| Clinical Orthopaedics and Related Research |
| © The Association of Bone and Joint Surgeons 2008 |
| 10.1007/s11999-007-0105-3 |
| (1) | Clinical Orthopaedics and Related Research, 1600 Spruce Street, Philadelphia, PA 19103, USA |
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Richard A. Brand Email: dick.brand@clinorthop.org |
Received: 23 October 2007 Accepted: 17 December 2007 Published online: 10 February 2008
“Based on the…observations, one can reasonably construct the natural history of periarthritis of the shoulder. It is apparent that aging is an important etiological factor, and with aging certain changes take place in the connective tissue elements of the musculotendinous cuff…it is also apparent that in slowly developing lesions of this nature compensating adjustments in the mechanics of the joint take place so that severe alterations in the mechanics of the joint do not appear. However, one must admit that such a joint is very vulnerable and, if subjected to minor trauma, the existing degenerative lesion would be extended and aggravated.”
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| 2. | DePalma AF. Origin and comparative anatomy of the pectoral limb. In: DePalma AF, ed. Surgery of the Shoulder. Philadelphia: JB Lippincott; 1950:1–14. |
| 3. | DePalma AF. Recurrent dislocation of the shoulder joint. Ann Surg. 1950;132:1052–1065. |
| 4. | DePalma AF. Diseases of the Knee: Management in Medicine and Surgery. Philadelphia, PA: JB Lippincott Company; 1954. |
| 5. | DePalma AF. The Management of Fractures and Dislocations—An Atlas. Philadelphia: WB Saunders Company; 1959. |
| 6. | DePalma AF. Surgical anatomy of the rotator cuff and the natural history of degenerative periarthritis. Surg Clin North Am. 1963;43:1507–1520. |
| 7. | DePalma AF. A lifetime of devotion to the Janus of orthopedics. Bridging the gap between the clinic and laboratory. Clin Orthop Relat Res. 1991;265:146–169. |
| 8. | DePalma AF, Rothman RH. The Intervertebral Disc. Philadelphia: WB Saunders Company; 1970. |
| 9. | Derkash RS. History of the Association of Bone and Joint Surgeons. Clin Orthop Relat Res. 1997;337:306–309. |
| 10. | Harris WH. Traumatic arthritis of the hip after dislocation and acetabular fractures: treatment by mold arthroplasty. An end-result study using a new method of result evaluation. J Bone Joint Surg Am. 1969;51:737–755. |
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A survey of the literature on the pathogenesis of recurrent dislocation of the shoulder reveals that there is total lack of agreement on the causative factors responsible for this lesion. It is interesting to note that most investigators, when considering the pathology of this disease, fail to evaluate the glenohumeral joint in its entirety but rather restrict themselves to some local irregularity observed in the labrum glenoidale, fibrous capsule or head of the humerus. Another observation that is outstanding by its very inconsistency is that these same workers believe and teach that stability of the glenohumeral joint is directly dependent upon the surrounding intricate muscular apparatus that motivates it; yet, when a state of instability exists, local defects in other components of the joint are credited as causative agents.
Bankart stoutly defends his belief that the pathology in all instances is either a detachment of the labrum from the anterior glenoid brim or a tearing away of the capsule from the labrum. He goes so far as to express the view that the recurrent lesion is a different entity from the ordinary acute traumatic dislocation. The recurrent lesion, according to his view, is invariably an anterior dislocation which tends to recur because the fibrocartilaginous labrum fails to re-attach itself to the glenoid margin. The acute traumatic lesion is an inferior dislocation, the head being forced through a rent in the fibrous capsule which heals readily to bone, thereby preventing recurrences. These features of the morbid anatomy of recurrent dislocation were recorded by Broca and Hartman as far back as 1890. These observers also noted a defect on the posterior aspect of the humeral head which they believed facilitated intracapsular subluxation of the head of the humerus.
Some observers are convinced that defects in the humeral head are capable of producing dislocation and believe that the frequency of the dislocation depends upon the size of the humeral defect. As the defect increases in size, the tendency to dislocation becomes greater.
