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Although many researchers haveconsidered the etiology of frozenshoulder,1-4 few have presented anorganized treatment approachbased on the underlying diagnosisas well as on variations in naturalhistory related to the specific diag-nosis. The purpose of this article isto present an organized overviewof the various causes of motion lossin the shoulder and the treatmentoptions available for each.

Epidemiology and NaturalHistory

“Frozen shoulder” is a generalterm denoting all causes of motionloss in the shoulder. The conditionis one in which there is both activeand passive limitation of motiondue to soft-tissue contracture thatresults in a mechanical block. Thissoft-tissue contracture can occur incombination with other conditions,such as rotator cuff tear and degen-erative arthritis. In the latter, jointincongruity may also limit motion.In all cases, the soft-tissue contrac-tures must be treated concurrently

with the other underlying or asso-ciated disorders. This article willaddress all causes of motion lossthat involve soft-tissue contractureand scarring about the region ofthe glenohumeral joint.

When discussing the idiopathicform of motion loss in the shoul-der, the term “primary adhesivecapsulitis” is preferable to “frozenshoulder,” as it more preciselydescribes the pathologic changes inthe joint capsule. The pathogenesisof this idiopathic condition remainsa subject of debate. Possible causesinclude immunologic, inflammato-ry, biochemical, and endocrinealterations.1,3 Systemic disorders,such as diabetes mellitus, cardio-vascular disease, and neurologicconditions, can also be contributingcauses. In particular, patients withdiabetes are at greater risk of adhe-sive capsulitis than the generalpopulation; the condition is oftenbilateral and resistant to all formsof treatment.1,5

Regardless of the biologic cause,adhesive capsulitis is characterizedby thickening and contracture ofthe joint capsule,6 which results in

decreased intra-articular volumeand capsular compliance so thatglenohumeral motion is limited inall planes. The natural history ofprimary adhesive capsulitis is welldescribed and has been termedbenign because it tends to resolveover the course of 1 to 3 years.3,7

Despite this favorable natural his-tory, some patients are unwilling toendure the painful limitation ofmotion while they wait for resolu-tion of the condition. Most patientswill have some residual loss ofmotion even after many years,although the literature suggeststhat most do not have serious func-tional limitations or pain.7

Secondary, or acquired, shoul-der stiffness develops when there isa known intrinsic, extrinsic, or sys-temic cause.8-11 Examples includepostsurgical and posttraumaticstiffness, which can occur with orwithout an associated fracture.Both types of shoulder stiffnessusually occur in association withprolonged immobilization. Whilethe management of primary adhe-

Dr. Warner is Director, Shoulder Service,University of Pittsburgh Medical Center, andAssociate Professor of Orthopaedic Surgery,University of Pittsburgh School of Medicine.

Reprint requests: Dr. Warner, ShoulderService, Center for Sports Medicine, 4601Baum Boulevard, Pittsburgh, PA 15213.

Copyright 1997 by the American Academy ofOrthopaedic Surgeons.

Abstract

“Frozen shoulder” comprises a group of conditions caused by different process-es. Effective treatment depends on recognition of the underlying pathologic dis-order in each individual case. Idiopathic adhesive capsulitis usually responds tononoperative therapy or closed manipulation, but shoulder stiffness due to trau-ma or surgery may necessitate either an arthroscopic or an open-release proce-dure. Both of these technically demanding techniques are effective in restoringmotion in cases of frozen shoulder refractory to nonoperative treatment.

J Am Acad Orthop Surg 1997;5:130-140

Frozen Shoulder: Diagnosis and Management

Jon J. P. Warner, MD

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sive capsulitis is usually conserva-tive with physical therapy, mostsurgeons believe that acquiredstiffness of the shoulder after surgi-cal procedures for instability meritsmore aggressive treatment becauseof the potential unfavorable conse-quences.1,8-14 For example, if an ex-cessively tight anterior soft-tissuerepair for instability causes an in-ternal rotation contracture, it mayresult in chronic posterior subluxa-tion of the humeral head, leadingto incongruity of the joint andrapid deterioration of articular car-tilage.8,9 In the case of motion lossafter immobilization of a trauma-tized shoulder, a supervised thera-py program might be successful inrestoring motion.

