Shoulder impingement is a common cause of shoulder pain, described by Neer in 1972 as a ridge of proliferative spurs on the undersurface of the anterior process of the acromion. These spurs allow for repeated contact of the rotator cuff and humeral head with traction of the coracoacromial (CA) ligament. The concept of impingement has since evolved to encompass four types of impingement: primary, secondary, subcoracoid, and internal.
Neer’s classic definition describes primary subacromial impingement, which can be further broken down into two main types: intrinsic and extrinsic. Intrinsic primary impingement implies that the structures beneath the CA arch enlarge and abut against it (thickening of the rotator cuff, bursa, or calcium deposits within the rotator cuff). Extrinsic primary impingement occurs when the space available for the rotator cuff diminishes (subacromial spurring, acromioclavicular [AC] joint osteophytes, greater tuberosity exostoses). In secondary impingement, glenohumeral instability allows anterior translation of the humeral head, and the rotator cuff contacts the CA arch.
Subcoracoid impingement is a controversial term describing anterior shoulder pain with forward flexion, internal rotation, and horizontal adduction of the humerus. In subcoracoid impingement, the subscapularis and lesser tuberosity impinge upon the posterior aspect of the coracoid process.
Internal impingement is typically described in overhead athletes and involves internal contact of the rotator cuff with the posterosuperior aspect of the glenoid and superior glenoid labrum. Specifically, the supraspinatus-infraspinatus junction and the humeral head contact the posterosuperior glenoid/superior glenoid labrum when the arm is abducted, extended, and externally rotated.
Patients with subacromial impingement typically present with the insidious onset of shoulder pain exacerbated by overhead activities. Patients may also present with rotator cuff-related symptoms such as anterolateral arm pain. Exacerbation of symptoms is frequently reported with shoulder elevation at or above 90 degrees or with lifting items away from the body. Patients with subcoracoid impingement present with anterior shoulder pain and difficulty with internal rotation, with or without symptoms of associated biceps pathology. Patients with internal impingement have difficulty with overhead activities, throwing, and symptoms related to superior and or posterior labral pathology.
Physical examination is critical to distinguishing between the different types of impingement. Every physical examination of the shoulder must include an evaluation of range of motion (ROM), rotator cuff strength, and provocative testing. Neer and Hawkins tests are typically used to evaluate for evidence of impingement; these tests are highly sensitive but not specific.
In Neer’s test, the examiner raises the affected arm in forced forward elevation while stabilizing the scapula. This causes the greater tuberosity to impinge against the acromion. This motion reproduces pain with impingement lesions of all stages, and it can elicit pain in many other conditions (adhesive capsulitis, osteoarthritis, calcific tendinitis, and bone lesions). Pain reproduced by this maneuver is referred to as a positive “Neer Impingement Sign”. After injection of 10 mL of 1% lidocaine, the maneuver is repeated. If the pain is significantly reduced or eliminated, then this is likely subacromial impingement and is referred to as a positive “Neer Impingement Test”. Pain caused by other conditions is not relieved (perhaps with the exception of calcific tendinitis).
The Hawkins-Kennedy test is performed by forward flexing the humerus to 90 degrees and forcibly internally rotating the shoulder. This maneuver drives the greater tuberosity further under the CA ligament, reproducing impingement pain. This test is highly sensitive and specific for bursitis and cuff abnormalities. O’Brien’s active compression test assesses labral pathology and involves flexion of the affected arm to 90 degrees while keeping the elbow fully extended. The arm is then adducted 10-15 degrees across the body. The patient then pronates the forearm so the thumb is pointing down, and the examiner applies downward force to the wrist with the arm in this position while the patient resists. The patient then supinates the forearm so the palm is up and the examiner once again applies force to the wrist while the patient resists. This test is positive when there is pain over the posterior shoulder while the forearm is pronated but not when the forearm is supinated, indicating labral pathology. Anterior pain may involve labral, rotator cuff, or AC pathology.
Subcoracoid impingement typically demonstrates palpable tenderness in the region of the coracohumeral interval. The coracoid may or may not be tender to palpation, and subscapularis testing, including belly press, lift-off, and bear hug tests may cause pain. Hawkins impingement testing with a cross-body component frequently elicits localized pain in the anterior aspect of the shoulder near the coracoid region. Biceps testing, including the Speed’s test and/or Yergason compression test may be positive if there is associated biceps pathology. One should palpate for biceps instability with dynamic testing.
