DIAGNOSIS AND TREATMENT OF
CALCIFIC TENDINITIS OF THE
SHOULDER
ARTHROPLASTY TEAM CME

INTRODUCTION
• classified as enthesopathy, is a self-limiting disease
• deposition of calcium phosphate crystals in the rotator cuff tendons.
• commonly occurs between the ages of 30 and 50 and is rare in those older than 70
years
• twice as likely to occur in women as in men
• more common in the right shoulder than in the left, and involves both shoulders in
10% of patients
• Most common site of occurrence is 1.5–2 cm away from the supraspinatus tendon
insertion site on the greater tuberosity

INTRODUCTION
• Location:
• 63% of cases occur in the supraspinatus tendon
• 20% in both the supraspinatus and subscapularis tendons
• 7% in both the infraspinatus tendon and subacromial bursa
• 3% in the subscapularis tendon
• diabetes and gout are considered to be risk factors for calcific tendinitis
• endocrine diseases, and conservative treatment is likely to fail in such cases
• rotator cuff tear present in approximately 25% of patients – A/W small VS large
calcific deposits

THREE MAIN THEORIES
A.Reactive calcification - involves an active cell-mediated process, usually followed by
spontaneous resorption by phagocytosing multinucleated cells showing a typical osteoclast
phenotype
B.Calcium deposits are formed by a process resembling endochondral ossification. The
mechanism involves regional hypoxia, which transforms tenocytes into chondrocytes
C.Ectopic bone formation from metaplasia of mesenchymal stem cells normally present in
tendon tissue into osteogenic cells.
As no single theory is satisfactory to explain all cases, calcific tendinopathy is currently
believed to be multifactorial.

ETIO-PATHOLOGY
Degenerative
Posits accumulate with age
Leading to ↓ blood vessels
↓ local oxygenation 🡪 hypoxia
Thinning & early tearing of tendon 🡪
necrosis & calcification
Reactive
Precalcific – metaplasia of tenocytes
into chondrocytes
Formative – calcium deposits form &
↑ size
Resting – calcific deposition stops
Resorptive – Ca deposits absorbed by
phagocytosis by Macrophages &
Giant cells
Postcalcific – remaining space
replaced by granulation & remodels

*Schematic representation of tendinopathy pathogenesis.
various risk factors
- mechanical overuse
- intrinsic and extrinsic factors
-trigger the development of tendinopathy in a continuous
manner
*the first step is that these risk factors impair proper
tendon repair leading to early reactive tendinopathy
- harbors the capacity for healing
- accumulation and increase of risk factors lead to
tendon disrepair
- subsequently results in tendon degeneration
* Poor function and load capacity of the tendon finally
end up in the end-state of tendinopathy leads to tendon
tearing or rupture.
Based on Cook and Purdam and Shearn et al.

CLASSIFICATIONS
Time
Acute
(2 weeks)
Subacute
(3-8 weeks)
Chronic
>3 weeks
Neer
(Pain)
Irritation
Local
pressure
Impingement
Chronic
stiffness

CLINICAL TYPES
• Type I – Idiopathic (Responds to conservative mx)
• Type II – Secondary - endocrine-related disorders of thyroid,
oestrogen and glucose metabolism (usually requires surgical
treatment)

MORPHOLOGY
Bosworth
Small
<0.5cm
Medium
0.5-1cm
Large
>1cm
DePlama &
Kruper
Type I – fluffy, ill
defined margins ,
resorptive
(acute pain)
Type II –
homogenous, well
defined margins
(No pain)
Mole
(French)
A – dense
homogenous,
sharp
B – dense,
segmented,
sharp
C – soft
contour,
heterogenous
D – dystrophic,
calcification @
the insertion RC
Gartner
Type I: Well
demarcated, dense
Soft, dense
Or Sharp transparent
Soft, translucent &
cloudy

