Hip pain is a common complaint in patients, regardless of age, seen in primary care clinics. The condition comprises 10% to 24% of pediatric sports injuries, occurs in 30% to 40% of adult athletes, and affects approximately 14% of the population over age 60.1-3 Determining the cause of pain can be challenging for any healthcare provider. Differential diagnoses include intra-articular and extra-articular pathologies and referred pain from lumbar, sacroiliac, and visceral regions. Providers need to ascertain whether the source of pain is from the anterior hip and groin, posterior gluteal region, lateral hip, or overlapping sources.3
Pain in the anterior hip and groin are commonly from intra-articular pathologies such as femoroacetabular impingement (FAI) syndrome, labral tears, dysplasia, osteoarthritis (OA), and avascular necrosis.3 Posterior gluteal pain is often due to lumbar spine pathology, sacroiliac joint dysfunction, piriformis syndrome, the femoroacetabular joint, or proximal hamstring tendinopathy.3 Patients who complain of lateral hip pain may suffer from greater trochanteric pain syndrome, including gluteal tendinopathy. Other causes of pain include muscular strains, entrapment neuropathies, and myofascial pain.3
This review includes the pathophysiology, diagnosis, clinical manifestations, and treatments for the most frequently encountered hip pain presentations. The pathologies discussed include OA, gluteal tendinopathy, FAI syndrome, and labral tears. Assessment techniques, plans, and treatments are explained and described.
Patients who present to a clinician with hip pain commonly report struggles with activities of daily living. The pain may have begun after a traumatic injury or over a period of time.3 The discomfort may limit the patient's ability to walk up or down stairs, get in and out of cars, run, and walk. Some patients will have issues sleeping on one side or both sides due to pressure on the hip.3 Hip disability and OA questionnaires such as the lower extremity functional scale can be used to evaluate functional limitations related to hip pain to determine therapeutic intervention goals.4
Interview. The history and physical exam are essential in identifying the patient's source of pain and dysfunction. The NP should start by obtaining the chief complaint, history of present illness (HPI), past medical history, and review of systems. This information is critical in discerning past injuries, illnesses, and chronic disease states that may have precipitated the patient's hip pain and in developing an accurate list of differential diagnoses. For example, history of low bone density, history of a recent fall, or family history of rheumatoid arthritis can aid the provider in developing an evaluation plan that includes appropriate diagnostic studies and in narrowing down the differential diagnosis. “Do not miss” diagnoses such as cancer, fractures, septic arthritis, and dislocations should always be at the forefront of the clinician's mind.3 Asking questions about the pain's onset, location, duration, character, aggravating and relieving factors, radiation, timing, and severity (OLD CARTS) can aid in determining if the pain is related to a coexisting condition or other disease process.5 The HPI should include the patient's limitations and details such as whether the pain is worse with certain activities, sitting for long periods, twisting, or ascending/descending stairs.3 The history may also include asking what the patient has tried in an effort to resolve the pain and whether they have seen another provider for the pain.
Exam. After a thorough history, the NP should determine the location of the pain and which position(s) reproduce the patient's symptoms. Patients may localize their pain by placing their thumb posterior to the greater trochanter with fingers extending to the groin area on the affected hip, referred to as the “C-sign,” which often indicates intra-articular pathology such as OA, labral tears, and FAI syndrome.6 Clinicians should visually inspect the hip joint, keeping in mind that the pain may result from a non-hip condition such as lumbar spine disease, athletic pubalgia, or an autoimmune disease such as rheumatoid arthritis.7 The skin around the hip should be assessed for bruising, erythema, and muscle atrophy.7 Next, the clinician should have the patient stand in order to observe posture along with pelvic and spinal alignment. The patient's gait should be assessed for symmetry; speed and antalgic gait patterns should be noted.6,7 The clinician should understand the intricacies of mechanical load transfer that take place during ambulation in order to distinguish compensation for pain and hip instability.6
The clinician should have the patient perform flexion, extension, and side bending (lateral flexion) of the lumbar spine as well as single-leg stance (Trendelenburg sign) while standing to see if their pain is reproduced or if there is any weakness.7 Next, with the patient in supine, prone, and side-lying positions, the clinician should assess the patient's active, passive, and resistive range of motion (ROM).7 It is typically recommended that the clinician perform palpation, including examination of lymph nodes, femoral pulses, bony landmarks, soft tissues, and muscles, noting any tenderness, at the end of the exam.7 The neurovascular exam should include assessment of peripheral pulses and sensation.7 Examination of the hip should also include a quick screen of the lumbar spine and sacroiliac joint to rule out their involvement (see Exam techniques).
