Calcific Tendinopathy

Introduction

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.

Procedures

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.

Patient History

• RCCT can be asymptomatic. The prevalence of calcific deposits in the rotator cuff in asymptomatic patients is 7.8%. Women between the fourth and sixth decades of life have the highest chance of suffering from symptomatic RCCT.

• When symptomatic, the main complaint is shoulder pain. The patient’s history will typically follow the three-stage natural history of the pathology:

  • Acute: characterized by severe pain, tenderness, and functional disabilities, generally for 1 to 6 weeks.

  • Chronic recurrent: common in the calcific stage of the pathology. It is characterized by waxing and waning pain. It may occur as such, without being preceded by an acute painful bout. Generally, it persists for 6 weeks to 6 months.

  • Persistent chronic pain: characterized by presence of a constant, dull pain, with no phases of remission or exacerbation, which occurs for more than 6 months.

  • Spontaneous resolution of symptoms. The pain and other symptoms are self-limited, and the natural history of the disease is for pain to improve over time.

Patient Examination

• A detailed history is of crucial importance. A medical history positive for diabetes or thyroid disease may increase suspicion for RCCT.

• A thorough physical examination is demanded when evaluating a patient with shoulder pain. It includes:

  • Active and passive range of motion (ROM) of the shoulder. A restricted ROM and external rotation may be suspicious of adhesive capsulitis, which can be associated in patients with RCCT.

  • Manual muscle testing to assess for weakness that may be related to pain inhibition, a rotator cuff tear, or neurologic injury.

  • Special test for rotator cuff tears (external rotation lag sign [ERLS], Jobe test, drop arm test, lift-off test, belly-press or Napoleon test, internal rotation lag sign [IRLS], Speed test, palm-up test).

  • Provocative impingement tests (Hawkins impingement test, Neer sign test, and the Yocum test).

  • Sensation and reflexes should also be assessed if nerve damage is suspected.

Treatment Options

• Physical therapy, pendular movement, passive mobilizations of the shoulder, and gentle exercises

• NSAIDs

• Cimetidine

• Corticosteroid injections

• Therapeutic US

• Extracorporeal shockwave therapy (ESWT)

• Needle lavage technique

• Shoulder arthroscopy

Surgical Treatment

Step-by-Step Guide to Surgical Technique

• An ultrasound scan is performed first to locate calcific deposit. The area of the deposit can be marked with a surgical skin marker.

• The surgical field is prepared in the usual sterile fashion.

• First the needle is inserted with the syringe containing 10 mL of 2% mepivacaine and the ultrasound probe is placed on the path to be followed. The local anesthetic is injected into the subacromial space.

• A 20G needle is inserted into the calcific deposit. The needle is introduced in-plane with the ultrasound beam, allowing visualization of the needle throughout its path to the calcium deposit.

• A second 20G needle is introduced to aspirate the introduced fluid.

• Once inside the calcium deposit, a small quantity of warm saline solution is injected into the calcific deposit. A cloudy fluid containing calcium usually comes out from the second needle. The procedure is repeated until the aspirated fluid is clear and the calcium deposit appears smaller on ultrasound images.

• Once the lavage is completed, the second needle is removed, while the first needle is either drawn back into the subacromial space. Two milliliters of triamcinolone are administered to prevent subsequent bursitis.

• A surgical dressing is applied.