IMAGING CLASSIFICATION
Farin
hyperechoic focus
with a well-
defined shadow
hyperechoic focus
with a faint
shadow
hyperechoic
focus with no
shadow
Chiou
calcific plaques
arc-shape (echogenic arc
with clear shadowing)
fragmented (at least two
separated echogenic
plaques
punctuated (tiny
calcific spots without
shadowing),
nodular (echogenic
nodule without
shadowing)
cystic (bold echogenic
wall with echo-free
content
Sansone
granular, calcifications with
partially defined margins and
irregular echogenicity
nodular, cystic
appearance with a
sediment-type content
linear, slight thickening
following the course of the
collagen fascicle
Loewet
(CT Scan)
A: compact &
homogeneous one-
part structure, clearly
defined outline
B: subdivided homogen
eous structure, clearly d
efined outline
C: diffuse area of low
signal intensity, no defin
ed outline in the tendon

ARTHROSCOPIC CLASSIFICATION
The French society of arthroscopy divided the condition into
four types:
• Type A (20%) with homogenous deposits with well defined
edges;
• Type B (45%) with heterogeneous fragmented deposits with
well defined edges;
• Type C (30%) with heterogeneous deposits with ill defined
edges
• Type D which is not calcific tendinitis but degenerative
dystrophic calcifications at the rotator cuff

CLINICAL EVALUATION
•Severe, acute pain is typically seen in the resorptive phase
• 2.7%–20% are asymptomatic, 35%–45% are discovered inadvertently on
radiograph developed symptoms
• Patients will describe waking up with a sharp stabbing pain in the
shoulder at night
• There is absence of any inciting trauma or overuse
•Acute pain due to rupture of calcific deposits into the subacromial bursa
causing an inflammatory bursitis

CLINICAL EVALUATION
• Formative phase – asymptomatic, found by chance, chronic intermittent pai,
discovered occasionally
• Resorptive phase – severe acute pain, worsen @ night, difficult lying on affected
side, limited ROM, characterised by internal rotation to relieve pain & ED visit
• The resorptive phase causes local edema and cyto-proliferation leads to increase
pressure within the tendon substance, directly triggering pain
• May accompanied by local heat, redness & oppressive pain (DDx: Septic
Arthritis)

INVESTIGATIONS
• radiographic images
• shoulder anteroposterior view
• internal and external rotation views
• supraspinatus outlet views
• axillary views
• should be acquired to determine the location of calcific deposits and predict the possibility of
collision symptoms.
• follow-up images are acquired, changes in the disease stage can be assessed
• the size of the calcific deposits does not change significantly over time, although a previous study
reported that 18% of patients experienced an increase in the size of calcific deposits after follow-
up for an average of 16 months

INVESTIGATIONS
• ultrasonography - used to assess calcific deposits.
• shows hyperechoic areas and an obvious posterior acoustic shadow in the formative or resting
phase
• resorptive phase, on the other hand, hyperechoic areas are relatively reduced, and the posterior
acoustic shadow is also reduced or not observed
• MRI is not a routine evaluation - helpful in identifying lesions in the shoulder joint,
including the location of calcific deposits and the condition of the rotator cuff.
• T1-weighted images, calcific deposits show a low signal intensity, whereas
• T2-weighted images, the edema pattern surrounding the calcific deposits can show a high signal
intensity

TREATMENTS – PRIMARY
Non–Operative Management
• Rest
• Physiotherapy
• NSAIDs
• Corticosteroid injection
• When there are signs of collision or the patient is in the resorptive phase, subacromial
steroid injections are effective in alleviating pain
• Extracorporeal shock wave therapy (ESWT)
• Ultrasound guided needle lavage (barbotage technique)
• PRP INJECTION
30 -80 % success rate

AjR,2007

NEEDLE THERAPY
• Needling and lavage has been reported to augment the relief of acute pain
• Multiple perforations of the lesion can decrease pressure within the tendon substance
• A two-needle technique which facilitates lavage and deposit outflow can be performed
• During the procedure, lidocaine can be injected, followed by administration of a
corticosteroid

SURGICAL TREATMENT
• Surgery is indicated in patients with severe symptoms persisting for more than 6
months
• Surgery 🡪 conservative treatment failure ~ 10% of patients, best effects in patients
with chronic calcific tendinitis - symptoms was > a year prior to surgery
• Chronic calcific tendinitis often requires surgical treatment, which can take the
form of open surgery or arthroscopic surgery.
• Arthroscopic surgery has the advantages of a short rehabilitation period and
cosmetic superiority, and it is a less invasive method 🡪 protect surrounding tissues
and can be used to treat comorbidities such as frozen shoulder and rotator cuff tears

