Acute calcific tendinitis of the gluteus medius: An uncommon source for back, buttock, and thigh pain

Seminars in Arthritis and Rheumatism ] (2013) ]]]–]]]

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Acute calcific tendinitis of the gluteus medius: An uncommon source for back, buttock, and thigh pain Nam Chull Paik, MD Department of Radiology, Arumdaun Wooldul Spine Hospital, Ulsan, Republic of Korea

a r t i c l e in fo

Keywords: Gluteus medius Calcific tendinitis Hip pain Back pain Greater trochanter Reactive calcification Hydroxyapatite deposition

a b s t r a c t Objective: This study was conducted to describe the imaging features and clinical manifestations in acute calcific tendinitis (CaT) of the gluteus medius muscle (GMe). Methods: A retrospective analysis was conducted, aimed at six patients with acute calcific tendinitis of the gluteus medius muscle (CaT-GMe), who were seen between January 2011 and December 2012. Clinical presentations, radiologic data (radiography, CT, and MRI), and laboratory reports were all subject to review. Results: All patients presented with pain and decreased range of motion (ROM) at the hip. Two of the six patients experienced pain in the anterolateral thigh and groin, with antalgic gait (anterior group). The other four complained of low back, buttock, and posterolateral thigh pain, accompanied by difficulty in standing and antalgic gait (posterior group). Edema within the GMe or effusion surrounding the muscle was regularly identified on MRIs. Calcific deposits were conspicuous in the gluteus medius tendon attachments to the lateral (anterior group) and superoposterior (posterior group) facets of the greater trochanter on radiography, CT, or MRI. Complete resolution of symptoms was uniformly achieved in 5–10 days with conservative management. Conclusions: Acute CaT-GMe should be considered in any patient suffering lateral hip pain (with either groin or low back pain) and ROM limitation. Images of the hip characteristically show edema of the gluteus medius and calcifications lateral or superior to the greater trochanter. & 2013 Elsevier Inc. All rights reserved.

Introduction Nearly every tendon in the body is susceptible to calcific tendinitis (CaT), but the shoulder joint is particularly vulnerable, especially the distal supraspinatus tendon. Less commonly stricken are the hip, knee, elbow, wrist, foot, and neck locations [1–3]. Aside from the shoulder, the hip joint is one of the more frequently affected sites, although the rectus femoris, vastus lateralis, piriformis, iliopsoas, adductor magnus, biceps femoris, gluteus maximus, gluteus minimus, and gluteus medius are potentially at risk [1–14]. Calcific tendinitis of the gluteus medius (CaT-GMe) is only reported sporadically, and magnetic resonance imaging (MRI) is barely established through a few case presentations from the last decade [3,10,12]. Herein, we report six patients with CaT-GMe, whom we grouped (anterior and posterior) according to symptomology and calcific localization on imaging. Our intent was to bolster recognition of this uncommon condition by clinicians and radiologists.

Materials and methods By searching the database of the hospital, the author retrospectively identified six patients with a diagnosis of CaT-GMe, who were seen between January 2011 and December 2012. This study was E-mail address: [email protected] 0049-0172/$ - see front matter & 2013 Elsevier Inc. All rights reserved. http://dx.doi.org/10.1016/j.semarthrit.2013.12.003

approved by our institutional review board. The following data were retrieved from the hospital information system for analysis: (1) clinical presentations, including demographics, histories, symptoms, physical examinations, and treatments; (2) radiologic data; and (3) laboratory reports for C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), and white blood cell (WBC) count (Table). All patients were initially evaluated by radiography and subsequently examined with MRI scans, and three subjects had additional computed tomography (CT) scans of the pelvis. All images were evaluated by a single radiologist, who has experience in prior research of calcific tendinitis of the longus colli [15]. The scan parameters of MRI and CT were described in the Appendix.

