Keywords
calcific tendinopathy - shoulder - ultrasound - lavage
Calcific tendinopathy involving the substance of the tendon is particularly common
in the rotator cuff, whereas insertional calcific tendinopathy involving the deposition
of calcium at the enthesis affects predominantly the Achilles tendon, the common extensor
tendon at the elbow, the gluteus medius and minimus at the greater trochanter, and
the patellar tendon. Calcific tendinopathy and insertional calcific tendinopathy appear
to be caused by two distinct pathogenetic mechanisms.[1]
Epidemiology, Pathogenesis, and Clinical Presentation
Epidemiology, Pathogenesis, and Clinical Presentation
Calcific tendinopathy of the rotator cuff is a common disorder that affects predominantly
the 40- to 60-year-old age group. Women appear to be more commonly affected than men,
and contrary to popular belief, individuals involved in strenuous manual labor or
athletic activities are not more commonly affected than those leading a sedentary
life.[2] There appears to be a slight preponderance in the dominant shoulder, but the nondominant,
and even both shoulders, may be affected.
Rotator cuff calcific tendinopathy is caused by the deposition of hydroxyapatite crystals,[3] most commonly in the supraspinatus and infraspinatus tendons. The subscapularis
and teres minor tendons may also be involved, but these calcific deposits tend to
be less frequently symptomatic unless they are very large.
The pathogenesis of calcific tendinopathy is still a matter of controversy. According
to Uhthoff and colleagues, the deposition of calcium apatite crystals within the substance
of the tendon is not a degenerative process but one that is actively mediated by cells
in a viable tendon.[4] The theory proposed by Uhthoff et al considers the clinical course, the morphological
aspects, and the histologic features of the disease. Uhthoff and colleagues described
three distinct stages in the disease process, namely the precalcific, calcific, and
postcalcific stages. Depending on the stage of the disease, the imaging appearance
and physical consistency of the calcification differ significantly as do patient symptoms.[5]
According to this theory, during the precalcific stage, fibrocartilaginous metaplasia
of tenocytes with the production of proteoglycan occurs in generally avascular areas.
This concept appears to be supported by histologic examinations.[6] Conversely, the stimuli that cause the initiation of the precalcific stage remain
unknown.
The following calcific stage consists of three phases: the formative, resting, and
resorptive phases. During the formative phase, calcium crystals are deposited into
matrix vesicles that coalesce and gradually form foci of calcification. During the
resting phase, the deposition of calcium is terminated and fibrocollagenous tissue
encircles and isolates the foci of calcification. As demonstrated at surgery, during
these two phases, the calcium deposits have a chalk-like appearance.[4] The formative and resting phases are chronic, usually lasting for a few years, and
they may be associated with intermittent or constant varying degrees of pain at rest
or with movement, especially abduction. Many individuals with radiographic evidence
of calcific tendinopathy, however, are asymptomatic.[2] In our experience, the larger calcifications and those located at the confluence
of the supraspinatus and infraspinatus tendons tend to be most symptomatic. The symptomatic
calcific deposits may cause focal thickening of the tendon ([Fig. 1]), they may elicit pain when probed percutaneously, and they may mechanically contribute
to a subacromial (supraspinatus, infraspinatus) or a subcoracoid (subscapularis) impingement
syndrome. When associated with an impingement syndrome, a concomitant subacromial
bursopathy is often present. Some authors have showed that the presence of a power
Doppler signal near the tendon calcification is more common in patients with symptomatic
calcifications than in individuals with asymptomatic calcifications.[7] During the resting phase of the disease, the calcifications tend to be well circumscribed
and discrete when examined radiographically ([Fig. 2]), and they often produce significant acoustic shadowing at ultrasound (US)[8] ([Fig. 3]).
Fig. 1 Sagittal ultrasound scan of the infraspinatus tendon shows an intratendinous calcific
deposit (between cursors) causing focal thickening and a convexity of the superficial
surface of the tendon.
Fig. 2 (a) Anteroposterior and (b) lateral radiographs of the left shoulder demonstrate a large multilobular calcific
deposit (arrow) in the infraspinatus tendon.
Fig. 3 Sagittal ultrasound scan of the posterosuperior cuff demonstrates a large hyperechoic
calcific deposit (long arrow) located at the confluence of the supraspinatus and infraspinatus
tendons, causing significant acoustic shadowing on the humeral cortex (short arrow).