Internal impingement is tested with the patient supine. The shoulder is abducted to 90 degrees and maximally externally rotated (late cocking phase of throwing) with extension. If this maneuver reproduces posteriorly located pain experienced during throwing, then the test is considered positive. This test is further confirmed with relief upon performing the relocation test, where the test is repeated in abduction and maximum external rotation with the elbow in front of the plane of the body. If the pain disappears, then internal impingement is likely. In addition, the O’Brien’s active compression test will often be positive and patients will show signs of loss of internal rotation of the shoulder. Internal impingement is often associated with scapular dyskinesia and poor posture, which should be evaluated and noted as well.
Radiographs should be obtained for the affected shoulder, with focus on any bony abnormalities of the CA arch. Routine radiographs include anteroposterior (AP) and Grashey views (i.e. AP radiograph of the shoulder in the plane of the scapula) as well as outlet and axillary views of the shoulder. Outlet views provide visualization of acromial morphology. Contralateral outlet views should be considered to compare the CA arches to assess pathological anatomy. Axillary views best demonstrate evidence of an os acromiale, which may be a source of secondary impingement. AC joint osteoarthritis with inferior osteophyte formation, acromial enthesophytes or sclerosis, and cystic changes of the humeral head are common findings associated with impingement. Acromiohumeral distance may better reflect the clinical status of patients with subacromial impingement than the acromial shape.
MRI provides detail of potential sites of subacromial impingement through the supraspinatus outlet. Ossification of the CA ligament or the presence of a subacromial spur can be best identified in the sagittal view. However, differentiation of a pathologic spur and the normal CA ligament can be difficult. One should also look for signs of subacromial bursitis on MRI: bursal thickness >3 mm, fluid in the anterior aspect of the bursa, and the presence of fluid medial to the AC joint.
The role of imaging in the diagnosis of subcoracoid impingement is controversial; however, several anatomical relationships associated with subcoracoid impingement can be analyzed using either CT or MRI. Coracoid overlap is the perpendicular distance between the most prominent tip of the coracoid to the line representing the plane of the glenoid fossa. Coracoid index is measured in a similar fashion, but the point of reference is the base of the coracoid. Coracohumeral distance is the shortest distance between the coracoid process and the subchondral bone of the humeral head. In our experience, a coracohumeral interval less than 10 mm may predispose a patient to coracoid impingement. Coracoid overlap and a coracoid index of more than 15-20 mm may also contribute to progressive subcoracoid impingement. In addition, a thickened conjoined tendon (frequently at its confluence with the CA ligament along the lateral aspect of the coracoid tip) may contribute to the soft-tissue component of subcoracoid impingement.
For internal impingement, magnetic resonance (MR) arthrography is routinely ordered because it improves detection of labral and capsular abnormalities as well as partial thickness rotator cuff tears. MR arthrogram in the position of abduction and external rotation (ABER view) is ideal to visualize impingement of the rotator cuff (supraspinatus-infraspinatus junction and the humeral head) with the posterosuperior aspect of the glenoid and superior glenoid labrum.
Special Diagnostic Tests
Targeted injection with lidocaine can be useful in differentiating the etiology of shoulder pain. The Neer impingement test involves an injection of 1% lidocaine into the subacromial space. If the patient has no pain with forced forward flexion with the scapula stabilized, this is diagnostic for subacromial impingement.
Subcoracoid impingement can be evaluated with injection of local anesthetic into the subcoracoid region, under direct ultrasound guidance or with the arm at the side in external rotation (avoiding accidental injection into the subscapularis or biceps tendon). The coracoid tip is palpated, and the needle is projected deep to this area just lateral to the coracoid tip. If resistance is felt during injection, the needle is slowly withdrawn until the resistance dissipates. Infiltration of lidocaine into the subcoracoid space is then performed. The Hawkins-Kennedy and cross-arm adduction tests are performed immediately following the injection to determine the extent of relief, confirming the diagnosis of subcoracoid impingement.
Relief of pain after injection of lidocaine in the AC joint indicates AC joint pathology as a source of pain. Similarly, relief of pain after injection of lidocaine into the bicipital groove supports a diagnosis of biceps tendinitis.