The great discrepancy in the etiologic factors responsible for the lesion, and the lack of uniformity in the surgical principles employed to effect a cure, prompted this investigation. Observations noted herein lead one to conclude that the local pathologic abnormalities recorded above are not the true causative agents, and that many of the surgical procedures performed to cure this malady are based on erroneous interpretations of normal or variational anatomy. Moreover, this investigation provides an explanation for the numerous failures which occur in procedures utilizing the principle of suspension to effect a cure, and for the success of those procedures which shorten the structures on the anterior aspect of the glenohumeral joint. The conclusions arrived at in this investigation are based on: (1) a study made on 36 recurrent dislocating shoulders. These shoulder joints were thoroughly explored and all abnormalities of the inside of the glenohumeral joint recorded; (2) gross and microscopic observations noted in 88 shoulder joints explored postmortem of 44 individuals ranging in age from 18 to 79 years who, prior to their death, gave negative histories and showed no clinical evidence of dysfunction of the shoulders; (3) determination of the range of external rotation of the arms in 800 normal individuals, 100 for each decade, from the first to the eighth inclusive; and (4) a postoperative end-result survey of 23 recurrent dislocating shoulders treated by the Magnuson (modified) procedure, the shortest interval since operation being 17 months, the longest three and a half years.
It becomes apparent that it is impossible for the head to pierce the capsule in the anterior portion of the joint unless it is forced through a rent below the subscapularis muscle. The head, therefore, in recurrent dislocations lies within the subscapularis recess or recesses, which are stretched to accommodate it. Both the middle and inferior glenohumeral ligaments may be the only feeble barriers to dislocation.
Thirty-six individuals provided the 36 recurrent dislocating shoulders studied; there were 35 males and one female; the age ranged from 18 to 36 years.
An observation of considerable significance was the pronounced laxity of the musculotendinous cuff in all cases. It appeared as if the short rotators were unduly stretched and lacked normal tonicity. Mild traction in all instances, with the cuff intact, readily separated the articulating surfaces of the humeral head and glenoid cavity. Such laxity in the musculotendinous cuff is not demonstrable in normal shoulders even under deep anesthesia.
Varying degrees of erosion and eburnation were found on the anterior lip of the glenoid fossa in cases in which there were labral detachments. In one instance a large irregular defect was demonstrable, leading to the conclusion that a fragment of bone had been sheared away from this area (Fig. 7b). Some osteophytes were observed on the anterior surface of the neck in three cases with extensive labral detachment.
It was interesting to note that the alterations noted above in the labrum glenoidale, fibrous capsule, and glenoid cavity did not essentially differ from the degenerative lesions observed in normal shoulder joints. Also, the lesions found in the normal shoulders were identically the same, in the respective decades, as those discernible in the aforementioned investigation, Variational Anatomy and Degenerative Lesions of the Shoulder Joint, a study conducted on cadavers on which no medical histories or physical examination prior to death were available.
Both the biceps tendon and the glenohumeral ligaments blend with the fibers of the labrum; any traction on these structures will tend to tear away the labrum from its bony anchorage on the glenoid (Fig. 1). Comprehension of this mechanism is facilitated by the knowledge that the glenohumeral ligaments act as check reins to external rotation of the limb. It becomes apparent that during normal joint function distracting forces are acting constantly on the labrum through the medium of the biceps tendon and glenohumeral ligaments; these forces achieve, gradually, separation of this triangular fibrocartilage from its bony attachment.
Progressive fibrosis of all capsular tissues, followed by restriction of external rotation, provides an explanation for the following clinical facts, namely, that recurrent dislocation of the shoulder is seldom encountered after the fourth decade and that the malady is a self-limiting disease. Many instances are known of individuals who had in early life numerous recurrences which, with out treatment, steadily decreased in frequency as the individual approached middle life; finally no more occurred. In other words, nature’s method of curing the disease is by producing scarring and fibrosis of the soft tissues sufficient to limit markedly external rotation.
Another observation of significance is that in those decades in which labral detachments are most frequent and most severe (after the fourth decade) recurrent dislocations are rarely encountered. In the light of these observations one is forced to conclude that local lesions such as labral defects and tears in the capsule and defects in the humeral head are not the causative agents of the disease, that a true Bankartian lesion does not exist, and that some other disorder is the responsible agent.