The resorptive phase is the last of the three phases in the calcific stage, during
which spontaneous resorption of calcium occurs with the formation of thin-walled vascular
channels that surround the calcific deposits, associated with a reaction driven by
macrophages and giant cells that phagocytose and remove the calcium. The factors that
trigger the resorptive phase also remain unknown. It has been demonstrated at surgery
that, during this phase, the calcific deposits have a toothpaste-like appearance.[4] During this phase, patients may present clinically with an acute inflammatory shoulder
syndrome characterized by severe pain and very limited range of motion caused by shedding
of calcium crystals into the adjacent subacromial bursa ([Fig. 4]), within the rotator cuff tendons or even into the adjacent bone ([Fig. 5]). This hyperalgic syndrome typically lasts for 2 weeks and is usually followed by
substantial clinical improvement. During this phase, the calcifications appear ill
defined on radiographs and produce little or no acoustic shadowing at US ([Fig. 6]). When percutaneously aspirated, these calcific deposits typically are soft with
a slurry-like consistency.[9] Finally, during the postcalcific stage, reparation of the tendon occurs with remodeling
by fibroblasts and new vascular channels that produce collagen and mature scar tissue.
Fig. 4 (a) Anteroposterior radiograph of the right shoulder shows ongoing resorption of a large
calcification into the subacromial-subdeltoid bursa (long arrow). (b) Corresponding coronal oblique T2-weighted with fat suppression MR image depicts
the hypointense calcification (short arrow) in the hyperintense subacromial-subdeltoid
bursitis (open arrows).
Fig. 5 (a) Anteroposterior radiograph of the right shoulder demonstrates a calcific deposit
in the resorptive phase that has eroded the humeral cortex and is migrating into the
bone (long arrow). (b) Corresponding coronal oblique T2-weighted MR image with fat suppression shows the
cortical erosion (short arrow) and the hyperintense reactive bone marrow edema (open
arrow).
Fig. 6 Longitudinal ultrasound scan of the left subscapularis tendon showing an almost isoechoic
calcification (between cursors). Note the absence of posterior acoustic shadowing.
This appearance suggests that the calcification has entered the resorptive phase.
Outcome and Treatment
In most cases, calcific tendinopathy is a self-limiting condition, in which the calcification
spontaneously resorbs after a period of a few years or is treated successfully conservatively.[10] In the formative and resting phases of the disease, if conservative measures fail
and the patient presents with progressive symptoms interfering with daily living activities,
removal of calcific deposits may be indicated.[4] The resolution of calcification has been shown to correlate well with clinical improvement
of symptoms, and therefore various treatments have been devised to promote their removal.
Arthroscopic removal of calcific deposits has shown successful results with significant
improvement in shoulder function at 24 months and progressive decrease in pain level
up to a year after the procedure.[11] There is evidence supporting the use of extracorporeal shock-wave therapy (ESWT)
in calcific tendinopathy of the rotator cuff. For instance, a randomized placebo-controlled
study, in which 134 patients (of 144 enrolled) completed the treatment and the 6-month
follow-up, suggested a beneficial effect of high-energy ESWT over 6 months for shoulder
function, self-rated pain, and diminished size of calcifications, compared with the
sham treatment.[12] Another randomized double-blind sham-controlled trial compared the effects of acetic
acid iontophoresis (AAI) and physiotherapy to physiotherapy alone in 27 patients (of
36 enrolled) with calcific tendinopathy.[13] This study concluded that treatment of calcific tendinopathy of the rotator cuff
with AAI and physiotherapy did not result in better clinical or radiographic effects
than those observed in patients treated with physiotherapy alone.
Fluoroscopy-guided needle lavage and aspiration of rotator cuff calcifications was
first described >30 years ago.[14] In 1995, Farin and colleagues described a two-needle US-guided technique to treat
calcific tendinopathy.[15] One year later, the same group presented their results in 61 shoulders with calcific
tendinopathy treated with this US-guided technique.[9] Their clinical results at 1-year follow-up were excellent in 74%, moderate in 16%,
and poor in 10% of patients, respectively. More recent studies using either a one-needle[16]
[17] or a two-needle[18] US-guided technique have reported that most patients experienced significant or
complete improvement in pain and disability. More recently, a study by Serafini and
colleagues suggested that treated patients had better outcomes than did untreated
patients at 1 year.[18] In a prospective study, Sconfienza and colleagues compared the use of room-temperature
saline to warm saline (42°C) in the US-guided lavage and aspiration treatment of rotator
cuff calcific tendinopathy in 462 patients.[19] Their study suggests that the use of warm saline reduces procedure time by improving
calcium dissolution. They also found a lower frequency of postprocedural subacromial-subdeltoid
bursitis in the warm saline group as compared with the group treated with room-temperature
saline.