|Standing exam techniques
Trendelenburg gait may indicate hip abductor weakness or proprioception disturbance
Antalgic gait may indicate traumatic injury, fracture, or synovial inflammation
Pelvic rotational wink may indicate an intra-articular etiology of pain or ligament injury
Foot progression angle with increased external rotation may indicate femoral retroversion, increased acetabular anteversion, torsional abnormalities, ligament injury, or effusion
Sitting exam techniques
|Range of motion
|Hip flexion contracture test
|Straight leg raise against resistance
Abbreviations: FADIR, flexion-adduction-internal rotation; FAI, femoroacetabular impingement.
Diagnostics. Diagnostic imaging should support the exam. It is not uncommon to find a second diagnosis that is not the actual cause of pain. Appropriate imaging for hip pain may vary depending on the characteristics and chronicity of pain. Plain radiographs are an inexpensive method for evaluating for fractures, degeneration of the spine, narrowing of joint spaces, and osteophyte formation.8 An anterior-posterior weight-bearing X-ray of the pelvis in addition to a lateral view of the symptomatic hip should be ordered.9 MRI or magnetic resonance angiography can be beneficial in assessing noninflammatory causes of pain and confirming diagnoses, such as herniated discs, and are highly sensitive in detecting degeneration of the labrum and labral tears.8 Lab studies are not routinely indicated during the diagnostic process for hip pain but can be considered if there are concerns of other contributing issues. For example, certain cases may warrant ordering a complete blood cell count to assess for infection, erythrocyte sedimentation rate and C-reactive protein to assess for inflammation, or synovial fluid aspiration to assess for crystals or send for culture (see Differential diagnosis of hip pain).
Arthritic hip pain
Pathophysiology. Hip OA is the most common source of hip pain among adults over 50 years of age, affecting 0.4% to 27% of this population, with a higher prevalence in males.10 Risk factors for developing hip OA are multifactorial. Risk factors include abnormal joint morphology such as FAI syndrome, developmental hip dysplasia, acetabular labral pathology, prior joint injury, and reduced hip ROM.10,11 Other risk factors include age over 50, higher bone mass, higher body mass index (BMI), and high-impact or prolonged joint loading physical activities and occupations.10,11 Likewise, the course of hip OA is multifactorial and involves all components of the joint. Altered biomechanical loads within the joint disrupt cellular homeostasis of the femur, leading to the thinning of subchondral and trabecular bone beneath the articular cartilage.11 Concurrently, the avascular and aneural articular cartilage begins to fibrillate and thin down to the tidemark transition from calcified cartilage and subchondral bone.11 Access to the subchondral bone facilitates the development of proinflammatory cytokines and subsequent synovitis.11 Hip OA can progress for months, years, or decades before the onset of pain or radiographic evidence, underscoring the importance of early clinical findings and screening.10,11
Differential diagnosis of hip pain2,10-20
||Common subjective findings
||Common objective findings
Diagnosis of cause of hip pain should never be made on imaging alone.
Obtain AP pelvis and lateral femoral head-neck radiographs initially. (Modified Dunn view may be indicated to evaluate cam-type morphology. Frog-leg or cross-table lateral view may be indicated in some cases.)
MRI/magnetic resonance arthrogram or CT arthrogram may be warranted in some cases to evaluate intra-articular structures and/or for 3D morphologic assessment.
Age >40 years
Lateral hip pain in region of greater trochanter
Pain with lying on side, standing, walking, stairs, and crossing legs
Groin pain (or may have back, buttock, or thigh pain)
Patient may describe clicking, catching, locking, stiffness, restricted ROM, or “giving way” of hip
Primarily groin pain (or may have back, buttock, or thigh pain)
A specific motion or position elicits hip or groin pain
Patient may describe clicking, catching, locking, stiffness, restricted ROM, or “giving way” of hip
C-sign often present
Deficits in hip strength and proprioception on single-leg balance
Limited passive IR of less than 30°
Positive FADIR, FlexIR, and deep squat tests
Abbreviations: AP, anteroposterior; CT, computed tomography; FABER, flexion-abduction-external rotation; FADER, flexion-adduction-external rotation; FADIR, flexion-adduction-internal rotation; FAI, femoroacetabular impingement; FlexIR, flexion/internal rotation; GMed, gluteus medius; GMin, gluteus minimus; IR, internal rotation; OA, osteoarthritis; ROM, range of motion; THIRD, The Hip Internal Rotation with Distraction.
