My Hip Hurts
Aaron Gipsman, MD
Eric Strauss, MD, FAAOS
Matthew A. Varacallo, MD
Dr. Strauss or an immediate family member is a member of a speakers’ bureau or has made paid presentations on behalf of Arthrex, Inc., Organogenesis, Smith & Nephew, and Vericel; serves as a paid consultant to or is an employee of Arthrex, Inc., Fidia, Flexion Therapeutics, Joint Restoration Foundation, Organogenesis, Smith & Nephew, Subchondral Solutions, and Vericel; has stock or stock options held in Better PT; has received research or institutional support from Cartiheal, Fidia, and Organogenesis; and serves as a board member, owner, officer, or committee member of American Academy of Orthopaedic Surgeons, American Orthopaedic Association, and Arthroscopy Association of North America. Dr. Varacallo or an immediate family member serves as a paid consultant to or is an employee of Arthrex, Inc. Neither Dr. Gipsman nor any immediate family member has received anything of value from or has stock or stock options held in a commercial company or institution related directly or indirectly to the subject of this chapter.
Introduction
Hip pain can be related to injury, overuse, arthritis, and other chronic conditions. Four categories of hip disorders are considered. Femoroacetabular impingement (FAI) is a common cause of hip pain in adolescents and adults; it is characterized by abnormal contact between the proximal femur and acetabulum. The iliopsoas functions as the strongest flexor of the hip joint. Injury to the iliopsoas can result in disabling hip and groin pain, particularly in athletic populations. Pathologic conditions of the iliopsoas include strain, tendinitis, tear, bursitis, and internal snapping
hip syndrome. Hamstring injury severity can range from partial-thickness or full-thickness avulsions and retracted ruptures to chronic degenerative pathologies. Greater trochanteric pain syndrome encompasses a range of pathologies from trochanteric bursitis and lateral hip pain and snapping hip to full-thickness gluteus medius/minimus tears and tendinopathy, of which tendinopathy is the focus of this chapter. Injuries to the hip abductor complex in many ways mimic and run parallel to the pathophysiologic cascade and natural history of rotator cuff tears in the shoulder, and thus, these structures are often referred to as the rotator cuff tears of the hip.
hip syndrome. Hamstring injury severity can range from partial-thickness or full-thickness avulsions and retracted ruptures to chronic degenerative pathologies. Greater trochanteric pain syndrome encompasses a range of pathologies from trochanteric bursitis and lateral hip pain and snapping hip to full-thickness gluteus medius/minimus tears and tendinopathy, of which tendinopathy is the focus of this chapter. Injuries to the hip abductor complex in many ways mimic and run parallel to the pathophysiologic cascade and natural history of rotator cuff tears in the shoulder, and thus, these structures are often referred to as the rotator cuff tears of the hip.
FEMOROACETABULAR IMPINGEMENT
Epidemiology
Most patients are younger than 40 years.
Etiology is unknown but FAI is thought to be due to a combination of genetic and mechanical factors.
Activities involving repetitive hip movements at the extremes of motion, particularly hip flexion, increase the mechanical stresses on the proximal femur and acetabulum and predispose these areas to the development of a reactive bony lesion. This effect is especially pronounced in adolescents, in whom the growth pattern of the proximal femoral physis can be altered
Athletics associated with risk for FAI include ice hockey, soccer, dance, and football.
Up to 60% of active adolescents and young adults have radiographic signs of impingement, with many remaining asymptomatic.
Males and females are at similar risk of the development of FAI but are predisposed to different patterns of impingement.
Pincer lesions are more common among females, which is likely related to sex-related differences in acetabular morphology.
Males, in contrast, are more likely to have cam lesions, which is thought to be activity related.
A unique subgroup of FAI is related to sequelae from pediatric hip conditions
Slipped capital femoral epiphysis classically is associated with the development of a cam lesion, whereas Legg-Calvé-Perthes disease can lead to complex deformity of the proximal femur and adaptive changes to the acetabular morphology.1
Despite the differences in etiology, these patients are treated similarly to those with more classic presentations of FAI.
