Subacromial Impingment and Confirmation Bias – PART 2: Alternative theories of “impingement” pain and specific anatomical findings

“Are you going to remove the “bone spur” that the radiologist found? I don’t want that digging into my rotator cuff.”

– Any misguided patient who thinks the spur might be the problem

You are encouraged to review part 1 of this series, included here for convenience:

The Impingement Trifecta

Patients with “shoulder impingement” present with what could be considered a “trifecta” of pathological findings:

  • Loss of internal rotation in abduction
  • Pathological thickening, roughness, and inflammation of the subacromial bursa
  • Articular sided partial thickness tearing of the supraspinatus

We should take a look at each of these findings, in an effort to describe the specific problem, as well as some potential treatment options. If we can identify which of the functional “4S” pillars is impaired, then treatment becomes quite targeted. Although many shoulder conditions fall into one of the “4S” categories, shoulder impingement seems to fall into three of them (stiffness, smoothness, weakness).

As recognized by a Dr. Bertram Zarins editorial in the Journal of Bone Surgery in 2005, rather than simply attributing pain to the shape of the acromion, we are best served by identifying the specific problem leading to loss of comfort and function of the shoulder:


Loss of Internal Rotation

Loss of internal rotation, or GIRD, could easily be confused for the “Hawkins impingment test”.

Hawkins Impingement Test: internal rotation in a position of abduction/forward flexion. This could easily be understood simply as a measure of internal rotation.

This commonly performed test is used to diagnose shoulder impingement – it is thought to be caused by pain generated by squeezing the rotator cuff tissue against the coracoacromial arch. And accordingly, can lead to failure of the rotator cuff. In truth, papers describe that in this position, the biceps and rotator interval are contacting the coracoacromial arch, and not the cuff1. Neer also explained that the supraspinatus contacts the anterior acromion only with the arm in near full forward flexion, but the the cuff is anterior to the acromion with the arm at rest by the side. Based on this information, it seems that the acromion may contact the biceps and rotator interval, but rarely the cuff tissue itself. How could the acromion itself lead to shoulder impingement, and should it be routinely assaulted at the time of surgery?

Recall that limited internal rotation in this “Hawkins” position will cause obligate translation of the humeral head into an anterosuperior position (as described by Doug Harryman in his classic paper.)2. Please refer to my prior post for explanation. It seems probable that pain may be caused by the loss of internal rotation disrupting the normal mechanics of the glenohumeral joint and subsequent increased pressure into the coracoacromial arch. This effect was also shown by Muraki in 2012, describing a mechanism for the very common anterior shoulder pain that is seen in patients with shoulder impingement and internal rotation deficiency.3

GIRD and Shoulder Impingement – the Stiffness problem of impingment
Photo taken from Matsen et al, Practical Evaluation and Management of the Shoulder, 19944

Neer recognized this loss of rotation in his classic paper, and his patients would endure at least 9 months of a diligent effort to restore normal motion to the shoulder prior to consideration of acromioplasty.5

Specific stretches to restore internal rotation are routinely prescribed by practitioners who correctly identify this loss of rotation. (link to my own PT script). The sleeper stretch in particular nicely targets the posterior band of the inferior glenohumeral ligament. Efforts at this exercise can quickly lead to gains in internal rotation. The sleeper stretch should be a foundational exercise for patients suffering from pain related to loss of internal rotation. However, don’t forget to stretch into cross body adduction, as this has some support in the literature as a more effective stretch to improve mobility.6,7 Specifically using a stretching program to treat impingement syndrome effectively improves both comfort and function.8


Subacromial Bursitis

Credit to Steve Lippitt, MD and University of Washington

Neer also described thickening of the bursa in his surgical treatment of shoulder impingement. Bursitis is also commonly seen on MRI and ultrasound studies as both a thickening of the tissue, and excess fluid in the bursal layer. This can alter the Smoothness principle that determines normal smooth articulation between the rotator cuff tissue and the overlying coracoacromial arch.

Bursal inflammation is a major contributor to pain. Attempts at calming the inflammation are indicated. NSAIDS, avoidance of aggravating activity, and judicious use of injections can help to settle down pain. The key may be in effectively allowing the patient to properly rehabilitate the shoulder.

Use of ultrasound may improve the accuracy and efficacy of the injection, although some controversy exists. A systematic review in 2015 suggested that ultrasound guidance results in greater clinical improvement than blinded injection.9


Partial Thickness Rotator Cuff Tear

Articular sided tearing commonly seen with “impingment” syndrome

The third finding in shoulder impingement is the prevalence of partial thickness supraspinatus tearing. Specifically – articular sided tears are commonly seen. Codman stated that this tear could not be explained by contact with the acromion, in his 1934 text.10 Intrasubstance tears can also be noted on MRI.

