Arthroscopic subacromial decompression has become a common procedure in the treatment of shoulder impingement problems. One has to be diligent, however, to preoperatively determine the appropriate indications for this technique lest it become over utilized. In addition, there are several technical considerations one should be aware of so as to avoid complications in its implementation.

Much of the controversy regarding ASAD involves the etiology of anterior superior impingement --- specifically "primary extrinsic impingement" popularized by Neer versus "secondary impingement" initially described by Codman and more recently championed by Nirschl. There are those who contend that all impingement is "secondary" and decompression is never indicated and others who believe that most impingement is "extrinsic" and almost always needs subacromial decompression. Review of the literature, common sense and arthroscopic experience would argue against both of these extremes.

The concept of secondary impingement originates with Codman who proposed an "intrinsic tendinous degeneration" as the essential lesion of rotator cuff disease, which is supported by a number of microvascular studies. The subsequent pain and weakness of the supraspinatus compromises its function as a humeral head depressor and allows the upward pull of the deltoid to dominate, producing a secondary impingement of the cuff into the acromion. Jobe enlarged this concept to include patients with underlying anterior glenohumeral ligament instability where the humeral head subluxes anteriorly, and the cuff is secondarily compressed against the coracoarcomial arch. More recently, Harriman argued that posterior capsular tightness with secondary anterior superior obligate translation of the humeral head is a common etiology of impingement.

Neer introduced the concept of primary extrinsic impingement of the anterior acromion, coracoacromial arch and the A-C joint on the underlying rotator cuff and biceps tendon when the arm is flexed or abducted greater than 90 degrees. He believed the impingement was due to acromial morphology or anterior osteophyte abutting on the bursal side of the cuff in elevation. Bigliani supported this concept noting increased cuff pathology with type III hooked acromion and Morrison found conservative treatment to be far less effective with type III vs. type I morphology. Even Codman described a subset of shoulders that exhibited "damaged tendon fiber 'straps', worn as if by friction" on the bursal surface of the supraspinatous. Os Acromial with its associated undersurface calcific and soft tissue ridges obviously wears and tears extrinsically on the bursal side of the cuff.

One needs to differentiate these anterior superior impingement pain syndromes from:

1) Gerber's anterior subcoracoid impingement which produces anterior mid arc pain from a congenital or iatrogenic laterally displaced coracoid tip and
2) Walsch's posterior superior "internal" articular-side cuff impingement with excess external rotation and extension.

The A-C joint also needs to he thoroughly evaluated preoperalively to determine whether it is playing a role in the symptom complex and will need to be addressed surgically.

One needs to treat all varieties of impingement with a diligent conservative treatment program including scapular and rotator cuff retraining, ROM exercises to regain full internal and external rotation, NSAIDs, differential subacromial/A-C joint injection and activity modification for 3-6 months in an effort to avoid operative intervention.

If conservative care proves unsuccessful, one then needs to try to differentiate primary extrinsic vs. secondary impingement vs. secondary impingement with pathologic adaptive subacromial changes and determine a preoperative plan. This distinction is based on the clinical picture, physical exam, imaging studies, differential injections and arthroscopic findings. In general, primary extrinsic impingement is seen in older patients with a type III acromion (where the acromio-humeral space narrows anteriorly) and associated A-C disease, a positive subacromial injection test, attrilional bursal or full thickness tears and significant fraying on the under surface of the acromion at arthroscopy. The literature and my own clinical experience suggests an extremely high success rate with ASAD/Mumford and arthroscopic cuff repair in this patient population.

Secondary impingement presents in a younger patient with a type I or II acromion (where the acromio-humeral space either widens or stays parallel anteriorly) associated anterior capsular laxity or posterior contracture, an equivocal injection test, articular side partial thickness cuff and SLAP tears and subacromial bursitis but no significant anterior acromial fraying. These patients require correction of the underlying gleno-humeral pathology and only a subacromial bursectomy, not a complete decompression, if the bursa is inflamed.

Chronic secondary impingement from whatever cause can gradually effectuate pathologic soft tissue and bony changes in the subacromial space. The unbalanced anterior superior abutment of the tuberosity against the anterior undersurface of the acromion stimulates the creation of a traction spur within the insertion of the coraco-acromial ligament - an "anterior acromial protuberance" best seen on the axillary and outlet view x-rays. This calcification in turn causes additional extrinsic impingement on the bursal side of the cuff and is often painful and inflamed like any other traction spur. If one deals only with the gleno-humeral pathology in this setting, the extrinsic impingement persists and failure can be expected. One needs to debride inflamed tissue, resect the traction spur and perform a more limited decompression (since the acromion is not as hooked) and avoid the A-C joint capsule.

The most commonly cited concern with ASAD is iatrogenic harm to the coracoacromial arch and destabilization of the gleno-humeral joint with anterior superior subluxation of the head. Although not uncommonly seen in open decompression surgery when the anterior deltoid is detached, there has been only one reported case with the arthroscopic technique using excess cautery ablation anteriorly. (Bonsell) In fact, this superior migration is not reported even with large os acromial resections. Some decrease in acromio-humeral distance after ASAD has been reported, however, when associated cuff tears are left unrepaired. (Kempt- Gleyzc)

When decompression is performed arthroscopically with a cutting block technique, a type I flat surface, a normal variant of acromial shape, is produced. One is not truly losing the "arch" but instead removing the excess congenital hook or protruding C-A ligament calcification blocking flexion. Since the deltoid is not detached, immediate motion can be instituted postoperatively so adhesions and stiffness are not a significant clinical problem.

Another argument against ASAD is that the results with minimal debridement and osteophyte resection equal decompression. (Nirschl) If one looks critically at this data, however, only one case out of 79 had an isolated bursal-side partial cuff tear (1.3%) with the rest having only articular (64.5%) or both side partial tears (34%). Obviously, this group of patients would require an extremely low number of decompressions using the rationale herein presented.

To simplify, one should only perform arthroscopic subacromial decompression if there is type II or 111 acromion (with or without an acromial traction spur) with documented subacromial pathology suggesting extrinsic pressure on the bursal side of the cuff (ie. bursal or complete cuff tears or undersurface anterior acromial fraying or calcification). Otherwise, debridement alone will suffice.

Technically, it is important to obtain a good quality outlet and axillary view for preoperative planning to determine the shape and thickness of the acromion. There is a small subset of patients with thin, broad acromion who are not candidates for the cutting block technique of ASAD and should only have a limited anterior acromial and spur resection. For the vast majority of patients, however, the cutting block technique produces the most consistent and reproducible flattening of the acromial undersurface and avoids the most common cause of acromioplasty failure which is inadequate resection. (Weber and Wolf) Care should be taken to keep the burr tightly on the undersurface of the posterior one half of the acromion as one comes forward on the "cutting block." If the portal is too low or soft tissue gets interposed posteriorly, the burr may falsely angle upwards resulting in excess anterior bone resection risking subsequent acromial fracture or deltoid detachment.

In summary, the key to successful results in impingement, cuff and A-C surgery is to avoid a dogmatic approach but instead tailor the treatment to the specific pathology noted in each individual patient. Then perform the appropriate operative procedure with consistency and precision.
 

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3/1/2006

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