Ultrasound-Guided Lavage and Aspiration Technique
Ultrasound-Guided Lavage and Aspiration Technique
US-guided lavage and aspiration techniques vary greatly, and there is no accepted
standardized methodology. At our institution, we use a one-needle technique ([Fig. 7]), and we routinely perform a complete shoulder US examination before any intervention.[16] This is done to ensure that there are no coexisting disorders such as rotator cuff
tears or adhesive capsulitis, and to confirm that the calcific tendinopathy is the
cause of the patient's symptoms. For the intervention, the patient is placed into
an oblique lateral decubitus position opposite the affected side. Depending on the
location of the calcification in the rotator cuff, the arm is positioned for adequate
visualization of the calcification (neutral or internal rotation for the supraspinatus
and infraspinatus tendons, external rotation for the subscapularis tendon).
Fig. 7 (a) Sagittal ultrasound scan of the posterosuperior cuff showing injection of lidocaine
1% into the subacromial bursa (arrow) using a 22-gauge needle, at the level of a large
rotator cuff calcification (open arrow). (b) Then, an 18-gauge needle connected to a 10-mL syringe filled with lidocaine 1% is
advanced into the calcification (arrow). Note the near-horizontal orientation of the
needle. (c) Progressive lavage and aspiration of the calcium has created a cavity inside the
calcification, leaving an irregular hyperechoic calcific rim. (d) After completion of the lavage, the 18-gauge needle is partly withdrawn and positioned
into the subacromial bursa for the injection of a mixture of cortisone and bupivacaine
5% (arrow). Note the residual decompressed, fragmented hyperechoic calcific deposit
(open arrow). (e) At the end of the procedure, the syringe showing the amount of calcium that was
retrieved.
After sterile preparation of the skin and equipment, the calcification is targeted
under US from a sagittal oblique posteroanterior approach using a 22-gauge needle
connected to a 10-mL syringe filled with 1% lidocaine. As the needle is advanced,
the skin, the subcutaneous tissues, and the subacromial bursa are injected with lidocaine
for local anesthesia. Approximately 4 to 6 mL of lidocaine are used. Then the 22-gauge
needle is retrieved and replaced by an 18-gauge needle, which, in turn, is connected
to the 10-mL syringe filled with 1% lidocaine, and using the same approach, under
US monitoring, the larger bore needle is advanced to penetrate into the calcification.
Importantly, the calcification should be punctured only once, and lidocaine is injected
into the calcification without first aspirating, to prevent the needle tip from becoming
obstructed. Starting the lavage, the first injection is usually forceful and creates
a cleavage in the substance of the calcification. The lavage is performed with several
short injections, each followed by release of pressure on the plunger to let lidocaine
and calcium fragments evacuate back into the syringe. The syringe can be held horizontal
or below horizontal to facilitate return of the aspirated calcific material. Also,
new lidocaine-filled syringes can be exchanged for the old one when it is filled with
calcium crystals. Lavage and aspiration should be continued until no more calcium
can be aspirated. It may not be possible to aspirate very hard calcifications, in
which case the calcification can be fragmented by injecting it and probing it gently
by moving the needle tip and rotating the syringe. At the end of the procedure, when
no more crystals are coming into the syringe, not all the calcifications will be gone.
The needle is then withdrawn into the subacromial bursa where a combination of 20
mg/mL of triamcinolone and 2.5 mL of bupivacaine 0.5% is injected to mitigate the
risk of postprocedural bursitis. The entire procedure usually lasts approximately
20 minutes. The procedure is usually not painful, although the patient may feel some
discomfort from the pumping effect of the lavage. Rarely, some patients may experience
a vagal reaction.
After the procedure, the patient is instructed to apply ice on the shoulder, intermittently
according to the usual protocol, as needed, and take analgesics as needed, although
most patients do not experience any significant postprocedural pain. Patients are
also instructed to limit strenuous exercises involving the shoulder for up to 4 weeks.
A follow-up appointment is scheduled for 8 weeks after the treatment and includes
assessment of clinical improvement and repeat US. If the patient presents with residual
pain and restricted range of motion, which is sometimes the case with larger calcifications,
a second percutaneous treatment is usually performed. Other patients may also present
with recurring pain after a period of complete resolution of symptoms. This is usually
caused by the dispersing calcium crystals inciting a subacromial bursitis. In those
cases, we perform a subacromial steroid injection.
Conclusion
Understanding the evolution of calcific tendinopathy, which correlates with the clinical
symptoms and the imaging features of the calcifications, helps to tailor management
and to determine prognosis of this disorder. Percutaneous calcium aspiration is a
minimally invasive and effective treatment of calcific tendinopathy. Rarely, if conservative
treatment fails, surgery may become necessary.
