Shoulder:Rotator Cuff Pathology/Rotator Cuff Tendinopathy
What would Codman have thought about this?
The pathology of the subacromial bursa and...
CHAPTER III THE PATHOLOGY OF THE SUBACROMIAL BURSA AND OF THE SUPRASPINATUS TENDON
I DO NOT propose to review in detail the pathology of such general conditions as tuberculosis and syphilis, which, of course, may occur in this region, but merely to attempt to describe such pathologic changes as I have myself seen at operation in about two hundred explorations of the bursa on living patients. I have kept no record of the number of times I have studied the bursa in the cadaver, but I am sure I have opened over five hundred subacromial bursae, perhaps a thousand. It is significant that most of the pathological changes which I have noted had not been previously described, at least, so far as this particular bursa is concerned; and, per contra, the conventional pathologic conditions, such as suppurative inflammation, "rheumatic changes," syphilis, tuberculosis, new growths, etc., have seldom been observed by me. In the shoulder these lesions are relatively rare. On the other hand, lesions peculiar to this region are so often present that I have observed some of them in probably one-third of all the bursae I have examined in the dead, and, of course, in nearly all of the living cases. Fortunately, within the last few years, I have had the privilege of studying a much more systematic series of observations made by Dr. I. B. Akerson of the pathologic staff of the Harvard Medical School and pathologist to the Long Island Hospital of the Institutions Department of the City of Boston. We have published together in the Annals of Surgery for January, 1931, an article on "The Pathology Associated with Rupture of the Supraspinatus Tendon." The following quotation is from this paper: "The present study has been made from autopsy material obtained at a large municipal hospital for chronic conditions. The patients sent to this hospital are people who are aged and down-and-out, and owing to the chronic character of their diseases, cannot be cared for at the other Boston hospitals. Dr. Akerson has made a study from one hundred specimens taken from fifty-two consecutive autopsies, and the percentage of cases showing evidence that the supraspinatus tendon had been ruptured at some time during the lives of these patients is high—39%. It may, therefore, be taken as a maximum, and it may be expected that pathologists performing routine autopsies in general hospitals for acute diseases, where the ages average considerably younger, will find a decidedly smaller percentage. We have made no attempt to correlate the past histories of these patients as to trauma or occupation with the autopsy findings. It would have been hardly possible under the circumstances. "As a routine method of examination of these cases, we recommend the pathologist to employ the form of incision which we use in operations on the living. A cut is made on the anterior aspect of the shoulder joint from the acromio-clavicular articulation downward for about two inches. The fibers of the deltoid are separated and retracted and the roof of the bursa is incised between two pairs of forceps as one opens the peritoneum. When the lips of the wound are retracted, the surface of the floor of the bursa can be made to pass in review by rotating the humerus. The base of the normal bursa is smooth and spherical and almost as colorless as the cartilaginous surface of the head of the bone, though it lacks the bluish luster of cartilage. Most rents in the tendons of the short rotators usually appear in this base as communications directly into the joint and are readily visible. Occasionally the tendon is ruptured beneath the base of the bursa, which is left intact. In the ordinary autopsy it would take but a few minutes' extra time to examine both bursa. If lesions are found, the head of the bone with the insertions of the short rotators can be removed and studied. This was the method used by Dr. Akerson and his findings are good evidence that some sort of pathological process has been at work in the subacromial bursae of these patients during their lifetime. One must understand that these findings are those accumulated by each individual subject in many years. They are end-results, not acute lesions." Dr. Akerson has continued his observations and at the present date (January, 1933) has recorded his findings on 200 shoulder joints in 102 subjects. I am greatly indebted to him for the opportunity of studying this material and the many microscopic sections he has made from it.
It seems best to list under five headings the pathologic conditions which may be found at autopsy or at operations on the living: Changes occurring: (A) In the bursa itself; (B) In the musculotendinous cuff itself; (C) In the tuberosities; (D) Within the joint; (E) When the musculo-tendinous cuff has been ruptured so that a free communication has been established between the joint and the subacromial bursa.
- In four of these cases the tendon was not found (i.e., had retracted).
A. CHANGES WITHIN BURSA
Normally the incised roof of the bursa is as thin or thinner than the peritoneum,- but when acute or chronic inflammation is present it may be as thick as blotting paper. It is apt to be especially firm in old, chronic cases of complete rupture of the cuff, when fluid is present. Normally it is transparent and film-like. In acute cases it may be opaque and reddish in color. In chronic cases it is whitish and firm.
(1) The roof of the bursa seldom shows any pathology, but in cases of long-standing bursitis from complete rupture of the supra-spinatus, one frequently sees by X-ray, or one can palpate from within the bursa, hypertrophic changes at the acromial edge. Such changes may also be found in muscular laborers without symptoms. (2) Calcified material in the bursa. Calcified deposits do not form in the bursa, but in the tendons. They may remain in the tendon substance for years, but the usual sequence of events is that they gradually work through to, or enlarge enough to reach, the base of the bursa, where they produce a mound-like swelling resembling a little boil, with a white center and a turgid zone about it. Up to this time there may have been no symptoms or very slight ones. Then some slight accident or unusual effort or even some customary action, as in turning over in bed, causes tension in the tendon resulting in rupture of a few superficial fibers, so that the little crater discharges into the bursa, where the calcified particles at once become diffused and may be readily delineated by the X-ray. An acute bursitis is produced; fluid is secreted with which the calcified particles mingle; fibrin appears and the specks of calcium become entangled in it. I have several times operated at this stage within a few days of the perforation and removed from the bursa a delicate film of fibrin shaped like a watch glass. Grossly the film is whitish in color and the microscope shows calcified particles scattered throughout its substance like stars in the sky.
FIGURE 34. PEFORATION INTO BURSA Diagrammatic illustration of a calcified deposit bursting into the subacromial bursa. This should be compared with Fig. 4 in Plate II, which was taken from the case alluded to below.