All patients with subacromial impingement should undergo a course of non-operative management for 3 to 6 months. Large retrospective studies show approximately 70% of patients with impingement will respond to conservative management. Initial rehabilitation goals include preventing overuse or re-injury with relative rest and activity modification. Control of subacromial bursal inflammation can be achieved with non-steroidal anti-inflammatory medication, hot and cold therapy, ultrasound, and corticosteroid injection when appropriate. Therapy is advanced as pain and inflammation subside, and the treatment goals shift toward regaining full ROM and eliminating capsular contractures. Posterior capsular contracture is addressed with progressive adduction and internal rotation stretching.
As pain continues to decrease and ROM improves, strengthening of the rotator cuff and periscapular musculature is initiated. Often, progressive resistance exercises are introduced at this point. In our patients, we stress avoidance of overhead weight training and long lever-arm exercises because these maneuvers can exacerbate impingement and place excessive torque on the glenohumeral joint.
Treatment of subcoracoid impingement is similar to that of subacromial impingement: avoidance of aggravating activities, including cross-body motions. A standard rehabilitation program focusing on scapular stabilization, rotator cuff strengthening, and correction of any pectoralis major contracture should be considered for a period of 3 to 6 months. Evaluation of the scapula is critical – malposition can have a role in functional coracoid impingement. A subcoracoid injection can provide pain relief and assist in a non-operative treatment regimen. To our knowledge, no study has documented outcomes following non-surgical management of subcoracoid impingement.
Symptomatic patients who have vague shoulder discomfort and demonstrate a glenohumeral internal rotation deficit (GIRD) are started on focused internal rotation stretches (“sleeper” stretches) to alleviate posterior inferior glenohumeral ligament (PIGHL) contracture and restore normal glenohumeral and periscapular biomechanics. Reducing GIRD and restoring total arc of motion decreases the risk for shoulder injury and generally allows return to preinjury function. Scapular reconditioning focuses on regaining scapular elevation and retraction control; progress is assessed by repeat examination for normalization of scapular symmetry. Up to 90% of athletes will decrease their GIRD deficit to an acceptable magnitude within 10 to 14 days of focused stretching (less than 20 degrees) with near normalization of total arc of motion.
Indications for Surgery
If a 3 to 6 month program of non-surgical treatment fails to resolve symptoms, MRI should be used to identify evidence of extrinsic impingement. Subacromial decompression can then be done using arthroscopic or open techniques. Arthroscopy provides an advantage for diagnosing and treating any intra-articular pathology (i.e. partial undersurface rotator cuff tear, or biceps tendon lesions) or early glenohumeral arthritis not otherwise visualized on imaging. Goals of subacromial decompression are to release the CA ligament, remove any thickened subacromial bursa, and achieve a flat, smooth, acromial undersurface. Subacromial decompression produces excellent long-term results in our experience.
Similar to subacromial impingement, failed non-surgical treatment is an indication for surgical decompression, either open or arthroscopic. Our preference is for arthroscopic subcoracoid decompression, where the posterior-lateral coracoid tip can be excised. In our experience, there is little risk of injury to adjacent neurovascular and soft tissue structures with careful debridement and instrument positioning. Presurgical imaging of the coracoid morphology can be useful in estimating the required extent of coracoid excision and determining whether an arthroscopic or open approach should be used. If resection of more than 10 mm of the coracoid tip is required, an open coracoid decompression allows the conjoined tendon to be approximated, with transosseous fixation into the residual coracoid.
Indications for surgical intervention for internal impingement include a failed capsular stretching and rotator cuff strengthening program, and persistent pain with or without symptoms related to associated labral pathology. In our opinion, it is best to treat any motion loss conservatively prior to addressing labral pathology in an overhead athlete with surgery.
Our arthroscopic set up and instrumentation is similar for subacromial, subcoracoid, and internal impingement. Necessary equipment includes a standard arthroscopy tower, 30-degree arthroscope, available 70-degree arthroscope, and standard arthroscopic instrumentation.
Examination under anesthesia of the affected shoulder is performed prior to patient positioning with the patient asleep and in the supine position. Passive ROM is documented in forward flexion, abduction, internal and external rotation at 90 degrees of abduction, and external rotation at the side in both the involved and uninvolved shoulders. Anterior and posterior glenohumeral translation is examined using a modified load and shift test. Inferior translation is evaluated with a sulcus test. Any side-to-side differences are noted and may be addressed at the time of surgery.
