Calcific Tendinitis of the Shoulder
Diagnosis and Simple, Effective Treatment
William B. Wolf III, MD
THE PHYSICIAN AND SPORTSMEDICINE - VOL 27 - NO. 9 - SEPTEMBER 1999
In Brief: Calcific tendinitis of the shoulder causes pain that is not activity dependent and often severe. Because its cause is uncertain and because calcium deposits can also be asymptomatic, diagnosis is made primarily by history and physical examination in conjunction with radiographs. Tenderness over the greater tuberosity generally differentiates calcific tendinitis from other conditions. For both the subacute and acute forms, needling, or using a hypodermic needle to disrupt the deposits, followed by corticosteroid injection into the subacromial space, can be diagnostic and therapeutic. If limitation of motion and weakness persist after this treatment, impingement syndrome or adhesive capsulitis may be the cause.
Calcium deposits around the shoulder can be an incidental radiographic finding, or they may play a role in calcific tendinitis, causing agonizing pain. Since the first radiographic description of calcific tendinitis in 1907 by Painter (1), many authors have described the condition as a common cause of shoulder pain.
Calcium deposits about the shoulder are sometimes mistaken for impingement syndrome or adhesive capsulitis. Unlike these conditions, however, this separate and identifiable process usually responds promptly to disruption of the deposits with a hypodermic needle, followed by injection of corticosteroid medication.
Calcium deposits around the shoulder most commonly develop in the supraspinatus tendon (figure 1). Calcific tendinitis is usually signaled by the rapid onset of pain that is unrelated to shoulder position or activity. The condition typically occurs in persons between the ages of 30 and 50, but a literature search revealed no data on its incidence or on its frequency relative to other causes of shoulder pain.
Little histologic or pathophysiologic research has been done on calcific tendinitis, and there is no consensus about its cause. Decreased local oxygen tension has been suggested as a possible factor in calcium deposition; in addition, it is uncertain whether inflammation is the primary process or a secondary response to microscopic tendon injury (1-3). Calcific tendinitis is clearly nondegenerative (1), and it does not appear to have a strong correlation with impingement syndrome (4).
Despite many investigations, the exact cause of pain in calcific tendinitis is unclear, and it is well documented that many patients have calcium deposits about the shoulder without any symptoms (5). Histologically, some authors have found relatively low concentrations of inflammatory cells; therefore, pain with this condition may have chemical and mechanical as well as inflammatory origins.
There is controversy about whether a subacute type of calcific tendinitis exists. Subacute calcific tendinitis and impingement syndrome may have similar symptoms, and often a patient may present with symptoms more characteristic of impingement syndrome, yet radiographic evaluation of the shoulder shows calcium deposition. Physical signs and symptoms, discussed below, can help to differentiate impingement accompanied by incidental calcium deposits from true subacute calcific tendinitis.
History. As mentioned, calcific tendinitis is usually characterized by an acute onset of intense shoulder pain that is neither position- nor activity-dependent. There is usually no history of recent trauma or overuse of the affected limb, and the onset of pain and loss of motion is usually quite rapid. The patient often relates simply awakening with a toothache-like pain in the shoulder that increases over a span of 24 to 48 hours to an intense and agonizing level that requires narcotics for relief.
The rapid onset of calcific tendinitis clearly differentiates it from impingement syndrome and adhesive capsulitis. Impingement syndrome generally starts gradually as low-grade pain with overhead activities and during sleep. At rest, symptoms of impingement may be completely absent (2). Adhesive capsulitis, or frozen shoulder, can be quite painful but, like impingement syndrome, has a gradual onset over weeks or months that is accompanied by a characteristic limitation of both active and passive range of motion.
Subacute calcific tendinitis can have an onset similar to that of impingement syndrome, but the combination of calcification on x-ray, greater tuberosity tenderness, and pain unrelieved by avoidance of overhead activity distinguishes the two diagnoses.
Physical exam. Physical examination of patients with calcific tendinitis yields several classic findings that leave little doubt as to the diagnosis. Most patients are in severe pain, hold their arm with the unaffected hand, and are unwilling to move their shoulder either actively or passively. Even slight movements may be extremely uncomfortable.