Soon after the material is thus forced into the bursa and becomes enmeshed in fibrin, the particles are rapidly eliminated, probably by the prompt action of leucocytes. This is not the case while they still remain in the tendon. When the operation on these cases was within a few days of the perforation, I have been able to readily remove the film of fibrin almost intact, but in one case, on the sixth day after perforation, I found the film so firmly adherent that no attempt was made to remove it, because I should have had to use a curette and feared that I might destroy the membrane and get obstinate adhesions in its place. Through the kindness of Dr. H. F. R. Watts, who followed the patient with weekly X-ray pictures, I found that absorption of all the calcified material took place within three weeks of the perforation. The patient was then free from symptoms. I was encouraged in making this decision in this case by the fact that I had previously had a number of cases in which rapid disappearance of the particles had taken place without any operation. I now feel that perforation is nature's method of getting rid of this condition and that the average case, where perforation into the bursa has occurred, if left entirely to nature without any treatment, would follow this course. I think this fact accounts for the encouraging results sometimes obtained by all sorts of treatment, whether diathermy, foreign proteids, alpine lamp or surgery. This favorable course is not always the outcome, however. The inflammatory reaction may be too intense, and adhesions and consequent "frozen shoulder" result. It may be months before the adhesions loosen and full motion returns. Sometimes the whole deposit is not discharged into the bursa and the residue may give trouble later. Under this heading we have discussed only the bursitis caused by the perforation of the calcareous material into the bursa. The study of the deposits themselves will be taken up again under Section B. (3) Defects in the base of the bursa. These defects are nearly always at the same critical point, almost in the center of the base, where the red zones, calcified deposits and "straps" occur. The description of these defects properly belongs under the next division of our subject, for they consist of lesions of the tendon itself, whether partial or complete. Should the reader undertake to verify my statements by observing the conditions found by incising the bursa in a series of autopsies, he will be surprised at first by the variety of appearances which tears in the tendons may cause. After he has seen the inside of fifty or a hundred bursae, the secondary appearances due to the synovitis set up by the lesion will cease to distract him and his surprise will then consist in seeing how much alike the fundamental lesions are. In other words, the superficial appearances of these defects vary with the extent of the rupture, the amount of joint cartilage exposed through the rent, the position of the lesions, the proliferation of the adjacent membrane, the extent of exposure of the biceps tendon, the degree of involvement of the adjacent tendons, the duration since the accident, the extent of formation of a falciform edge, the amount of recession or hypertrophy of the tuberosity, etc. Yet after sufficient experience, rupture of the tendon of the supraspinatus will be seen to be the basis of almost all the lesions. His chief doubt will be as to whether degeneration of the tendon always precedes rupture, although he will be convinced that rupture has certainly occurred whether the tendon was previously sound or senile in texture. (4) Synovial villi. These are the most common evidence of pathology one encounters in the bursa itself. It is difficult to say that a given degree of roughening of the serosa is abnormal. Is callus on the palm pathologic? It may be that in the same way some of these villi represent overuse rather than inflammation. On opening the bursa one sees strands of filmy tissue crossing the space after the air has been let in. Sometimes instead of being attached at their ends to both floor and ceiling, one end will be free so that the capillary villous will drift about in the bursa. In such cases the whole floor of the bursa is apt to be velvety with lesser villi and thickened nictitating folds. The center of this process is usually over the attachment of the supraspinatus to the tuberosity. In fact, this point seems to be the locus minoris resistentia of this bursa. We seldom find lesions of any kind in which this point is not involved. It seems to be the place where there is the most mechanical stress. It is here that the supraspinatus is at the greatest disadvantage in overcoming inertia in starting the upward motion of the arm. The sudden contraction of the deltoid may jam this point on the acromion or coraco-acromial ligament if the supraspinatus is not on the qui vive. Here also would come the greatest friction in occupations requiring repeated elevation of the arm. At any rate, lesions of the bursa as a rule are found on the base at this point. I have recorded none on the roof except a general synovial thickening. There is a vast difference in the appearance of these synovial villi in life and after death. In life they are often pink or red, but in the cadaver they are limp and colorless and do not readily attract notice. In my opinion their presence is evidence that there has been inflammation and adhesion of the bursal surfaces, followed by resolution of most of the adhesions. They are probably homologues of pleural bands and are remnants of organized exudate. They are very frequently found and are to be expected in the bursas of the type of human being usually found in the dissecting room. (5) Bands. In a few cases at operation I have found thick, cord-like bands of fibrous consistency similar to the bands one frequently finds in the olecranon or prepatellar bursa. One very typical case was in a man who had for years climbed electric light poles, usually carrying heavy weights as he did so. A very painful, chronic bursitis with loud friction sounds developed. Excision of the bands restored normal use of the arm. Such cord-like bands are relatively uncommon in this bursa although frequently found in the prepatellar bursa. They must not be confused with the film-like synovial villi spoken of above, nor with the " straps " alluded to under No. 9. (6) The normal nictitating folds formed by double layers of the movable periphery and described in Chapter I, page 27, may become inflamed and swollen. I have occasionally seen them bright red, resembling inflamed conjunctiva. They are sometimes the sole cause of a mild, chronic, non-adherent bursitis, giving intermittent, elusive symptoms such as twinges in certain motions. (7) Adhesions. As stated previously, I have come to believe that the bursa, like the peritoneum, possesses the function of rapidly forming protective adhesions to confine inflammation, and also the ability to absorb them and thus restore, in whole or in part, the mobility of the adjacent tissues. For instance, the diaphanous folds which often partially separate the subacromial and subcoracoid portions of the bursa may, when inflammation arises in one portion, wall off the affected part after the manner of water-tight bulkheads in a modern steamer. It is not uncommon to find blotches of calcareous deposit, which have escaped into the bursa, thus localized. In my experience adhesions never occur in the strictly subacromial portion of the bursa, and are most common in the subdeltoid portion and in the fold partially separating this from the subcoracoid portion. They are seldom very dense in any situation. They are always absorbed or rendered pliable in time by nature's own processes. Frozen shoulders from this cause invariably recover. I have probably relieved the minds of more patients by this assurance than by my best operative efforts on their bodies. (8) A slight amount of fluid in the bursa may occur in any acute or chronic bursitis, but if on opening the bursa and abducting the arm, a large amount, i.e., several drams spurt out, one may be quite confident that the supraspinatus is ruptured and that there is a free communication between joint and bursa. As in other joints where there is synovitis, we may assume that nature supplies this fluid to reduce friction. (9) Straps. These are damaged tendon fibers. One sees just over the supraspinatus insertion a circular area about an inch in diameter, which seems to be worn as if from friction. It is ragged and frayed. On close inspection there is a thin strap of fibers running in the same direction as the supraspinatus fibers and really composed of tendon tissue. The strap is perhaps a half inch square, attached above and below to the supraspinatus and lying on it or in it, but separated from it by a space. It is usually separable into a half dozen parallel strands. It can be lifted up except where it is attached at its two ends and perhaps by filmy material on its sides. It is very thin but quite firm. I have not been able to make out positively whether these lesions are caused by friction and consequent inflammation, or are remnants of the effect of the discharge of a calcified deposit in years gone by, or are the results of partial ruptures. If you abduct the arm this little strap will buckle up off the tendon on the top of the greater tuberosity like an inch worm. Section of such a case showed that the deeper parts of the tendon were a series of such "straps" on a smaller scale. The tendon seemed to be split in layers. Dr. Akerson is studying a series of normal supraspinatus tendons at different ages and has kindly allowed me to have some of his sections. At all ages there appears to be a tendency for the tendon fibers to lie in loosely attached planes or laminations parallel to the joint surface as in Fig. 9. In the pathologic tendon these rifts or separations become complete and "straps" are formed. One receives the impression that normally these bands of tendon may each in turn take the maximum strain as the arm is elevated. Also that any one of them singly may tear or evulse from the denser portion of the attachment. (10) A deep red, more or less circular zone of turgid membrane lying on the base of the bursa in the region of the supraspinatus facet is a not uncommon finding in the class of cases described on page 216 as tendinitis. Often this zone has a whitish central area which corresponds to the portion of the tendon just proximal to its insertion. The calcified deposits are usually surrounded by similar red, circular zones. Those referred to under this heading differ, because no white deposit is obtained when the whitish area is incised with the point of a knife, nor does any show in the X-ray. In one such case after puncture with the knife a few little rice-like grains of material popped out through the opening. Under the microscope the rice bodies appeared to be bits of necrotic tendon. In another case a little fluid came out under tension. In several other cases I have excised bits of tendon and found invariably the peculiar degenerated condition illustrated in Plate VI. It will be more appropriate to consider the cause of this condition in the tendon under heading B. The point which I wish to make under this heading is that the red, circular zones are visible from the bursa in both these cases and in the calcareous cases. The deep red, circular zone seen on the base of the bursa is due to congestion of the subsynovial vessels. It is very superficial and does not extend into the tendon, which itself is very anasmic. In fact, the gross appearance of the whitish center in both cases suggests there has been an infarction. The reader should refer in this connection to page 232.