Capsular, labral lesions and humeral head defects are not the prime causative agents of recurrent dislocation; they are changes associated with ageing but may be produced or aggravated by trauma. Neuromuscular imbalance, chiefly of the short rotator muscles, is the most single important causative factor. Such a neuromuscular state follows severe stretching of and direct injury to the involved muscles, particularly the subscapularis muscle, at the time of injury. Pronounced capsular stretching and enlargement of the bursal recesses to accommodate the head are secondary adaptive changes. Repeated dislocations increase the neuromuscular imbalance, hence increasing the tendency to recurrences until nature overcomes the laxity of all tissues by a progressive process of fibrosis which limits external rotation and stabilizes the glenohumeral joint.
If the aforementioned concept of the pathogenesis of recurrent dislocation is accepted, it becomes apparent that such a complication may follow any initial mechanism of anterior dislocation, provided the short rotators, particularly the subscapularis muscle, are severely stretched and traumatized, and if the primary dislocation has not been adequately treated. I am in total disagreement with Bankart’s postulate that recurrent dislocation is a different lesion than ordinary acute traumatic dislocation and that it can occur only in the presence of capsular or labral detachment.
Capsular and labral lesions, as well as defects in the humeral head, have been given an undeserved place of importance in the pathology of recurrent dislocation, because it has been clearly revealed in this study that they are normal degenerative changes associated with wear and tear and senescence—although it must be admitted that trauma plays a part in their formation.
A survey of the many operative procedures devised for re-dislocation reveals that the essential feature which affects a cure is restriction of external rotation. Regardless at what region of the glenohumeral joint, or at what components of the joint the operative attacks are aimed, limitation of external rotation will effect a cure in the great majority of cases. This is also nature’s method of eliminating the disability. Therefore, the simplest procedure which will bring about restriction of the arc of external rotation will eventually be uniformly adopted.
Magnuson points out that by the transference of the subscapularis tendon to the greater tuberosity a musculotendinous sling or cup is formed around the humeral head in both external and internal rotation which counter-balances the powerful pull of the adductor muscles (pectoralis major, latissimus dorsi, and teres major) which tend to force the head downward and forward. We are of the opinion that the Magnuson procedure properly performed will supplant all other operations.
The Magnuson procedure was modified in order to increase the efficiency of the musculotendinous sling. This has been accomplished by transferring the subscapularis tendon across the bicipital groove and anchoring it at a lower level than its original insertion onto the humeral shaft.
The greater tuberosity is visualized by internal rotation of the arm. The subscapularis is then pulled, by means of a suture through its substance, across the bicipital groove to a point below the greater tuberosity and its site of reattachment is determined. The tendon should be anchored to the humeral shaft below the level of its original insertion, under moderate but not severe tension. With a thin osteotome a slot one-quarter inch wide and as long as the width of the subscapularis tendon is made parallel to the posterior lip of the bicipital groove below the greater tuberosity. Four drill holes are then made in the posterior lip of the newly formed slot and the end of the tendon is buried in the bony trough with silk mattress sutures. The upper border of the subscapularis muscle is approximated to the supraspinatus muscle by side-to-side sutures, while its lower border is sutured to the capsular tissues under the head of the humerus.
Considerable restriction of external rotation is demonstrable at the completion of the procedure. The subscapularis muscle and tendon fibers can also be seen to form a sling under the head, on abduction of the arm in internal and external rotation. The procedure is completed by wound closure in layers with interrupted sutures.
For the first two weeks, the arm is fixed to the side with the forearm across the chest by a Velpeau dressing. For the next two weeks the arm is kept in a sling. Motion is then begun but not permitted above the horizontal plane for two more weeks. Forceful external rotation during this period is prohibited, but full resumption of all motions should be attained by the eighth week. As a rule, abduction is restricted a few degrees and external rotation may be restricted as much as 50 per cent. This, however, produces no functional disability and is assurance against re-dislocation. The amount of external rotation lost is but a small price to pay for the cure of such a disabling malady by so simple a surgical procedure.