Tenderness over the calcium deposit is the most important sign and is particularly important in differentiating subacute calcific tendinitis from impingement syndrome. Though finger pressure over the greater tuberosity of the humeral head is exquisitely painful with acute calcific tendinitis, it is an important sign to elicit because the treatment of calcific tendinitis differs from the treatment of impingement syndrome or any other condition.
In subacute cases, the presentation may be very similar to that of impingement syndrome: weakness of external rotation with the patient's elbow held at the side and a positive impingement sign consisting of pain on thumb-down resisted abduction with the arm abducted 90°. However, patients who have impingement syndrome generally do not have point tenderness over the greater tuberosity (2).
The patient may have some discomfort during range-of-motion examination of the cervical spine secondary to trapezius spasm, but with calcific tendinitis, full flexion and extension of the neck generally do not cause discomfort.
The neurovascular exam and skin are normal, and swelling is generally absent. In the presence of swelling, it is important to entertain the diagnosis of septic arthritis or bursitis because the course of treatment for a septic process is quite different.
Imaging. X-ray generally reveals single or multiple calcium deposits of variable size in the region of the greater tuberosity (figure 2). Magnetic resonance imaging, which may be used to rule out a rotator cuff tear, is unreliable for demonstrating calcification. The size of the calcium deposit on the x-ray does not correspond with presenting symptoms, and on rare occasions it may be difficult to identify any crystalline calcium deposition. There are also reports (2) of calcific tendinitis in which no calcium deposition was visible. Thus, it is important to remember that calcific tendinitis is a clinical rather than radiographic diagnosis. If deposits are an incidental radiographic finding, patients should be informed that these may or may not become problematic.
Lab tests. Laboratory data are usually not obtained unless septic arthritis is suspected. Patients who have acute calcific tendinitis may have a low-grade fever and mild leukocytosis, but high fever and significant elevation of the white blood cell count should increase the clinical suspicion of septic arthritis or bursitis. In the presence of local swelling and erythema in a febrile patient, a culture should be obtained before starting definitive treatment.
Treatment of calcific tendinitis should be based on symptoms alone, rather than on radiographic appearance (6-8). After resolution of symptoms, the calcium deposit may remain unchanged or may resorb.
Needling. In acute calcific tendinitis, treatment with a sling and oral narcotics without injection usually yields little relief. In my experience, "needling," or using multiple passes with a hypodermic needle to break up calcium deposits, along with injection of a combination of a local anesthetic and a corticosteroid, is generally effective for subacute and acute presentations. (See "Needling Technique for Calcific Tendinitis," below.)
In the patient who presents with agonizing pain and exquisite tenderness at the calcium deposit, I have found needling to be the most effective method for prompt pain relief and resolution of the problem. A literature search revealed no prospective, randomized trials comparing needling with other noninvasive treatments, but this strategy is the only one likely to be immediately effective in the patient who has an acutely inflamed calcific deposit (2).
Subacute calcific tendinitis can be treated with oral nonsteroidal anti-inflammatory medication and rest, but if signs and x-rays confirm calcific tendinitis, early needling of the deposit and injection of the area is appropriate because the response is frequently diagnostic. The patient who has subacute calcific tendinitis generally experiences prompt and permanent relief of symptoms with this treatment.
After needling treatment, shoulder function should return to normal within a few days. This contrasts with frozen shoulder or impingement syndrome, in which limitation of motion and weakness persist after resolution of pain. For this reason, if there is a question of calcific tendinitis versus impingement syndrome, continued symptoms on reexamination 2 or 3 weeks after injection indicate impingement syndrome.
Surgical excision. Surgical excision of calcium deposits is rarely indicated (9). The vast majority of patients who have symptomatic calcific tendinitis respond to appropriate nonsurgical treatment, and no patient should be considered for surgery until the calcific deposit in question has been needled at least twice by an experienced practitioner. Occasionally, symptoms of calcific tendinitis persist despite conservative treatment; for these patients, surgical excision should be considered.