B. CHANGES OCCURRING IN THE MUSCULO-TENDINOUS CUFF ITSELF
(1) Degeneration in the collagen of the tendinous fibers is so common that it is difficult to find in elderly subjects an example of normal tendinous substance. Even in the case which I have used as an illustration of the normal insertion of the supraspinatus (Fig. 9), a few of the fibers showed early changes. Fig. 5, in Plate VI, is taken from this case. It shows small areas of collagen which take a deep red stain with hematoxylin and eosin, and at first sight resemble muscle fibers. In practically all the bits of tissue which I have taken from the tendons at operation or from the specimens Dr. Akerson has examined, these same changes are found in some degree, whether the specimens came from tissue adjacent to calcareous bodies, partial or complete ruptures, or from the non-calcareous cases which I am disposed to call "tendinitis." Little pathologic work has been done on lesions of tendons in any part of the body, so there is not much in the literature to help us to interpret our findings. Indeed, there is little to say beyond the fact that hyaline degeneration occurs and is not accompanied by invasion of lymphocytes or leucocytes, or other usual inflammatorysigns. The degenerated areas vary greatly in their staining reactions, which may be as blue as cartilage or as red as muscle with hematoxylin and eosin. I am convinced that some of the central fibers of a tendon may tear without those which are superficial to it on the bursal side, or beneath it on the joint side, being ruptured. In one case in the living, I opened up a little cavity in the tendon which contained fragments of degenerated or necrosed fibers. There was no apparent opening from the cavity which contained these little bodies, either toward the joint side or the bursal side. They were not calcified. It seems to me highly probable that the calcareous deposits represent nature's failure to heal such internal lesions in the tendon. However, one might take the opposite view that central degeneration first took place; then fragmentation of the degenerated areas; still later calcification of the fragments; finally, discharge into the bursa and, soon after, absorption as described on page 69. We must at present confess that we do not know what the first step in the retrograde process is. It may be traumatic infarction, or perhaps due to a general toxic condition. It stands to reason that there must be a stage in the course of the calcified lesions just prior to the time when X-ray evidence can be obtained, when necrotic tendon fibers would be found without any calcium in them. Perhaps some day we shall be able to diagnose such cases, and by simply puncturing the tendon remove the tension and obtain prompt relief. This is certainly possible now as soon as the calcium is dense enough to show in the X-ray. In such cases the little cavity contains only a milk-white fluid. (2) Calcified deposits. These peculiar and interesting areas are probably the next most common lesions to villi, although in the dissecting room, partial ruptures of the supraspinatus will be found much more often. This is because the deposits are temporary and undergo natural absorption, leaving no evidence behind, unless perhaps defects in the tendons. Many partial and all complete ruptures, on the other hand, leave a permanent defect. In living patients the deposits are probably more common or at least more often diagnosed, because, when pronounced, they show in the X-ray. I am convinced, however, that many are small and escape notice, for I have seen some in very clear films which are not larger than a pin-head and others which cast but a faint shadow, easily missed if they had overlapped the contour of a bone. Many escape notice entirely and perhaps never give symptoms. Some are microscopic. (Plate VI.)
PLATE II. CALCIFIED DEPOSITS
Figure 1. The deposit appears to be double. The larger mass lies in the supra-spinatus tendon, while the smaller mass is in the portion of the infraspinatus tendon which lies, in part, anterior to it. (See Chapter I, Fig. 6.) The long diameter of the latter is probably perpendicular to the plane of the plate. The motions of this arm were free, and without symptoms, although the patient had acute symptoms in the other shoulder, shown in Fig. 2. Figure 2. The shadow of the deposit consists of a diffuse portion and a small dense portion. The diffuse portion was due to calcined material in the supraspinatus tendon, which had not yet perforated into the bursa, although it was on the point of doing so at the time of operation. It had infiltrated the substance of the tendon and muscle far beneath the acromion. In both shoulders the shadow of the deposit corresponds very well with the normal position of the tendon. The dense portion was probably in the infraspinatus. Figure 3. Shows a large, dense deposit in a patient with subacute symptoms, who still possessed a normal extent of motion in his shoulder joint, although he had acute pain during elevation when the mass impinged between the tuberosities and the acromion process. The calcified material had not yet escaped into the bursa, although the X-ray shows outlying specks of calcium in the superficial parts of the tendon. As is the case in most instances, the deposit was made up of small, dense masses. The tuberosity shows characteristic atrophy in the trabeculae. At operation in both this case and in that shown in Fig. 2, the floor of the bursa showed a red zone with a white center. Contrast these three figures with Figures 4 and 5, which show the bursa distended with the material. Figure 4. Should be compared with Fig. 34, for it shows a similar outline of the extruded particles. In some cases, e.g., Fig. 44, the lower portion of the bursa appears to be bilocular, the particles having accumulated by gravity in the fluid at the bottom of these pockets. One should understand that in these figures we detect merely the outline of the bursa, as if in section, but that in reality the bursa lies also in the antero-posterior plane and forms a concavo-convex cap over the tuberosities. Figure 5. As in the last case, one may be sure that the deposit has burst into the bursa if the bulk of the material shows external to the tuberosity in the unro-tated antero-posterior view. Figure 6. Illustrates a case alluded to in the text (p. 78) in which a second operation was done. There is a remnant of the deposit still left in the infraspinatus after the first operation, which was on the supraspinatus, but the long, oval deposit is in the subscapularis and was removed at the second operation. Compare this figure with another case where the deposit was in the subscapularis and is shown in the outline drawing, Fig. 43.