We do know, however, that tendon degeneration and progression of rotator cuff disease closely mirrors the passage of time as people get older. Aging has been strongly correlated with development of cuff tears, as has been shown in numerous studies. Cadaveric, arthrogram, MRI, and ultrasound studies all support this notion. (as discussed in previous post, which outlines the danger of obtaining routine MRI)

Sher data showing the increasing incidence of cuff tears in asymptomatic shoulders with age on MRI11
Templehof data utilizing ultrasound on asymptomatic shoulders12

We also know that changing the shape of the coracoacromial arch (with acromioplasty/subacromial decompression) does not seem to be protective of this natural aging process.13,14 It seems clear that use of this traditional intervention on the “bone spur” is not helpful in treatment of rotator cuff pathology.

Our best intervention for treatment of tendinosis and degeneration is physical therapy. The basic orthopedic maxim that soft tissue will respond favorably to eccentric loading of the tissue holds true in the shoulder, as in other areas.15

Rotator cuff weakness (the Strength principle) also leads to upward migration of the humeral head in relation to the glenoid – another source of secondary impingment against the arch. Cuff weakness should respond favorably to an appropriate rehabilitation program.’


What about the “spur”?

Unquestionably, imaging studies seem to show a prominent spur on the anteroinferior acromion. This easily raises concern that the bone is quite literally digging into the rotator cuff.

Cutout of sagittal MRI cut showing the acromion and apparent prominent “spur” coming from the antero-inferior corner, raising concern about cuff abrasion.

Neer described in his classic paper that the calcification of the CA ligament is likely a result of traction on the tissue. Burns, in an anatomical study of the subacromial space, also determined that the calcification of the CA ligament is likely an enthesopathy from chronic traction16. This is likely why the presence of a spur seems to correlate with age, as shown in a number of studies. Nicholson in 1996 described the presence of spurring to be 7% in patients <50, and 30% in patients >50.17 Similar numbers were shown by Liotard in 1998 (8% if <60, 27% if >60).18 Additionally, the presence of a cuff tear predicted the formation of a spur.

The formation of a spur could plausibly be due to long term traction on the CA ligament: anything causing superior migration could lead to its development. Several ideas come to mind:

  • Posterior capsule contracture (Harryman study)
  • Rotator cuff tear
  • Normal aging and its correlation with spur formation

It is plausible that the spur does not cause cuff disease. Rather, aging and tissue degeneration is the likely prevalent cause of cuff failure.

Proper understanding (as described in prior post) of the nature of the articulation between the coracoacromial arch above and the cuff below makes it easy to understand the following sequence of images, demonstrating the above spur sitting in its native MRI: this sequence shows the round humeral head, the matching curved cuff surface, and matching CA arch. One must look closely to find a spur. Finding the calcification of the CA ligament clearly shows the cuff is in no danger from the “spur”.


Summary

Impingement presents with a triad of internal rotation deficiency, inflammation of the subacromial bursa, and partial thickness articular sided supraspinatus tearing. The spur is likely not related to the development of shoulder pain or rotator cuff disease.

The next, and last post, in this series will present high level literature describing the ineffectiveness of spur removal in treating shoulder pain. It will also describe Confounding Bias, and how this challenges our ability to change historical treatment patterns despite this evidence.


