Calcific Tendonitis Barbotage/Lavage

Key Points

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Calcific tendonitis, or more appropriately tendinosis, of the rotator cuff is a relatively common cause of shoulder pain. Calcifications are usually self-limiting but can also be recurrent, progressive, and debilitating.
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Calcific deposits can develop in any rotator cuff tendon, but the vast majority occur in the supraspinatus tendon, followed by the infraspinatus and the subscapularis tendons.
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Calcific tendonitis is usually the most symptomatic during the resorptive phase, when there is an acute inflammatory reaction to the calcification.
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Radiographs of the shoulder are essential to confirm the diagnosis of calcific tendonitis, exclude other potential causes of shoulder pain, and allow planning for intervention.
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Conservative treatment, including nonsteroidal antiinflammatory drugs (NSAIDs), subacromial-subdeltoid (SASD) bursa corticosteroid injections and physiotherapy, should be the first line of therapy for calcific tendonitis.
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When conservative treatment fails, ultrasound (US)-guided barbotage/lavage is a safe, quick, and effective way to provide immediate and long-term relief of symptoms.
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A SASD bursa corticosteroid injection should be performed immediately following barbotage to prevent a calcific bursitis flare up due to some retrograde passage of calcium into the bursa during the procedure.
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Although the shoulder is the most common site for calcific tendinitis, other tendons can be affected, including at the elbow, knee (quadriceps and patella), gluteal tendons, Achilles, etc. The techniques described in this chapter can be adapted and applied to other areas.

Clinically Relevant Anatomy

The rotator cuff is composed of four muscles arising from the scapula that attach to the humeral head. The supraspinatus, infraspinatus, and teres minor tendons attach to the superior, middle, and inferior facets of the greater humeral tuberosity, respectively. The subscapularis tendon attaches to the lesser humeral tuberosity.

Pathophysiology

Calcific tendonitis is the result of hydroxyapatite crystal deposition in an otherwise healthy tendon. The exact etiology remains uncertain, with several proposed theories. ^, The multiphasic disease model posited by Uhthoff and Loehr is one of the most accepted and divides the cycle of calcific tendonitis into three stages :

1.

Precalcific stage: an unknown trigger, postulated to be a decrease in oxygen tension, induces fibrocartilaginous metaplasia of tenocytes into chondrocytes with formation of intracellular calcifications. This stage is asymptomatic.
2.

Calcific stage: this stage is further subdivided into three phases.
- 2.1.
  
  Formative phase: hydroxyapatite crystals rupture into the extracellular space and coalesce, taking on a chalklike consistency.
- 2.2.
  
  Resting phase : the calcific deposits are walled-off and quiescent. This phase is of variable length and usually asymptomatic, unless there is rotator cuff impingement caused by mass effect of large calcific deposits.
- 2.3.
  
  Resorptive phase : an unknown trigger induces angiogenesis, inflammation, and resorption of the calcific deposit, which becomes liquefied, taking on a toothpaste-like consistency. Increased internal pressure in the deposit due to increased volume from liquefaction may cause decompression of the calcification into the subacromial-subdeltoid (SASD) bursa, inciting bursitis. This phase corresponds to the most painful and symptomatic clinical stage, often characterized by sudden onset of severe pain.
3.

Postcalcific stage: fibroblasts migrate into the tendon defect and form a scar, with the tendon returning to a relatively normal appearance. This stage is again usually asymptomatic.

Several of the phases may occur concurrently within a calcific deposit, and the sequence of the stages may not always be regular.

Calcific tendonitis can occur in any rotator cuff tendon, but the vast majority (≈80%) of deposits are located in the supraspinatus tendon, usually in the so-called critical zone 1.5 to 2.0 cm from its insertion onto the greater tuberosity. The infraspinatus tendon is involved 15% of the time, followed by the subscapularis tendon in approximately 5% of cases. The teres minor tendon is rarely involved. ^,

Clinical Presentation and Epidemiology

Calcific tendonitis is a common disease with reported incidence rates ranging from 2.7% to 54%, accounting for 7% of cases of shoulder pain. ^, ^, It is usually symptomatic between the ages of 40 and 60 years and is more common in women and diabetic patients. ^, ^, ^, Calcific deposits in the rotator cuff are present on radiographs in 7.5% to 20% of asymptomatic individuals and in 6.8% of symptomatic individuals. ^, Deposits are bilateral in 10% to 20% of patients and become symptomatic in 50% of patients. ^, ^, Rotator cuff tears are generally not associated with calcific tendinitis.