Normal Anatomy andPathology

The inherently loose articulation ofthe normal shoulder joint is a nec-essary anatomic feature that per-mits the large range of multiplanarmotion required for normal shoul-der function. In this noncon-strained articulation, the largerhumeral head has a nearly perfectcongruity with the smaller osseousglenoid. The surface area of the

articulation is enlarged by thefibrous glenoid labrum attachedaround its periphery. The stabilityof this joint is largely maintainedby rotator cuff muscle action,which creates compression of theconvex humeral head into thematched concave articular glenoidfossa. The glenohumeral ligamentsand capsule, which are normallylax or under minimal tension dur-ing most shoulder rotations, func-tion mainly at the extreme posi-tions of rotation and translation tostatically constrain the joint againstexcessive movement of the humer-al head on the glenoid.15

During motion of the normalshoulder, the tightening and loos-ening of the glenohumeral liga-ments and capsule encircling thehumeral head are accompanied bylengthening and shortening of therotator cuff and deltoid tendonsand muscles.16 Loss of motion inthe shoulder can be the result ofany condition that directly affectsthese structures or their ability toglide relative to one another duringshoulder movements. A coexistingjoint incongruity, such as arthritisor an osseous block due to a mal-united or displaced greater tuber-osity fracture, may be present.Both arthritis and fractures are also

commonly associated with capsu-lar contracture and scarring be-tween soft-tissue planes.

The etiology of shoulder stiff-ness includes contracture or short-ening of the capsule and gleno-humeral ligaments, contracture orshortening of the extra-articulartissues, and scarring between the tis-sue planes of the shoulder (Fig. 1).The exact cause can usually be pre-dicted with some degree of accu-racy. For example, in primaryadhesive capsulitis, the soft tissueprincipally affected is the jointcapsule, while the rotator cuff andsoft-tissue planes remain normal(Fig. 1, A). In cases of postsurgicalstiffness, the specific disorder isrelated to the nature of the ante-cedent surgical procedure. Whensurgical treatment was for instabil-ity, capsular contracture and/orextra-articular constraint may bethe cause of the motion loss. Forexample, when a capsular shift ora Bankart procedure for recurrentdislocation results in excessiveloss of external rotation, the maincause of motion loss is capsularscarring rather than extra-articularconstraint. In most instances,arthroscopic treatment can im-prove motion, although subscapu-laris shortening can sometimes be

Fig. 1 Etiology of shoulder stiffness. A, Contracture of the capsule (cross-hatched areas) results in loss of all rotation (arrows). B, Extra-articular entrapment of the subscapularis (cross-hatched area) results in loss of external rotation (arrow). C, Scarring between tissueplanes (cross-hatched areas) results in loss of all rotation (arrows).

A B C

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a factor. In contrast, if stiffnessafter a Bristow procedure is due inpart to entrapment of the sub-scapularis, an open procedure isnecessary for definitive treatment(Fig. 1, B).9,17

If the shoulder has been immo-bilized for a prolonged period oftime after a traumatic event or sur-gical procedure, associated scarringbetween tissue planes may concur-rently restrict motion. For exam-ple, the motion loss that follows afracture and prolonged immobi-lization is usually characterized bymarked scarring in the tissueplanes between the deltoid and thehumerus, as well as in the deeperlayers of the rotator cuff and cap-sule (Fig. 1, C).

Clinical Evaluation

Assessment of MotionShoulder motion must be

assessed and documented carefullyand consistently to obtain an accu-rate and ongoing measure of theefficacy of a given treatment. Bothactive and passive motion lossesmust be recorded and compared,since concomitant conditions, suchas a rotator cuff tear, can result inloss of active motion in a shoulderthat is also stiff due to adhesions.In patients with glenohumeral stiff-ness, there may often be theappearance of relatively goodmotion due to increased scapu-lothoracic motion or trunk lean.The examiner must be careful toidentify and control these compen-satory motions in order to measureonly pure glenohumeral motion.Active shoulder flexion is mea-sured anterior to the scapularplane, with the patient seated, andis referenced to the patient’s tho-rax, not to a line vertical to thefloor. This avoids measurement ofany associated trunk tilt orincreased scapulothoracic contribu-

tion to overall motion. Active pain-free motion is recorded. Activeexternal and internal rotation aremeasured with the shoulder inadduction as well.

In some situations, pain inhibi-tion may result in poor activemotion. For example, in the caseof a subacromial disorder, an injec-tion of 1% lidocaine into thisregion will reveal the true activemotion possible when pain is elim-inated. Recording the increase inmotion after injection helps differ-entiate motion loss due to painfrom that due to a soft-tissue con-tracture. I perform this test onpatients with painful flexionthrough an arc of at least 90degrees. An individual with limit-ed motion due to painful flexionfrom rotator cuff disease will haverelief of pain with improvedmotion; an individual with a soft-tissue contracture will continue tohave limited motion.

