CASE REPORT |
https://doi.org/10.5005/jp-journals-11003-0130 |
Calcific Tendinopathy of Rotator Cuff Causing Frozen Shoulder: Case Report
1-4Department of Pathology, Army College of Medical Sciences, Delhi, India
5Department of Orthopedics, Hamdard Institute of Medical Sciences and Research, Delhi, India
Corresponding Author: Sharmila Dudani, Department of Pathology, Army College of Medical Sciences, Delhi, India, Phone: +91 9811778156, e-mail: drsdudani@hotmail.com
Received on: 09 February 2023; Accepted on: 15 May 2023; Published on: 28 June 2023
ABSTRACT
Calcific tendinopathy is common in females of age group 40–60 years causing severe pain and disability in shoulder movements causing a clinical picture of a frozen shoulder. Rarely the onset of pain may be subacute and chronic.
It is believed to be a degenerative process with the deposition of calcium hydroxyapatite crystals following the metaplastic transformation of tenocytes to chondrocytes in the tendons of the rotator cuff. Three stages have been described.
A 55-year-old female with a history of regular intake of calcium supplements came with complaints of excruciating pain and restricted mobility of the left shoulder joint. The patient was managed conservatively and regained the full range of movement. Other treatment modalities may be required in a subset of nonresponsive patients.
How to cite this article: Dudani S, Rautela A, Gulati R, et al. Calcific Tendinopathy of Rotator Cuff Causing Frozen Shoulder: Case Report. J Med Acad 2023;6(1):33-35.
Source of support: Nil
Conflict of interest: None
Patient consent statement: The author(s) have obtained written informed consent from the patient for publication of the case report details and related images.
Keywords: Calcific tendinopathy, Frozen shoulder, Pain, Rotator cuff
INTRODUCTION
Calcific tendinopathy or calcium deposition in the rotator cuff is a common cause of the nontraumatic acute onset of shoulder pain, marked stiffness, and restriction of range of motion. It commonly affects females between 40 and 60 years of age.1 The incidence is not higher in individuals who do heavy manual work.
The pathogenesis is unclear but it is believed to be due to dystrophic calcification following the metaplastic transformation of tenocytes to chondrocytes.2
Though it is a common condition, very few reports of this condition in Indian patients’ are available.3
We report a case of acute onset severe painful calcific tendinopathy of the left rotator cuff in a middle-aged Indian female. This entity should be included in the clinical diagnosis of “frozen shoulder” and should be kept in mind in patients consuming oral calcium and vitamin D supplementation.
CASE DESCRIPTION
A 55-year healthy female doctor with a fairly sedentary lifestyle presented to the orthopedic outpatient department with sudden onset of severe, excruciating pain and stiffness in the left shoulder. Pain was aggravated with the slightest movement which affected activities of daily living and was more severe at night. There was no history of associated trauma. The patient did not suffer from any comorbidities (diabetes/hypertension/hypothyroidism). There was no family history of a similar condition. O/E marked tenderness was noted in greater tuberosity. Active abduction and internal rotation were severely restricted due to extreme pain. Subscapularis musculotendinous belly press test could not be done. External rotation was possible for the full range. Routine baseline investigations done were normal. The serum calcium level was 9.9 mg/dL. Vitamin 25 (OH)D3 level was 45 ng/mL.
Patient did not report any drug intake except for calcium and multivitamin supplements.
X-ray showed calcific tendinitis of the left shoulder (Fig. 1). Patient was unwilling to get ultrasound (USG)/magnetic resonance imaging (MRI) of the shoulder and was managed conservatively with ice packs and rest. Analgesics were required in the first 5 days only. Complete recovery of a full range of shoulder motion was seen within 6 weeks of conservative treatment.
Fig. 1: X-ray left shoulder AP view showing marked soft tissue calcification overlying greater tuberosity near the site of insertion of rotator cuff
DISCUSSION
Calcific tendinitis of the shoulder was referred to as “painful periarthritis of the shoulder,” first described by Duplay in 1872.4 Codman in 1934 observed calcium deposits inside or around the tendon sheaths5 rather than the subacromial bursa as was earlier believed.
