
Calcific tendonitis of the rotator cuff
- 11/02/2019
Calcific tendonitis is a process in which intratendinous calcifications form. It is characterized by the deposition of calcium hydroxyapatite crystals within the tendon. It is a living, cell-mediated process that progresses over time and is self-limited. It can affect any tendon, with a preference for those without a synovial sheath: the FCU, finger extensors, or rotator cuff. Rotator cuff calcific tendonitis is a common condition in trauma clinics (10% of all consultations for shoulder pain). It is undoubtedly one of the most common causes of non-traumatic shoulder pain:
- The most commonly affected tendon is the supraspinatus tendon, with a frequency ranging from 2.7% to 10%, depending on the series studied.
- It is more common in women, especially those between 30 and 60 years of age.
- Bilateral involvement is present in 13–47% of cases.
- Up to 25% are related to diabetes mellitus.
WHY CALCIFICATIONS FORM?
There are theories that attempt to answer why these calcifications form:
- Codman's degenerative theory: degenerative processes of tendon fibers would cause necrosis and a process of dystrophic calcification.
- Uhthoff's calcific tendinitis theory: the calcification process would be cell-mediated, followed by a spontaneous process of phagocytic resorption, unrelated to previous injuries, occurring at an early age and with spontaneous resolution.
This accumulation of intratendinous calcium hydroxyapatite crystals occurs in three phases:
Phase 1 or precalcification phase: often asymptomatic. Tendon degeneration and changes in the subacromiodeltoid bursa occur, predisposing to the second phase.
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Phase 2 or calcification: Calcium pyrophosphate crystals accumulate, generating a significant inflammatory reaction, with inflammatory pain, generally unrelated to activity, more intense at night, and often interfering with the patient's rest.
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Phase 3 or post-calcification, in which calcium deposits may disappear through a reabsorption process.
DIAGNOSIS OF CALCIFYING TENDINITIS
The clinical presentation of calcific tendinitis varies widely. It may be an incidental finding in a patient presenting for another reason or be highly symptomatic, with severe pain and significant functional limitations. Intrinsic factors that may influence this include age and body mass index.
The diagnosis is usually clinical: inflammatory pain unrelated to trauma or overexertion, present throughout the day but exacerbated at night. A plain X-ray confirms the diagnosis, and in our case, ultrasound is preferred to confirm the lesion and determine its location (it avoids the radiation exposure caused by plain X-rays and CT).
From an ultrasound perspective, recent studies classify calcifications as granular (those with partially defined margins and irregular echogenicity), nodular (with a cystic appearance and sedimentary contents), and linear (thin and following the tendon course).
On the other hand, based on their density, we can classify them into calcifications:
- Type I or hard calcification: with a smooth, well-defined contour, a well-defined upper hyperechogenic line, and a significant posterior acoustic shadow that obscures the cortical surface of the humerus. These are usually incidental findings without significant clinical manifestations, although they can of course be clinically significant.
- Type II or intermediate: with characteristics intermediate between types I and III, with a less-defined upper shadow and less acoustic shadow, so they subtly obscure the humeral bone contour. They are usually more symptomatic than type I.
- Type III or soft: whose lumpy, pasty appearance gives them less hyperechogenicity and is less well-defined. They do not have acoustic shadows. They are usually associated with the resorptive phase of calcification and are the most symptomatic.
TREATMENTS FOR CALCIFICTIVE TENDINITIS OF THE SHOULDER
There are different treatments for calcific tendinitis of the shoulder:
Initially, joint rest, analgesic and anti-inflammatory medications, and exercises or rehabilitation regimens can improve the pain and prevent loss of mobility during the first few days.
Cases resistant to these measures may be treated with shock waves or ultrasound-guided therapies such as needle puncture lavage for thicker calcifications (type III) or barbotage in hard calcifications (type I).
Surgical treatment is reserved for cases in which all these measures do not improve the clinical picture. We recommend arthroscopic debridement of the subacromial space and calcium deposits.
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