Results Two males and four females were studied (age range: 33–62 years). All presented within 1–3 days of symptom onset, afflicted with pain and decreased range of motion (ROM) at the hip. Two patients presented with pain in the anterolateral thigh and groin, associated with antalgic gait (anterior group, patients 1 and 2). The others complained of low back, buttock, and posterolateral thigh pain; had difficulty in standing; and displayed antalgic gait (posterior group, patients 3–6). There were no pertinent underlying diseases, medical histories of significance, or preceding histories of trauma, although two patients were febrile. Initial

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Table Characteristics of patients (n ¼ 6) with acute calcific tendinitis of the gluteus medius

Gender/age (years) Pain location Symptom duration Motion limitation Laboratory finding

Patient 1 (Fig. 1)

Patient 2

Patient 3 (Fig. 2)

Patient 4

Patient 5 (Fig. 3)

Patient 6

M/54

F/35

F/33

F/54

F/62

M/62

Groin and anterolateral Groin and thigh anterolateral thigh 2 days 2 days

Low back, buttock, and posterolateral thigh 1 day

Low back, buttock, and Low back, buttock, and Low back, buttock, and posterolateral thigh posterolateral thigh posterolateral thigh 3 days 2 days 3 days

Walking

Walking

Walking and standing

Walking and standing

Walking and standing

Walking and standing

BT 36.5 ESR 22 CRP 2.6 WBC 9100 Lateral

BT 36.5 ESR 12 CRP 0.3 WBC 11,600 Lateral

BT 37.3 ESR 6 CRP 0.6 WBC 10,800 Superoposterior

BT 36.8 ESR 9 CRP 0.5 WBC 12,100 Superoposterior

BT 37.5 ESR 29 CRP 5.0 WBC 10,100 Superoposterior

BT 36.8 ESR 14 CRP 2.0 WBC 9700 Superoposterior

Ill-defined globular

Ill-defined globular

Aciniform

Ill-defined globular

Calcification location Calcification Oval/curvilinear Curvilinear morphology Pain Within 5 days with bed Within 5 days with resolution rest and NSAIDs bed rest and NSAIDs Follow-up No recurrence, No recurrence, 5 months 12 months Remarks From the formative to the resorptive phase

Within 5 days with bed rest Within 7 days with bed Within 10 days with and NSAIDs rest and NSAIDs bed rest and NSAIDs

Within 6 days with bed rest and NSAIDs

No recurrence, 22 months

No recurrence, 19 months

No recurrence, 15 months

Concurrent asymptomatic contralateral involvement

laboratory data were as follows: ESR elevation (reference range: o20 mm/h) in two patients (22 and 29 mm/h); CRP increase (reference range: o0.8 mg/dL) in three patients (2.0, 2.6, and 5.0 mm/h); and mild leukocytosis (reference range: o10,000 cells/ mm3) in four patients (10,100–12,100 cells/mm3). Calcific deposits were evident in the gluteus medius (GMe) tendon attachments to the lateral (anterior group) and superoposterior (posterior group) facets of the greater trochanter on radiographic, CT, or MR images, with appearances of curvilinear, ill-defined globular, and aciniform. Edema within the GMe or effusion (fluid with T1 hypointensity and T2 hyperintensity) surrounding the muscle was regularly identified on MRIs. Two patients even showed differing stages of CaT concurrently—one exhibiting serial changes, from the formative to the resorptive phase (patient 1), and the other having bilateral calcific deposits, asymptomatic on the right and painful on the left (patient 3). Complete resolution of symptoms was uniformly achieved within 5–10 days with the conservative management of nonsteroidal anti-inflammatory drugs (NSAIDs) and immobilization (bed rest in hospital or/and at home). Clinical, imaging, and laboratory findings are summarized in the Table. Representative case A 54-year-old man (patient 1, Fig. 1) with a history of intermittent low back pain presented with pain in the left groin and lateral thigh and difficulty in walking for 2 days. There was marked tenderness over the greater trochanter, with decreased range of motion of the left hip due to severe pain. He had no history of recent trauma or medical illness. He had been evaluated and treated for low back pain 3 months earlier in our hospital. He had a temperature of 36.51C and a leukocyte count of 9100 per mm3. His ESR was 22 mm/h and CRP was 2.6 mg/dl. Laboratory studies showed normal calcium and alkaline phosphatase levels and normal liver and renal function. Urinalysis was within normal limits. Plain radiographs at presentation revealed an ill-defined, fluffy, curvilinear soft tissue calcification adjacent to the greater trochanter (Fig. 1B). On radiographs obtained 3 months earlier, there was a dense, well-circumscribed, ovoid calcification lateral to the greater trochanter (Fig. 1A). CT scan confirmed calcification in the tendon of gluteus medius at the lateral facet of the greater trochanter and showed no cortical erosive change (Fig. 1C and E).