Pertinent Anatomy/Pathoanatomy
FAI occurs as a result of abnormal contact between the anterior femoral head-neck junction and anterosuperior acetabular rim with hip flexion and internal rotation. Over time, the increased contact pressure at the acetabular rim leads to injury to the cartilage and labrum.
Cam and pincer lesions are the characteristic deformities of FAI (Figure 1).
Cam deformity is characterized by the loss of the normal spherical contour of the proximal femur at the junction of the femoral head and neck.
Pincer deformity occurs when the acetabular rim covers too much of the femoral head. Less commonly, a prominent anterior inferior iliac spine can also act like a pincer.
Approximately half of patients with FAI have mixed-type impingement with both a cam and pincer lesion, with most of the remaining patients having an isolated cam deformity.1
Atraumatic hip instability is associated with FAI. Anterior bony impingement between the proximal femur and acetabulum can lever the femur posteriorly. This can worsen as the stabilizing effects of the anterior capsule and labrum attenuate, particularly among female patients with ligamentous laxity.
Although frank hip dislocation is uncommon, patients may experience recurrent subluxation events leading to functional limitations of hip motion and eventual posterior chondrolabral injury.
 Figure 1 Illustration shows that pincer impingement (red arrow) results from abnormal acetabular morphology, whereas cam impingement (black arrow) is caused by loss of the spherical contour of the proximal femur. (Reproduced with permission from Miller MD: Operative Techniques in Sports Medicine Surgery. Wolters Kluwer, 2022, Figure 50.1.) |
Pertinent History/Physical Examination Findings
Patients with FAI report a gradual onset of hip and/or groin pain, typically without an inciting event.
Pain is worse with hip flexion, including sporting activities and sitting for prolonged periods. Mechanical symptoms, such as clicking or locking, can be indicative of a labral tear, subtle instability, or associated snapping hip syndrome.
Examination is significant for painful and limited hip flexion and internal rotation.
Gait is often normal but can be antalgic in severe cases, characterized by a shortened stance phase on the affected side.
Figure 2 Photograph showing the flexion/adduction/internal rotation (or FADIR) impingement test. (Reproduced with permission from Johnson D: Operative Arthroscopy, ed 4. Wolters Kluwer, 2013, Figure 45.7.)
Impingement tests have a high sensitivity with moderate specificity for FAI.2
Flexion/adduction/internal rotation (FADIR) test (Figure 2): Examiner passively flexes the patient’s hip and knee to 90°, then adducts and internally rotates the hip. Pain and reproduction of the patient’s symptoms is suggestive of anterior hip impingement.
Flexion, abduction, and external rotation, known as FABER or Patrick test (Figure 3): Patient’s affected leg is placed in a figure-of-4 position, with the hip flexed, abducted, and externally rotated. The examiner stabilizes the pelvis with one hand, while applying an external rotation force to the affected limb. Hip and groin pain are suggestive of FAI, whereas buttock and low back pain are more reflective of sacroiliac or lumbar pathology.
In patients with suspected instability, an assessment of global ligamentous laxity is obtained using the Beighton criteria.
The dial test can also be used to specifically evaluate for hip capsular laxity. With the patient lying supine and the knee extended, the examiner holds the limb into terminal internal rotation, then releases the force. Positive result: foot subsequently falls into more than 45° of external rotation beyond neutral
 Figure 3 Photograph showing the flexion, abduction, and external fixation test, also known as FABER or Patrick test. (Reproduced with permission from Johnson D: Operative Arthroscopy, ed 4. Wolters Kluwer, 2013, Figure 45.9.) |
Relevant Imaging
Radiographic examination for FAI begins with an AP view of the pelvis and a frog-lateral view of the affected hip.
The Dunn and false-profile views are frequently used to obtain additional information about the bony morphology of the hip.
To obtain the Dunn view, the patient is positioned supine with the hip in neutral rotation, 45° or 90° of flexion, and 20° of abduction.
The false-profile view is obtained with the patient standing and facing away from the imaging plate at an angle of 65°.
