This article describes calcific tendinitis of the rectus femoris treated with a local injection of a mixture of steroid and local anesthetic under C-arm control. From March 2004 to May 2005, 6 patients were treated for calcific tendinitis of the rectus femoris at our institution and followed for at least 2 years. The male:female ratio was 1:5, and mean patient age was 41 years (range, 33-49 years). Calcifications were located in the direct head in 1 patient and in the reflected head of the rectus femoris in 5. One patient underwent open surgical removal and 5 were treated with a local steroid and anesthetic injection. The patient undergoing surgical removal obtained immediate pain relief but reported discomfort in the wound area for 10 days postoperatively. The 5 patients receiving injections achieved dramatic pain relief within 2 days; follow-up radiographs revealed complete calcification disappearance within 16 weeks of treatment in all 5. No patient had experienced recurrence or complications at >2-year follow-up. Prompt diagnosis and early treatment with a local injection of a mixture of steroid and local anesthetic under C-arm control successfully relieved symptoms and facilitated a return to normality.
Periarticular calcific tendinitis is an acute inflammatory reaction and one of a subgroup of calcium hydroxyapatite crystal deposition disease processes1 that usually affects the shoulder rotator cuff.2 Pain or tenderness around the affected area can be so extreme that range of motion is severely limited. Fever, local edema, and elevated levels of acute-phase reactants may be present. Misdiagnosis has been reported and may lead to inappropriate treatment and adversely affect recovery.3 Computed tomography (CT) allows proper visualization and localization of the lesion and facilitates accurate injection if required.4 Magnetic resonance imaging (MRI) is useful to rule out other conditions such as infection, fracture, or bone tumor, and to illustrate the intense inflammation associated with this condition.5
Hip joints are also often affected by calcific tendinitis, which usually causes pain in the posterolateral aspect of the thigh that may simulate radicular pain from a prolapsed intervertebral disk.6 Most commonly the area around the greater trochanter is affected at the insertion of the gluteus medius and minimus.7 Calcific tendinitis of the rectus femoris,6 vastus lateralis,4 piriformis,1 iliopsoas, adductor magnus,8 biceps femoris, and gluteus maximus4 have been also previously reported.
To the best of our knowledge, no report has been published on clinical and radiological response to the C-arm-guided injection of steroid and local anesthetic agent for the treatment of calcific tendinitis in the hip. This article describes 6 patients with calcific tendinitis of the rectus femoris treated with a local injection of a mixture of steroid and local anesthetic under C-arm control.
Materials and Methods
From March 2004 to May 2005, 6 patients were treated for calcific tendinitis of the rectus femoris at our institution and followed for at least 2 years. The male:female ratio was 1:5, and mean patient age was 41 years (range, 33-49 years). No patient had a history of a previous problem in the hip or any injury of note. All patients reported being more comfortable holding their hips in 20° to 30° of flexion and reported pain during examination, especially with the hip in extension. All patients exhibited limping on the affected side during ambulation. Tenderness was reported in the inguinal area that radiated to the thigh distally. Body temperatures were within the normal range. Sedimentation rates, rheumatoid latex test findings, serum uric acid level, white blood cell count, and blood chemistry were all within normal limits. Mean C-reactive protein level was 1.65 mg/dL (range, 0.95-2.24 mg/dL; normal level <0.5 mg/dL).
Hip radiographs revealed an area of variable calcification with an irregular border close to the superior lip of the acetabulum in all patients, and subsequent CT scans confirmed the presence of calcification within the origin of the rectus femoris in all patients and excluded the possibility of an intra-articular lesion. Magnetic resonance images detected inflammatory edematous changes in the soft tissue adjacent to the calcific rectus tendon in all patients.
Pretreatment diagnosis was calcific tendinitis of the rectus femoris, located in the direct head in 1 patient and in the reflected head in 5. Pain control was achieved with an intramuscular injection of nepafenac and oral nonsteroidal anti-inflammatory drugs (NSAIDs). Because conservative treatment was unsuccessful at alleviating symptoms, other treatment options were planned. Specifically, 1 patient with an acute-on-chronic pattern of hip joint pain of 30 days duration was considered a chronic case and underwent open surgical removal by an anterolateral hip approach under spinal anesthesia. A calcific lesion was confirmed in the reflected head of the rectus femoris. The calcific deposit was removed and inflamed soft tissue was debrided (Figure 1).