References

  1. Tucker S, Taylor NF, Green RA. Anatomical validity of the Hawkins-Kennedy test–a pilot study. Man Ther. 2011 Aug;16(4):399-402. doi: 10.1016/j.math.2011.02.002. Epub 2011 Mar 4. PMID: 21377402. ↩︎
  2. Harryman DT 2nd, Sidles JA, Clark JM, McQuade KJ, Gibb TD, Matsen FA 3rd. Translation of the humeral head on the glenoid with passive glenohumeral motion. J Bone Joint Surg Am. 1990 Oct;72(9):1334-43. PMID: 2229109. ↩︎
  3. Muraki T, Yamamoto N, Zhao KD, Sperling JW, Steinmann SP, Cofield RH, An KN. Effects of posterior capsule tightness on subacromial contact behavior during shoulder motions. J Shoulder Elbow Surg. 2012 Sep;21(9):1160-7. doi: 10.1016/j.jse.2011.08.042. Epub 2011 Nov 12. PMID: 22079765. ↩︎
  4. Matsen, Lippitt, Sidles, Harryman. Practical Evaluation and Management of the Shoulder, 1994. ↩︎
  5. Neer CS 2nd. Anterior acromioplasty for the chronic impingement syndrome in the shoulder. 1972. J Bone Joint Surg Am. 2005 Jun;87(6):1399. doi: 10.2106/JBJS.8706.cl. PMID: 15930554. ↩︎
  6. McClure P, Balaicuis J, Heiland D, Broersma ME, Thorndike CK, Wood A. A randomized controlled comparison of stretching procedures for posterior shoulder tightness. J Orthop Sports Phys Ther. 2007 Mar;37(3):108-14. doi: 10.2519/jospt.2007.2337. PMID: 17416125. ↩︎
  7. Salamh PA, Kolber MJ, Hegedus EJ, Cook CE. The efficacy of stretching exercises to reduce posterior shoulder tightness acutely in the postoperative population: a single blinded randomized controlled trial. Physiother Theory Pract. 2018 Feb;34(2):111-120. doi: 10.1080/09593985.2017.1376020. Epub 2017 Sep 13. PMID: 28901811. ↩︎
  8. Tahran Ö, Yeşilyaprak SS. Effects of Modified Posterior Shoulder Stretching Exercises on Shoulder Mobility, Pain, and Dysfunction in Patients With Subacromial Impingement Syndrome. Sports Health. 2020 Mar/Apr;12(2):139-148. doi: 10.1177/1941738119900532. Epub 2020 Feb 4. PMID: 32017660; PMCID: PMC7040949. ↩︎
  9. Wu T, Song HX, Dong Y, Li JH. Ultrasound-guided versus blind subacromial-subdeltoid bursa injection in adults with shoulder pain: A systematic review and meta-analysis. Semin Arthritis Rheum. 2015 Dec;45(3):374-8. doi: 10.1016/j.semarthrit.2015.05.011. Epub 2015 May 21. PMID: 26590864. ↩︎
  10. Codman, EA. “The Shoulder: Rupture of the Supraspinatus Tendon and other lesions in or about the subacromial bursa”. 1934 ↩︎
  11. Sher JS, Uribe JW, Posada A, Murphy BJ, Zlatkin MB. Abnormal findings on magnetic resonance images of asymptomatic shoulders. J Bone Joint Surg Am. 1995 Jan;77(1):10-5. doi: 10.2106/00004623-199501000-00002. PMID: 7822341. ↩︎
  12. Tempelhof S, Rupp S, Seil R. Age-related prevalence of rotator cuff tears in asymptomatic shoulders. J Shoulder Elbow Surg. 1999 Jul-Aug;8(4):296-9. doi: 10.1016/s1058-2746(99)90148-9. PMID: 10471998. ↩︎
  13. Hyvönen P, Lohi S, Jalovaara P. Open acromioplasty does not prevent the progression of an impingement syndrome to a tear. Nine-year follow-up of 96 cases. J Bone Joint Surg Br. 1998 Sep;80(5):813-6. doi: 10.1302/0301-620x.80b5.8533. PMID: 9768891. ↩︎
  14. Kartus J, Kartus C, Rostgård-Christensen L, Sernert N, Read J, Perko M. Long-term clinical and ultrasound evaluation after arthroscopic acromioplasty in patients with partial rotator cuff tears. Arthroscopy. 2006 Jan;22(1):44-9. doi: 10.1016/j.arthro.2005.07.027. PMID: 16399460. ↩︎
  15. Kuhn JE, Dunn WR, Sanders R, An Q, Baumgarten KM, Bishop JY, Brophy RH, Carey JL, Holloway BG, Jones GL, Ma CB, Marx RG, McCarty EC, Poddar SK, Smith MV, Spencer EE, Vidal AF, Wolf BR, Wright RW; MOON Shoulder Group. Effectiveness of physical therapy in treating atraumatic full-thickness rotator cuff tears: a multicenter prospective cohort study. J Shoulder Elbow Surg. 2013 Oct;22(10):1371-9. doi: 10.1016/j.jse.2013.01.026. Epub 2013 Mar 27. PMID: 23540577; PMCID: PMC3748251.  ↩︎
  16. Burns WC 2nd, Whipple TL. Anatomic relationships in the shoulder impingement syndrome. Clin Orthop Relat Res. 1993 Sep;(294):96-102. PMID: 8358951. ↩︎
  17. Nicholson GP, Goodman DA, Flatow EL, Bigliani LU. The acromion: morphologic condition and age-related changes. A study of 420 scapulas. J Shoulder Elbow Surg. 1996 Jan-Feb;5(1):1-11. doi: 10.1016/s1058-2746(96)80024-3. PMID: 8919436. ↩︎
  18. Liotard JP, Cochard P, Walch G. Critical analysis of the supraspinatus outlet view: rationale for a standard scapular Y-view. J Shoulder Elbow Surg. 1998 Mar-Apr;7(2):134-9. doi: 10.1016/s1058-2746(98)90223-3. PMID: 9593091. ↩︎


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