The AP view should be carefully evaluated for joint space narrowing and subchondral sclerosis, indicative of early osteoarthritis.
The contour of the proximal femur should be evaluated on the frog-lateral and Dunn views, with loss of sphericity resembling a pistol grip being characteristic for a cam lesion.
Signs of acetabular retroversion, classically associated with pincer deformity, include the crossover sign, posterior wall sign, and the ischial spine sign.
The alpha angle is calculated using the frog-lateral or Dunn views.
A best-fit circle that is centered on the femoral head is used to determine the point on the anterolateral femoral neck where a loss of sphericity occurs.
The alpha angle is calculated between this point and a line parallel to the longitudinal axis of the femoral neck, with a value greater than 55° reflective of cam deformity.
Multiple parameters are used to evaluate for pincer impingement.
On the AP view, the lateral center-edge angle is calculated between a vertical line centered over the femoral head and the lateral edge of the acetabulum.
Similarly, the anterior center-edge angle can be calculated on the false profile view. A center-edge angle greater than 40° is suggestive of overcoverage and pincer impingement.
The Tönnis angle can also be used to evaluate for femoral head coverage on the AP view. It is determined using a horizontal line connecting the acetabular teardrops and a line tangential to the weight-bearing portion of the acetabulum, with an angle less than -10° being reflective of overcoverage.
MRI is frequently obtained to further evaluate the patient’s three-dimensional bony anatomy and identify associated soft-tissue pathology involving the labrum, cartilage, and hip musculature.
Bone marrow edema and cystic changes are frequently visualized on the anterosuperior aspect of the femoral neck. Chondrolabral detachment and degenerative tearing of the labrum with associated bony edema of the acetabular rim are commonly identified within its anterior and superolateral portions.3
Arthroscopic studies have found that the acetabular labrum is abnormal in greater than 90% of hips with FAI.1
Nonsurgical Measures
Always begin with nonsurgical measures, including activity modification, physical therapy, and NSAIDs.
Patients are instructed to avoid sitting for extended periods as well as squatting and other activities involving positions of high hip flexion.
Physical therapy focuses on strengthening of the hip flexors, hamstrings, abductors, and core musculature. Patients who do not improve with these initial treatments should receive an image-guided intra-articular corticosteroid injection.
Symptomatic relief can be expected as quickly as 6 weeks in responsive patients.
However, the success of nonsurgical treatment is mixed and appears to vary according to patient age.4
Up to 85% of adolescents experience a positive response to nonsurgical treatment and can return to sports, whereas closer to 50% of adults can expect to return to normal physical activity with nonsurgical treatment alone.5
Treatment response is not associated with the presence of labral tears or the magnitude of bony deformity.5
For patients who do not obtain any symptomatic relief from an injection, an alternative diagnosis of FAI should be considered.
Surgical Intervention
Surgery is indicated for patients with FAI in whom a trial of 3 to 6 months of nonsurgical treatment has failed, including a corticosteroid injection.5
The elements of surgery to correct FAI include femoroplasty to restore the normal spherical contour of the femoral head-neck junction, acetabuloplasty to remove the pincer lesion, and labral repair to redistribute contact pressures and restore the stabilizing suction seal.
Hip arthroscopy is performed with the patient in the supine position (Figure 4).
The hip is distracted using a perineal post and traction boots.
Fluoroscopic guidance is used to localize the anterolateral portal, immediately anterior to the tip of the greater trochanter.
The 70° arthroscope is inserted into the joint to visualize the articular surface of the femoral head and acetabulum, also known as the central compartment.
An anterior working portal is then made under direct visualization of the arthroscope, slightly distal to the level of the anterolateral portal and lateral to the anterior superior iliac spine to avoid injury to the lateral femoral cutaneous nerve.
Figure 4 Photograph showing typical portals used for hip arthroscopy, which include the anterolateral (dashed arrow) and anterior (solid arrow) portals. The posterolateral portal (white arrow) is commonly used for posterior labral repair and reconstruction. (Reproduced with permission from Miller MD: Operative Techniques in Sports Medicine Surgery. Wolters Kluwer, 2022, Figure 50.4.)