The deposits do not arise in the bursa itself, but in the tendons beneath it. Most instances occur in the supraspinatus tendon close to its insertion, but a considerable number are found in the tendon of the subscapularis and in the tendons of the infraspinatus and of the teres minor. I formerly did not identify them in these tendons. As will be seen later, one does not see these tendons in operating, and at first I contented myself with removing the deposit and making no particular effort to determine its exact situation. It took me some years to realize how easy it is to determine the situations of the tendons when operating by placing the arm in exactly the mid-position between external and internal rotation and palpating the bicipital groove. Since, after the bursa is opened, one usually has no difficulty in locating the deposit by the circle of blood-red congestion about its whitish or yellow center, it has seemed superfluous to ascertain which tendon contained it. I later learned that there might be two or more deposits each in a different tendon. In one patient failure to remove both at the first operation resulted in a second attack of acute symptoms and a second operation. On page 230 the importance of accurate X-ray localization is emphasized. The size of the deposit varies greatly, ranging from that of a pinhead to a shadow, two or three inches long, of the supraspinatus tendon and muscle as in Plate II. Such large shadows are very rare, and the deposit is seldom bigger than a lima bean. The consistency varies also and may be that of a milk-white fluid or of a hard, yellowish crystalline substance. Usually it closely resembles in color and consistency ordinary zinc ointment. Sometimes it is cheesy and yellowish, like the contents of a wen. In acute cases- it is not difficult to remove, but in some chronic cases of long standing it is very gritty and seems incorporated in the fibers of the tendon so that one cannot curette it all out without removing much semi-normal tendon with it. One sees whitish, stringy fibers in the little pit from which it is being removed. Sometimes it shells out very easily with a definite contour. In my own operations I have avoided removing any tendon, preferring to leave some of the deposit in the fibers, than to excise tendon which might return to normal and become of use in future function. Brickner has removed enough for sections, and Moschcowitz has studied them. Harbin has not hesitated to remove some tendon and reports good results in spite of this. On a few occasions I have found the deposit surrounded by a small amount of granulation-like tissue, largely composed of foreign-body giant cells, but in these eases the deposit had probably perforated into the bursa. Several times I have had careful chemical analyses made. Dr. James L. Stoddard made for me an analysis of the material from one of these cases. "The following report on the bursal deposit shows it to be a mixture of calcium phosphate, calcium oxalate, and organic matter, mostly fibrin. Gross: A pasty, white mass, in part blood tinged, springy and a little elastic on stretching, moist, with an extremely fine, even texture, and with no evident structural elements which hinder division at any point. Microscopic: Small ovoid colorless bodies, varying enormously in size. Some are at the limit of vision with an oil immersion lens, and show marked Brownian motion; all gradations exist up to bodies several times the diameter of a red cell. They are all the same in qualitative appearance. They are slightly refractive, less so than fat, have usually a somewhat irregular oval shape, but the edge is always smooth and even. Nothing but the bodies is visible in the specimen.
Chemical—Qualitative: No color with Sudan 3; hence not fat. Insoluble in acetic acid, alcohol or ether. Soluble for the most part in fairly strong HC1. On heating to yellow heat, chars, smokes, and burns briefly with a yellow flame, and gives a burnt feather odor. Leaves a gray ash.
Ash dissolves easily in weak acetic acid with evolution of C02, showing original substance to have contained oxalate. Gives no murexide test for uric acid. No test for cholesterol (Lieberman-Burchard test). Solution in strong KOH acidified with acetic acid gives off slight trace of H2S, detected on lead acetate paper. This is probably due to presence of fibrin, which also explains the consistency of the deposit. Solution of ash gives heavy phosphate test with ammonium molybdate. Chemical—Quantitative: A small sample of the deposit was ashed, weighed (weight 86 mg.), dissolved in HC1, filtered from char, ammonium oxalate added, the solution neutralized, and the precipitate analyzed quantitatively for calcium as in the blood calcium method (Clark's modification of the Kramer-Tisdall method). The filtrate was made acid with acetic acid, and a calcium acetate solution added to precipitate the excess oxalate which would interfere with the phosphate determination. The filtrate from this precipitation was analyzed for phosphate by the blood phosphate method (Brigg's modification of the Bell-Doisy method). "Result: Calculated back to Ca3(P04)2 and Ca204, H20 gives respectively: calcium phosphate 55.8%, and calcium oxalate 44.2% of the inorganic matter of the dried, unashed specimen. The amount of organic matter was not determined. Of the ash there was 14% not to be accounted for by figuring all the phosphate as calcium phosphate, and the remaining calcium as carbonate. Part or all of this 14% was due to char, and part may have been due to other inorganic matter (perhaps some magnesium salts, etc.). (The ashing was done at the lowest possible heat, but of course some of the calcium carbonate may have decomposed into oxide, which would raise a little the undetermined fraction.) One of the most interesting features is the peculiar microscopic appearance of the specimen, with this non-crystalline precipitate of fairly definite shape." Maxwell Harbin (Arch, of Surg., Vol. 18, No. 4, P. 1491, Apr., 1929) reports a case which from the X-ray film is very clearly a case of perforation of one of these deposits into the bursa. He made a rather extensive excision and gives the following report of the chemical analysis of the specimen, together with a low power photomicrograph. "The bursa, as well as the necrosed tendon (Fig. 8), was excised. It is of interest to note the considerable variety of earthy substances which exist in the necrosed tendon. Inorganic phosphates were present to a considerable degree. Calcium was easily discernible with a trace of calcium, iron, carbonates and chlorides. The specimen was composed of tough, white fibrous substance covered in certain areas by a cream-colored cheesy substance. A few grit-like particles were found in the cheesy material. Some hardened blood was present. Analysis of tissue removed from the supraspinatus tendon showed the following:
"The white fibrous substance was apparently dense fibrous connective tissue. The yellow cheesy substance was composed of fat, protein and a fair amount of calcium phosphate." Comment by E. A. C.: Confessedly Dr. Harbin had excised some tendon and fat, and the analysis was not made from the pure deposit as in my case. One of my assistants, Dr. T. W. Stevenson, made the following observations:
Study of a Calcareous Deposit
A little of the material was suspended in normal saline and observed under the microscope. Many small bodies of variable size, mostly round or oval in shape, were seen. The smallest were the size of bacteria or smaller and the larger ones were about the size of white blood cells. Scattered over the slide were many large, round or oval bodies 10-15 times the size of a white cell. They presented a peculiar appearance in that they were concentrically striated. The appearance resembled that of the gall stones pictured in MacCallum's Pathology. The center of these bodies is slightly clearer than the periphery. This central nucleus (?) resembles a white cell and is about that size. The concentric rings are very distinct, but two or three in each body are more pronounced than the others. When a little of the material was suspended in concentrated sodium hydroxide solution, the bodies were turned slightly more yellowish. The striations were more marked. No dissolution or other change occurred up to one hour.