Clinical manifestations. Patients with symptomatic hip OA report an insidious onset of pain during prolonged standing, walking, squatting, and crossing their legs. Pain is often localized to the anterior proximal-medial hip or thigh, lateral hip, or posterior hip, typically with minimal referral beyond the hip. In OA, the C-sign is often present and patients frequently use pain descriptors such as “deep,” “ache,” “stiff,” and occasionally “sharp.” Other associated symptoms can include joint crepitus with hip motion. Objectively, hip OA frequently presents with antalgia noted from midstance to terminal phase of gait, decreased hip ROM, and hip muscle weakness. Guidelines recommend observation of gait; flexion, abduction, and external rotation (FABER) test or Patrick test; passive hip ROM; and hip muscle strength.10 Additionally, a clinical cluster, or a collection of key objective and subjective findings that raise index of suspicion for a particular diagnosis, for hip OA includes complaints of anterior or lateral hip pain during weight-bearing; painful passive hip internal rotation; hip internal rotation ROM less than 24° or hip internal rotation and flexion 15° less than the uninvolved side; morning stiffness lasting less than 60 minutes; and age over 50. Symptoms of hip OA often do not correlate with radiographic findings.10
Treatment. Treatment of OA depends on severity and duration and consists of nonpharmacologic and pharmacologic management. Guideline-based recommendations for conservative management of hip OA is multimodal, beginning with patient education on activity modification and weight loss to mitigate excessive weight-bearing stress to the joint.10 Encouraging physical activity can help alleviate pain and improve mobility. Referral to physical therapy may be needed to help with joint mobilization for overall improvement of mobility. Physical therapy can provide patients who have OA with exercises aimed to improve hip flexibility by improving muscle strength and soft tissue mobilization. They may also recommend gait training with assistive devices such as canes or crutches. Mainstay pharmacologic treatment for OA includes acetaminophen and nonsteroidal anti-inflammatory drugs (NSAIDs). Oral duloxetine is a serotonin and norepinephrine reuptake inhibitor that has an indication for chronic musculoskeletal pain in adults and can help decrease pain.12 Topical agents commonly used for hip pain include capsaicin and topical NSAIDs such as diclofenac. Intra-articular corticosteroid injections can help alleviate inflammation. Patients typically need a combination of pharmacologic and nonpharmacologic treatment through a multidisciplinary approach to improve quality of life.
Nonarthritic hip pain
Pathophysiology. The primary complaint of lateral hip pain in the greater trochanter region is commonly seen in postmenopausal women over 40 years old. Formerly referred to as trochanteric bursitis, gluteal tendinopathy is now the most prevalent cause of lateral hip pain.13 Gluteal tendinopathy is viewed as a degenerative process involving the continuum of the bone, bursa, and tendons. Ultrasound studies of individuals with greater trochanteric pain have elucidated the high prevalence of degenerative tears of the gluteus medius (GMed) and gluteus minimus (GMin) tendons and low prevalence of bursal involvement.13 Intrinsic risk factors include female sex, age greater than 40, and muscle imbalance between GMed/GMin and other hip abductors.13,14 Additionally, decreased femoral neck-shaft angle of less than 134° is associated with increased severity of gluteal tendinopathy.13 The strongest extrinsic risk factor is abnormal tensile and compressive loading of the GMed and GMin tendons leading to catabolic matrix degenerative changes with subsequent reduced load-bearing capacity and increased susceptibility to degenerative tendon tears.13,14
Clinical manifestations. Symptoms of gluteal tendinopathy include insidious onset of lateral hip pain in the greater trochanter region aggravated by lying on the painful side at night, standing, walking, ascending or descending stairs, and sitting with legs crossed.13 Objectively, gluteal tendinopathy frequently presents with antalgia during the single-limb stance phase of gait. Grimaldi et al. recommend clustering provocation of lateral hip pain with single-leg stance; resisted abduction with the hip in end-range adduction; resisted hip internal rotation at end-range flexion-adduction-external rotation; and palpation of the GMed/GMin tendon insertions.15 If a patient does not have pain on palpation of the GMed/GMin tendons or greater trochanter, the clinician should consider other diagnoses.15
Treatment. Initial treatment includes limiting patient activity and eliminating any activity that reproduces the pain. NSAIDs may be helpful in the acute phase of gluteal tendinopathy and may provide short-term pain relief. Local injectable corticosteroids may also help control acute pain but should not be used for the long term. For chronic gluteal tendinopathy, referral to physical therapy is recommended for further evaluation and treatment.
