1. Adhesive Capsulitis of the Shoulder
Diagnosis and Management
Brad Register MD
Athens Orthopedic Clinic
August 26, 2017

2. Disclosures (none)

3. My History Georgia Native University of Georgia MD-Johns Hopkins
3-year Football Letterman
MD-Johns Hopkins
Baltimore, Maryland
Residency-Emory
Atlanta, GA
Fellowship-Sports Med
Steadman Clinic
Vail, CO

4. Objectives
Develop a basic understanding of causes, natural history, and treatments
Be able to distinguish adhesive capsulitis from other conditions
Know when to refer to a shoulder specialist

5. Adhesive Capsulitis
Painful, gradual loss of active and passive shoulder motion
Leads to stiffness in all 4 planes
Due to contracture and fibrosis of shoulder capsule
Often self limiting, but natural history controversial

6. History Described by Duplay in 1872 as “scapulohumeral periarthritis”
Believed to result from subacromial bursitis
Pasteur wrote about “tenobursite” in 1932
Bicipital tendinitis?
Codman coined the term “Frozen Shoulder” in 1934
Neviaser named the condition “Adhesive Capsulitis” in 1945
Fibrosis, inflammation, contracture
This term, which was first used by Codman,1 does not denote a specific pathology. Rather, it applies to what he described as “many conditions which cause spasm of the short rotators
or adhesions about the joint or bursae.” A diagnosis of frozen shoulder is as vague as calling a gait abnormality a limp and should be avoided.

7. What is a frozen shoulder?
Specific entity
Inflammation of capsular subsynovial layer
Produces thickening, fibrosis, and adherence of capsule
To itself and neck of humerus
Dec. GH volume
Shortened capsule can lead to pain
Adhesive capsulitis is a specific pathologic entity in which chronic inflammation of the capsule subsynovial layer produces capsular thickening, fibrosis, and adherence of the capsule to itself and to the anatomic neck of the humerus.2 The contracted, adherent capsule causes pain, especially when it is stretched suddenly, and produces a mechanical restraint to motion.

8. Anatomy
Describe the rotator cuff and the flexibility provided by the glenohumeral ligaments

9. What causes a frozen shoulder?
In short, we don’t know!
Most pts report no cause
Some report remote, minor trauma
Unknown if this actually incites process
We know what it is, and who develops it

10. Who develops a frozen shoulder?
Most common patient: Female between 40 and 60
Endocrinopathies
Diabetes (incidence between 10-36%)
Thyroid
Autoimmune
CVA, MI, Breast CA tx
Trauma
Prolonged immobilization
Sedentary occupations
Incidence around 3-5%

11. What conditions mimic a frozen shoulder?
Multiple conditions present in a similar fashion
Glenohumeral OA
Full and PTRCT’s
Calcific Tendinitis
Cervical radiculopathy
“Secondary adhesive capsulitis”
Misleading
Prefer “stiff and painful shoulder”
These include full andpartial-thickness rotator cuff tears, calcific tendinitis, glenohumeral or acromioclavicular arthritis, and cervical radiculopathy. In these conditions, motion loss is typically multifactorial rather than the result of isolated capsular restriction.3 Some authors have advocated describing this type of stiffness as “secondary adhesive capsulitis” to distinguish it from the idiopathic (ie, primary) form.4

12. Presentation Can be very difficult to diagnoses early in the process
Pain for several months with insidious onset
Occ minor trauma
Often starts as night pain with normal motion
Pain often located Anteriorly, at deltoid insertion
Early stages report constant pain
Occ. Radiates down arm
Gradually progresses through 3 distinct stages
Freezing, Frozen, Thawing

13. Stages (1) 3 distinct clinical phases 1) “Freezing”
Starts with pain at night, normal ROM
Progressive pain initially, then gradual LOM
Acute adhesive synovitis
Initially: Fibrinous inflammatory Synovial reaction
no adhesions
Eventually: Proliferation of synovium and early adhesions
Pain out of proportion as Stage 1 progresses
Stage 1, the preadhesive stage, consists of a fibrinous inflammatory synovitic reaction without adhesion formation (Figure 2, A). At this stage, patients typically have full motion but report
pain, particularly at night. Symptoms are nonspecific, and misdiagnosis is common. Stage 2 is marked by acute adhesive synovitis with proliferation of the synovium and early formation of adhesions (Figure 2, B), most notably in the dependent inferior capsular fold. Pain is a prominent feature, and motion loss is present but typically mild. Stage 3, the maturation stage, involves less synovitis and more fibrosis (Figure 2, C). The axillary fold is obliterated. Pain may be less severe than in stages 1 and 2, but motion is significantly restricted. In stage 4, the chronic stage,
adhesions are fully mature, and motion is severely reduced. Because of the marked fibrosis, intra-articular structures may be difficult to identify at arthroscopy (Figure 2, D). Patients may have painless, limited range of motion in stage 4, but pain occurs when the arm is suddenly moved beyond the limits of the scarred capsule.