The other 5 patients were treated with an injected mixture of steroid and local anesthetic. Each patient was placed supine on the fracture table. An 18-gauge spinal needle was used to localize the calcification with the aid of a C-arm. Aspiration was performed and 80 mg of methylprednisolone and 2 mL of 0.5% bupivacaine was injected (Figure 2). Calcific materials were aspirated in 3 of 5 patients.
The single patient who underwent open surgical removal obtained complete relief immediately, but reported discomfort in the wound area for 10 days. The 5 patients treated by injection also obtained dramatic pain relief within 2 days, and follow-up radiographs revealed complete disappearance of all calcifications. They remained asymptomatic with no radiographic evidence of calcification after a minimum 2-year follow-up.
Calcium hydroxyapatite crystal deposition disease involves the presence of painful periarticular calcific deposits in tendons and soft tissues and tends to affect people between 40 and 70 years of age. The condition is usually monoarticular, although polyarticular involvement has also been reported.9 As other periarticular soft tissues may also be involved, calcific tendinitis constitutes a subgroup of the calcium hydroxyapatite crystal deposition disease process.1 Although calcific tendinitis has been well described, soft tissue calcification may be misinterpreted as an accessory bone or avulsion fracture.3
The etiology of calcium hydroxyapatite crystal deposition is not clearly understood, and the only disorders that have been associated with calcific periarthritis are chronic maintenance hemodialysis for renal insufficiency and diabetes mellitus.10 Traumatic,7 genetic,9 and metabolic11 factors have been proposed as etiologies, and historically it was assumed that these deposits resulted from trauma around involved joints, although no specific mechanism was elucidated.7 Repetitive trauma has been cited as a factor, especially in the shoulder region,7 and tendinous tears of hip abductors have been proposed to be related to calcific tendinitis.5 Recently, tendinous tears of hip abductors were compared to rotator cuff tears, and in this case, a history of overuse was presumed to be related to the patients symptoms.7 The influence of an inherited genetic factor in some patients with calcific periarthritis appears certain, but no association with the human leukocyte antigen system has been established.9,10 Uhthoff et al,11 after performing histological studies on surgically treated patients, proposed that local hypoxia leads to fibrocartilage formation and subsequent calcium deposition, vascular proliferation, and resorption of deposits by macrophages, which restores normal perfusion and oxygen tension to tissue.
According to the literature,5 periarticular calcific tendinitis can be classified as acute or chronic. In acute calcific tendinitis, most attacks last <2 weeks and calcification disappears from radiographs 4 weeks to 8 months post-onset. Despite its self-limiting nature, mild or moderate pain persists for 2 to 24 months in chronic disease. Kandemir et al1 recommended arthroscopic treatment for chronic cases. In our study, 1 patient had an acute-on-chronic pattern of hip joint pain of 30 days duration. In this case, we considered this long-lasting symptom as an indicator of chronicity, decided that steroid injections were not a good option, and opted for open excision.
Calcific tendinitis of the rectus femoris may appear linear, rounded, or amorphous, and is present adjacent to the superior acetabular lip (in the region of the origin of one of its heads).7 Typically the condition produces hip pain, but it may be asymptomatic. Its physical signs are identical to those of acute synovitis of the hip, which suggests that acute episodes are precipitated by the rupturing of deposits within tendons into the hip joint. Sarkar et al6 reported 6 cases of calcific tendinitis that developed in the reflected head of the rectus femoris close to the hip capsule, suggesting that acute episodes are precipitated by the rupturing of deposits, but they were unable to explain the clustering of 6 patients with this rare condition in 1 geographic region. In our 6 cases, calcific tendinitis developed in the direct head of the rectus femoris in 1 and the reflected head in 5, and similarly, we are unable to explain the clustering of these 6 patients; however, calcific tendinitis in the reflected head of the rectus femoris is more prone to produce an acute episode than that in the direct head because of the proximity to the hip capsule and ease of clinical detection.