Conservative interventions emphasize patient education and tendon load management.13,16 Patient education should include reducing high compressive or tensile loads through the GMed/GMin tendons via modification or elimination of activities such as asymmetrical standing with the painful hip in adduction, sitting with the involved leg crossed over the uninvolved leg or with the painful hip in internal rotation, and sleeping in side-lying position with the upper hip in flexion and adduction. Coupled with activity modification, progressive, pain-free GMed/GMin strengthening exercises are recommended.16
Pathophysiology. Chronic hip pain occurs in 30% to 40% of adult athletes, and patients with intra-articular hip pathology see an average of three clinicians before receiving an accurate diagnosis.2 FAI syndrome has been found to be the cause in 40% of cases of anterior hip and groin pain, surpassing labral injuries (33%) and hip OA (24%), and is also considered a primary contributor to idiopathic hip OA.2,17,18 FAI pathomorphologies fall into three categories relating to the femoroacetabular joint: cam, pincer, and mixed. The mixed-typed morphology is the most common form of FAI syndrome and involves both the cam and pincer morphologies.17 The cam-type morphology impinges on the superior acetabulum with hip flexion and internal rotation along the femoral head-neck junction (FHNJ). The cam-type impingement is caused by a bump on the anterior or anterior-lateral femoral head or insufficient concavity of the FHNJ.2,18 Cam morphologies are more common in men and are three times more likely to occur in athletes. Cam deformities have been associated with FAI progression to labral tear and, when coupled with internal rotation deficit, an increased risk of OA, according to moderate evidence.18 The pincer-type morphology results from an acetabular overcoverage of the femoral head. Four patterns have been identified: global acetabular overcoverage, focal anterior rim overcoverage, acetabular retroversion, and focal posterior rim overcoverage.17,18 The pincer-type morphologies are more common in women and are found less often in athletes.2
Clinical manifestations. Individuals with FAI often report anterior hip and groin pain, although pain may also present in the lateral hip, anterior thigh, low back, and buttock. Activities involving flexion, adduction, and internal rotation such as squatting and getting up from a low seat or out of the car may cause discomfort. Individuals are usually limited in those motions and have decreased strength of the hip adductors, abductors, flexors, and external rotators. The flexion-adduction-internal rotation (FADIR) and flexion/internal rotation (FlexIR) tests may be the best clinical tests for FAI, with the deep squat test starting to show promise.18 Plain radiographs are recommended initially with anterior-posterior pelvis and lateral femoral head-neck views. The modified Dunn view best visualizes the anterior-superior aspect of the FHNJ, where the cam-type morphology is commonly found.2,18
Treatment. Treatment of FAI may include conservative care, rehabilitation, and/or surgery. Nonsurgical management of FAI syndrome often consists of activity modifications, home exercises, mobility and strengthening with a rehabilitation clinician, and intra-articular injections. Rehabilitation techniques focusing on core and pelvic stability, strengthening, and mobility have demonstrated significant improvement in symptoms for up to 2 years.2
High-level evidence supporting rehabilitation is limited, but research has shown promising outcomes that warrant consideration of nonsurgical approaches before electing for surgical intervention.17-20 Neuromuscular training focusing on strengthening the lumbopelvic region while limiting the total hip ROM along with facilitating a posterior pelvic tilt during lunging and squatting activities to reduce impingement is beneficial.17 Studies have also reported the identification and correction of biomechanical errors, technique development, and avoidance of irritating activities in sports that demand extreme hip flexion, internal rotation, and adduction to be promising in delaying surgical intervention.21 Return to activities such as running should gradually progress after symptoms are minimized and faulty movement patterns have been addressed.18 It is important for clinicians to be realistic with patients regarding time frames for returning to normal activity and to quantify those expectations to help patients make informed decisions. If pain is not relieved with rehabilitation, the clinician may consider referring the patient to an orthopedic surgeon for surgical options.