Passive motion should be evalu-ated with the patient supine, whichrestricts excessive scapulothoracicmovement, therefore providing amore accurate assessment of pureglenohumeral rotation. Passiveflexion, external rotation in adduc-tion (arm at the side), external andinternal rotation in abduction (armto 90 degrees abduction), andcross-chest adduction must be mea-sured.

Patterns of Motion LossPrimary adhesive capsulitis is

usually associated with globalmotion loss, whereas postsurgicalor posttraumatic shoulder stiffnessmay present with global loss ofmotion in all planes or with a morediscrete limitation of motion affect-ing some planes while relativelysparing others. Recognition ofthese different patterns of motionloss is important in planning surgi-cal treatment when shoulder stiff-ness is refractory to nonoperative

care. Motion loss often correlateswith the location of a capsular con-tracture. For example, limitation ofexternal rotation of the adductedshoulder is associated with contrac-ture in the anterosuperior capsularregion and the rotator interval;release of this area will usuallyimprove the arc of motion.12-14,18

Limitation of external rotationwhen the shoulder is abducted isusually associated with scarring inthe anteroinferior region of the cap-sule. Limitation of internal rotationin adduction and abduction is asso-ciated with scarring of the posteriorcapsule, which is also reflected inloss of horizontal or cross-chestadduction.15

Even though these observationsare useful guidelines for surgicaltreatment, it should be remem-bered that any capsular contracturewill limit motion in more than oneplane. Extra-articular contractures,such as subscapularis entrapmentand scarring between tissue planes,may also contribute to globalmotion loss.

Secondary FindingsBoth postsurgical and posttrau-

matic shoulder stiffness are char-acterized by the presence of someintrinsic shoulder disorder, suchas rotator cuff disease, postsurgi-cal scarring, or trauma to the softtissues with or without fracture.The key finding in this setting ispassive motion loss. Therefore,the physical examination shouldcarefully document motion loss inall planes. Prolonged immobiliza-tion of the shoulder may also be afactor.

Some patients with postsurgicalor posttraumatic shoulder stiffness,as well as those with primary adhe-sive capsulitis, will have pain pat-terns that suggest impingement orrotator cuff disease or another con-comitant condition, even thoughthere is no objective evidence. The

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plain radiographs (specifically, thesupraspinatus outlet view) mayshow a flat acromion (Bigliani typeI),19 but the magnetic resonanceimaging study may be normal.

The biomechanical conse-quences of soft-tissue contracturesmay be “nonoutlet”-type impinge-ment, in which the capsular con-tracture causes excessive transla-tion of the humeral head on theglenoid during attempted shoulderrotation. Both anterior and poste-rior capsular contractures havebeen shown experimentally tocause increased superior transla-tion of the humeral head duringattempted flexion.15,18 This abnor-mal superior movement of thehumeral head has the effect ofcompressing the rotator cuff andsubacromial bursa between thecoracoacromial arch and thehumeral head, thus causing theimpingement-type symptoms.Some patients have partial painrelief with a subacromial injectionof lidocaine. Experimental work byHarryman et al18 has shown thatcapsular release eliminates abnor-mal translation and restores nor-mal ball-and-socket kinematics(concentric rotation) to the gleno-humeral joint.

Loss of glenohumeral motionwill not only profoundly restrictoverall upper extremity functionbut also alter the normal kinematicrelationship of the glenohumeraland scapulothoracic joints. A com-pensatory increase in scapulotho-racic motion can create additionalsymptoms, described by the pa-tient as discomfort medial to thescapula.

Radiologic Studies

Plain RadiographyIn most cases, but particularly in

instances of primary adhesive cap-sulitis, radiographic studies do nothelp to clarify the causation of stiff-

ness of the shoulder, but they doconfirm the presence of a normalglenohumeral joint by identifyingfractures, arthritis, or metallicimplants that may be contributingto motion loss. Disuse osteoporosismay occasionally be evident, espe-cially in patients who have the clin-ical features of reflex sympatheticdystrophy.

ArthrographyMany authors have asserted that

arthrographic confirmation ofdecreased joint capacity, defined asthe inability of the joint to acceptmore than 5 to 10 mL of contrastmedium, is essential to a definitivediagnosis of adhesive capsuli-tis.3,5,20 However, it has beenshown that there is no direct corre-lation between arthrographic find-ings and motion loss.20 Therefore, Ido not use this test unless I want torule out the possibility of a con-comitant full-thickness rotator cufftear.