The differential diagnoses of calcifications in the rectus femoris include os acetabuli, avulsion fractures, sesamoid bones in the rectus femoris, myositis ossificans, and malignancies (eg, juxtacortical sarcoma, chondroma, chondrosarcoma, and synovial sarcoma). Differentiation of diagnosis is usually based on the size, characteristic ovoid shape, bony trabeculation, and painlessness of the ossicle. A comet-tail appearance to a calcific deposit suggests that it lies within a tendon. Malignancies must be considered, but CT allows proper lesion visualization and localization4 and facilitates accurate injection if required.6 Magnetic resonance imaging can be a useful tool to rule out other conditions and to illustrate inflammation intensity.5
Treatment options include conservative treatment with rest (eg, NSAIDs, local applications of heat and cold, diathermy, ultrasonic therapy),12,13 arthroscopy,1 local surgical excision,3,13,14 and local steroid injection.6,14 Local steroid and anesthetic injections are rapid and provide long-lasting pain relief and a shortened clinical course, but the mechanism involved is uncertain.6 Sarkar et al6 reported that a prompt diagnosis and early treatment with a local injection of corticosteroid under CT control successfully relieved symptoms in 6 patients with calcific tendinitis of the rectus femoris. We performed a local injection under C-arm control rather than CT control, because CT is expensive and exposes the patient to as much as 10 to 15 times more radiation than other radiographic techniques.15
Physicians should be aware of acute calcific periarthritis during the differential diagnosis of acute severe pain related to joints, as misdiagnosis leads to inappropriate treatment and delays recovery. Injections administered at the early stages of the disease invariably lead to rapid symptom relief and return of function.3
- Kandemir U, Bharam S, Philippon MJ, Fu FH. Endoscopic treatment of calcific tendinitis of gluteus medius and minimus. Arthroscopy. 2003; 19(1):E4.
- Neviaser RJ. Painful conditions affecting the shoulder. Clin Orthop Relat Res. 1983; (173):63-69.
- Johnson GS, Guly HR. Acute calcific periarthritis outside the shoulder: a frequently misdiagnosed condition. J Accid Emerg Med. 1994; 11(3):198-200.
- Hodge JC, Schneider R, Freiberger RH, Magid SK. Calcific tendinitis in the proximal thigh. Arthritis Rheum. 1993; 36(10):1476-1482.
- Sakai T, Shimaoka Y, Sugimoto M, Koizumi T. Acute calcific tendinitis of the gluteus medius: a case report with serial magnetic resonance imaging findings. J Orthop Sci. 2004; 9(4):404-407.
- Sarkar JS, Haddad FS, Crean SV, Brooks P. Acute calcific tendinitis of the rectus femoris. J Bone Joint Surg Br. 1996; 78(5):814-816.
- Holt PD, Keats TE. Calcific tendinitis: a review of the usual and unusual. Skeletal Radiol. 1993; 22(1):1-9.
- Hayes CW, Rosenthal DI, Plata MJ, Hudson TM. Calcific tendinitis in unusual sites associated with cortical bone erosion. AJR Am J Roentgenol. 1987; 149(5):967-970.
- Cannon RB, Schmid FR. Calcific periarthritis involving multiple sites in identical twins. Arthritis Rheum. 1973; 16(3):393-396.
- Hajiroussou VJ, Webley M. Familial calcific periarthritis. Ann Rheum Dis. 1983; 42(4):469-470.
- Uhthoff HK, Sarkar K, Maynard JA. Calcifying tendinitis: a new concept of its pathogenesis. Clin Orthop Relat Res. 1976; (118):164-168.
- Greene TL, Louis DS. Calcifying tendinitis in the hand. Ann Emerg Med. 1980; 9(8):438-440.
- Rowe CR. Calcific tendinitis. Instr Course Lect. 1985; (34):196-198.
- Braun-Moscovici Y, Schapira D, Nahir AM. Calcific tendinitis of the rectus femoris. J Clin Rheumatol. 2006; 12(6):298-300.
- Moore DC, Bush WH, Burnett LL. Celiac plexus block: a roentgenographic, anatomic study of technique and spread of solution in patients and corpses. Anesth Analg. 1981; 60(6):369-379.
Drs Yun, Park (Jung Ho), Park (Jong Woong), and Lee are from the Orthopedic Department, Ansan Hospital, Korea University, Ansan, South Korea.
Drs Yun, Park (Jung Ho), Park (Jong Woong), and Lee have no relevant financial relationships to disclose.
Correspondence should be addressed to: Ho Hyun Yun, MD, Orthopedic Department, Ansan Hospital, Korea University, Danwon-Gu, Ansan, 790825, South Korea.