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

Disclosures (none)

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

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

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

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.

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.

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

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

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%

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

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

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.

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

Stages: Arthroscopic Neviaser, Neviaser. JAAOS 2011.

Stages

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

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

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.

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

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?

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 24-26 wks relief Intra-artic vs subacromial? Mention subacromial vs intra-articular benefits Mention dose studies

Treatment: Invasive Manipulation under anesthesia Complications Manual release of capsule along with CSI Frequent PT postop 95% satisfied @ 6 mos Dodenhoff. JSES 2000 Excellent results in 70% @ 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

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

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

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

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!

Thank you