Concentrated nitric acid caused no change. Glacial acetic acid caused no change. Thin smears were made and fixed by heat. They were stained and the following results noted: Gram's Stain: No organisms were seen. The calcareous bodies decolorized and were stained an even red with no striations visible. Methylene blue stained the bodies an even blue and concealed the striations. Ziehl-Neilson stain showed no acid fast organisms or bodies.
Stern of Cleveland has reported that these deposits are modified fat, but I can find no evidence to support his contentions. Dr. Robert Chambers was kind enough to investigate some of the small bodies for me with his dissecting microscope. He found, when he attempted to pull them apart, that they were quite elastic and sprang back to their original shape.
I have repeatedly made microscopic examinations of fresh specimens of the material removed and they always consist chiefly of the little, round and ovoid bodies above described. I have never succeeded in dissolving them in ether. Their real character remains a mystery to me, but I am satisfied they are not fat. Moschcowitz in 1915 said: "The calcification is present either in the form of discrete, sharply circumscribed, sand-like masses, embedded as it were in a cavity within the tendon; or as diffuse, finely granular masses, shading imperceptibly into the surrounding tissue structure; or as finely granular amorphous material, lying within the tendon or the granulation tissue." Concerning another case he said: "In no specimen was the slightest tissue reaction noted, in the form of round cell infiltration, granulation tissue or the formation of new blood vessels." It seems to me that the latter statement is more characteristic of the early uninflamed stages in the tendon when the trouble is forming and the bursa is not yet involved. The first description is that of a more acute case when the deposit has caused a reaction in the base of the bursa. It seems to me probable that new blood vessels, etc., proceed into the tendon from the synovia. In such cases, unless the bursa is involved, it is striking that blood vessels, lymphocytes and the usual microscopic phenomena of inflammation are lacking, and yet there is clear evidence of degenerative change. I hazard the suggestion that it may be found that tendon repair differs from the repair of other tissues in this respect; i.e., that necrosis must first proceed to a point where it involves an adjacent vascular tissue before vascularization will take place. Moschcowitz did not definitely state his opinion on the question of precedence of lesion or trauma, for he was evidently influenced by Brickner's belief that this calcification process was a prompt reaction to a trauma. My own belief is that the deposit has probably been present long before the trauma with which it is associated by the patient. Moschcowitz continues: "The necrotic tissue can have only two sources: (1) Degeneration of the blood and serum consequent upon the primary trauma. (2) The breaking down by coagulation necrosis of the tendinous structures." He excludes the first because there is no blood pigment; the tissue is too homogeneous and plastic in appearance; the line of continuity of the necrosed portions with the solid portions is a gradual one. He also states that it used to be generally accepted that calcification never occurs in any but dead or inert tissue, but that in consequence of recent experiments, which he quotes, it seems that calcification may be a matter of only a few days in areas rendered anaemic by tying arteries. Yet he says it does not follow experimental suture of tendons. It seems to me that we are indebted to Moschcowitz for the best statement of the pathologic findings, but that he has been too strongly influenced by Brickner's clinical belief that in these cases calcification is an immediate result of trauma. He also quotes me as believing this, but I do not recall that I ever did believe it, and I certainly did not state this in my writings. I did believe, and do still, that some slight injury, long before, may have pulled the fibers apart and started the process. Since tendons contain few blood vessels, evidence of hemorrhage is not required to support the likelihood of this theory. There are two other interesting points in Moschcowitz' paper. One is that he was unable to find in the literature of pathology that any effort had been made to study the minute pathology of these lesions. He was only able to find Wright's report (on one of my cases, and which I had quoted) and another by Wrede, which was inconclusive. The second is that he prophesies that since in other tissues where one finds calcification one eventually finds some ossification, we should presently find ossification in an instance of this lesion. I have not yet been able to find such an instance proved microscopically. One must not be deceived by bits of the tuberosity in a retracted supraspinatus tendon. Similar formations are sometimes found in other tendons, as in the quadriceps and the gluteus medius, and I know of one case in the flexor carpi ulnaris. Dr. .J. H. Wright told me that a similar pathologic process was found in the heart valves. The question of whether infection has anything to do with the condition has ceased to interest me, as I have always closed the wounds and have never seen even mild sepsis develop. Many times I took cultures which were always negative. Nor have I been able to definitely associate the condition with distant foci as evidence of toxaemia. Of course, many patients have bad teeth, but in no instance has there seemed to be any association, for as soon as the deposits are removed the patients promptly recover, whether the teeth have been extracted or not. In one instance extraction of a tooth was at once followed by acute symptoms in the shoulder, which soon subsided and disappeared altogether. However, I strongly recommend every patient with bad teeth to have them attended to, although I do not consider the causative connection scientifically established. There is no constitutional condition which I have associated with the lesions, for they occur in the lean or the fat, in the active or sedentary. My chief reason for believing that they are primarily due to trauma or overuse is that their pathology may best be accounted for on this hypothesis. Furthermore, I do associate them to some extent with occupation, for they occur in people who habitually use their arms in semi-abduction, as stenographers, accountants, machine operators and surgeons. I think that automobile driving may have a tendency to encourage this formation. In fact, any occupation or avocation which requires undue use of the abducted or elevated arm. (3) Defects due to ruptured supraspinous tendons. In spite of my known interest in the subject and the goodwill of many friends in active surgical practice, I have never seen, either on the operating or autopsy table, a fresh rupture of the supraspinatus tendon. It merely happens that no one recognizes these cases in time. I have seldom operated within three weeks after the injury, although I strongly believe in immediate operation. The earliest case was three days after the injury, and in this case, unfortunately, there had also been a prior one. Decided changes occur in the first few weeks, so that one finds the ends of the torn surfaces covered with fresh tissue which disguises the exact anatomic relations of the parts. However, experience in operating at varying intervals after the trauma, combined with dissections on the cadaver, has given me a fair idea of the method of healing which nature attempts. We must examine again the normal anatomy. The continuity of the semi-circular conjoined insertion of the four muscles (see p. 17) is interrupted by the groove for the biceps tendon which separates the two tuberosities and theoretically the insertions of the subscapularis and supraspinatus. The facets of insertion of these two muscles are widely separated in anatomic diagrams, but as a matter of fact, their common expansion bridges the groove and makes them continuous, although thin just over the groove. Ruptures almost always involve this portion over the groove and it is very often the internal limit of the rupture, which as a rule extends from this point outward, involving the portions of the cuff made up of the supraspinatus and part of the infraspinatus expansions. Occasionally the tear crosses the bicipital groove and involves the subscapularis portion of the conjoined tendon. In at least one dissecting room specimen the tear extended inward from the groove and involved the subscapularis portion alone. When one opens the bursa in these cases the biceps tendon may or may not be exposed, according to whether or not the tear extends across above the bicipital groove. It is usually to be found just under the edge of the inner side of the rent. If it is exposed it is seen as a bright pink band crossing the bluish surface of the shining articular cartilage. It is not only pink and inflamed looking, but may be twice its natural size. One finds that below and above the point