Calcific tendonitis is a painful inflammatory condition involving the resorption of calcium hydroxyapatite deposits in or around a tendon, traditionally involving the rotator cuff tendons of the shoulder and most commonly the supraspinatus tendon.
Patients present with an acutely painful shoulder. The pain may be severe and usually presents around the great tuberosity, depending on which tendon is involved. The prototypical patient is a white female between the ages of 30-50. The severity of the pain often triggers the patient to present to the emergency room, and the symptoms often mimic septic arthritis of the shoulder.
Pain is most often associated with use of the shoulder, particularly with forward elevation and abduction (reaching and overhead activity as is similar to other pathology of the rotator cuff). They may report that the shoulder is tender as well. The pain may interrupt their sleep. The onset is often sudden with an insidious onset. In about 10% of the time the calcific tendonitis may be bilateral, although the patient may not be having symptoms at the same time in each shoulder.
Some patients have a prolonged course of pain which may be marked by periods of waxing and waning pain. In rare cases symptoms may last for years. Generally, the acuity of the symptoms correlates to the duration of symptoms. It is thought that the pain and symptoms correlates to the rate of calcium resorption, and likewise the inflammatory response created. A patient coming in with more severe initial pain and symptoms will be more likely to have a short clinical course because the calcium deposits will be absorbed more quickly.
Physical exam findings are dependent on the severity of the disease and pain, but generally mimic subacromial impingement. Patients may be tender to palpation near the insertion of the tendon. They may also have limited range of motion of the shoulder both actively and passively secondary to the pain.
About half of the time, the supraspinatus is involved. The next most common tendon to be involved is the infraspinatus followed by the teres minor and less than 5% of the time in the subscapularis.
Most cases of calcific tendonitis can be differentiated from septic arthritis from laboratory markers and X-ray findings. However, it is important to rule out septic arthritis in patient who present with an acutely painful and inflamed shoulder with no history of trauma – particularly in immune compromised patients or patients with prior known shoulder pathology.
Overall incidence of calcific tendinitis ranges from 2.5-20%. However, the condition is generally only painful in only about 1/3 to 1/2 of patients with the deposits in their tendons. Of patients with shoulder pain, about 7% is due to calcific tendinitis. Patients may have bilateral calcific tendinitis in 24-66% of the time, but it is usually only symptomatic bilaterally about 10% of the time.
The condition mostly affects individuals between 30 and 50 with a slight predilection in women and Caucasians. It is also more common in insulin dependent diabetics and patients with thyroid disease. The condition also appears to be more common in people with relatively sedentary professions such as desk jobs and housewives and less common in heavy labourers.
Pathology and pathophysiology
Calcific tendinitis occurs as a multifocal, cell-mediated calcification inducing metaplasia from tenocytes to chondrocytes and subsequent calcification inside the tendon. This is followed by phagocytosis of the metaplastic areas in the tendons by multinucleated giant cells. Ultimately, the tendon remodels and reforms normal tendon.
There are three phases of calcific tendonitis: precalcifying stage, calcifying stage, and postcalcifying/resorptive stage. The precalcifying stage involves the metaplasia of the tenocytes to chondrocytes and is usually asymptomatic. During the calcifying stage the calcium deposits in the metaplastic tissue and consolidates into dense homogenous and well delineated areas of calcium. This stage is also usually asymptomatic, but patients may experience symptoms similar to mild subacromial impingement. The final, resorptive stage is the stage during which most patients seek attention for their symptoms. During this phase there is a proliferation of blood vessels and vascularity into the calcified area. As the body phagocytoses the calcium deposits, the resultant inflammatory response creates increasing intratendinous pressure and subsequent pain. The body initially lays down primarily type III (scar) collagen, but then remodels the tendon into type I collagen typical in tendons as the phagocytosed metaplastic tissue is replaced by normal tissue.
In the acute, painful phase of calcific tendonitis the presentation is similar to conditions such as septic arthritis, adhesive capsulitis (frozen shoulder), and gout. In less severe cases the condition may be confused with a rotator cuff tear or shoulder impingement syndrome. However, calcific tendonitis is a non-degenerative condition which generally does not result in the tendon becoming torn or otherwise pathologic after resolution. Parsonage-Turner syndrome may also create an acutely painful shoulder, but usually causes neurologic or pain symptoms further down the arm rather than isolated to the shoulder. The characteristic findings on x-ray should be able to distinguish calcific tendonitis from the other conditions. If there is any doubt, an aspiration and synovial fluid analysis will be able to rule out a septic arthritis.
The cause of the calcific tendonitis is not well understood. However, there are theories that temporary tissue hypoxia and localized increased pressure cause pathologic changes in the tissue leading to the calcium deposits. The deposits are most commonly found 1.5-2cm from the insertion of the supraspinatus tendon, the “critical portion.” There are debates about the vascularity of this region with different authors arguing the area is well-vascularized versus a watershed region.