Clinical symptoms vary significantly depending on the stage and location of calcific deposits. Sudden and excruciating pain often occurs during the resorptive phase. Pain is usually referred to the deltoid region, and limitation in range of motion and function can clinically mimic adhesive capsulitis or a rotator cuff tear. ^, If the calcific deposit decompresses into the SASD bursa during the resorptive phase, the resultant crystal-induced SASD bursitis will usually dominate the clinical picture. During more quiescent stages of calcific tendonitis, larger calcific deposits can cause symptoms of impingement.

Imaging and Sonographic Evaluation

Given the multiple clinical presentations of calcific tendonitis, and the aforementioned overlap of symptoms with those of other shoulder pathologies, a differential diagnosis should always be considered clinically; however, calcific tendonitis can usually be readily distinguished from the other diagnostic considerations based on a combination of appropriate history, physical exam, and correlative imaging.

Confirming the clinical suspicion of calcific tendonitis requires imaging of the shoulder. Radiographs ( Fig. 24.1A ) can help to confirm the presence of calcific deposits. Dystrophic insertional calcifications, or enthesophytes, should not be confused with calcific tendonitis. Enthesophytes are usually significantly smaller in size, linear in morphology, and located directly above, or in contact with, the greater humeral tuberosity, whereas calcific tendonitis is generally located 1 to 2 cm away from the greater humeral tuberosity with no osseous contact and is typically ovoid in morphology. Further cross-sectional imaging of the shoulder with either magnetic resonance imaging (MRI) or ultrasound (US) (see Fig. 24.1B and C ) is recommended to assess the integrity of the rotator cuff and exclude other possible etiologies for shoulder pain.

US can also help to confirm and localize the calcifications. The sonographic appearance of a calcific deposit correlates with its consistency. In the formative and quiescent phases, calcific deposits have a high density of hydroxyapatite crystals, which cause strong reflection of sound waves. This results in the calcific deposits appearing solid and echogenic with pronounced posterior acoustic shadowing, making them easy to delineate from the surrounding tendon. As liquefaction proceeds in the resorptive phase, the calcific deposit becomes progressively less echogenic with diminished posterior shadowing.

Treatment Options

Symptomatic calcific tendonitis can be highly debilitating, limiting activities of daily living and resulting in a significant economic impact due to missed work. ^, Calcific tendonitis is often described as a self-limiting entity, which usually resolves spontaneously ^, ^, ; however, a significant portion of patients will continue to remain symptomatic for an extended period or may experience a cyclic clinical course, with repeated episodes of acute, disabling pain and progressive loss of function. ^,

There is general agreement that conservative management should be the first line of treatment in the acute phase of calcific tendonitis. ^, ^, ^, ^, Conservative management usually involves a combination of nonsteroidal antiinflammatory drugs (NSAIDs) and corticosteroid injections into the SASD bursa for symptom relief, and occasionally physiotherapy to prevent loss of joint mobility. Conservative therapy can be effective, but residual significant symptoms persist in approximately 30% to 50% of patients. Many authors suggest a trial of conservative therapy for a period of at least 3 to 6 months; however, this could vary on an individual basis depending on the severity of pain and the patient’s ability to tolerate a conservative approach.