where the biceps tendon is exposed by the retraction of the ruptured supra-spinatus, it is still of normal size and white and shiny. When not exposed, but lying just under the edge of the portion not ruptured, it is not abnormal looking. Frequently it cannot be found, for it has been torn off its attachment on the glenoid and has been pulled by its own muscle belly down into the bicipital groove. The proximal end sometimes sticks in the upper portion of the groove, and at other times retracts way down it and curls up in a coil just above the muscle belly. Occasionally it is found to be much frayed, which probably indicates repeated jamming between the head of the humerus and the acromion. Sometimes the frayed edges are adherent in the groove, and have little rice-like bodies attached to them. From what I have said about the cuff of conjoined tendon in which the tendons of each muscle and the capsule are welded intimately, and since ruptures always occur in this portion, it will be more readily understood that when I speak of any one tendon as rupturing I mean the portion of the cuff represented by that tendon. Since the gap of the rupture is held on each of its edges by the conjoined tendon, the retraction of the muscle makes the rent triangular. The interweaving expansions of the tendon on each side still hold it to a certain extent, and the pull of the muscle is distributed on the conjoined tendon on each side as if it had a Y attachment. The middle of the inverted Y retracts farthest and the sides slope toward the base on the tuberosity. The shape of the whole rent is therefore roughly an equilateral triangle, with its base on the tuberosity and its apex disappearing under the acromion. The width of the tear is the width of the base; restoration would be made if the apex were sutured to the middle of the base. The base itself is inflexible, being either the bony seat on the tuberosity from which the tendon was evulsed or an inelastic stub of tendon still attached to the tuberosity. The size of this triangular rent varies from a half inch to an inch and a half base. Sometimes only a few fibers are torn, and at other times most of the conjoined tendon. In one case I found that the whole cuff with all the tendons had been evulsed, and that the head of the humerus was free under the deltoid. (See case report on pp. 389, 390, 391.) A skin wound of triangular shape healing by second intention, i.e., granulation and epithelialization from the edges, becomes rounded before it heals; so do these triangular defects in the supra-spinatus, so far as the edge of the rent is concerned. They differ from the skin defect because there is no bottom or bed of granulations, so must heal entirely from the periphery, and complete closure of the hole is therefore unlikely. In the skin ulcer this peripheral healing is epithelial and spreads over the surface of the granulations on the base as ice, beginning at the edges, skims over a pond. In the tendon defect the peripheral tissue is fibroblastic not epithelial, and fibroblastic reconstruction is dependent on a new formation of blood vessels instead of mere multiplication of cells to skim over another tissue which will feed them. Now it happens that tendon is a tissue in which there are exceedingly few blood vessels to form the basis of new granulations, so that the conditions for healing are still more unfavorable. I have already stated that it is my own belief that tendon repair does not usually take place from within, but from the synovial or areolar tissues adjacent to it. It is likely, therefore, that the synovial covering acts in these cases something like epithelium to cover the edges, and also as an agent to expedite the new supply of blood vessels. At any rate, I have had the opportunity to see on the operating table the appearance of these rents at various stages from a few days to two years after the accident. Even three weeks after the rupture, the triangular appearance is sometimes a little rounded by bridging of the corners and extension from the sides of an almost transparent new tissue, presenting a falciform edge toward the center. In later cases this edge is harder and more extensive, but always presents the falciform margin, which lies on the cartilaginous joint surface in the manner of the semilunar cartilages of the knee joint—clearly to avoid friction. Obviously, as this circle gets smaller, either by the contraction of the tissue of which it is composed (cf. contraction of surface scars), or by more tissue forming toward the center, the smaller and more circular the defect becomes, until possibly the hole between the bursa and the joint might be entirely closed. Assuming that there is still a stub of tendon attached to the tuberosity, it seems possible that healing in this manner would eventually occur in young, well-vitalized tissues, but in the aged, with barely vitalized tendons, little change would tike place after the first few weeks. This supposition is strengthened by reference to the age table, which shows that I have never operated on a young man and demonstrated a rupture of the tendon. In those cases in which the tendon is actually evulsed from the facet, a complete circle with a falciform edge is not formed as healing progresses, for the bone forms a defect in the circle. The base of the former triangle is the bone of the tuberosity. It may be bare and as a rule has no granulations; sometimes there is a little velvety tissue on it. On microscopic section of the bare facet, one finds a little skim of fibrous tissue over the spongiosa, and that is all. As a rule there is a little plaque of dense bone beneath this, and at the periphery of the defect some raised "productive" bone. These bony changes are shown in the X-ray. Healing in these cases would appear to be at still more of a disadvantage than when a stub of tendon is left on the tuberosity. It is not unusual to find both, some stub and some bony defect. From the operator's point of view a stub of tendon is a great advantage, for where evulsion has occurred he must drill the tuberosity in order to suture the tendon. A knowledge that a falciform edge is present is also important for the operator, for in most cases he must remove it and pare down to the real tendon tissue before he sutures. The new tissue in this falciform edge is seldom strong enough to hold a suture, and would be in the way of the sound tissue. (Fig. 12.) Referring to Fig. 6 will help the reader to understand the points at which rupture or evulsion is likely to take place. The figure shows that the insertion of the tendon into the bone is very superficial, and the shell of the surface of the bone is very thin. Under high magnification very many minute prolongations of the tendon are inserted into this thin shell of bone. (The structure suggests to my mind a room full of people hanging to the ceiling by having all their fingers deeply thrust into the plaster as into finger holes in a bowling ball.) As a practical matter this network of attachment to the tuberosity does hold against excessive pull except in elderly people when the attachment is pulled out. In most of the cases I have seen at operation it was apparently evulsed at the line of junction, but soon after the injury a stub of tendon would probably have been found. Such stubs probably slowly disappear. Referring again to Fig. 9, it will be seen that stress on the supra-spinatus tendon in the direction of its normal pull may result in four different forms of break in continuity: a. The tuberosity, facet and all may be pulled away. This may occur without making a communication between the base of the bursa and the joint. Since the fixed portion of the base of the bursa is on both tuberosity and tendon, it is likely that the whole bursa follows the displaced tuberosity, and the bony gap is filled in by callus from the peripheral torn periosteum. (See p. 317.) I am quite sure that this is the rule, although my opinion is formed on that very untrustworthy guide, "clinical experience." Cases of fracture of the tuberosity get well much more promptly and with less pain than do ruptures of the tendon, and differ in their minor symptoms from the latter. Moreover, in the two cases cited I have opened the bursa and felt beneath its unruptured base the fragment of tuberosity. In most fracture cases the bursa is not involved because it is higher than the usual line of fracture. (See p. 273.) It seems to me probable that in all cases where the tuberosity is involved, whether it is broken off alone or with several fragments, that the line of cleavage in the bone is just external to the firmly attached base of the bursa, which in fact strengthens the bone locally like a patch. In other words, I think that if one opened the bursa by my routine incision in a series of fresh cases of fracture of the tuberosity, he would not find the bursa full of blood and communicating directly with the two raw fractured surfaces and thus into the joint. Sometimes this would be true when the fragment as shown by the X-ray is drawn inward as far as in Fig. 35, but not in the usual case as in Plate IX.
