AP (a), Y view (b) and axillary (c) radiographs obtained after 6 months of shoulder pain show a large homogenous calcific deposit measuring 22 × 7 mm in the subacromial space. Compared with X-rays obtained 5 months previously, the deposit is unchanged
The patient assents to a trial treatment of corticosteroid injection into the subacromial space and home exercises intended to strengthen the rotator cuff and stabilize the scapula. She reports back in 8 weeks with continued pain. An MRI is ordered to further assess her soft tissues and demonstrates a hypo-intense body on the bursal surface of the supraspinatus tendon that measures 19 × 6 mm. There is mass effect on the supraspinatus tendon but the rotator cuff tendons are all intact (Fig. 2.2a–c).
Coronal (a), sagittal (b), and axial (c) T2-weighted images demonstrate a hypo-intense , marginated mass consistent with the calcific deposit (arrow) on the bursal side of the rotator cuff with mass effect on the deltoid. It is impossible to tell the degree to which the calcific deposit has replaced or displaced the supraspinatus tendon
This patient presents with a classic history, physical exam, and diagnostic studies consistent with rotator cuff calcific tendonitis (RCCT) , also referred to as hydroxyapatite or crystalline calcium phosphate tendon deposition . It is important to take into account the patient’s symptoms, signs, and imaging findings, because not all calcific deposits cause pain . The natural history of RCCT can be positive with expected improvement in clinical symptoms and possible eventual absorption of the calcific deposits. We informed our patient that people can respond to conservative treatments consisting of relative rest, anti-inflammatory medications, histamine blockers, and physical therapy and home exercise regimens . Other nonsurgical but invasive management options are reviewed including therapeutic ultrasound, extracorporeal shock wave therapy, and ultrasound-guided barbotage and aspiration [3–5]. However, we also discussed that patients can fail conservative care and may continue to have unchanging pain, which would be an indication for surgical management. Level II evidence found that while radiographically inhomogeneous deposits responded well to both surgical and nonsurgical treatments, homogenous deposits responded better to arthroscopic removal . The current thinking on RCCT pathogenesis and pain generators is metaplasia of tenocytes leading to cell-mediated calcification with pain mediated by swelling, neoinnervation, and neovascularization [7, 8].
Calcium deposits of the rotator cuff occur most commonly in the supraspinatus tendon, followed by the infraspinatus tendon . Rarely, the deposit can occur in the subscapularis tendon . The primary surgical goal is to express the calcific body to hasten the recovery process of the tendon and thus alleviate pain. Arthroscopically assisted removal of calcium deposits has largely replaced traditional open approaches to calcium removal.
The patient underwent shoulder arthroscopy after 7 months of failed conservative management. Preoperatively, the patient’s MRI is reviewed. Axial, sagittal, and coronal plane MRI cuts are used in conjunction to map out the location of the calcium deposit. Most deposits will be encountered on the bursal side and/or within the substance of the tendon; rarely deposits can be visualized from the articular side, but secondary changes of inflammation may be noted from the articular view [1, 11].
We position the patient in the beach chair as for standard rotator cuff-related arthroscopies. First, an arthroscopy of the glenohumeral joint is performed to evaluate for associated pathologies and to evaluate for partial articular sided or complete rotator cuff tears. If articular sided calcifications are visualized, they are tagged with a monofilament stitch outside to inside using a spinal needle that is inserted off the lateral edge of the acromion.
The arthroscope is then placed into the subacromial space. The subacromial arthroscopy is performed with anterolateral and posterolateral portals, with the arthroscope placed in the posterolateral portal and the anterolateral portal as the primary working portal. This optimizes visualization of the rotator cuff and facilitates an efficient bursectomy. After bursectomy, the calcium deposit is visualized on the bursal side of the rotator cuff tendon. Calcium deposits are detected as white or yellow patches on the cuff with surrounding areas of hyper-vascularity on the cuff, as well as hemorrhagic bursa (Fig. 2.3a, b). Most deposits present as topographic bulges adjacent to normal rotator cuff, but depending on their depth, hidden calcifications may also be present.
