Calcific Tendinopathy
Introduction
Procedures
Patient History
Patient Examination
Imaging
Treatment Options
Surgical Indications
Surgical Treatment
Ultrasound-guided Percutaneous Irrigation of Calcific Tendinopathy (US-PICT)
Positioning
Possible Pearls
Possible Pitfalls
Equipment
Step-by-Step Guide to Surgical Technique
Postoperative Care
Shoulder Arthroscopy
Positioning
Possible Pearls
Possible Pitfalls
Equipment
Step-by-Step Guide to Surgical Technique
Postoperative Care
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Calcific Tendinopathy
Chapter 17
A. Evaluation and Management of Calcific Tendinopathy
Nicola Maffulli, Francesco Oliva, and Alessio Giai Via
Rotator cuff calcific tendinopathy (RCCT) is a common cause of nontraumatic shoulder pain, characterized by calcium deposits in the substance of the tendon, first described by Painter in 1907. Calcific deposits can be found in up to 22% of patients during routine shoulder examination. A study from Louwerens et al. in 2015 found that in symptomatic patients with acute or chronic nontraumatic shoulder pain, the prevalence of calcific deposits in the rotator cuff was 42.5%. In most instances, the calcific deposits are located in the supraspinatus tendon (70%–87%), followed by the infraspinatus tendon (9%–20%) and the subscapularis tendon (4%–7%). Calcific tendinopathy of the subscapularis tendon is less common, and it may be the cause of secondary subcoracoid impingement. Women aged between 30 and 50 are the most frequently affected, and the pathology is bilateral in 10% of patients.
The pathogenesis is still not completely understood, and many theories have been developed. Codman first tried to explain the pathogenetic process of RCCT, proposing that the degeneration of rotator cuff tendons caused by overuse or aging is the first step that precedes calcification. Sandstrom proposed that degeneration of the tendon fibers, secondary to local ischemia, was the leading factor that induces the deposition of calcific deposits. More recently, Uhthoff and Loehr hypothesized that a favorable environment permits an active process of cell-mediated calcification, usually followed by spontaneous phagocytic resorption. Degenerative changes cannot be solely responsible because calcific tendinopathy has been reported in twin brothers and in children, which makes it difficult to fully explain these phenomena with a reactive degenerative theory.
The association between calcific tendinopathy and metabolic diseases, such as diabetes mellitus and thyroid disorders, has been pointed out, but the precise mechanism is still unknown. Patients with associated endocrine disorders present with earlier onset of symptoms, longer natural history, and undergo surgery more frequently compared with a control population. More than 30% of patients with insulin-dependent diabetes present with tendon calcification. A recent study demonstrated that thyroid hormone nuclear receptors are present on tenocytes, and that, in vitro, thyroid hormones enhance tenocyte growth and counteract apoptosis in healthy tenocytes isolated from tendons in a dose- and time-dependent manner. Hypothyroidism causes accumulation of glycosaminoglycans in the extracellular matrix (ECM), which may predispose patients to develop tendinopathy and tendon ruptures. However, the relationship between tendinopathy and metabolic disorders is still under investigation.
Most RCCT can be treated successfully conservatively, Nonsteroidal antiinflammatory drugs (NSAIDs) are widely prescribed to control pain, often before the radiographic diagnosis of calcific tendinopathy.
Shockwave therapy is widely used for the management of calcific tendinopathy. A recent systematic review showed good evidence of the benefit of high-dose focused extracorporeal shockwave therapy (F-ESWT) in calcific tendinopathy of the rotator cuff in reducing pain and improving shoulder function at 6-month follow-up.
Although most patients with calcific tendinopathy respond well to conservative management, approximately 10% of patients require surgical removal of the calcium deposits. Surgery is indicated in patients with severe, disabling symptoms that have persisted for more than 6 months, but there is no consensus regarding the optimal operative treatment. Needle lavage is a minimally invasive effective treatment for patients with acute painful RCCT. Shoulder arthroscopy is indicated in patients with large calcific deposits and long-standing symptoms.
The patient is advised to continue normal daily activities, avoiding overloading and sport activities involving the upper extremities during the first weeks after the treatment. Ice and oral analgesics are prescribed for the first 48–72 hours after the procedure.
A physiotherapy program consisting of pendular exercises, stretching, and gradual strengthening of the rotator cuff muscle is indicated for the first 4–6 weeks.
The patient follows a standard postoperative rehabilitation protocol for rotator cuff repair. Ice and oral analgesics are prescribed for the first 48–72 hours after the procedure.
The affected shoulder is immobilized in a shoulder brace in a neutral position for 4 weeks.
At 2 weeks after surgery, gentle passive-assisted mobilization and pendular exercises are allowed twice a day. Active mobilization, recovery of the range of movement, and gradual stretching are allowed after 4 weeks. The patient begins muscle-strengthening exercises 6 weeks after surgery.
B. Management of Calcific Tendonitis