD. Outcomes of endoscopic gluteus medius repair with minimum 2-year follow-up. Am J Sports Med. 2013 May;41(5):988-97. [PubMed: 23524152]

41.

Thomassen PJB, Basso T, Foss OA. Endoscopic Treatment of Greater Trochanteric Pain Syndrome - A Case Series of 11 Patients. J Orthop Case Rep. 2019 Jan-Feb;9(1):6-10. [PMC free article: PMC6588147] [PubMed: 31245309]

42.

Brinks A, van Rijn RM, Willemsen SP, Bohnen AM, Verhaar JA, Koes BW, Bierma-Zeinstra SM. Corticosteroid injections for greater trochanteric pain syndrome: a randomized controlled trial in primary care. Ann Fam Med. 2011 May-Jun;9(3):226-34. [PMC free article: PMC3090431] [PubMed: 21555750]

Disclosure: Laura Pumarejo Gomez declares no relevant financial relationships with ineligible companies.

Disclosure: Daniel Li declares no relevant financial relationships with ineligible companies.

Disclosure: John Childress declares no relevant financial relationships with ineligible companies.