Radiographic and laboratory findings
Patients generally have normal appearing labs such as white blood cell count (WBC), C-reactive protein (CRP), and erythrocyte sedimentation rate (ESR) but some patients with a severe inflammation reaction from the calcium resorption may demonstrate an elevated ESR and mildly elevated WBC with relative neutrophilia.
X-ray findings in calcific tendonitis are the hallmark findings in calcific tendonitis and confirm the diagnosis. Once the patient has reached the calcifying stage, a homogeneous, well-demarcated calcium mass is seen within one of the tendons. As the patient moves into the resorptive stage, radiographs demonstrate a fluffy, poorly delineated deposit of calcium within the tendon.
It is important to analyze multiple x-ray views of the shoulder to confirm the diagnosis of calcific tendonitis. The calcification may be missed with one view of the shoulder, particularly with subscapularis involvement so AP radiographs in internal and external rotation as well as scapular Y and/or axillary views of the shoulder are recommended as a complete series to evaluate the shoulder in any suspected shoulder pathology.
Above is a typical example of calcium deposits seen on AP (top) and “scapular Y” lateral (bottom) images of a left shoulder in the supraspinatus tendon in a patient with calcific tendonitis.
Risk factors and prevention
There are no known modifiable risk factors for calcific tendonitis. Even if a calcium deposit is found incidentally such as during a chest x-ray, there is no intervention recommended if it is asymptomatic.
Calcific tendonitis is a self-limited disorder which resolves on its own over a period of time. Therefore, the mainstay of treatment is conservative, nonoperative management with symptom control. A corticosteroid/local anesthetic combination injection into the shoulder joint is usually very helpful in relieving much of the pain with few adverse effects. Some physicians recommend needling the calcium deposits percutaneously with or without a concomitant injection of local anesthetic +/- corticosteroid to accelerate the healing in the tendon.
NSAIDs should be tried for pain management as well. When the patient has impingement type symptoms and is in an early stage of calcific tendonitis, a physical therapy regimen is generally successful at relieving the patient’s pain. Furthermore, therapy is important to help the patient maintain their shoulder range of motion.
Radiotherapy has been attempted to treat calcific tendonitis, but the results are not conclusive enough to justify the cost and potential adverse effects. Ultrasound on the other hand has been shown to bring patients short term relief of their pain, but there has been no long term benefit found.
Extracorporeal shock wave treatment (ESWT) has also been found beneficial in the treatment of calcific tendonitis. Some studies have found that high-pulse energy is beneficial over low-pulse energy but others have found no difference. The theory is to break apart the calcifications just as in the treatment of kidney stones. Patients are generally not recommended for ESWT until they have failed conservative treatment for at least 3 months and preferably 6 months. Adverse effects seem to relate to blood flow disruption and include intramuscular hematoma, bone marrow edema, and a few case reports of osteonecrosis of the humeral head - so its use is not completely benign.
Surgical management of calcific tendinitis involves excising the calcified deposits arthroscopically or in an open fashion. Surgery is best indicated for symptomatic patients in the calcifying stage and for chronic or worsening symptoms after failure of conservative measures. Therefore, surgery is indicated for relatively few patients with calcific tendonitis. It is controversial whether a subacromial decompression is beneficial concomitantly with excision of the calcium deposits. Authors have shown that it does prolong the recovery from surgery, but there may be a role for it in patients demonstrating chronic impingement symptoms without a homogenous, well-circumscribed lesion.
Outcomes are variable given that the clinical course is so variable between patients. Again, generally the disease is self-remitting over a short period of time and most patients are symptom-free in a few weeks after the onset of symptoms. Reported rates of recovery from symptoms without intervention range greatly in the literature from 30-90%. However, results of complete resorption of the calcium is lower meaning many patients with residual calcium after an acute calcific tendonitis attack may be symptom free despite X-rays continuing to show calcium in the tendon. About 10% or less of patients with calcific tendonitis will need surgical or more aggressive management of their condition.
Chronic calcific tendonitis treatment is also fairly efficacious. Needling has been shown to have favourable results in 70-90% of patients treated. ESWT is successful 50-80% of the time in relieving symptoms despite the chronicity of the disease. Surgical management of calcific tendonitis is successful 80-90% of the time in relieving symptoms.
Untreated calcific tendonitis is likely to resolve on its own. It is important to explain the disease process to patients so that they understand that the sometimes severe pain they are experiencing is neither life or limb threatening and will likely abate on its own. Patients may continue to perform any task or activity of daily life they please, pain allowing.
Understanding the genesis of the metaplasia in calcific tendonitis and the initial trigger of calcific tendonitis may help guide future treatment and prevention methods. So far we have begun to understand the pathology but not the trigger of calcific tendonitis. There is work to be done to fully understand how prevention may be successful.
- · Calcific tendonitis
- · Rotator cuff
- Subacromial impingement
Skills and competencies
- Understand the presentation and be able to recognize calcific tendonitis
- · Know the differential diagnosis and work up for an acutely painful shoulder
- · Understand and be able to recognize the hallmark findings on x-rays
- Understand the treatment options and algorithm for calcific tendonitis
. _In: OrthopaedicsOne - The Orthopaedic Knowledge Network. Created
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