14. Stages (2&3) 2) “Frozen” 3) “Thawing” Persistent stiffness
Pain only at extremes
Primarily fibrosis with less synovitis
Axillary fold adhesed
3) “Thawing”
Minimal pain
Motion gradually improves
Adhesions mature

15. Stages: Arthroscopic
Neviaser, Neviaser. JAAOS 2011.

16. Stages

17. Exam Stage 1 (Freezing) Stage 2 (Frozen) Stage 3 (Thawing)
Initially pain, normal ROM
Progressive pain with motion, provocative tests
Stage 2 (Frozen)
Moderate limitations in ROM (all 4 directions)
Pain only at extremes of motion
Stage 3 (Thawing)
Gradual resolution of stiffness, pain
Mention normal range of motion in each plane, compared with frozen shoulder

18. Exam Decreased ROM in all four directions
One of the only conditions (with normal XR) that causes this
Hallmark is decreased ER with the arm by the side

19. Natural History Controversial
Traditionally thought to be self-limiting
Tx not necessary
Studies show better results with Subjective c/w Objective findings
90% satisfied
Griggs et al JBJS 2000
Residual pain in 50%
Persistent stiffness 60%
Shaffer et al JBJS 1992
The natural history of adhesive capsulitis remains a matter of debate. Some have suggested that adhesive capsulitis is self-limiting and need not be treated. Codman1 counseled his patients that their symptoms would gradually subside. Miller et al20 recommended patience and reported complete resolution of symptoms 4 years after onset in 50 patients treated with only minimal home exercise and heat. There may be a natural trend toward symptomatic improvement, but reported outcomes of minimal treatment vary considerably and are highly dependent on how they are measured. Results tend to be more favorable with subjective outcome measures than with objective outcome measures.
Uncertainty regarding the ultimate progression of adhesive capsulitis hampers efforts to measure the effectiveness of new treatments. Given the prolonged disability these patients face, interventions should be focused on hastening recovery of motion and diminishing pain.

20. Imaging Radiographs normal
If dx in doubt, MRI helpful to rule out other conditions
RCT
MRI may show thickening of GH ligaments
Typically in axilla and RI

21. Treatment-PT PT combined with HEP frequently started initially
Gentle (nonaggresive) stretching
Aggressive PT often non-effective, painful
RCT showed worse results with aggressive PT
Diercks JSES 2004
Other authors rec. high-grade PT
Vermeulen, Phys Ther 2006
Strengthening typically unnecessary
Diercks et al. in an RCT of 77 patients showed that intensive physical rehabilitation can be counter-productive comparing one group performing passive stretching and mobilization beyond pain limits (intensive physiotherapy group) with a second group performing active and actively assisted exercises within pain limits (supervised neglect group). At two years only 63% of the first group and 89% of the second group had good shoulder function
Do you know what’s always good for shoulder pain?

22. Treatment-Pharmacologic
NSAID’s often used first line
May help symptoms, but do not alter disease process
Intra-articular and oral steroids show transient relief
Improved pain relief with inj c/w NSAIDs
Ranalletta. AJSM 2016
Some evidence that image guided injections superior
Lorbach KSTA 2010
Wide range of results from intra-articular injections
3-6 vs wks relief
Intra-artic vs subacromial?
Mention subacromial vs intra-articular benefits
Mention dose studies

23. Treatment: Invasive Manipulation under anesthesia Complications
Manual release of capsule along with CSI
Frequent PT postop
95% 6 mos
Dodenhoff. JSES 2000
Excellent results in 15 yrs
Farrell. JSES 2005
No difference between intra-artic inj vs MUA?
Jacobs. JSES 2009
Complications
Recurrence
10-25% (DM)
Fracture, Dislocation
Rare
Hydrodilation also described
No clear advantage over CSI
Corbeil. Can Assoc Rad J 1992

24. Treatment: Invasive Arthroscopic release
Shown to be effective by several authors
Debate as to effectiveness compared with MUA alone
Thought to be beneficial with controlled release, decreased risk of SS rupture

25. My preferred treatment
PT with gentle stretches and HEP
NSAIDs as needed
Intra-artic inj if no improvement
MUA+CSI in pts after 6 mos. Failed tx
MUA, Scope + CSI in high-risk patients
DM, CVA
Aggressive PT after procedures

26. Summary Adhesive capsulitis a distinct entity of unknown origin
More common in certain groups
Women (>40 and <60)
DM, Thyroid, BrCa
Progresses through 3 distinct stages
Very diff. to dx in early “freezing” stage
Often (but not always) resolves on its own

27. Summary PT (formal and HEP) is the mainstay
NSAID’s, oral CS can hellp with pain
If fails 6 months of cons. care, consider surgery
MUA with CSI can be effective
Scope LOA used more frequently
Postop PT critical!

28. Thank you