Several researchers have investigated risk factors for predicting poor outcomes from conservative management of calcific tendonitis, although results have been mixed. In general, female gender, dominant arm involvement, bilateral disease, longer duration of symptoms at presentation, and larger number of calcifications were found to be negative prognostic factors. In contrast, the significance of common radiographic parameters, such as size, morphologic features (based on the Gartner classification ), and location of the calcific deposits, have been more inconsistent in the literature. ^, ^,

Given the often self-limiting nature of calcific tendonitis, an ideal intervention should not only be effective at removing the culprit calcification and improving the patient’s symptoms but should also be as minimally invasive and of as short a duration as possible; relatively comfortable for the patient; have minimal associated complications; and be cost-effective. ^, ^, Several treatments have been investigated and employed when conservative management of calcific tendonitis fails. Acetic acid iontophoresis is one potential treatment shown to be no more effective than physical therapy or placebo. The efficacy of other treatments has been demonstrated, although they are not without their own drawbacks. They include the following procedures.

Shockwave Lithotripsy

Shockwave lithotripsy, or extracorporeal shock wave therapy (ESWT) uses shock waves to dissolve the calcifications. This treatment has been demonstrated to be effective at resolving calcific deposits and significantly improving clinical symptoms. ^, ^, However, the utility of ESWT is limited due to several factors, including: a protracted treatment course requiring at least three sessions separated by 2 to 4 weeks, during which the patient often remains symptomatic; significant pain often experienced by patients during the procedure; and the need for specialized equipment, which increases the cost of offering this treatment. ^, ^,

Open or Arthroscopic Surgical Excision of Calcifications

Surgical excision of calcifications can provide significant clinical improvement, but prospective randomized controlled trials are limited. Surgical resection has been shown to be more effective than ESWT in reducing pain and radiographic resolution of calcifications, but studies are inconclusive as to whether this difference is significant by 2 years post treatment. ^, No study has compared surgical outcomes with US-guided barbotage. Although surgery is an effective treatment for calcific tendonitis, controversy remains over the optimal surgical management, with ongoing debate regarding repairing the resultant tendon defect. ^, Surgery has significant potential drawbacks, including higher risk of complications such as infection, adhesive capsulitis, reflex sympathetic dystrophy, protracted recovery and rehabilitation period, and significantly increased costs. ^, ^, For these reasons, surgery is currently considered the option of last resort, to be used only when other less-invasive methods have failed.

Barbotage/Lavage

Two-needle barbotage under fluoroscopic guidance was first described by Comfort and Arafiles in 1978, and Farin et al. first demonstrated the feasibility of US-guided barbotage in 1995. ^, ^, These studies described a barbotage technique with fenestration, which involves puncturing the calcific deposit with a needle multiple times. Citing concern regarding the potential risk of tendon injury caused by fenestration, Aina et al. first described a modified US-guided single-needle technique in 2001. No high-quality studies have compared the efficacy of lavage with simple fenestration, but subsequent double-needle approaches have also largely forgone fenestration. ^, More recent randomized controlled studies have demonstrated no significant difference in clinical outcomes up to 1 year between the single- and double-needle lavage technique, with the main difference being a slightly shorter procedure time treating denser calcifications using the double-needle technique. ^,

Clinical trials have generally shown significant pain relief and improvement of symptoms with US-guided barbotage both in the short term and at 1 year post treatment. ^, ^, Barbotage also results in a statistically significant decrease in the size of calcific deposits versus conservative therapy at 1 year post treatment. The self-limiting natural history of calcific tendonitis becomes more relevant during a more protracted time frame, and longer-term follow-up studies have shown that clinical outcomes of patients who were treated with barbotage are not significantly different from patients treated conservatively at 5 and 10 years post treatment. ^,

Equipment

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High-frequency (>10 MHz) linear US
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18- to 20-gauge 1.5-inch needle for lavage
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25-gauge 1.5-inch needle for initial anesthetic
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Optional: 30-gauge 0.5-inch needle for initial skin anesthetic
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10-mL syringes with 50:50 mixture of anesthetic and bacteriostatic sterile saline for lavage
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10-mL syringe for initial anesthetic
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5-mL syringe for corticosteroid

Common Injectates

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Anesthetic: 1% lidocaine for barbotage, 0.5% ropivacaine for SASD bursa injection
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For SASD bursa injection : corticosteroid (40 mg triamcinolone acetonide or methylprednisolone acetate) and local anesthetic

Author’s Preferred Technique: