Evaluation and Nonsurgical Management of Rotator Cuff Calcific Tendinopathy




Rotator cuff calcific tendinopathy is a common finding that accounts for about 7% of patients with shoulder pain. There are numerous theories on the pathogenesis of rotator cuff calcific tendinopathy. The diagnosis is confirmed with radiography, MRI or ultrasound. There are numerous conservative treatment options available and most patients can be managed successfully without surgical intervention. Nonsteroidal anti-inflammatory drugs and multiple modalities are often used to manage pain and inflammation; physical therapy can help improve scapular mechanics and decrease dynamic impingement; ultrasound-guided needle aspiration and lavage techniques can provide long-term improvement in pain and function in these patients.


Key points








  • Rotator cuff calcific tendinopathy is a common asymptomatic finding on imaging studies that accounts for shoulder pain in approximately 7% of cases.



  • Most patients can be managed conservatively with a combination of nonsteroidal anti-inflammatory drugs, modalities, physical therapy, and injection therapy.



  • The goal of physical therapy is to improve scapular mechanics and decrease subacromial impingement.



  • Ultrasound-guided needle aspiration and lavage of calcium deposits in the rotator cuff tendons have been shown to decrease the size of deposits and improve pain and function on a long-term basis.






Introduction


Rotator cuff disease is a common cause of shoulder pain. The differential diagnosis of rotator cuff disease includes tendinitis, tendinopathy, subacromial impingement, partial and full thickness tendon tears, and calcific tendinopathy. Although calcific tendinopathy is a common incidental finding on imaging studies, it can also be a cause of significant shoulder pain and disability. The supraspinatus tendon is most commonly involved, which can lead to significant subacromial impingement and limit activities at or above shoulder level. Like many other rotator cuff problems, most patients respond well to relative rest, nonsteroidal anti-inflammatory drugs (NSAIDs), physical therapy, and subacromial bursa injections with corticosteroids. There is growing interest and use of ultrasound-guided injection procedures in musculoskeletal medicine. One novel technique for the treatment of rotator cuff calcific tendinopathy (RCCT) involves advancing a larger-gauge needle under live sonography into the calcium deposit, fragmenting it, and aspirating its contents. This technique has been shown to provide excellent long-term pain relief and may be a good alternative to surgical intervention.




Introduction


Rotator cuff disease is a common cause of shoulder pain. The differential diagnosis of rotator cuff disease includes tendinitis, tendinopathy, subacromial impingement, partial and full thickness tendon tears, and calcific tendinopathy. Although calcific tendinopathy is a common incidental finding on imaging studies, it can also be a cause of significant shoulder pain and disability. The supraspinatus tendon is most commonly involved, which can lead to significant subacromial impingement and limit activities at or above shoulder level. Like many other rotator cuff problems, most patients respond well to relative rest, nonsteroidal anti-inflammatory drugs (NSAIDs), physical therapy, and subacromial bursa injections with corticosteroids. There is growing interest and use of ultrasound-guided injection procedures in musculoskeletal medicine. One novel technique for the treatment of rotator cuff calcific tendinopathy (RCCT) involves advancing a larger-gauge needle under live sonography into the calcium deposit, fragmenting it, and aspirating its contents. This technique has been shown to provide excellent long-term pain relief and may be a good alternative to surgical intervention.




Epidemiology


There have been several studies on the epidemiology of RCCT. One of the most famous of these studies was done in 1941 by Bosworth, who looked at 5061 office employees and found the prevalence of calcium deposits in the rotator cuff to be 2.7% on fluoroscopic examination. Several other studies have reported prevalence rates ranging from 2.7% to 22%, mostly affecting people ranging from 30 to 50 years of age. It is often an asymptomatic finding on imaging studies. However, when considering people with shoulder pain, RCCT is a finding 6.8% of the time. When one shoulder is affected, the other shoulder will also be affected 14% of the time. Similar to other rotator cuff pathologic abnormalities, the supraspinatus tendon is most likely to be affected.


People with sedentary lifestyles experience a higher risk of developing RCCT. Ischemic heart disease, hypertension, diabetes, and thyroid disease are known associated medical conditions that seem to predispose patients to developing calcific tendinopathy for reasons not well understood. There is a known correlation with calcific tendinopathy and endocrine disorders. These patients have an earlier onset of symptoms, a longer disease course, and ultimately undergo surgery more frequently than people that do not have these conditions. Interestingly, RCCT is rarely associated with metabolic disorders related to calcium or phosphorus.




Pathophysiology


The mechanism of the pathogenesis of calcific tendinopathy has remained elusive. There are several competing theories. It has been suggested that one of the reasons the pathogenesis remains unknown is that biopsies obtained are done near the end of the natural history of the disease. The other theories on the pathogenesis of calcific tendinopathy that will be discussed in this article include degenerative calcification, reactive calcification, endochondral ossification, and chondral metaplasia ( Table 1 ).



Table 1

Summary of different theories on pathogenesis of calcific tendinopathy



















Theory Proposed Mechanism
Degenerative calcification Intracellular calcium accumulated from old, damaged, and necrotic tenocytes
Reactive calcification Metaplastic fibrocartilage with calcium deposited through an inflammatory mechanism
Endochondral ossification Metaplastic fibrocartilage becomes vascular from underlying bone marrow and calcium deposited without evidence of inflammation (similar to bone spur formation)
Chondral metaplasia Erroneous differentiation of tenocytes into bone cells, mediated by BMP-2


In degenerative calcification, it has been proposed that tendon fibers deteriorate over time. It is thought that aging tenocytes become progressively more damaged with time as a result of decreased vascular flow and tendon fibers become hypocellular and eventually undergo necrosis from the damage. As a result, intracellular calcium builds within the tenocytes in the form of psammoma bodies during the beginning phases of calcification; this in turn becomes larger over time until there are macroscopic areas of calcification that will be apparent on imaging and possibly symptomatic in affected patients.


Reactive calcification proposes the cause of calcification as a multistage process beginning with tenocyte metaplasia, which leads to calcification and ultimately a cell-mediated inflammatory reaction. Uhthoff and colleagues proposed dividing the process into 3 main stages: precalcific, calcific, and postcalcific ( Table 2 ). In the precalcific stage, the tenocytes undergo metaplasia into fibrocartilaginous tissue, acting as a substrate for calcium deposition, which is thought to be mediated by chondrocytes. The calcific stage is when actual calcium deposition occurs in the tendon and the body’s subsequent reaction to a calcified tendon. Uhthoff and Loehr further subdivide the calcific stage into the formative and resorptive phases. In the formative phase, calcium crystals deposit into the affected tissue, which is mediated by the chondrocytes of the metaplastic fibrocartilagenous tissue, that eventually combine into larger areas of calcified tissue. Uhthoff further comments that if surgery is done during this stage of the disease, the calcified areas will be chalky and need to be “scooped” out. The resorptive phase begins after a varying period of dormancy in the disease course. The affected area develops “vascular channels” wherein macrophages phagocytose and eliminate the calcium. Finally, the postcalcific phase describes the process whereby fibroblasts in granulation tissue remodel the affected tissue following calcium removal.



Table 2

Summary of different stages of calcific tendinopathy



















Stages of Calcification Pathophysiology
Precalcific stage Tenocytes undergo metaplasia into fibrocartilagenous tissue
Calcific stage: formative phase Calcium crystals deposit onto metaplastic tissue
Calcific stage: resorptive phase Phagocytosis of deposited calcium
Postcalcific stage Remodeling of affected tissue


Another mechanism proposed by Benjamin and colleagues, who studied Achilles tendons of rats, suggested that endochondral ossification of fibrocartilage is the pathogenesis of calcific tendinopathy. Again, fibrocartilage first develops in affected sites through the process of metaplasia. The fibrocartilage then develops vascular flow from underlying bone marrow. As the fibrocartilage becomes increasingly vascular, deposits of calcium form. What develops is essentially a bone spur in the tendon tissue. An important note, through this process no inflammatory reaction was seen to take place. Unfortunately, Benjamin and colleagues did not report on the process of resorption and changes that take place in the rat tendons.


The fourth mechanism discussed here is that of chondral metaplasia. Rui and colleagues think the calcification of tenocytes is a result of erroneous differentiation of tendon stem cells into bone cells. Hashimoto and colleagues showed that injection of bone morphogenic protein (BMP-2) into tendons produced ectopic bone formation in the tendon, suggesting tendon stem cells were responsive to proteins thought to induce bone growth. The exact mechanism by which tendon stem cells differentiate themselves incorrectly into bone is not clear at this point.


To complement the discussion, it has been proposed that there are genetic components that predispose certain populations to developing calcific tendinopathy. It should also be mentioned again that there are several endocrine and vascular disorders that are associated with calcific tendinopathy. However, it is not clear how they affect the natural history of the disease.


Although the exact mechanism of the pathophysiology remains elusive, there are a few important points to take into consideration:




  • There are several things that likely contribute to the development of calcific tendinopathy.



  • There are several medical conditions that can predispose a person to this condition.



  • There may be a genetic component and familial predisposition.



It is tempting to think there is some sort of injury that first occurs to the tendon cells, whether it is an acute clinically apparent injury or a series of subclinical microtraumas over the span of several years. Certainly, something must occur to induce metaplasia of the tenocytes that ultimately lead to the development of calcific tendinopathy. Furthermore, it is unclear if the calcification and resorption process are a part of normal healing that takes place in an injured tendon.




Clinical presentation


Calcific tendinopathy of the shoulder may present in several different ways; however, the main complaint when patients are symptomatic is pain. As previously discussed, epidemiologic studies have shown that many cases of calcific tendinopathy of the shoulder will be asymptomatic or an incidental finding on imaging studies. However, Bosworth reported that 34% to 45% of patients with rotator cuff calcifications were found to be symptomatic.


A good way to look at RCCT, and its typical natural history, is that the disease progresses through 3 stages: the precalcification stage; the calcification stage, which includes the formative and resorptive phases; and the postcalcific stage (see Table 2 ).


Often, the pain is worse in acute presentations than in chronic presentations. In some chronic forms, there may be periods whereby patients are asymptomatic and a relapsing remitting pattern will be observed. Uhthoff and Loehr and Speed and Hazleman have commented that it is during the resorptive stage that patients are most likely to develop symptoms and this was attributed to the process of resorption of calcium itself. When osteolysis of the greater tuberosity is observed in calcific tendinopathy of the shoulder, it has been reported that there is an association with worse outcomes, more pain, more functional impairment, and less success with surgery. In most cases, the pain and other symptoms will be self-limited and the natural history of the disease is for pain to improve over time without the need for aggressive interventions.




History and physical examination


A complete history is important when evaluating a patient with shoulder pain. Questions to ask relate to pain with overhead activities, night pain, a history of trauma, or sports participation. It is also helpful to ask about numbness, tingling, burning, or weakness, because this may suggest a cervical radiculopathy or brachial plexopathy. A medical history significant for diabetes or thyroid disease may increase suspicion for calcific tendinopathy.


A thorough physical examination is also important when evaluating a patient with shoulder pain. The examination should begin with inspection and palpation of the painful shoulder. Active and passive range of motion of the shoulder should also be assessed. Manual muscle testing should be done to assess for weakness that may be related to pain inhibition, a rotator cuff tear, or neurologic injury. Sensation and reflexes should also be assessed if nerve damage is suspected. Finally, provocative tests should be done.


Tests classically used to assess shoulder pain related to subacromial impingement include the Hawkin impingement test, Neer sign test, and Yocum test. These maneuvers have in common the idea that when performed correctly, the subacromial space is compressed. For all of the above impingement tests, reproducible pain with the maneuver is considered a positive sign. In the Hawkin test, the shoulder is passively flexed to 90° and internally rotated by the examiner. In the Yocum test, the patient places their hand on the contralateral shoulder and elevates their elbow without elevating the shoulder in the process. The Neer sign test is performed by passively forward flexing an internally rotated shoulder.


Occasionally, a patient will have constitutional symptoms of fever and malaise. In these patients, elevated inflammatory markers may be found on blood work such as C-reactive protein, erythrocyte sedimentation rate, and serum white blood count. In these patients, it is important to consider septic arthritis, gout, and pseudogout. Ultimately, to make the diagnosis of calcific tendinopathy of the rotator cuff, imaging studies will be needed.




Imaging studies


Plain films are often adequate to diagnose calcific tendinopathy of the rotator cuff. Anteroposterior, outlet view, internal rotation, and external rotation views are routinely ordered ( Fig. 1 ). MRI can be a useful adjunct study to see if there is an associated rotator cuff tear and to evaluate for suspected osteolysis of the greater tuberosity. In addition, MRI has a distinct advantage for evaluation of the glenoid labrum, subcortical bone, and deep soft tissues when compared with other imaging modalities.


Oct 6, 2017 | Posted by in ORTHOPEDIC | Comments Off on Evaluation and Nonsurgical Management of Rotator Cuff Calcific Tendinopathy
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