Magnetic Resonance Imaging andComputed Tomography

Magnetic resonance imagingcan be of use in selected cases inwhich there is a question of anassociated disorder, such as a rota-tor cuff tear. Contrast medium–enhanced computed tomographycan also provide information aboutarticular injury and placement ofhardware about the joint thatmight be impinging on the articu-lar surface.

Physical Therapy

For most patients, a supervisedphysical therapy program will besuccessful in treating primaryadhesive capsulitis,1,2,4,7 but therehas never been a careful study ofthe cost-effectiveness of thisapproach. Some orthopaedic sur-geons do not believe that super-

vised therapy is important for thesepatients, and instead prefer a homeprogram. In cases of idiopathicadhesive capsulitis, I combine ahome program with supervisedphysical therapy three times aweek for an initial 6-week trial. Ifthe patient is making progress, thecombined program is continued foran additional 6 weeks, followed bya home program.

In contrast to primary adhesivecapsulitis, postsurgical or posttrau-matic shoulder stiffness is oftenmore resistant to a conservativeapproach.1,8-11 The likely naturalhistory can be predicted from anunderstanding of the pathologicfeatures and the potential forfuture articular injury, such as thatassociated with a fixed subluxationof the joint. Although the litera-ture clearly shows that limitationof external rotation to less thanneutral can be associated with thedevelopment of arthritis, the mini-mal acceptable external rotationloss remains unclarified.8,9,11 It ismy impression that after instabilitysurgery, limitation of external rota-tion to less than 60% of that of thecontralateral shoulder should betreated aggressively to avoiddevelopment of arthritis fromeccentric articular contact. Asupervised physical therapy pro-gram is tried first, but my experi-ence has been that even an aggres-sive stretching program by aknowledgeable shoulder therapistis often ineffective when there is ahistory of surgery or trauma. Thelength of time for which the super-vised physical therapy program iscontinued depends on the cause ofthe motion loss and the patient’sresponse to this treatment. If after12 to 16 weeks the patient is get-ting progressively worse or therehas been no improvement, anoperative intervention is recom-mended. The risks and benefits ofthe operative approach have been

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carefully described and mayinclude fracture, neurovascularinjury, residual stiffness, instabili-ty, and infection.

Selection of OperativeTreatment

It is important to emphasize thattreatment of primary adhesive cap-sulitis should not be consideredwhile the patient is experiencingsevere pain in addition to motionloss because this may represent theinflammatory phase of the disease.Neviaser and Neviaser3 have point-ed out that any surgical treatmentin this stage will likely exacerbatethe patient’s motion loss byincreasing capsular injury. It is im-portant to wait until pain is presentonly at the end of the range ofmotion, indicating that the activeinflammatory process has resolved.

When an operative approach iscontemplated, it is also importantto reemphasize that the diagnosiscan be used to predict the likeli-hood of extra-articular scarring aswell as capsular contracture. Thesurgical treatment must be tailoredto address all of these factors. In allcases of refractory primary adhe-sive capsulitis, closed manipulationshould be the initial approach.This approach is also used in rela-tively acute cases of motion lossafter surgery or trauma when ther-apy has failed to restore motion.However, when there is a suspect-ed or known extra-articular con-tracture (e.g., after a Bristow orPutti-Platt procedure), an openapproach is usually required, andclosed manipulation should not beattempted.

Closed Manipulation

Closed manipulation is performedwith the patient under general

anesthesia with drug-induced com-plete muscle relaxation. However,if the patient has marked osteope-nia or underwent an antecedentsurgical repair within the previous3 months, this approach is con-traindicated because of the risk offracture, disruption of the soft-tissue repair, nerve injuries, andpostmanipulation instability.1,3-5

The anesthetic technique is anextremely important aspect of theoverall treatment. There must becomplete muscle paralysis duringthe procedure. In my experience,while general anesthesia is an ade-quate method, patients often havesubsequent pain that interfereswith their therapy in the immedi-ate postoperative period. It istherefore recommended that aninterscalene block with a long-acting agent (bupivacaine) beused. The block is administeredeither as a single percutaneousinjection or by placement of an in-dwelling interscalene catheter.21-23

If a simple block is performed, it isrepeated in the morning on thefirst and second postoperativedays. Use of 0.5% bupivacainewill provide about 12 hours ofanalgesia, which will markedlyreduce the patient’s requirementfor narcotics while increasing tol-erance to physical therapy. If aninterscalene catheter is used, a con-tinuous slow drip of bupivacaineis administered.