The patient is positioned in the lateral decubitus position using a standard boom and making sure all bony prominences are well padded and an axillary float is in place. The arm is suspended in-line with 10 lbs for females and 15 lbs for males in general. In our experience, the lateral decubitus position provides the advantages of joint distraction, 360-degree shoulder access, and decreases the need for additional assistants while allowing for full access to the entire shoulder joint and subacromial space.
Step-by-Step Description of Procedure
Standard anterior, posterior, and lateral arthroscopic shoulder portals are used to perform the diagnostic arthroscopy and subacromial decompression.
The bony anatomy of the acromion, clavicle, coracoid process, and AC joint are marked on the skin with a skin marker. Proposed sites of the posterior, anterior, and lateral portals are marked. The posterior portal is located 2 cm medial and 2 to 3 cm distal to the posterolateral corner of the acromion. The anterior portal is typically marked 1 cm lateral and 1 to 2 cm cephalad to the coracoid process. The lateral portal is marked 2 to 3 cm distal to the lateral border of the acromion at the junction of the anterior and middle thirds of the acromion.
The glenohumeral joint is insufflated with 50 cc of arthroscopic solution, and the posterior portal is established with a 5 mm skin incision and trocar placed into the glenohumeral joint. The arthroscope is inserted and flow is established. Under direct arthroscopic visualization, an 18-gauge spinal needle is used to confirm the location of the anterior portal. A 5 mm skin incision is made and a probe is placed through this anterior portal.
A diagnostic arthroscopy is performed, inspecting the biceps tendon, rotator interval, glenohumeral joint, glenoid labrum, glenohumeral ligaments, and rotator cuff. Disease processes that may clinically mimic subacromial and subcoracoid impingement (glenohumeral arthritis, rotator cuff tears, subscapularis tears) are noted. The camera should be shuttled between the posterior portal and anterior portal to complete the intra-articular inspection in order to properly evaluate the posterior capsulolabral structures. A 70 degree lens may be utilized to best evaluate the integrity of the subscapularis attachment to the lesser tuberosity and the subscapularis recess.
A blunt arthroscopic trocar is used to redirect the posterior portal from the intra-articular position to the subacromial space. The trocar is swept through the subdeltoid bursa to assist in opening up the subacromial space while palpating the coracoacromial ligament with the tip of the trocar. The arthroscope is introduced and an initial assessment of the subacromial space is performed. A 5 mm skin incision is used to establish the lateral portal, 2 to 3 cm distal to the mid-lateral border of the acromion under localization with a spinal needle. Care is taken to avoid injury to the axillary nerve.
Visualization is often difficult because of the thickened and inflamed subacromial bursa. An arthroscopic shaver is introduced into the lateral portal and when its cutting flutes are visualized, bursectomy is performed.
Pearl: Early removal of the “posterior veil” will offer the best visualization. The bursectomy should be carried to the subdeltoid recess to complete the decompression and allow for full visualization of possible additional pathology. Additional anterior superolateral and posterior superolateral portals may be employed as needed.
The tip of the anterolateral aspect of the acromion is palpated with the arthroscopic shaver to confirm the correct subacromial orientation. Acromial resection is completed in an anterior-to-posterior and lateral-to-medial direction via the lateral portal with an arthroscopic shaver or burr. The desired depth of resection, estimated from the preoperative films, is obtained by measuring with the diameter of the burr. To smooth out any ridges or rough edges, the burr may be placed in the “reverse cutting” position – this provides less aggressive resection and is often easier to control in hard, sclerotic bone. As a gross guideline, after acromioplasty with the camera at the level of the mid acromion one should visualize one third of the arthroscopic screen each to be bone, rotator cuff, and open subacromial space.
Care must be taken to avoid resection of the highly vascular bursal tissue medial to the musculotendinous junction of the rotator cuff.
Electrocautery is used to coagulate any bleeding and remove the remaining soft tissue from the undersurface of the acromion, starting at the anterolateral corner of the acromion. The CA ligament is peeled off from the undersurface of the acromion and the remaining ligament stump is completely excised using the shaver or cautery. Beware of the acromial branch of the thoracoacromial artery within the CA ligament. Do not cut the CA ligament if rotator cuff pathology is present to avoid the risk of anterosuperior escape.
After an adequate portion of the acromion is removed, the shoulder is taken through its ROM to confirm the adequacy of resection. The arthroscope may be placed in the lateral portal to look for any residual osteophytes from the undersurface of the AC joint, which should be resected if necessary to achieve adequate decompression. Electrocautery should be used to resect the highly vascular soft tissue on the undersurface of the AC joint. The arthroscopic shaver or the burr is used to coplane the distal portion of the clavicle with the acromion from the lateral portal if necessary.