FIGURE 35. RETRACTED FACET AND DROPPING SHOULDER I have found this Rontgenogram, unlabeled among my papers, so that I cannot give, as I usually have in my other illustrations, a statement that the condition was proved by operation. However, the picture is so characteristic of a retracted supraspinatus facet that I do not hesitate to use it. Such a condition is far more serious than most of the major fractures (Fig. 59). Even without knowing the history in such a case I should be confident in saying, from the X-ray alone, that the patient has a post-dislocation condition, where there is "dropping shoulder" due to deltoid paralysis and where the supraspinatus facet of insertion lias been pulled by the muscle beneath the acromion. It also shows some bone formation from shreds of periosteum retracted to a lesser degree by the adjacent tendons. As in cases 71 and 115, the dislocation has probably not been really reduced. These appearances indicate operation.
b. Evulsion may occur at the point of insertion and the superficial part of the facet be carried inward by the retracted tendon. Since this little shell of bone would show very faintly in the X-ray, and also since it would have been absorbed in the long-standing cases which form the bulk of my experience, I cannot speak very positively about it. In a few cases I have seen remnants of it attached to the retracted end of the tendon, and I have often noted its absence on the tuberosity. In some cases it seems that the minute, finger-like processes are evulsed from the bone without taking the bone with them. Occasionally part of the tendon is evulsed, leaving bare bone, while the remaining portion leaves a small stub on the tuberosity. c. True rupture of the tendon leaving a stub on the tuberosity usually occurs at the narrowest place shown in Fig. 6, leaving the broad, semi-cartilaginous fibro-cartilage still attached to the bone as' a stub. This amount is barely sufficient to permit a good hold with a stitch. I have occasionally seen a larger stub, perhaps three-quarters of an inch in length. In these few cases this larger stub was very vascular and of deep purplish red color like a cock's comb. On one occasion such a stub popped out of the wound as soon as the roof of the bursa was incised. The vascularity of such a stub sug gests that there must be a considerable blood supply in the bony facet. The desiccated bone shows many vascular channels in the sulcus, and near the upper end of the bicipital groove. Both those cases in which there is evulsion and those in which a stub is left necessarily have a direct communication established between the joint and the bursa. In cases where bursa and joint communicate there is always more or less straw-colored fluid in the joint which washes back and forth into the bursa, rising in the bursa when an effort is made to raise the arm, and falling back into the joint as the arm is relaxed and lowered. This process dilates the bursa and in extreme cases leads to hygroma of the shoulder, as described on p. 478. d. A fourth condition of great clinical importance consists of those cases in which a portion of the tendon is torn to a degree insufficient to tear the base of the bursa itself, so that a film of tissue is left between the joint and the bursa. I allude to these cases as "partial" ruptures or "rim rents." Repair takes place to a certain degree from the thickening of the film of bursal base. I have found few such cases in the living, probably because they do not cause a degree of disability to make me advise operation, but I have frequently seen this condition at autopsy. If one removes the head of the humerus with the short rotators attached and examines the sulcus which surrounds the articular edge, one finds the attachment of the supraspinatus extremely thin, so that when held up to a bright light the attachment is found to be Y-shaped and the central portion between the limbs of the Y is diaphanous. The sulcus at this point is correspondingly broad instead of being a cleft, as it is in the normal joint (Fig. 10). It appears that the portion of the tendon on the joint side, together with its joint synovial lining, has pulled off, leaving the bone bare. I believe this fourth division accounts for many of the industrial shoulder injuries which recover after a few weeks or months, and which I have in the past classified as relatively trivial cases of traumatic subacromial bursitis (see Plates III and IV, pp. 101 and 102). It seems legitimate to assume that in such injuries as almost or quite cause a dislocation of the shoulder, the synovial reflexion and the portion of the tendon on which it is reflected, might be torn away from the articular edge, leaving the bone trabecule bare at this point. There would be slight bleeding, which might gradually fill the joint and distend it. This hemorrhage would in turn be replaced by an excess of synovial effusion, which might be kept up by the individual continuing to use the arm. Motion might prevent the formation of fibrin to act as a basis for new granulations and fibrosis in the bed of bone. Even if pain were sufficient to start scapulohumeral spasm, the effusion might hold the parts apart and prevent proper healing. If the patient were old, and the tissues already weak, healing would be even more unlikely. At any rate, it is very common to find at autopsy that the sulcus is bare.
FIGURE 86. VOLCANOES AND CAVERNS Deeper section through the same tuberosity as that shown in Plate V, Figure 1. The ends of the canals of invasion of vascular tissue appear as caverns. As these caverns and volcanoes are frequently found in X-ray films in cases of tendinitis, as well as in cases primarily due to rupture of the tendons, intensive study should be given to them.