The subacromial space is viewed from the posterior lateral portal. After bursectomy, the calcific deposit is revealed as a large, white plaque bulging from the bursal side of the rotator cuff (a). Surrounding area of hyper-vascularity is also seen (b). An 18-gauge spinal needle is introduced into the deposit (c), and the toothpaste-like calcium initially fountains out as if under pressure (d) (arrow). The process is repeated with the spinal needle several times, re-creating several “geysers of toothpaste” and a “snowstorm” appearance in the subacromial space. Calcium hydroxyapatite is completely expressed with a blunt instrument such as a probe or Wissinger rod (d). The expressed deposit is collected and the surrounding abraded rotator cuff edge is trimmed and lavaged with an arthroscopic shaver (e)
An 18-gauge needle is introduced percutaneously off the lateral edge of the acromion and the deposit is needled (Fig. 2.3c). The needle can be connected to a syringe and aspirated, but in this case the needle is withdrawn and the deposit expressed itself as stream of putty, similar to “toothpaste” (Fig. 2.3d). The paste is expressed with a Wissinger rod producing a snowstorm appearance within the subacromial space , which is removed with a shaver (Fig. 2.3e). Care is taken to preserve rotator cuff tendon at the expense of complete removal of the calcium deposits. Despite our care to maintain integrity to the cuff, a high-grade partial-thickness tear of the supraspinatus tendon was identified.
The high-grade rotator cuff tear on the bursal side is repaired with an arthroscopic Mason-Allen stitch (Fig. 2.4a–d) . Antegrade passage of rotator cuff stitches with a suture lasso device through Neviaser’s portal does not require takedown of intact articular sided rotator cuff fibers (Fig. 2.4b).
A high-grade bursal sided tear with intact articular supraspinatus tear is discovered after removal of the deposit from the footprint (a). After preparation of the denuded footprint, a 4.75 mm double-loaded anchor is placed into the tuberosity. A sturdy suture lasso (Banana SutureLasso, Arthrex, Naples, FL, USA) is used to penetrate the cuff in antegrade fashion (b) (upper right corner). Both limbs of the black and white suture and one limb of the blue and white suture are passed sequentially in a modified arthroscopic Mason-Allen configuration; in this picture the black and white suture creates a horizontal mattress after which the passed limb of the blue and white suture is thrown on the unpassed limb medial to the horizontal mattress (c); when tied this creates a rip-stop suture repair (d)
The need for acromioplasty is determined by the morphology of the acromion, wear on the coracoacromial (CA) ligament, condition of the bursa, and dynamic evaluation of the rotator cuff (Fig. 2.5a, b). There is abrasion of the undersurface of the CA ligament and passive elevation of the arm reveals abutment between the cuff and the lateral acromion are signs suggesting impingement and indications for acromioplasty. The subacromial decompression is performed with the use of an arthroscopic electrocautery wand and a 5.0 mm barrel burr (Fig. 2.5b). A final lavage is performed to remove any remaining bone fragments and calcium crystals.
Arthroscopic evaluation after rotator cuff reveals a downsloping acromion (dotted line), which upon dynamic evaluation shows impingement on the cuff near the site of repair as well as abrasion of the coracoacromial ligament (arrow) suggesting signs of chronic impingement (a). Near-identical view after arthroscopic decompression shows impingement-free arc of rotation (b)
The patient was immobilized in a sling for 4 weeks. During that time she was allowed passive supine straight-arm raises. Gentle active range of motion was started at 4 weeks and strengthening at 10 weeks following repair.
The patient’s pain resolved over the first 8 weeks and her motion returned to normal by 12 weeks. The ASES score at 4 months was 94. The patient’s 2-week postoperative X-ray showed diminished but residual calcifications within the rotator cuff tendon (Fig. 2.6).
AP X-ray obtained at the 2-week postoperative visit shows residual calcification
In a radiographic cross-sectional study, Bosworth found that the prevalence of calcific deposits was 2.7% in a group of asymptomatic patients . The finding emphasizes the need to methodically rule out other sources of pain such as adhesive capsulitis, biceps tendinopathy, and rotator cuff dysfunction. The disease is more common in middle-aged women, and those with a history of diabetes mellitus, thyroid disorders, hypertension, and heart disease, but it is not associated with calcium or phosphate disorders [9, 14]. It is important to distinguish calcific tendinitis from dystrophic calcification of the rotator cuff as the latter is age related and not generally a painful finding. Louwerens and coworkers compared the prevalence of calcifications of the rotator cuff in an asymptomatic cohort with another group of patients with impingement symptoms. The asymptomatic group had a lower overall rate of calcifications present (7.8% versus 42.5%), and the symptomatic group had larger deposits . These authors did not distinguish between dystrophic and reactive calcifications. The history and physical exam of RCCT match those of subacromial impingement, but pain with RCCT is typically more severe and may resemble gout or other reactive arthritis. Past authors have suggested that there are different stages of calcification, which have different radiographic and clinical characteristics [1, 15]. However, a patient may fail nonoperative treatment at any point along the continuum of disease [1, 12, 15, 16]. It is our opinion that staging the disease is not as important as clinically correlating the disease to the patient’s symptoms, treating with appropriate conservative measures, and offering surgery to those who have failed a course of conservative care.