No recurrence, 10 months Extensive aciniform calcification

MRI scan showed inflammatory edematous change in the gluteus medius muscle and curvilinear calcification as a low signal in the tendon at the lateral facet of the greater trochanter but no bone marrow edema, bursal distension, or joint effusion (Fig. 1D and F). Given the clinical presentation and imaging findings, a diagnosis of calcific tendinitis of the gluteus medius was made. The patient was treated conservatively with NSAIDs and advised bed rest for immobilization of the hip joint for 4 days. There was marked resolution of his symptoms in the first 2 days. On day 5, he was able to walk alone without any assistance, his ESR and CRP returned to normal limits (6 mm/h and 0.3 mg/dl, respectively), and he was discharged. Follow-up at 5 months showed no recurrence of symptoms.

Discussion The three major crystal-induced musculoskeletal disorders seen in clinical practice are as follows: (1) CaT, due to basic calcium phosphate deposits (predominantly hydroxyapatite); (2) gout, from monosodium urate deposition; and (3) pseudogout, where deposits consist of calcium pyrophosphate dehydrate [1,6,15]. Acute CaT is diagnosed by integrating clinical presentation with distinctive findings on imaging, namely the coexistence of tendinous calcification and edema or effusion within the symptomatic muscle and adjacent soft tissue [6,12,15]. It is usually signaled by sudden onset of extreme pain, so that ROM is severely limited. Due to its inflammatory nature, mild fever, leukocytosis, and ESR or CRP elevations may be present. The symptoms gradually and spontaneously subside [6,12,15]. The above features were characteristics of the six patients described here. We believe that our stratification of patients into anterior and posterior groups reflects the anatomic and functional configuration of the gluteus medius. The greater trochanter has four facets: anterior, lateral, superoposterior, and posterior. The GMe tendon attaches at the lateral and superoposterior facets, the gluteus minimus tendon inserts at the anterior facet, and the trochanteric bursa covers the posterior facet [16,17]. In addition to its two sites of insertion, the GMe muscle has three anatomically distinct segments (posterior, central, and anterior), each with clear biomechanical roles. The posterior segment, arising from the central

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Fig. 1. Patient 1: A 54-year-old male with a 2-day history of groin pain and difficulty in walking; images show lateral tendon involvement, progressing from the formative (A) to the resorptive (B–F) phase. Anteroposterior radiograph obtained 3 months ago (A) harbors dense, well-circumscribed, ovoid calcification (small arrow) lateral to the greater trochanter, consistent with the formative phase. Anteroposterior radiograph at presentation (B) reveals ill-defined, fluffy, curvilinear calcification (arrows) of the resorptive phase. Computed tomography (CT) scans (C and E), each with curvilinear calcific density (arrows) in the tendon of gluteus medius at the lateral facet of the greater trochanter. Fat-suppressed proton density magnetic resonance imaging (MRI) scans (D and F) marked by edema of the gluteus medius muscle; note curvilinear calcification as low signal in tendon (arrows) at the lateral facet of the greater trochanter.

posterior muscle, has a thick, round tendinous insertion at the superoposterior facet. With its coronal oblique orientation (aligned with femoral neck), it stabilizes the acetabular mooring of the femoral head during motion and gait. The central segment arises from the muscle's undersurface, attaching vertically to the junction of the superoposterior and lateral facets. This portion is thought to initiate hip abduction. The anterior segment inserts broadly at the lateral facet and functions as a hip abductor (aided by the central segment) and an external rotator of the pelvis [16,17]. To the best of knowledge, there has been no histopathologic documentation of CaT-GMe. Prior studies have detailed structural and functional similarities between glenohumeral and hip joints, spawning the concept of a hip joint “rotator cuff” that incorporates the gluteus medius and minimus tendons [18,19]. Thus, it might be expected that CaT-GMe and CaT of the shoulder would bear clinical, radiologic, and histopathologic resemblances. As such, Uhthoff and Loehr [20] have outlined a 5-stage progression of shoulder joint CaT, assigning precalcific, calcific (formative, resting, and resorptive), and postcalcific phases. The precalcific phase (stage 1) involves a fibrocartilaginous transformation (metaplasia of tenocytes to chondrocytes), with no overt radiologic changes. During the formative calcific phase (stage 2) (patient 1, Fig. 1A; and patient 3, Fig. 2A, C, and E), calcium crystals are deposited between the strands of fibrocartilage, gradually eroding the latter and becoming chalk like. These deposits are well defined, dense, and homogeneous on radiographs. They correspond clinically with pain that is chronic or possibly absent. The resting calcific phase