The method of closed manipu-lation has been described byNeviaser and Neviaser3 andHarryman.1 The scapula is stabi-lized by one hand while thehumerus is grasped with the otherhand just above the elbow. Theforearm should not be used as alever in this manipulation. Anattempt is first made to recoverexternal rotation with the arm atthe side. As firm pressure is grad-ually exerted, palpable and audibleyielding of soft tissue occurs and

motion improves. Although theremay be some concern about frac-ture with this initial rotatory force,I attempt this motion first becauseit is easier to recover flexion andabduction if the greater tuberositycan be rotated out from under theacromion. If external rotation can-not be recovered, flexion isattempted, followed by abductionand then external and internal rota-tion. Finally, the arm is broughtback into adduction and internallyrotated. Motion is usually restoredin all planes.

Arthroscopic Release

Although most patients with pri-mary adhesive capsulitis respondto physical therapy, some willrequire closed manipulation toachieve and maintain sufficientimprovement in motion. A smallpercentage of those patients willcontinue to have motion loss thatis refractory even to manipulationof the shoulder under anesthesia. Ihave found the technique of arthro-scopic capsular release very help-ful in this situation. Similarly, incases of postsurgical or posttrau-matic shoulder stiffness in whichclosed manipulation fails, arthro-scopic release can also be attempt-ed, provided there is no extra-articular component to the motionloss.9-14

This approach continues to becontroversial, however. Some sur-geons suggest that arthroscopy isof little diagnostic and therapeuticvalue in treating patients with ad-hesive capsulitis of the shoulder.3Others suggest that the arthro-scope may be helpful in delineat-ing pathologic changes, document-ing the results of closed manipula-tion, and treating concomitantintra-articular and subacromial dis-orders.23,24 Over the past 4 years, Ihave used arthroscopic release in

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selected cases in which motion lossappeared to be principally due tocapsular contracture that was unre-sponsive despite closed manipula-tion. This technique has the ad-vantage of allowing the detectionof coexisting disorders, as well aspermitting a controlled and precisecapsular release. It also allowsconcurrent treatment of concomi-tant subacromial disease, as docu-mented by preoperative temporaryrelief from local anesthetic injectionand the intraoperative finding ofan inflamed subacromial bursa.Furthermore, in cases of both idio-pathic and postsurgical motionloss, I have found that the force ofmanual manipulation required toregain motion is greatly reducedby arthroscopically releasing thecapsule before manipulating theshoulder. The arthroscopic tech-nique also has the advantage overan open release of avoiding themorbidity associated with an

extensive open surgical dissection.If motion loss remains unchangedintraoperatively after attemptedarthroscopic release and manipula-tion, conversion to an open releaseis possible.

Anesthetic technique is an im-portant component of the surgicalplan for arthroscopic capsularrelease. The method of obtainingcomplete muscle paralysis with aninterscalene block, as alreadydescribed for closed manipulation,is recommended for both anteriorand posterior release procedures.

Anterior ReleaseAnterior capsular release (Fig. 2)

is performed with the patient seat-ed in the “beach chair” position.25

With use of this position, arm trac-tion is unnecessary, although somesurgeons prefer the added joint dis-traction produced when traction isapplied with the patient in a lateraldecubitus position. It is always dif-

ficult to insert the arthroscope intoa stiff shoulder because of the cap-sular contracture and decreasedjoint volume, and articular injuryfrom forceful insertion of thearthroscope is a concern. Chondraldamage can be avoided by gentlyinserting the arthroscope over thehumeral head. Although some sur-geons24 recommend use of a small-er arthroscope (3.9-mm diameter),such as that used for small-jointarthroscopy in the wrist, I haveused the standard 30-degreearthroscope (5.5-mm diameter)without difficulty.

The biceps tendon is the firstanatomic landmark that should beidentified. It marks the upper edgeof the “rotator interval region,”which is formed by the anterioredge of the supraspinatus tendonand the cranial border of the sub-scapularis tendon.18 This region isusually composed of a thick bandof scar tissue, which obscures the

Fig. 2 Anterior arthroscopic capsular release is performed through an anterosuperior portal (G = glenoid; HH = humeral head). A, Leftshoulder as viewed through a posterior portal. An arthroscopic probe is placed onto the thick wall of scarred capsule in the anterosuperi-or (rotator interval) region of the capsule. B, An arthroscopic electrocautery device has divided the anterosuperior region of the capsule,and the subscapularis tendon (S) and the remaining thickened inferior glenohumeral ligament (IGHL) are visible. B = biceps tendon. C, Ifnecessary, the anteroinferior capsule is released down to the bottom of the glenoid, but not through the axillary pouch (AP).

