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Snapping Hip Syndrome

  • Author: Joseph P Garry, MD, FACSM, FAAFP; Chief Editor: Craig C Young, MD  more...
Updated: Nov 24, 2014


Snapping hip syndrome is characterized by an audible snap or click that occurs in or around the hip. This syndrome is well recognized but poorly understood. Snapping hip syndrome may be due to an external cause (eg., snapping of the iliotibial band or gluteus maximus over the greater trochanter) or an internal cause (eg., snapping of the iliopsoas tendon over the iliopectineal eminence, acetabular labral tear, intra-articular loose body). Acetabular labral tears and intra-articular loose bodies are relatively uncommon causes of internal snapping hip syndrome and are not discussed in detail. Snapping hip syndrome may be painful or painless. While some athletes may seek attention for a painless audible snap, most do not seek medical attention unless the snapping hip is painful.




United States

No data are available on the prevalence or incidence of snapping hip syndrome. The syndrome occurs most often in individuals aged 15-40 years and affects females slightly more often than males.[1] In one clinic, the rate of some form of snapping hip syndrome in female ballet dancers with hip complaints was 43.8%, and approximately 30% noted pain with this condition.[2]


Functional Anatomy

The pelvis is the link between the trunk and the lower extremities. The ball-and-socket joint of the hip allows for three degrees of freedom; approximately 120° of flexion, 20° of extension, 40° of abduction, 25° of adduction, and 45° each of internal and external rotation. The lateral hip's greater trochanteric region is a complex region with the convergence of several tendons (insertion of the gluteus minimus, medius and overlying gluteus maximus), the tensor fascia lata, the greater trochanteric bursa and the overlying iliotibial band. The iliotibial band is a ligament that originates from the iliac crest and inserts on the lateral proximal tibia. Crossing two joints, this ligament functions to flex and rotate the thigh medially.

The most common cause of a snapping hip is the iliotibial band snapping over the greater trochanter. This may be associated with trochanteric bursitis or with increased varus of the hip. The finding of a tight iliotibial band is common. Sudden loading of the hip (eg., landing after a jump) may reproduce this sensation of the iliotibial band subluxing over the greater trochanter. With sudden loading, the hip typically is flexed, causing the iliotibial band to move anteriorly followed by the tendon snapping backward as the individual recovers and extends the hip.

The gluteus maximus is the largest of the gluteal muscles and functions as an extensor and external rotator of the hip. Originating along the posterior ilium, dorsal surface of the sacrum, and gluteal aponeurosis, the gluteus maximus inserts on the iliotibial tract and gluteal tuberosity of the femur. During extension of the hip, the distal border may snap over the greater trochanter of the femur. Jacobsen et al. described the finding of hip abductor weakness in eccentric strength as compared to healthy matched controls.[3] Whether this finding is causal or simply associated with symptomatic external snapping hip is unknown at this time.

The psoas and iliacus muscles originate from the lumbar spine and pelvis, respectively, and are innervated by the L1, L2, and L3 nerve roots. These muscles converge to form the iliopsoas muscle and insert onto the lesser trochanter of the proximal femur as the iliopsoas tendon. The psoas major tendon exhibits a characteristic rotation through its course, transforming its ventral surface into a medial surface and its dorsal surface into a lateral surface.[4] The iliac portion of this tendon has a more lateral position and the most lateral muscle fibers of the iliacus muscle insert onto the lesser trochanter of the femur without joining the main tendon.[4] The iliopsoas muscle passes anterior to the pelvic brim and hip capsule in a groove between the anterior inferior iliac spine laterally and the iliopectineal eminence medially.[4] The musculotendinous junction is consistently found at the level of this groove.

The iliopsoas muscle functions as a hip flexor and external rotator of the thigh. Furthermore, an iliopsoas-infratrochanteric muscular bundle has been described, which likely relates to the iliopsoas tendon. This muscular bundle arises from the anterior inferior iliac spine (above the origin of the rectus femoris muscle), courses along the anterolateral aspect of the iliacus muscle, and inserts without a tendon onto the anterior surface of the lesser trochanter of the femur.[4] The iliopsoas bursa lies between the musculotendinous junction of the iliopsoas and the pelvic brim. An internal cause of snapping hip has been described as the iliopsoas tendon snapping over the iliopectineal eminence, hip capsule itself, or less likely the lesser trochanter. The motion of extending a flexed, abducted, and externally rotated hip reproduces the snapping phenomenon.