For patient positioning and standard portal placement see subacromial impingement above. A standard posterior arthroscopy portal is established as described previously for subacromial impingement. In addition a low rotator interval portal may also be used.
While viewing from posterior, the rotator interval tissue is debrided using an arthroscopic shaver and electrocautery device exposing the undersurface of the coracoid. The coracoacromial ligament and conjoined tendons are identified. Caution is used with use of the electrocautery device in the area of the conjoined tendon, to avoid injuring the musculocutaneous nerve, and while debriding inferior and medial to the coracoid to avoid injuring the axillary nerve and artery. The subscapularis tendon is thoroughly examined for partial tearing caused by the tight subcoracoid space using both the 30 and 70-degree lenses. In addition, the biceps tendon is examined for instability and tearing.
One then proceeds with mechanical coracoplasty. We find that the coracoid tip tends to be amenable to using a standard full radius shaver on forward and reverse in performing an adequate bony resection. The amount of bone resected is dependent upon pre-operative planning and intra-operative testing. Internal and external rotation of the shoulder will allow intra-operative assessment of any obvious impingement and allow one to judge resection depth. After completion of subcoracoid decompression and coracoplasty, any additional intra-articular pathology should be addressed followed by standard subacromial space evaluation.
During examination under anesthesia, special attention is paid to loss of glenohumeral internal rotation and total arc of motion. Loss of internal rotation in the setting of loss of total arc of motion is pathologic and should be addressed at the time of surgery. Pre-operative radiographs and MR arthrogram should be scrutinized for signs of capsulolabral pathology, posteroinferior glenoid Bennett’s traction osteophytes, and internal impingement-related partial articular-sided tendon avulsion (PASTA) lesions.
Standard anterior and posterior glenohumeral portals are used as noted above. Careful evaluation of the superior labrum, posterior labrum, capsule, and the undersurface of the rotator cuff (particularly the supraspinatus-infraspinatus junction) are performed. The camera must be moved from the posterior to the anterior portal to completely evaluate all possible pathology.
In the setting of internal impingement associated with loss of total arc of motion and loss of internal rotation that has not responded to conservative measures, a posterior inferior capsular release should be performed. If a Bennett’s lesion is present, it should be addressed by performing a resection with a mechanical shaver or burr.
Pearl: Use of a 70-degree lens from the anterior portal and a 4 mm round burr from posterior is the best combination to excise a Bennett’s lesion.
Any rotator cuff or labral pathology should also be addressed concurrently. Subacromial decompression is not necessary in the absence of signs of subacromial impingement.
Pearls and Pitfalls of Technique
Inadequate bone resection: Avoided by pre-operative assessment of the amount of bone to resect (supraspinatus outlet view).
Inadequate bursectomy and subacromial debridement: Bursal-sided rotator cuff tears or continued mass effect from retained bursal tissue or calcific lesions may compromise surgical outcome. Bursectomy should be complete through the subacromial and sub deltoid spaces.
Retained CA ligament: May be a cause for persistent impingement. Complete excision is confirmed by visualization of the undersurface of the deltoid across the anterior aspect of the acromion. DO NOT resect the CA ligament if rotator cuff pathology is suspected, as this may lead to superior escape.
Hemostasis: Excessive bleeding obscures adequate visualization and may lead to inadequate bone resection. Placing 20 cc of 1:300,000 diluted epinephrine into the arthroscopic solution can limit bleeding. Keeping mean arterial pressure low, i.e. below 70, via hypotensive anesthesia can be effective if the patient has no contraindication.
Error in diagnosis: The most common cause of failure of subacromial decompression; subacromial impingement in isolation is a rare diagnosis, have a high index of suspicion for additional pathology, i.e. rotator cuff, superior labrum-biceps tendon, AC joint, etc. MRI or additional imaging is indicated prior to surgery to rule out concomitant pathology. AC arthritis, instability, glenohumeral arthritis, rotator cuff tears, and biceps lesions commonly coexist with impingement and may mimic it clinically.
Careful pre-operative examination and examination under anesthesia are key to success.
Avoid excessive release when performing posterior inferior capsular release to avoid instability.
Be sure to address superior labral and rotator cuff pathology to achieve maximum results.