A B C

G G

G

B

S

HH

HH

AP

IGHL

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normally visible upper edge of thesubscapularis tendon. A varyingamount of synovitis may also bepresent.

An arthroscopic cannula isinserted just beneath the bicepstendon, and the capsular scar tissueis divided with the use of an elec-trocautery device and a motorizedshaver (Fig. 2, A). The capsulardivision begins superiorly fromjust anterior and inferior to thebiceps tendon and continues inferi-orly until the discrete upper edgeof the subscapularis tendon is en-countered (Fig. 2, B). This is a sur-gical release of the rotator-intervalregion of the capsule.18 Both Ozakiet al14 and Neer et al12 have shownthat such a release performedthrough an open approach is suc-cessful in restoring external rota-tion in shoulders with refractoryadhesive capsulitis.

After release of this region ofthe capsule, the humeral headmoves inferiorly and laterally,allowing more space in the jointfor the arthroscope to be movedboth anteriorly and inferiorly. Thearthroscope is removed, and amanipulation is performed torestore motion in all planes.External rotation in adduction isusually restored with almost nomanipulation force. The shouldercan then be manipulated into otherplanes with minimal force, usuallyaccompanied by an audible andpalpable yielding of tissue andimproved motion. If there contin-ues to be minimal or no improve-ment of motion in the remainingplanes, the arthroscope is reinsert-ed into the joint, and the remain-der of the anteroinferior capsule isreleased. The capsular release isperformed in the midcapsularregion, extending down to the five-o’clock position for the right gle-noid and down to the seven-o’clock position for the left glenoid(Fig. 2, C).

Some surgeons have expressedconcern about risk to the axillarynerve with a capsular release inthis region,23 but I have notencountered any neurologic com-plications. The subscapularis isinterposed between the anteroinfe-rior capsule and the axillary nervewhen the arm is adducted. Itshould be reemphasized that theaxillary pouch should not bereleased with this technique.Release of the anteroinferior cap-sule will usually restore externalrotation in abduction, but somepatients will still lack internal rota-tion in abduction after release ofthe entire anterior capsule; if that isthe case, the posterior capsule mustbe released as well.

When the capsular release isbegun in the rotator interval re-gion, it is extremely important toidentify a discrete subscapularistendon. If this structure cannot be

identified, the procedure must beconverted to an open release.Failure to curtail the arthroscopicrelease in this situation can resultin division of the subscapularis ten-don as well as the anterior capsule.When such a conversion has beennecessary, distortion and scarringof the subscapularis and extra-articular scarring were identified,all of which were successfully man-aged with open release.

Posterior ReleaseIn those few instances in which

there is continued loss of internalrotation and flexion after an anteri-or release, arthroscopic release ofthe posterior capsule is also neces-sary to accomplish a global capsu-lar release (Fig. 3). This technique isindicated when the loss of internalrotation in abduction exceeds 40degrees compared with the contra-lateral side.

A B

Fig. 3 Technique of arthroscopic posterior capsular release, depicted in a right shoulderviewed through an anterosuperior portal (G = glenoid; HH = humeral head; PC = posteri-or capsule; RC = rotator cuff). A, An arthroscopic shaver has been placed through thethickened posterior capsule. B, After release of the posterior capsule, the rotator cuff mus-cle can be seen.

G

HH

PC

RCG

HH PC

RC

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A small subset of patients mayhave an isolated posterior capsularcontracture characterized bymotion loss primarily limited tointernal rotation, cross-chest (hori-zontal) adduction, and flexion withrelative preservation of externalrotation. These patients often haveimpingement-type pain and insome cases have undergoneacromioplasty or other surgerywithout relief. Their capsular con-tracture may result in a form ofnonoutlet-type impingement bycausing increased obligate antero-superior translation during shoul-der flexion and internal rotation.This condition is treated with aposterior capsular release to restorelost motion and normal kinematics.