Pathophysiology. The labrum is triangular fibrocartilage that runs circumferentially around the rim of the acetabulum.20 It increases the surface area of the acetabulum by deepening the socket and is vital to the stability of the hip joint. The injured labrum is often identified as the culprit in groin pain and is hard to distinguish from FAI syndrome, which often coexists.18 The leading causes of labral tears are FAI syndrome, trauma, dysplasia, capsular laxity, and degeneration that produce significant shear forces eventually leading to failure of the labrum.20 The pain more often occurs with hip extension or signs of instability. If left untreated, labral tears will contribute to the development of OA.18,20
Clinical manifestations. Like FAI syndrome described above, the most common symptom is anterior hip or groin pain that may radiate to the knee. The pain is generally described as a constant dull pain; however, sharp pain may occur with specific movements. Positive anterior hip impingement tests such as the FADIR and FlexIR tests may imply anterior labral tear. Other clinical tests may include the FABER or Patrick test and, more recently, The Hip Internal Rotation with Distraction (THIRD) test.20 The posterior hip impingement test may be positive if the patient experiences pain when lying prone with hip and knee extended while the examiner passively extends, adducts, and externally rotates the hip.20
Treatment. Patients with groin pain from a suspected labral tear are often prescribed rest, NSAIDs, other pain medications, activity modification, rehabilitation, and intra-articular injection. Nonsurgical management of labral tears is a reasonable initial strategy considering the prevalence of asymptomatic patients.18 One study found that a significant portion of adults with prearthritic intra-articular hip pain improved with nonoperative therapy focused on limitation of hip extension, acetabular rotation on the femur, and anterior hip translation.19,22 Neuromuscular training focusing on the lumbopelvic region should also be emphasized, including training the trunk stabilizers; GMed, GMin, and gluteus maximus; deep lateral rotators; and iliopsoas muscles while minimizing the quadriceps and hamstring contribution during exercise.18 In individuals with labral tears along with FAI syndrome, lateral and inferior traction mobilizations may be beneficial. Sometimes the patient should receive an intra-articular injection, which usually includes an anesthetic agent and a corticosteroid, for diagnostic and therapeutic purposes; a positive response can help distinguish between a labral tear and other pathologies such as psoas bursitis. Research shows that 85.7% of patients with labral pathology respond positively to intra-articular injection, with more than half reporting immediate relief of pain.20 Early pain relief enables patients to better tolerate strengthening and mobility restoration work with a rehabilitation specialist. If nonsurgical management is unsuccessful at improving pain and mobility, then labral debridement or repair by an orthopedic surgeon may be needed.
Treatment guidelines for hip pain
Conservative treatments for hip pain include the use of activities such as aquatic exercises, stretching, weight training, and aerobics, which can be beneficial.10,12,16 Dietary counseling and subsequent weight reduction can significantly improve hip pain for individuals with a BMI greater than 25.10,12 Patients should also have proper footwear and may need referral to a podiatrist.9 Activity should be modified to decrease the cause of the pain, and the use of a supportive device such as a cane can help offload the hip and reduce the pain.10
Pharmacologic interventions for hip pain can include the use of acetaminophen, NSAIDs, and/or duloxetine to decrease pain.12 Topical agents commonly used for hip pain include capsaicin and topical NSAIDs such as diclofenac. However, there is not strong enough evidence to recommend for or against the use of these products with hip pain. Opioids, including tramadol, should not be used as first-line agents but may have a role in select instances of pain resistant to other methods.
Intra-articular corticosteroid injections can be beneficial in relieving some types of hip pain. Intra-articular hyaluronic acid injections can be effective for knee but not hip pain due to OA.12 Platelet-rich plasma injections and cell therapy lack evidence-based studies to support their use in patients with hip pain.12 Intra-articular injections of the hip should be guided by ultrasound, computed tomography (CT), or fluoroscopy.12
Rehabilitation therapy remains one of the most beneficial recommendations for patients with hip pain who are not undergoing surgery. Rehabilitation is helpful in identifying the impairment, strengthening muscles, and relieving pain. Surgical intervention may be indicated in patients who have not had functional improvement and whose pain is not controlled with conservative methods, including physical therapy, intra-articular injections, and pharmacotherapy.
Hip pain is a common complaint, especially among patients over the age of 60 years, that primary care NPs see. NPs are often the first point of contact for patients with musculoskeletal pain. Important components of management of hip pain include completing an in-depth history and thorough physical exam, ordering appropriate diagnostic tests, and implementing an appropriate pharmacologic or nonpharmacologic intervention. The NP should have a thorough understanding of different types of hip pain and their respective treatments.
Interprofessional care is essential to improving healthcare outcomes. Interprofessional collaborative practice allows a holistic approach through the involvement of multiple healthcare professions. Collaborative practice involves shared responsibility and use of effective communication among interprofessional team members when caring for patients with hip pain.23 Patients may have encounters with multiple disciplines including nurses, NPs, physician assistants/associates, physicians, and/or rehabilitation therapists, who all share the responsibility of improving outcomes for patients with hip pain.
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