Bleeding: Aggressive medial debridement, CA ligament release-acromial branch of the thoracoacromial artery.
Over-resection of the acromion: acromial fracture.
Os acromiale: Acromioplasty in the setting of os acromiale may destabilize the os and cause pain.
Bleeding: Axillary artery (inferior and medial branches).
Nerve Injury: Musculocutaneous nerve in the conjoined tendon, axillary nerve inferior to the subscapularis tendon.
Coracoid Fracture: Exuberant coracoid resection.
Instability: Excessive capsular release.
Nerve Injury: Axillary nerve with inferior extension of the release, use meniscus biter to perform inferior extent of the release to avoid thermal injury
Patients are placed in a sling for comfort post-operatively but are encouraged to discontinue the sling when the interscalene block wears off. Most will use the sling for comfort for up to 2 weeks. Initially, passive ROM is started. Therapy is advanced to active ROM with terminal stretching as comfort allows. Rotator cuff strengthening and periscapular strengthening is started once full ROM is achieved. Activities may be advanced as tolerated once full active motion is achieved and strength is 85% of the opposite side.
Post-operative rehabilitation of internal impingement focuses on normalization of periscapular and glenohumeral biomechanics with a focus on maintaining internal rotation and total arc of motion. Early aggressive passive and active ROM is recommended. Once ROM is achieved, progression from isometric to open chain strengthening with a focus on normalization of periscapular kinematics is possible. Once full strength and motion is achieved, one may consider advancement to a formal return to play program including a throwing progression. Return to play should be delayed until completion of a formal throwing program.
Outcomes/Evidence in the Literature
Neer, CS. “Anterior acromioplasty for the chronic impingement syndrome in the shoulder: a preliminary report”. J Bone Joint Surg Am. vol. 54. 1972. pp. 41-50. (Classic article describing the relevant anatomical findings and the rationale, indications, technique, and preliminary results of anterior acromioplasty. Neer proposed that the spurs on the undersurface of the anterior acromion, resulting from impingement of the rotator cuff and humeral head against the undersurface of the anterior acromion and CA ligament were primarily anterior, not lateral.)
Park, HB, Yokota, A, Gill, HS, El Rassi, G, McFarland, EG. “Diagnostic accuracy of clinical tests for the different degrees of subacromial impingement syndrome”. J Bone Joint Surg Am. vol. 87. 2005. pp. 1446-1455. (This Level I study assessed diagnostic values of the commonly used clinical tests for subacromial impingement in varying severity of rotator cuff disease. Sensitivity, specificity, positive predictive value, negative predictive value, and overall accuracy of the eight tests studied varied considerably. The combination of the Hawkins-Kennedy, the painful arc sign, and the infraspinatus muscle test yielded the best post-test probability (95%) for any degree of impingement syndrome.)
Roberts, CS, Davila, JB, Hushek, SG, Tillett, ED, Corrigan, TM. “Magnetic resonance imaging analysis of the subacromial space in the impingement sign positions”. J Shoulder Elbow Surg. vol. 11. 2002. pp. 595-599. (This study used MRI to identify and measure the changes in anatomic structures in the subacromial space as the arm was moved from complete rest to 160 degrees of forward flexion during the Neer and Hawkins impingement sign maneuvers. The rotator cuff insertion was closest to the anteroinferior acromion at 90 degrees of flexion (Hawkins sign position), not at full elevation (Neer sign position). This data suggests that a clinically positive Hawkins sign is consistent with external shoulder impingement.)
Valadie, AL, Jobe, CM, Pink, MM, Ekman, EF, Jobe, FW. “Anatomy of provocative tests for impingement syndrome of the shoulder”. J Shoulder Elbow Surg. vol. 9. 2000. pp. 36-46. (Cadaveric study describing the extra- and intra-articular anatomic relationships present during the Neer and Hawkins tests. Cadavers were placed in the provocative position and sectioned. The greater tuberosity and rotator cuff tendons contacted the acromion more commonly in the Neer position. In the Hawkins position, the rotator cuff more consistently contacted the CA ligament and more medial structures of the CA arch.)