(stage 3) is a variable period of disease inactivity, followed by the resorptive calcific phase (stage 4) (patient 1, Fig. 1B–F; patient 3, Fig. 2B, D, and F; and patient 5, Fig. 3A and B), where activity clearly resumes. Vascular ingrowth, phagocytic activity (macrophages and multinuclear giant cells), and inflammation at the periphery of deposits are subsequently indicative of calcium resorption. At this juncture, painful symptoms and reduced mobility also seem to peek. Calcifications that are fluffy, cloud like, ill defined, amorphous, or irregular in density on radiographs are compatible with the resorptive phase, as well as dramatic osseous changes (cortical erosion, bone marrow edema, etc.) and extensive soft tissue edema. Upon surgery, the calcific material is thick and pasty. In the postcalcific phase (stage 5), normal tendinous collagen is ultimately restored by fibroblasts. Soft tissue calcification at points of tendon insertion on radiographs or CT scans should raise suspicion of CaT. When calcification occurs in para-osseous soft tissues, the differential diagnosis further includes myositis ossificans, periosteal chondral tumors, osteogenic or synovial sarcomas, progressive systemic sclerosis, and heterotopic ossification [7,21]. Calcification near the greater trochanter may also be associated with gluteal tendon tear, trochanteric bursitis, or tendinitis with an unerupted deposit (the above-mentioned formative calcific or resting calcific phases) [10,22,23]. CT enables better detection and more precise localization of intratendinous calcification, which is often missed on radiographs, and readily delineates the calcific (rather than osseous) composition [4,8,15]. Ultrasonography, although not

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Fig. 2. Patient 3: A 33-year-old female with a 1-day history of low back, buttock, and posterolateral thigh pain on left (B, D, and F); images illustrate concurrent asymptomatic calcific deposit in the superoposterior tendon of the right gluteus medius (A, C, and E). Fat-suppressed proton density coronal MR images with effusion (arrowheads) surrounding the left gluteus medius muscle and low-signal calcifications (arrow) in the tendon (B). On asymptomatic right side (A), note intratendinous calcification as low-signal area with high-signal rim (small arrow) but no muscle edema or effusion. Coronal and sagittal CT images depicting well-circumscribed asymptomatic calcification (small arrows) of homogeneous density (C and E) and symptomatic calcifications (arrows) with fluffy, ill-defined edges (D and F) in the superoposterior tendons of the gluteus medius, bilaterally.

performed in this series, is also helpful in identifying intratendinous calcification appearing as hyperechoic foci with possible posterior acoustic shadowing. Generally, tendinitis appears as diffuse hypoechogenicity and thickening of the tendon [24]. However, edema of the tendon, muscle, and adjacent soft tissue is imaged well in MRI sequences, and MRI is invaluable in ruling out other pathology that may present as lateral hip pain [6,7,10,12,13,15,16,22,23]. Often referred to as greater trochanteric pain syndrome, lateral hip pain is a common clinical complaint in a wide range of disorders. Trochanteric bursitis and tendon abnormalities of the

gluteus medius or minimus are generally responsible [18,19, 25–27], but a host of conditions, such as degenerative hip arthropathy, stress fractures, tumors, infectious processes, avascular necrosis, entrapment neuropathies, and fibromyalgia may present similarly and should be differentiated [19,27,28]. Lumbar spinal disease may also be manifested as lateral hip pain, referred from disc herniation, spinal stenosis, facet syndromes, or compression fractures [19,26,29]. Conversely, lesions of the GMe may result in low back pain (LBP) [30,31] as seen in patients 3–6 and also mimic the radicular pain of a herniated lumbar intervertebral disc [32]. Hip function

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Fig. 3. Patient 5: A 62-year-old female with a 2-day history of low back, buttock, and posterolateral thigh pain; images highlight extensive calcification of the superoposterior tendon. Anteroposterior radiograph of so-called aciniform calcifications, presenting as multiple, ill-defined, ovoid deposits (arrows) superior to the greater trochanter (A). Fat-suppressed T2-weighted coronal MR image, with effusion (arrowheads) surrounding the gluteus medius muscle and numerous low-signal aciniform calcifications (arrows) of the superoposterior tendon (B).

has been shown to be an important contributor to both trunk and spine function, and therefore it likely plays a role in the development and response to LBP. For example, in an electromyographybased experimental study of individuals without a history of low back pain, Nelson-Wong et al. [33] showed that participants who developed LBP demonstrated co-activation of the left and right GMe muscles from the beginning of standing, whereas those who did not develop LBP showed synergistic, reciprocal activation of these muscles. Thus, the inflammation of the GMe in our patients may have contributed to the development of LBP. Distinguishing GMe pathology and lumbar radiculopathy requires an awareness of both entities, with carefully taken histories and thorough physical exams. Normally, pain from gluteal lesions is limited to the proximal tibia, whereas in lumbar radiculopathy, pain radiates to the lower leg and foot. In addition, patients with lumbar radiculopathy will not respond to thumb pressure over the greater trochanter, resistance to leg abduction, or extreme external rotation of the thigh [32]. Treatment of CaT must take into account that this is a self-limited process, likely to resolve spontaneously within 1–2 weeks of symptom onset. NSAID medications and relief from load bearing (at affected tendon) helps to alleviate symptoms [3,6,7,12,15]. As with CaT at other sites, our patients improved in 5–10 days with this approach. Occasionally, patients with severe symptoms may require a short course of intravenous or peroral steroids [15]. Percutaneous steroid injection [5,10,13,14] and needle aspiration of deposits [3,9,20] have also been advocated. With intractable CaT, endoscopic treatment or open surgical removal of calcific debris may be needed [11,20]. The true incidence of CaT-GMe is difficult to ascertain. In our experience, it appears more common than formerly presumed. Radiologists and clinicians, as caregivers in this setting, should be cognizant of related features to ensure prompt diagnosis and proper management. In summary, acute CaT-GMe is suspected clinically, confirmed radiologically, and rightly should be considered in patients troubled by lateral hip pain [with either anterior (groin) or posterior (low back) radiation] and ROM limitation. Images of the hip typically show edema of the GMe and calcification lateral or superior to the greater trochanter. Conservative treatment with NSAIDs and bed rest is usually quite effective.

Appendix Noncontrast CT scans were obtained with a 16-slice scanner (BrightSpeed, General Electric, Milwaukee, WI) and then

reformatted in axial, coronal, and sagittal planes in 3.0-mm slice thickness. MRI scans were unenhanced examinations using a 1.5-T scanner (Signa HDe, General Electric). The sequences consisted of coronal T1-weighted (TR range/TE range, 483–616/12–16), coronal fat-suppressed proton density (TR range/TE range, 2333–2866/36– 44), axial T1-weighted (TR range/TE range, 466–616/12–14), and axial fat-suppressed proton density (TR range/TE range, 2166– 2683/37–43) images. In one instance (patient 5), only coronal fat-suppressed T2-weighted imaging (TR/TE, 4133/86) was performed. TR/TE (ms)

Coronal 483–616/ T1WI 14–16 2333– Coronal 2866/ FS PWI 36–44 Axial 466–616/ T1WI 12–14 2166– Axial FS 2683/ PWI 37–43

Slice thickness (mm)

Matrix

FOV (mm) Acquisition time

4.8

416  256 330  370 3 min 52 s

4.8

352  224 330  370 4 min 22 s

4.5

352  224 370  370 3 min 01 s

4.5

352  256 370  370 4 min 15 s

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