The incidence of calcific tendinitis ranges from 2.7 to 20%. Nearly 90% of the calcification occurs in the supraspinatus and infraspinatus tendons. The commonest age group afflicted is 40–60 years with a predilection for women.6 It is rarely seen in individuals younger than 40 years of age as calcium tends to deposit in degenerated tendons. There is no association with trauma noted.3
The etiopathogenesis of calcific tendinitis is unclear. However, it is widely believed to be a degenerative process with the metaplastic transformation of tenocytes into chondrocytes with subsequent dystrophic calcification.2 Some workers have postulated that degeneration of tissue follows ischemic injury.5 whereas others believe it could be a result of aberrant differentiation of tenocytes into osteocytes as an injection in the rabbit of recombinant bone morphogenetic proteins-2 induced ectopic bone formation.6 Some authors believe that calcific tendinopathy of the rotator cuff is associated with decreased intratendinous oxygen concentration promoting fibrocartilaginous metaplasia and necrosis and secondary calcium deposition.7 A genetic predisposition to calcific deposition as well as abnormal activity of the thyroid gland, and diabetes have been postulated to have a role in the etiopathogenesis.1
Uhthoff and Loehr have described three stages for calcific tendinopathy as follows:7
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Precalcific stage: characterized by fibrocartilaginous metaplasia of tendon which acts as a nidus for subsequent calcium deposition.
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Calcific stage: Two phases are seen—formation and resorption. In the former stage, deposition of calcium hydroxyapatite crystals in the tendons is seen. There are no calcium deposits in the bone. The resorptive phase is seen after a variable silent period, starting with neoangiogenesis and phagocytosis of calcium by macrophages causing edema, increased intratendinous pressure, and extrusion of calcium crystals in subacromial-subdeltoid bursa. This phase is associated with disabling acute pain which may even be unresponsive to analgesics.
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Postcalcific stage: starts simultaneously with the resorptive phase and may last several months. Granulation tissue is formed and remodeling of the tendon by fibroblasts is seen with resultant complete healing.
Patients’ with calcific tendinitis present with severe acute disabling pain associated with stiffness mimicking the clinical presentation of a frozen shoulder. Pain can be anteriorly in a bicipital groove or posteriorly situated below the spine of the scapula.
At times the patient is asymptomatic or develops a subacute low-grade pain in the shoulder that increases at night in 50% of patients with a restricted range of motion. Symptoms may last for 2–3 weeks in the acute phase and >3 months in the chronic phase.
In a study by Rouhani et al. on 250 patients with calcific tendinopathy, approximately 76.7% of patients reported an intake of supplemental calcium. All were females and they reported more pain and higher disabilities of the arm, shoulder and hand scores. However, patients who did not consume calcium supplements suffered from a longer duration of pain.8-10
The role of oral supplemental calcium and vitamin D in causing calcific tendinopathy is not clear as most females in the older age group are routinely prescribed these for good bone health and this gender commonly reports calcific tendinopathy.
This was also the case with our patient also had a regular oral supplemental intake of calcium.
The incidence of this disease is not higher in athletes or in individuals undertaking manual labor involving the upper limbs.1
In 10–20% of patients, the deposits may be bilateral and are not related to any physical activity.11
The differential diagnosis of calcific tendinopathy of the shoulder is subdeltoid bursitis, subacromial impingement, rotator cuff tears, and adhesive capsulitis.
Calcific tendinitis can be evaluated by various imaging techniques. X-ray, USG of the shoulder is useful in detecting and classifying the pathology. As X-ray delineates the pathology quite distinctly, various authors have proposed classification of the calcium as seen on X-ray—anterior posterior (AP) and axillary views based on the size of deposits, disease phase, and morphological appearance.1 On USG, the calcium deposits usually appear hyperechoic with the presence or absence of posterior shadowing. These have been classified depending on the different percentages of calcium.2 USG also allows the additional advantage of therapeutic intervention like needling under guidance The calcification may be poorly visible on MRI and if it is edematous, can be mistaken for a tendinous tear.12
Most patients respond to conservative treatment including rest, physical therapy, and oral analgesic administration. However, other therapeutic options available are intraarticular injection of steroids, aspiration of calcium deposits under USG guidance, and extracorporeal shock wave therapy. Surgical treatment for the removal of calcium deposits is indicated in patients who have had severe persistent pain for >6 months.1
A variant of calcific tendinopathy with osteolytic involvement of greater tuberosity needs to be recognized due to its poor clinical outcome both with conservative as well as surgical treatment.1
Besides the conventional treatment, a healthy diet rich in anti-inflammatory foods may help considerably in reducing the intensity of pain as well as in shortening the duration of the disease.
More studies are required from different racial and ethnic populations to better understand the demographics, pathophysiology, imaging, and therapeutic responses of this acute painful condition.
CONCLUSION
Calcium deposits in the rotator cuff are an acute condition with painful restriction of shoulder rotator cuff movement. An increased incidence is seen in patients taking calcium supplements. It is a complex cell-mediated process that usually responds to conservative treatment. Surgery is resorted only in cases that fail to respond to conservative therapy.
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