SURGICAL DILEMMAS
• No significant differences in the clinical outcomes after complete and incomplete
removal of calcific deposits
• patients whose radiographic findings after surgery indicated a removal or reduction
of calcific deposits showed better prognoses than those whose calcific deposits
remained unchanged
• Whether rotator cuff repair after the removal of calcific deposits affects clinical
outcomes remains controversial
• Several authors have suggested that rotator cuff repair can facilitate rehabilitation
treatment in patients with a combined full-thickness rotator cuff tear

SURGICAL TECHNIQUES -
GLENOHUMERAL JOINT
posterior portal 🡪 2 cm inferior and 1
cm medial to the posterolateral
corner of the acromion
anterior portal 🡪 lateral to the
coracoid process and anterior to the
acromioclavicular joint
Assess for capsular adhesion,
expansion, swelling or fibrillation of
articulation side of SST
Polydioxanone (PDS)

SURGICAL TECHNIQUES -
SUBACROMIAL JOINT
• After adequate glenohumeral joint exploration,
arthroscope moves into the subacromial space.
• Arthroscopic treatment of calcific tendinitis is
mostly performed in the subacromial space.
• In general, moderate inflammatory changes, as well
as hyperproliferation and thickening of the bursa,
can be observed.
• Afterward, a lateral working portal is made at the
anterolateral area of the acromion

SURGICAL TECHNIQUES –
BURSECTOMY AND DECOMPRESSION
• Decompression is conducted by
thoroughly removing the bursa using a
shaver with a suction opening through
the lateral working portal.
• If no lesion is visible in the articular
joint or if calcific deposits are located
on the bursal side, comprehensive
bursectomy is performed first.

SURGICAL TECHNIQUES –
CALCIFIC DEPOSIT REMOVAL
• In acute or resorptive phases 🡪 calcific deposits have a toothpaste-like appearance. In the chronic or
formative phases, they have a chalk-like appearance - calcific deposits can be observed as creamy or
snowy.
• Larger deposits or if there are difficulties removing them, a small incision can be made in the
long axis of the tendon using a scalpel

ROTATOR CUFF TENDON REPAIR
AND ACROMIOPLASTY
• Controversial 🡪 if tear is 2 cm or larger and involves more than 70% of the thickness of the
tendon, tendon repair is performed
• Tear near the SST repaired with anchor sutures
• Musculotendinous junction tear side-to-side 🡪 suture lasso
• Acromioplasty is not required

AUTHORS’ PREFERRED
TREATMENTS
• Sometimes difficult to identify the location of calcific deposits even after bursa removal
• Calcific deposits 🡪 located by gently needling the rotator cuff tendon at suspicious areas with a 16-
gauge spinal needle
• After removing calcific deposits, large partial or small full-thickness rotator cuff tears are not
repaired
• Rotator cuff repair is performed only for medium or large full-thickness rotator cuff tears.

POST OP REHAB
•Immediate passive ROM of shoulder
•Arm sling for 3/52 for those undergone decompression
•Passive & active ROM 6-12 weeks post op
•Light duty office work & moderate labour after 6-12 weeks
•Shoulder abduction brace for post rotator cuff repair 🡪 4/52
• Passive ROM post op
• Muscle strengthening after 6-12 weeks depending on the size of tear

CONCLUSION
• PRIMARY CHOICE CONSERVATIVE – ESPECIALLY IN ACUTE
CALCIFIC TENDINITIS
• EXPECTANCY OF POST OP RECOVERY TAKES UP TO 6/12 FOR FULL
RECOVERY
• DELAYED OF IMMEDIATE PAIN MAY OCCUR FOR 2 YEARS OR MORE
POST OP
• CONTINUAL FOLLOW-UP FOR PAIN CONTROL AND RECURRENCE OF
SYMPTOMS IS NECESSARY AFTER SURGERY

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