Analysis by many observers of the different types of operations performed discloses that the Bankart and Putti-Platt procedures give a high percentage of cures while the Nicola and Henderson operations result in a high percentage of failures. Adams recorded the following data in III cases under observation not less than two years from the time of operation. Re-dislocation occurred in 21 (36 per cent) of 59 cases, in which the Nicola operation was employed; in two of 37 cases in which the Putti-Platt operation was done and in one of 18 cases in which the Bankart procedure was performed. Leeds reported recurrences of dislocation in nine out of 13 cases treated by the Henderson operation. Re-dislocation occurred in all cases in which the sling was constructed of fascia lata and in four of seven cases in which the tendon of the peroneus longus muscle was used as a sling.
|
Name |
Sex |
Age |
Date operation |
Number recurrences |
Pain |
Satisfied |
|---|---|---|---|---|---|---|
|
C.F. |
M |
28 |
5/26/48 |
1 |
Yes |
No |
|
R.M. |
M |
23 |
11/22/47 |
0 |
No |
Yes |
|
R.C |
M |
30 |
5/30/48 |
0 |
No |
Yes |
|
G.H. |
M |
24 |
10/3/47 |
0 |
Occasionally |
Yes |
|
W.M. |
M |
24 |
6/28/48 |
0 |
No |
Yes |
|
A.A. |
M |
23 |
2/30/48 |
0 |
No |
Yes |
|
M.K. |
M |
21 |
3/21/48 |
0 |
No |
Yes |
|
E.H. |
M |
22 |
4/29/48 |
0 |
No |
Yes |
|
J.C. |
M |
29 |
6/25/48 |
0 |
No |
Yes |
|
J.F. |
M |
26 |
7/30/48 |
0 |
No |
Yes |
|
W.V. |
M |
20 |
7/19/48 |
0 |
Yes |
Yes |
|
A.V. |
M |
25 |
8/24/48 |
6 |
After dislocation |
No |
|
W.S. |
M |
21 |
3/3/48 |
0 |
No |
Yes |
|
J.N. |
M |
18 |
11/15/47 |
0 |
No |
Yes |
|
T.J. |
M |
36 |
8/4/48 |
0 |
No |
Yes |
|
D.L. |
M |
17 |
5/21/45 |
0 |
No |
Yes |
|
W.B. |
M |
30 |
1/21/48 |
0 |
No |
Yes |
|
C.M. |
F |
29 |
3/26/48 |
0 |
Slight |
Yes |
|
J.C. |
M |
19 |
8/24/47 |
0 |
No |
Yes |
|
L.B. |
M |
33 |
6/12/47 |
0 |
No |
Yes |
|
T.N. |
M |
22 |
8/18/46 |
0 |
No |
Yes |
|
D.O. |
M |
29 |
10/15/47 |
0 |
No |
Yes |
|
J.N. |
M |
22 |
2/23/48 |
0 |
No |
Yes |
|
Analysis of cases: |
||||||
|
Total number of cases |
23 |
|||||
|
Age range |
17 to 33 years |
|||||
|
Males |
22 |
|||||
|
Females |
1 |
|||||
|
Recurrences of dislocation |
2 cases (8.7 per cent) |
|||||
|
Pain present in |
2 cases |
|||||
|
Not satisfied with operation |
2 |
|||||
|
Satisfied with operation |
21 |
|||||
|
Period of observation |
17 months to 3½ years |
|||||
Success of the modified Magnuson and Bankart procedures can be directly attributed to the known restriction of external rotation which is achieved by these operations. Failure of the Henderson operation can be explained on the basis that it fails to limit external rotation while the high percentage of failures occurring in the Nicola procedure results from failure to restrict external rotation and pulling away of the labrum from the glenoid rim when the weight of the extremity acts upon it through the medium of the proximal end of the biceps tendon which now functions as a suspensory ligament.
| 1. | Local lesions of the labrum glenoidale, fibrous capsule, glenoid cavity, and humeral head are not the causative agents responsible for recurrent dislocation of the shoulder. |
| 2. | These lesions are observed in normal shoulders and are manifestations of wear, tear, and senescence. |
| 3. | Trauma does play a role in their formation. |
| 4. | They occur most frequently and exhibit the greatest severity in decades in which recurrent dislocations are seldom encountered. |
| 5. | Recurrent dislocation of the shoulder is a self-limiting disease; nature affects a cure by a progressive process of fibrosis which restricts external rotation. |
| 6. | Operative procedures which mimic this mechanism are favored by a high percentage of cures; those that do not, result in a high percentage of failures. |
| 7. | The modified Magnuson operation is offered as a simple and effective method to achieve the desired restriction of external rotation. |