Dumontier, C, Sautet, A, Gagey, O, Apoil, A. “Rotator interval lesions and their relation to coracoid impingement syndrome”. J Shoulder Elbow Surg. vol. 8. 1999. pp. 130-135. (This study demonstrated that the soft-tissue thickening on the lateral coracoid tip representing the fibrous falx in the anteroinferior portion of the coracoid arch also may contribute to narrowing of the coracohumeral interval. The fibrous falx is formed by coalescence of the lateral part of the CA ligament and the conjoint tendon. This soft tissue thickening is better identified on axial MRI than on CT scan.)
White, EA, Schweitzer, ME, Haims, AH. “Range of normal and abnormal subacromial/subdeltoid bursa fluid”. J Comput Assist Tomogr. vol. 30. 2006. pp. 316-320. (This study used MRI to determine the range of normal and abnormal subacromial/subdeltoid (SA/SD) bursal fluid. After analysis of 71 shoulders, this study concluded that normal SA/SD bursa fluid is rarely thicker than 2 mm and tends to be located posteriorly. An abnormal amount of fluid is present when the thickness exceeds 3 mm, fluid is present medial to the AC joint, and fluid is seen in the part of the bursa anterior to the humerus.)
Cummins, CA, Sasso, LM, Nicholson, D. “Impingement syndrome: temporal outcomes of nonoperative treatment”. J Shoulder Elbow Surg. vol. 18. 2009. pp. 172-177. (This is a level I prospective study analyzing patients with impingement syndrome to look at outcomes of non-operative treatment on a temporal basis. Patients underwent a standardized, non-operative treatment protocol consisting of subacromial steroid injection, followed by physical therapy. Of patients with impingement syndrome treated non-operatively, 79% did not require surgery after two-year follow up. Predictors of patients going on to surgical intervention included the total number of subacromial steroid/lidocaine injections and patient response to the initial subacromial injection. Of the patients not undergoing surgery, 30% continued to have some shoulder pain.)
Davis, AD, Kakar, S, Moros, C, Kaye, EK, Schepsis, AA, Voloshin, I. “Arthroscopic versus open acromioplasty: a meta-analysis”. Am J Sports Med. vol. 38. 2010. pp. 613-618. (This level III meta-analysis addressed the persistent controversy over the efficacy of arthroscopic vs. open acromioplasty. No statistically significant differences were found in clinical outcomes or complications between arthroscopic and open acromioplasty. However, open acromioplasty was associated with longer hospital stays and a greater length of time until return to work.)
Burkhart, SS, Morgan, CD, Kibler, WB. “The disabled throwing shoulder: spectrum of pathology. I: pathoanatomy and biomechanics”. Arthroscopy. vol. 19. 2003. pp. 404-420. (Review of the biomechanics and pathogenesis of internal impingement. The authors argue that the most important pathologic process that occurs in throwers is a loss of internal rotation in abduction. They propose that an acquired internal rotation loss caused by a posteroinferior capsular contracture is the essential lesion that results in increased external rotation. This, they argue, can occur with or without anterior capsular stretching.)
Warner, JJ, Allen, AA, Marks, PH, Wong, P. “Arthroscopic release of postoperative capsular contracture of the shoulder”. J Bone Joint Surg Am. vol. 79. 1997. pp. 1151-1158. (This study describes a technique for posterior capsule release for isolated loss of internal rotation. Electrocautery is used to divide the posterior capsule from the posterior portal beginning posterior to the biceps tendon origin at the 11 o’clock position, continuing inferior to the 8 o’clock position. The depth of the capsular division is complete when the muscle fibers of the rotator cuff are visible. A shaver is then used to create a sider gap in the resected capsule to avoid recurrence.)
The term “shoulder impingement” involves a spectrum of disease, encompassing subacromial impingement, subcoracoid impingement, and internal impingement. Diagnosis is aided by a detailed history and physical exam, followed by targeted diagnostic injection and further imaging studies. While the pathology driving these disease processes may differ, the approach to their treatment is similar: an initial course of non-operative treatment for 3 to 6 months, with a focus on prevention of overuse or reinjury with relative rest and activity modification. Therapy is advanced as pain and inflammation subside, and the treatment goals shift toward regaining full ROM and eliminating capsular contractures. Failed non-operative treatment is an indication for surgical intervention in all forms of impingement, with arthroscopic surgery now the preferred surgical approach.
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- The Problem
- Clinical Presentation
- Diagnostic Workup
- Non–Operative Management
- Indications for Surgery
- Surgical Technique
- Pearls and Pitfalls of Technique
- Potential Complications
- Post–operative Rehabilitation
- Outcomes/Evidence in the Literature