A capsulotomy is made between the two portals to facilitate access to the joint.
A diagnostic arthroscopy is done in the central compartment to evaluate the cartilage and labrum.
Detachment of the labrum at the chondrolabral junction is typically identified between the 10-o’clock and 2-o’clock positions on the acetabular rim.
A radiofrequency ablation device is used to débride soft tissue from the anterolateral acetabular rim, with care taken to avoid iatrogenic damage to the labral tissue.
A motorized burr is used to resect a pincer lesion if it is present, and fluoroscopy is used to confirm adequate resection.
In cases without a pincer, the burr is used to remove sclerotic cortical bone at the level of the planned labral repair.
Figure 5 Arthroscopic labral repair. The arthroscope is looking down at the acetabular rim (A) and femoral head (FH). Suture repair of the labrum (L) has been performed. The articular cartilage of the acetabulum is seen in the depth of the image to the left of the femoral head. (Reproduced with permission from Johnson D: Operative Arthroscopy, ed 4. Wolters Kluwer, 2013, Figure 48.11G.)
The labrum is repaired (Figure 5) using suture anchors, with knot-tying and knotless techniques providing similar clinical results.
The entry angle of the anchor should be away from the joint to minimize the risk of iatrogenic cartilage damage.
Repair of posterior labral tears often requires a posterolateral portal that is placed posterior the tip of the greater trochanter.
Management of chondral lesions of the acetabulum and femoral head remains controversial, with isolated débridement and microfracture most commonly used.
With work in the central compartment complete, traction is released and the hip is flexed to 45°.
The 70° arthroscope is directed into the extra-articular, intracapsular portion of the hip known as the peripheral compartment.
A radiofrequency ablation device is used to elevate adherent capsule off the femoral neck and femoral head-neck junction.
A motorized burr is then used to resect the cam lesion.
The hip is internally and externally rotated to access the lateral and medial edges of the lesion.
Adequate resection with restoration of the normal spherical contour of the proximal femur is confirmed with fluoroscopy.
Under direct visualization of the arthroscope, the hip is brought into high flexion and internal rotation to confirm that there is no residual impingement.
Closure of the hip capsule can then be performed with a suture passer, although the efficacy of capsular repair remains unclear.
Postoperative rehabilitation includes toe-touch or foot-flat weight bearing on the surgical extremity with an assistive device for the first 4 weeks postoperatively.
Hip flexion range of motion exercises can begin immediately, with supervised physical therapy beginning by the second week.
Many surgeons use a hinged hip brace in the early postoperative period to prevent positions of extreme hip extension, rotation, and abduction that can place excessive tension on the labral repair.
By 4 weeks postoperatively, patients can be advanced to weight bearing as tolerated. Hip and core strengthening exercises are introduced and progressively increased by week 8.
Running and sport-specific exercises can begin between 3 to 6 months postoperatively, with return to sport expected by 1 year.
Although hip arthroscopy is a safe and effective treatment for FAI, there is a steep surgeon learning curve that is associated with patient outcomes and the development of complications.
Iatrogenic chondral injury is the most common complication and occurs secondary to difficulty accessing the central compartment joint and/or improper surgical technique.
Neurapraxia of the pudendal nerve can result from prolonged traction time or improper positioning, whereas errant placement of the anterior portal results in transient or permanent injury of the lateral femoral cutaneous nerve. Less common complications include infection, venous thromboembolism, and broken instrumentation within the hip joint.
Postoperative hip instability is rare but can occur from extensive capsulotomy and acetabular resection in the setting of capsular laxity.
Following hip arthroscopy, most patients can reliably expect significant reduction in pain and improved function of the hip.
Return to sport is high among athletes, with rates approaching 90%.6
Poorer outcomes have been reported among older patients with early osteoarthritis, particularly those with less than 2 mm of joint space remaining.
