Retrocalcaneal Bursitis Workup

Updated: Feb 22, 2018
  • Author: Patrick M Foye, MD; Chief Editor: Sherwin SW Ho, MD  more...
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Workup

Laboratory Studies

If the retrocalcaneal bursitis cannot be explained by local factors (eg, poorly fitting shoes, increased running, high heels), or if systemic symptoms or signs of rheumatologic involvement exist, consider laboratory studies to evaluate the possibility of gout (hyperuricemia), rheumatoid arthritis (rheumatoid factor [RF]), and seronegative spondyloarthropathies (eg, human leukocyte antigen [HLA] B-27, erythrocyte sedimentation rate [ESR], C-reactive protein [CRP]).

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Imaging Studies

Plain radiographs of the calcaneus may reveal a Haglund deformity (increased prominence of the posterosuperior aspect of the calcaneus). However, on weight-bearing lateral radiographs, the retrocalcaneal recess often appears normal even in patients with retrocalcaneal bursitis, limiting its usefulness in making this diagnosis. [9]

Radiographs may be used as a diagnostic measure to support a clinician’s diagnosis of retrocalcaneal bursitis. Individuals with retrocalcaneal bursitis may have an absence of the normal radiolucency (ie, blunting) that is seen in the posteroinferior corner of the Kager fat pad, known as the retrocalcaneal recess or bursal wedge. This may occur with or without an associated erosion of the calcaneus. [10, 11]

Evaluation of the soft tissue in the retrocalcaneal space on conventional lateral radiographs is less reliable in assessing for retrocalcaneal bursitis in patients who have previously undergone endoscopic calcaneoplasty, making it difficult to use radiographs diagnostically in evaluating for recurrent retrocalcaneal bursitis in such patients. [12]

Plain radiographs can be used to evaluate for stress fracture of the calcaneus. If the studies are negative for a stress fracture, but a stress fracture remains a significant diagnostic consideration, the clinician may wish to pursue 3-phase bone scanning or computed tomography (CT) scanning of the calcaneus.

Magnetic resonance imaging (MRI) may demonstrate bursal inflammation, but this modality probably does not offer much more information than that found by careful physical examination. Theoretically, MRI could help the physician to determine whether the inflammation is within the subcutaneous bursa, the subtendinous bursa, or even within the tendon itself; however, such testing is generally not necessary.

If MRI imaging is needed for confirmation of retrocalcaneal bursitis, the retrocalcaneal bursa will appear as an enlarged, fluid-filled structure with low signal intensity on T1-weighted images and high signal intensity on fluid-sensitive images. Further, there may be associated marrow edema in the calcaneus or the distal Achilles. Edema in the tissues surrounding the retrocalcaneal bursa may be indicative of chronic mechanical irritation. [13]

Hybrid imaging modalities, most specifically single-photon emission CT (SPECT)/CT, may assist with early detection of bursitis by offering a precise, accurate, and highly localizing diagnostic image. However, little research exists on the cost benefit of this modality, and, therefore, it is not frequently used for this type of soft-tissue injury. [14]

Ultrasonography may be a potentially useful tool for diagnosing pathologies of the Achilles tendon. [15] (See the Procedures section below.) Some clinicians have suggested that ultrasonography can be used in place of MRI in cases in which imaging is desired to investigate pathology at the posterior heel. One study concluded that extended field-of-view sonography (EFOVS) when combined with traditional gray-scale sonography has similar sensitivity and specificity to MRI for diagnosing calcaneal bursitis in addition to more rapid results, lower cost, and lack of contraindications. [16]

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Procedures

Many clinicians advocate the use of corticosteroid injection(s) into the affected bursa, with particular care to avoid injection within the Achilles tendon.

Although there is a theoretical risk of tendon rupture, prospective, randomized studies have not been performed to definitively establish a causal relationship between steroid injections and such tendon ruptures. Instead, the association between steroid injections and subsequent tendon ruptures is mostly based on retrospective case reports. Thus, the cases that were more likely to go on to rupture were potentially those in which a more severe presentation prompted the steroid injections in the first place.

A case report by Sofka et al demonstrated that retrocalcaneal bursitis can be diagnosed and treated with ultrasonography. [17] This modality can be used to guide injection into the retrocalcaneal bursa with a combination of local anesthetic (eg, lidocaine, with relief within minutes and duration of several hours) and corticosteroid (eg, triamcinolone [Kenalog; Bristol-Myers Squibb Company, Princeton, NJ], with anti-inflammatory effect within 24-48 hours and a relief duration of weeks to months). In contrast, in an animal study, Hugate et al demonstrated the adverse effects of local corticosteroid injections (both within the tendon substance and into the retrocalcaneal bursa) on the biomechanical properties of the Achilles tendon. [18] The authors stressed that ultrasonographic guidance helps to ensure reliable and accurate delivery of medication into the bursa, while concurrently avoiding intratendinous injection.

Diagnosing retrocalcaneal bursitis requires a multifaceted approach based on patient history and physical and radiographic imaging. [19] In current practice, no definitive diagnostic measures exist, as many pathogenic features are not entirely understood. It has been speculated, however, that heel pain in Haglund deformity (which can be associated with retrocalcaneal bursitis) may be secondary to increased bursal pressure. Based on this, a recent pilot project developed minimally invasive technology (butterfly needle and water column) that precisely measured bursal pressure in cadaveric specimens and may serve to aide in the diagnosis of retrocalcaneal bursitis if further studies lend support to the “hypothesis of pressure-induced pathogenesis.” [20]

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