You are on page 1of 2

ADHESIVE CAPSULITIS

Definition
- Adhesive capsulitis or periarthritis, AKA frozen shoulder, is the extreme thickness or immobility in the shoulder
joint, usually following injury and caused by the adhesions and inflammation in the shoulder joint capsule
- A disorder in the shoulder capsule, the connective tissue surrounding the glenohumeral joint of the shoulder,
wherein it becomes inflamed and stiff, greatly restricting motion and causing chronic pain

Relevant anatomy
- The glenohumeral joint is comprised of the scapula and humerus. The joint cavity is cushioned by articular
cartilage covering the head of the humerus and face of the glenoid. The scapula extends up and around the
shoulder joint at the rear to form a roof, called the acromion, and around the shoulder joint at the front to form the
coracoid process.
- The end of the scapula called the glenoid meets the head of the humerus to form a glenohumeral cavity that acts as
a flexible ball-and-socket joint. The joint is stabilized by a ring of fibrous cartilage surrounding the glenoid, called
the labrum.
- The biceps tendon attaches the biceps muscle to the shoulder and helps to stabilize the joint. Four short muscles
originate on the scapula and pass around the shoulder where their tendons fuse together to form the rotator cuff.
- All of these components of the shoulder, along with the muscles of the upper body, work together to manage the
stress the shoulder receives as it moves.
- 3 bony articulations: SC, AC, GH

Etiology
- Usually an idiopathic condition but can be associated with DM, inflammatory arthritis, trauma, prolonged
immobilization, thyroid disease, CVA, or autoimmune disease.

Epidemiology
- Middle-age women and diabetic patients are at higher risk for spontaneous idiopathic adhesive capsulitis
- Usually occurs between ages 40-60 y/o
- Occurs in approximately 2% to 5% of the general population and 2-4x more common in women than in men

Pathophysiology
- Can either be idiopathic or associated with internal derangement such as trauma, tendonitis and tears. This leads to
the development dense adhesions, capsular thickenings, and capsular restrictions, especially in the dependent folds
of the capsule. Perivascular inflammation, but predominant abnormality is fibroplastic proliferation with increased
collagen and nodular band formation.

Braddom’s classification
Stages Symptom duration Sign and symptom
1 1-3 months Painful shoulder movement, minimal restriction in motion
2 3-9 months Painful shoulder movement, progressive loss of glenohumeral joint motion

3 9-15 months Reduced pain with shoulder movement, severely restricted glenohumeral joint motion

4 15-24 months Minimal pain, progressive normalization of glenohumeral joint motion

Kisner and Colby classification


Stages Symptom duration Sign and symptom
Freezing 10-36 weeks Pain even at rest and limitation of motion by 2-3 weeks
Frozen 4 – 12 months Pain only with movement, significant adhesions, and limitation GH motions, atrophy of the
deltoid, rotator cuff, biceps and triceps
Thawing 2- 24 months No pain and no synovitis but significant capsular restriction from adhesion, some patients
may never recover

Clinical manifestation
 Usually affects the non-dominant shoulder although it can occur in either shoulder
 Night pain and disturbed sleep during acute flares
 Pain on motion and often at rest
 Decreased joint play and ROM, usually limiting ER and ABD with some limitation of IR and flexion
 Possibly faulty postural compensation with protracted and anteriorly tilted scapula, rounded shoulders, and elevated
protected shoulder
 Decreased arm swing during gait
 General muscle weakness and poor endurance in the glenohumeral muscles with overuse of the scapular muscles
leading to pain in the trapezius, levator scapulae, and posterior cervical muscles; reverse scapulohumeral rhythm
 (+) substitution for limited GH motion with increased scapular motion, especially elevation
 Shoulder hiking on active movement

PT evaluation

Diagnosis
Criteria: 1. Decreased GH motion and loss of synchronous shoulder girdle motion
2. Restricted elevation (<135/90 degrees)
3. ER 50-60% percent of normal
4. Arthrogram findings of 5 mL-10 mL volume with obliteration of the normal axillary fold

Differential diagnosis
a. Trauma – fracture in shoulder region, misdiagnosed posterior shoulder dislocation, hemarthrosis secondary to
trauma
b. Soft tissue disorder – tendonitis of rotator cuff or long head of biceps, subacromial bursitis, impingement, TOS
c. Joint disorder – arthritis
d. Bone disorder – avascular necrosis of the head of humerus, paget’s disease, primary bone tumor

Prognosis
- Most patients will have restoration of normal function over 12-14 month period. In patient who do not improve
after 6 months of nonoperative treatment, more aggressive approach are advised.

PT management
Goals: 1. Relief of pain
2. Restoring proper arthrokinematics
3. Restoration of ROM
4. Strengthening of shoulder muscle

Stage I (interrupt cycle of pain)


- Postural training
- Modalities to control pain: ES, TENS, iontophoresis, cryotherapy, US
- Grade 1 and 2 joint mobilization technique and AAROM on pain free range
- CKC to promote rotator cuff function
- Scapular stabilization exercise to to activate scapular muscles
- Scapular taping can be used
Stage II (interrupt cycle of pain, minimize capsular restrictions)
- ROMEs
- Strengthening of the rotator cuff, serratus anterior, middle and lower traps to establish coordinated force coupling
- Taping of ST joint to limit scapular substiture patterns and force greater mobility at GH joint during activity
Stage III and IV (improve GH mobility and restore SH rhythm)
- Aggressive stretching and joint mobilization – full AROM is needed because any residual limitation may reinitiate
the cycle
- Heat and US to increase tissue extensibility
- Strengthening of rotator cuff and SH muscle to establish coordinated force coupling

You might also like