Longer duration of symptoms, lower patient activity level, higher alpha angles, and limited preoperative range of motion all have been associated with worse outcomes.
Reoperation rates by 4 years postoperatively are approximately 6%, with most patients requiring total hip arthroplasty secondary to osteoarthritis.6
Top 10 Knowledge Drops for Your Rotation
Individuals at the highest risk of the development of FAI are athletes performing hip movements at the extremes of motion, including ice hockey, soccer, dance, and football.
Females are more likely to have pincer impingement, whereas males are more likely to have cam lesions.
Slipped capital femoral epiphysis is associated with the later development of a cam lesion.
Patients with FAI have pain with active hip flexion and sitting for prolonged periods.
Radiographic examination for FAI includes an AP view of the pelvis and frog lateral, Dunn, and false-profile views of the affected hip.
The alpha angle is used to identify loss of sphericity of the proximal femur reflective of cam deformity, whereas the lateral center-edge and Tönnis angles are used to identify acetabular overcoverage indicative of pincer deformity.
Chondrolabral detachment and degenerative tearing of the labrum are commonly identified at the anterior and superolateral portions of the acetabular rim between the 10-o’clock and 2-o’clock positions.
Surgical correction of FAI includes femoroplasty to restore the normal spherical contour of the femoral head-neck junction, acetabuloplasty to remove the pincer lesion, and labral repair to redistribute contact pressures and restore the stabilizing suction seal.
The most common complications of hip arthroscopy for FAI include iatrogenic chondral injury, traction injury to the pudendal nerve, and damage to the lateral femoral cutaneous nerve from anterior portal placement.
Patients with less than 2 mm of remaining joint space have poorer outcomes following hip arthroscopy for FAI.
ILIOPSOAS DISORDERS
Epidemiology
The iliopsoas is involved in 40% of patients with acute groin injuries, frequently in conjunction with an injury to the adductor musculature.7
In the chronic setting, iliopsoas conditions are present in 10% of patients presenting with hip or groin pain.
Female patients are more likely than males to have iliopsoas pathology, which is thought to be associated with increased hip motion secondary to underlying ligamentous laxity.
Activities that involve repetitive hip flexion and/or stretching to the extremes of motion, including dancing, soccer, hockey, gymnastics, and track and field, can predispose certain athletes to iliopsoas conditions.
Pertinent Anatomy/Pathoanatomy
The iliopsoas is a composite musculotendinous structure consisting of the psoas major muscle and the iliacus muscle, which have unique origins in the lower abdomen and pelvis before combining into a single tendon distally.
The psoas major muscle originates from the vertebral bodies, intervertebral disks, and transverse processes of T12 through L5, and is directly innervated by the L1, L2, and L3 branches of the lumbar plexus.
The iliacus muscle arises from the upper two-thirds of the iliac fossa on the inner aspect of the pelvis and the lateral aspect of the sacrum and is innervated by the femoral nerve.
Deep to the inguinal ligament, the musculotendinous portion of the iliacus and psoas major muscles converge to form the iliopsoas tendon.
Proximal to the hip joint, the tendon sits within a bony groove between the anterior inferior iliac spine laterally and the iliopectineal eminence medially.
The tendon then courses directly superficial to the hip capsule and labrum before it inserts on the lesser trochanter of the femur. The iliopsoas tendon is therefore an extracapsular, extra-articular structure.
A large synovial bursa exists between the iliopsoas tendon and the anterior hip capsule, which helps to reduce friction between these structures with hip motion.
The bursa is thin and nearly collapsed under normal conditions. In patients with iliopsoas bursitis, however, the bursa becomes inflamed and swells with fluid.
The close anatomic relationship between the iliopsoas tendon, hip capsule, labrum, and iliopsoas bursa frequently results in concomitant pathology between these structures.
Snapping hip syndrome, also known as coxa saltans, is typically caused by the abnormal movement of a tendon over a bony prominence with hip motion.
Internal snapping occurs when the iliopsoas tendon rubs against the iliopectineal eminence, whereas external snapping happens when the iliotibial band (ITB) moves over the greater trochanter.