Excision can be done arthroscopically (figure 3) on an outpatient basis with the patient awake under interscalene block, and the results are generally quite good. The calcium deposit need not be removed in its entirety, because relief is excellent with partial removal, which tends to preclude extensive damage and the need for rotator cuff repair.
Concomitant acromioplasty is not indicated. Such treatment is reserved for patients who have impingement syndrome, and there is extensive evidence that calcific tendinitis and impingement syndrome rarely coexist (4). Acromioplasty in this setting increases the possibility of adhesion formation, requires a more prolonged rehabilitation, and offers no demonstrated benefit over simple excision of the calcific deposit (2).
Rehabilitation. Patients who have undergone successful needling and injection for acute calcific tendinitis rarely require supervised rehabilitation. Because the condition is of sudden onset, patients experience little loss of muscle tone. With prompt resolution of symptoms, subsequent physical examinations usually reveal a normal shoulder.
Patients who have subacute calcific tendinitis may require some work on endurance and balance of their rotator cuff muscles, but they can do this at home (10). Rarely, a patient with persistent subacute calcific tendinitis develops symptoms of adhesive capsulitis; such patients may benefit from supervised physical therapy. The vast majority of patients regain normal shoulder function with a simple home exercise program.
Pointing to Relief
Fortunately, the clinical signs of calcific tendinitis are usually clear, and the response to treatment is often dramatic. With practice and attention to detail, needling treatment is safe and can yield lasting and gratifying relief.
Needling Technique for Calcific Tendinitis
Needling is the use of a hypodermic needle to break up calcium deposits in patients who have calcific tendinitis of the shoulder. This procedure, together with injection of corticosteroids, is extremely effective in resolving calcific tendinitis. It is believed that needling allows the encapsulated, pressurized deposit to decompress and permits vascular contact for calcium resorption and neovascularization.
A variety of needling techniques are mentioned in the literature (1). The elements presented here are common to most, however, and this simple stepwise approach yields excellent results with minimal risk. Some authors suggest aspiration of the calcium deposits (1), but simple needling is equally effective with less potential for complication.
Corticosteroid injection into tendons can cause significant damage (2) and should therefore be avoided.
Step 1: Locate the injection site. With the patient seated and the hand of the affected extremity resting in his or her lap, palpate the anterior and posterior borders of the acromion process (solid outline) to identify its midpoint (dashed line). Mark a point approximately 2 cm inferior to the lateral border of the acromion at its midpoint.
Step 2: Apply povidone-iodine to the skin.
Step 3: Anesthetize the site. Using a 25-gauge needle for patient comfort, inject 1 mL of 1% or 2% lidocaine hydrochloride.
Step 4: Needle the deposits. Use a separate, 10-mL syringe containing 6 mL of lidocaine, 2 mL of 0.25% bupivacaine hydrochloride, and 2 mL of a corticosteroid (eg, triamcinolone hexacetonide or betamethasone sodium phosphate) with an 18- or 20-gauge needle. To attempt to encounter the calcium deposits, direct the needle perpendicular to the surface of the skin. The needle will pass through the deltoid muscle into the firm tissue of the rotator cuff. If further anesthesia is necessary for patient comfort, withdraw the needle from the cuff tissue just until it is free of resistance, and inject a small amount of the mixture. Then, make passes with the needle into the rotator cuff to locate the calcium deposit, which will have a gritty texture. Insert the needle into the deposit four or five times to break it up, taking care not to inject any of the solution into the tendon.
Step 5: Inject the corticosteroid medication into the subacromial space. Withdraw the needle just until it clears the rotator cuff tissue and redirect it into the subacromial space. Then inject the mixture of lidocaine, bupivacaine, and corticosteroid into the subacromial bursa.
Dr Wolf is chief of orthopedics at Shady Grove Hospital and a partner at the Orthopaedic Center, both in Rockville, Maryland. Address correspondence to William B. Wolf III, MD, The Orthopaedic Center, PA, 9711 Medical Center Dr, Suite 201, Rockville, MD 20850.