Among ballet dancers, those with snapping hip have a narrow bi-iliac width, greater range of movement in hip abduction, decreased range of motion in external rotation, and greater strength in the external rotators of the hip.[5] These findings suggest that skeletal or biomechanical conditions may predispose an individual to the development of a snapping hip.


Sport-Specific Biomechanics

In snapping hip syndrome, slightly different biomechanics are involved with the iliotibial band than with the iliopsoas musculotendinous unit.[6] This condition may develop as the result of an acute injury leading to subsequent bursitis, tendinitis, or biomechanical changes. More commonly, snapping hip syndrome is the result of repetitive overuse.

External snapping hip syndrome may be caused by either the iliotibial band or gluteus maximus snapping over the greater trochanter. Subluxation of the iliotibial band over the greater trochanter may occur while the hip extends from a flexed position (in which the iliotibial band moves from a position anterior to the greater trochanter to a position posterior to the greater trochanter). This action is most pronounced with sudden loading of the hip joint into a flexed position, such as occurs when landing a jump (eg. dismounting from an apparatus in gymnastics, rebounding in basketball, long jumping in track-and-field competitions).

The gluteus maximus is a powerful extensor of the thigh and trunk when the lower extremities are fixed. However, it is posturally unimportant, relaxed with standing, and used little in walking. The gluteus maximus is used in activities such as running, climbing, and rising from a seated or stooped position. It also regulates flexion at the hip (a paradoxical action).[6]

Internal snapping hip syndrome is most commonly caused by a snapping of the iliopsoas tendon over the iliopectineal eminence. As an overuse phenomenon, this condition may occur in any activity resulting in repeated hip flexion or external rotation of the femur. Activities that may predispose to iliopsoas tendinitis include dancing, ballet, resistance training (eg. squats), rowing, running (particularly uphill), track and field, soccer, and gymnastics.

During the adolescent growth spurt, a tendency exists for the hip flexors to become relatively inflexible. For younger athletes, this can lead to problems as increased stress is placed on the iliopsoas musculotendinous unit and general biomechanics are altered. Tightness of the iliopsoas, tensor fascia lata, or rectus femoris can lead to inhibition of the gluteus maximus, allowing for an anterior pelvic tilt, which can lead to adverse affects on the kinetic chain.

Excessive anterior tilt due to a tight iliopsoas muscle, tight hip adductors, and a relatively weak rectus abdominis can lead to increased lumbar lordosis with subsequent increased stress on the lower lumbar disks, facet joints, and sacroiliac joints. This also may result in increased knee flexion during gait at the heel-strike and midstance phases. The increase in eccentric load across the knee extensor mechanism may result in patellar tendon injuries (eg. patellar tendinitis, Osgood-Schlatter disease). With increased knee flexion, compressive forces at the patellofemoral articulation increase and may predispose to patellofemoral problems.

Contributor Information and Disclosures

Joseph P Garry, MD, FACSM, FAAFP Associate Professor, Department of Family Medicine and Community Health, University of Minnesota Medical School

Joseph P Garry, MD, FACSM, FAAFP is a member of the following medical societies: American Academy of Family Physicians, American Medical Society for Sports Medicine, Minnesota Medical Association, American College of Sports Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Russell D White, MD Clinical Professor of Medicine, Clinical Professor of Orthopedic Surgery, Department of Community and Family Medicine, University of Missouri-Kansas City School of Medicine, Truman Medical Center-Lakewood

Russell D White, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Family Physicians, American Association of Clinical Endocrinologists, American College of Sports Medicine, American Diabetes Association, American Medical Society for Sports Medicine

Disclosure: Nothing to disclose.

Chief Editor

Craig C Young, MD Professor, Departments of Orthopedic Surgery and Community and Family Medicine, Medical Director of Sports Medicine, Medical College of Wisconsin

Craig C Young, MD is a member of the following medical societies: American Academy of Family Physicians, American College of Sports Medicine, American Medical Society for Sports Medicine, Phi Beta Kappa

Disclosure: Nothing to disclose.

Additional Contributors

Andrew D Perron, MD Residency Director, Department of Emergency Medicine, Maine Medical Center

Andrew D Perron, MD is a member of the following medical societies: American College of Emergency Physicians, American College of Sports Medicine, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.


Walter L Jenkins, MS, PT, ATC Interim Chair, Clinical Professor, Department of Physical Therapy, East Carolina University

Walter L Jenkins, MS, PT, ATC is a member of the following medical societies: American Orthopaedic Society for Sports Medicine

Disclosure: Nothing to disclose.

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