Intra-articular snapping is less common but occurs when a loose body within the hip joint itself interferes with the smooth movement of the femoral head within the acetabulum.
Acute injury of the iliopsoas will lead to a strain of the iliacus muscles or the iliacus and psoas muscles, with isolated psoas strains being uncommon.7
In the chronic setting, iliopsoas tendinitis is related to overuse and can be associated with partial tearing of the tendon.
An acute tendon tear of the iliopsoas tendon is rare in adults. In children and adolescents, however, an avulsion fracture of the lesser trochanter can occur because of the greater strength of the iliopsoas muscle and tendon relative to that of the developing bony apophysis.
Pertinent History/Physical Examination Findings
Patients with iliopsoas strains, tendinitis, tears, and bursitis frequently complain of hip and/or groin pain.
The pain can radiate into the lower abdomen, lower back, and the upper thigh. Pain is provoked with activities that involve hip flexion and extension.
An injury or inciting event is frequently reported, often involving forceful hip flexion.
The dominant leg is more commonly involved than the nondominant leg, particularly in kicking and running athletes.
Recurrent injury is common, and up to 50% of patients can have a prior injury to the hip or groin.7
Patients with internal snapping hip syndrome will report an audible and/or palpable snapping sensation in the inner aspect of the hip that is associated with pain.
Symptoms are provoked by activity, particularly those involving hip flexion.
Up to 40% of active individuals can have hip snapping, but most do not have symptoms.
Physical examination should include a complete evaluation of the hip.
Tenderness to palpation can be present over anteromedial aspect of the hip and upper thigh.
Range of motion is typically normal.
Strength testing often elicits pain with resisted hip flexion in the seated position.
Evaluation of the snapping hip should attempt to identify the anatomic location of the pathology.
Many patients can voluntarily reproduce the snapping with certain movements, which is accompanied by an audible popping or clicking noise.
Internal snapping can be provoked by the examiner by passively moving the hip from a position of flexion, abduction, and external rotation to one of extension and internal rotation. In contrast, external snapping of the ITB over the greater trochanter occurs as the hip is flexed in neutral rotation.
In the evaluation of the patient with hip and groin pain, it is important to differentiate iliopsoas pathology from other conditions.
Adductor injuries will present with pain over the medial thigh that is worsened with resisted hip adduction.
Sports hernia, also known as athletic pubalgia, is an overuse syndrome of the abdominal and adductor muscles that can be provoked by examination maneuvers that increase intra-abdominal pressure, such as sit-ups and Valsalva.
Patients with FAI and labral tears have decreased and painful motion of the hip, particularly in flexion and internal rotation.
In skeletally immature patients with hip or knee pain, a slipped capital femoral epiphysis should always be ruled out with diagnostic imaging.
Iliopsoas pathology is frequently seen in conjunction with other conditions.
Acute strains to the iliopsoas can also involve the hip adductors, abductors, hamstrings, and/or secondary hip flexors including the rectus femoris and sartorius.
In the chronic setting, labral tears can occur secondary to impingement of the labrum and capsule by a pathologic iliopsoas tendon. Alternatively, inflammation of the iliopsoas bursa and tendon can occur as a result of underlying FAI and labral tearing.
Relevant Imaging
Evaluation of a patient with suspected iliopsoas pathology should begin with standard anterior-posterior and frog-lateral hip radiographs.
Fracture should always be ruled out in the acutely injured patient.
In the chronic setting, cam and pincer lesions are reflective of underlying FAI, whereas joint space narrowing, osteophyte formation, subchondral sclerosis, and/or bony cysts are cardinal signs of hip osteoarthritis.
The need for advanced imaging is dictated by multiple factors related to the patient and the suspected pathology.
MRI can identify iliopsoas strains, tendinitis, and bursitis. Furthermore, it can evaluate for intra-articular pathology involving the cartilage and labrum.
In certain situations, dynamic ultrasound examination is used to evaluate for a snapping iliopsoas tendon as the hip is brought through a range of motion.8Related posts:
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