I typically perform posteriorrelease with the patient in thebeach-chair position, although lat-eral decubitus positioning may beused alternatively. The arthro-scope is placed through a cannulain an anterosuperior portal, whilethe arthroscopic sheath in the pos-terior portal is removed over aswitching stick and is replacedwith an operative cannula. Anelectrocautery device and a motor-

ized shaver are then used to releasethe posterior capsule from just pos-terior to the biceps tendon origindown to the posteroinferior rim ofthe glenoid. The posterior capsuleis always observed to be markedlythickened and without the redun-dancy seen in a normal shoulder, inwhich it is no more than 1 mmthick and is redundant when thearm is adducted and in neutralrotation (Fig. 3, A).

The arthroscopic release of theposterior capsule must be just atthe glenoid rim. Because the mus-cle of the infraspinatus is superfi-cial at this point, this is taken as theendpoint for capsular division (Fig. 3, B). If the capsular divisionis performed more laterally, thereis a risk of dividing the infraspina-tus tendon, because it conjoins withthe capsule lateral to the joint line;this would potentially weakenexternal rotation by creating a tearin the infraspinatus tendon.

Open Release

In cases in which arthroscopicrelease is contraindicated or fails to

restore motion, an open release canbe performed.8-13 Since arthros-copy is performed with the patientin a seated position, immediateconversion to an open approach isfeasible.

As with closed manipulationand arthroscopic release, use of an interscalene block is the pre-ferred anesthetic technique. Adeltopectoral incision is used.Extensive scarring through all lay-ers of the dissection is often identi-fied. The deltopectoral interval isgently dissected, and the adhe-sions between the deltoid and thehumerus are sharply released (Fig. 4, A). This must be donewith care, as the axillary nervemay be at risk. The axillary nervecan often be palpated on the deepsurface of the deltoid muscleapproximately 3 to 5 cm below thelateral border of the acromion.The dissection is easier if theshoulder is abducted (Fig. 4, B),which allows the deltoid tobecome lax and more easilyretracted. Internal rotation of thearm while gently retracting thedeltoid muscle will allow anterior-to-posterior release of subdeltoid

Fig. 4 Release of subdeltoid scar. A, Scar obliterates the plane between the deltoid and the proximal humerus and rotator cuff. B,Abduction of the shoulder allows the deltoid to relax and makes release of scar tissue easier.

A B

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adhesions until the deltoid canmove freely over the proximalhumerus when the arm is rotated.

The dissection then proceedsmedially into the subacromialspace. After the coracoacromialligament is excised, the subacromi-al space may be found to be filledwith dense scar adhesions betweenthe rotator cuff and the acromion,which should be sharply released.Care must be taken with deltoidretraction, as overzealous retrac-tion can either tear the muscle oravulse it from its origin or inser-tion. The conjoined tendon is thenseparated from the scarred areajoining it to the underlying sub-scapularis and retracted medially.This can usually be accomplishedwith a combination of blunt andsharp dissection. The surgeonshould be mindful of the musculo-cutaneous nerve; it is essential tokeep the dissection lateral to thebase of the coracoid process to pre-vent injury to neurovascular struc-tures.

The superior border of the sub-scapularis tendon is identified, andthe rotator interval is released,extending from the humerus to thecoracoid.12-14 As the dissectionproceeds from superficial to deepbetween tissue layers, the shouldershould be gently manipulated toregain motion. If there is stillmarked limitation of external rota-tion due to scarring in the intervalbetween the subscapularis and thecapsule, the subscapularis is splitbetween its fibers, and an elevatoris used to release adhesions be-tween its tendon and the underly-ing capsule. If there is still limita-tion of external rotation, a coronalZ-plasty lengthening of the sub-scapularis and capsule is per-formed (Fig. 5). This is done bydividing the scarred capsule andsubscapularis tendon in the coro-nal plane so that the superficialhalf of the tendon remains attached

to the muscle; the remaining deephalf is divided at the glenoid andremains attached to the lessertuberosity. The orientation of thiscoronal dissection can be guidedby determining the thickness of thescarred tendon and capsular tissueonce the rotator interval region isopened. The surgeon can usuallyboth see and palpate the thicknessof the anterior tissues through thisinterval.

When the anterior capsule andsubscapularis have been dissected,the subscapularis is usually foundto be entrapped in scar tissue. Toachieve full mobility, it may be nec-essary to visualize and dissect theaxillary nerve (Fig. 6, A and B). Avessel loupe is placed around theaxillary nerve, and the subscapu-laris is released globally on itssuperior, inferior, deep, and super-ficial surfaces.

If abduction and internal rota-tion are still limited, the inferiorand posterior capsule can bereleased through the joint. To dothis, I place a humeral head retrac-tor to displace the humeral headposteriorly and also put a bluntretractor beneath the inferior cap-sule to protect the axillary nerve(Fig. 6, C). The capsule is thenreleased from inferior to posteriorand superior under direct vision.The retractors are removed, andthe shoulder is placed through therange of motion to evaluate motiongains. The arm is positioned in themaximum external rotation thatwill allow secure closure of the Z-plasty of the anterior capsule andsubscapularis tendon with the useof large, nonabsorbable, braidedsuture. The patient usually gainsat least 40 degrees of external rota-tion; however, this depends on thequality of the tendon and capsulartissue. Range of motion is assessedagain to determine where there istension on the soft-tissue repairand thus define a “safe zone” forearly passive range-of-motionactivity.

Postoperative Treatment

On the morning of the first postop-erative day, either a repeat inter-scalene block is instituted or theinterscalene catheter infusion iscontinued. Therapy is performedtwice a day, in the morning and the

Fig. 5 Coronal Z-plasty lengthening ofsubscapularis and capsule. A, Entrapmentof the subscapularis causes loss of externalrotation (arrow). B, The subscapularis andcapsule are divided in the coronal plane,beginning laterally at their insertion anddeveloping a superficial layer. C, The cap-sule (deep layer) is then divided at the gle-noid, and the arm is externally rotated forcompletion of the Z-plasty lengtheningprocedure.

A

B

C

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Vol 5, No 3, May/June 1997 139

afternoon. The patient is dis-charged after the second therapysession on the second postopera-tive day. Narcotic analgesia isused as necessary to supplementthe interscalene analgesia. Therapyconsists of an aggressive stretchingprogram in all planes, and thepatient is instructed in self-assistedstretching exercises as well. As theinterscalene block usually results inonly partial muscle paralysis, thepatient can perform some stretch-ing independently.

When a soft-tissue repair hasbeen performed, as with a Z-plastylengthening in the front of theshoulder, motion should be onlypassive for 4 weeks. The positionsat which resistance is felt and therepair is observed to be under ten-sion should be noted at the time ofsurgery and specified for the treat-ing therapist as the limits of pas-sive motion. After 4 weeks, anaggressive active-motion programwith therapist-assisted stretching isbegun.

The patient who has under-gone an arthroscopic capsular re-

lease is discharged on the after-noon of the second postoperativeday. The patient is encouragedto use the surgically treated armfor activities of daily living, anda sling is not worn. The patientcontinues a home program withself-assisted stretching and a pul-ley device, as well as supervisedphysical therapy on an outpa-tient basis five times per weekfor the first 2 weeks and thenthree times per week for the next2 weeks.

After 4 weeks, the patient’sprogress is assessed, and the needfor additional therapy is individu-alized. I do not recommend useof a continuous passive motionmachine, as it has been my experi-ence that this device is not reliablefor maintaining motion gains.Whether the patient was treatedarthroscopically or with openrelease, the strengthening phaseof the postoperative therapy pro-gram is delayed until a nearly fullpain-free arc of motion has beenachieved. This usually takesabout 3 months.

Summary

Proper treatment of motion loss inthe shoulder depends on an initialrecognition of the causative disor-der and its natural history.Although a nonoperative approachof supervised or unsupervisedtherapy is usually successful intreating adhesive capsulitis, it mayfail in patients whose stiffness isdue to surgery or trauma. Closedmanipulation restores motion inmost cases of idiopathic adhesivecapsulitis, but is often ineffective inthe treatment of postsurgicalmotion loss. An arthroscopicrelease technique allows preciseand controlled release of capsularcontractures in cases of both idio-pathic adhesive capsulitis and post-surgical motion loss. When there isan extra-articular component to thesoft-tissue contracture, an openapproach will improve motion.Postoperative treatment mustemphasize pain control and main-tenance of motion gains achievedat the time of manipulation orsurgery.

Fig. 6 Subscapularis mobilization in a left shoulder (humeral head omitted from drawing for better visualization). A, Sutures are placedinto the contracted and shortened subscapularis tendon. An elevator protects the axillary nerve as the inferior and anterior capsules aredivided. The coracohumeral ligament (dotted line) is also divided. B, After the capsular release and coracohumeral ligament division, thesubscapularis is mobilized. C, An inferior and posterior capsular release can be performed if the axillary nerve is carefully mobilized andprotected (shown elevated with a vessel loupe around it and an elevator beneath it).

A B C

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Journal of the American Academy of Orthopaedic Surgeons140

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