C. CHANGES IN THE GREATER TUBEROSITY
(1) Excrescences. Pathologic changes in the tuberosity may readily be detected by the X-ray. In many cases of old, complete ruptures of the supraspinatus and in some cases of partial rupture, the relative thickness of the tendon and of the tuberosity is changed, so that there is a notch in the base of the bursa. Thus the tuberosity forms a distinct eminence and may cause a jog and friction as it passes upward under the acromion. The result is a stimulation of the bone cells in the tuberosity and irregular excrescences form at the region where undue friction occurs. This new formed bone is very spongy and probably later atrophies, because in the very old cases one finds that complete recession of the whole tuberosity has taken place. Atrophy of the tendon without actual rupture might cause enough irregularity in the base of the bursa to begin a little irritation. A vicious circle of atrophy of tendon, inflammation of tuberosity, osteitis, excrescences, greater jog and greater friction, greater atrophy, etc., might be established. At the same time hypertrophic changes on the acromial edge are stimulated. (2) Caverns. Very frequently where this superficial osteitis occurs on the tuberosity, there is also absorption of the bone beneath its surface. This absorption of the bone results in the formation of little caverns which contain vascular tissue. I am inclined to think that they represent the early stages of what I call recession. (3) Eburnation. By eburnation I mean an increased deposit of lime salts which result in the hardening of a definite area of the bone. Such areas of eburnation are frequently found at the insertions of these tendons in working men. In the X-ray a heavy plaque of bone is shown where the tendon is inserted in the sulcus. In some cases where the fibers of insertion have been damaged, there appears to be an increase of this bony deposit, so that when this is found in a case of suspected rupture, it is a confirmatory sign. It is not, however, of much importance practically. In my opinion, this appearance is evidence of the existence of low-grade, chronic inflammation, and I think that it is possible that the increase of this bony substance may interfere with the nutrition of the finger-like processes which hold the tendon in the bone at this point and tend to weaken the hold which these processes have there. (4) Bursal osteitis. Osteitis caused by this irritation on the tuberosity may sometimes involve the outer side of the tuberosity as well as its tip. The base of the bursa may be the seat of chronic inflammation, so that irregularities will be shown by X-ray on the appropriate portion of the tuberosity, external and below the insertion of the tendon, on the outer aspect of the bone. (5) Recession. I have referred above to the atrophic changes which take place in the sulcus and tuberosity long after ruptures of these tendons have occurred. It is highly probable that most ruptures occur at the line of junction of the tendon tissue with the palisade-like fibrocartilage adjacent to the bone shown in Fig. 9. When I have operated within a few weeks after the accident, this stub of tendon was usually present. In the very late cases, however, the tuberosity has usually been found to be quite bare, and not only bare, but atrophic. Instead of showing a normal sulcus and tuberosity, these structures are more or less leveled off, or, as I prefer to say, there has been a gradual recession of the tuberosity after the stub of tendon has worn away or been absorbed. The sulcus and tuberosity were no longer of use, but were actually an impediment to elevation of the arm. Without the pull of the tendon to fulfill its normal functional demand, the tuberosity had gradually disappeared. In the very old cases, such as many of those Dr. Akerson found at autops}', or the case mentioned on page 108, the recession of the tuberosity was so marked that one could hardly tell, by superficial examination, where the old cartilaginous edge ended, or where the area normally occupied by the sulcus and tuberosity had been. This region now wa.s smooth, covered with a thin fibrous layer, and continued the rounded contour of the articular head. This recession of the tuberosity may be detected also by the X-ray. Note the dotted line in Diagram C and also Plate IV. (6) Trabecular atrophy. In all long-standing lesions of the bursa, whether or not they are due to rupture of the tendons, the X-ray shows that the trabeculae beneath the base of the bursa are more or less atrophied. This produces a dark area in the X-ray film which corresponds with the portion of the tuberosity on which the base of the bursa rests. In the normal bone the trabeculae are, to be sure, less dense in this region than in other parts, but where the atrophy is pathologic, the outline of this more translucent area is indefinite and not as plainly marked as in the healthy bone. I presume that the trabecular are absorbed because there is chronic congestion of the small vessels of the marrow spaces in the region. This kind of atrophy is sometimes very marked in acute cases of bursitis due to calcified deposits. In such cases it slowly disappears after the lesions have healed.
D. CHANGES WITHIN THE JOINT ITSELF
(1) The common lesions of the long tendon of the biceps have been alluded to on p. 85. (2) Rupture on the joint side of the tendons (rim rents). We have already considered under B, lesions of the tendons at this point, but since they do occur here, they necessarily involve the joint. Normally the true joint cartilage forms a very sharp angle with the insertions of the tendons, as shown in Fig. 10. Fig. 9 shows some of the fibers beginning to tear at this synovial reflection. Diagram D shows an extensive tear so that the rent-has come through to the most superfici fibers of the tendon. The reader should visualize this vertical section so as to understand that the rent also extends along the curve of the edge of the joint cartilage to a considerable extent, leaving the sulcus bare, perhaps for an inch or more. This condition I like to call a "rim rent," and I am confident that these rim rents account for the great majority of sore shoulders. It is my unproved opinion that many of these lesions never heal, although the symptoms caused by them usually disappear after a few months. Otherwise, how could we account for their frequent presence at autopsy? (3) Eburnation of the sulcus has already been spoken of under the last heading, but it is unavoidably listed here again because it lies at the periphery of the joint. (4) Raised articular edge. Not infrequently we find in elderly subjects, a very slight, rounded, corona-like elevation of the edge of bone under the articular cartilage. It is difficult to say whether it is really pathologic in character. It might be regarded as evidence of a chronic arthritis. However, it is frequently present as shown by X-ray, in joints of which the patient makes no complaint. So far I have been unable to attribute any clinical significance to it. (5) Adhesions of the extensions of the joint. The reader will recall the so-called bursal extensions of the joint which lie beneath the infraspinatus and subscapularis. It is highly probable that the margins of these, especially the margins of the one beneath the subscapularis, may be stretched or torn so that habitual dislocation may readily occur. On the other hand, adhesions between their surfaces would necessarily limit the motions of the joint. I mention these extensions because some future investigator may be able to make some observations of clinical importance concerning them, but my personal experience with them is nil, for I have not even studied the question systematically on the cadaver. Albert (1893) mentions a case of tumor in the axilla caused by distention of the subscapularis bursa, but I have never observed such a case. (6) Fluid in the shoulder joint is considered on page 115. The chief point which I wish to make in regard to it at present is, that in elevation of the arm the lower portion of the capsule is stretched tight and fluid is forced upward into the rim rents or, if there is a communication through the whole tendon, into the bursa itself. Theoretically, if there is fluid in the joint and the tendon is not ruptured, elevation of the arm should also tend to dilate the bursae beneath the subscapularis and infraspinatus.
E. WHEN THE MUSCULO-TENDINOUS CUFF HAS BEEN RUPTURED So THAT A FREE COMMUNICATION HAS BEEN ESTABLISHED BETWEEN THE JOINT AND THE SUBACROMIAL BURSA
The considerations under this heading are merely presented as a review of the others, with the particular idea of accentuating what I believe is nature's method of compensating for these lesions, i.e., dilatation of the bursa by joint fluid, gradual absorption of the tuberosity and atrophy of the stub of tendon in order to form a new, smooth surface. (1) Indicates the fibro-synovial edge which is formed very soon after the injury and which must be pared away before the tendon is sutured. (2) Erosion of articular cartilage. It is obvious from what has been said that after rupture of the musculo-tendinous cuff, more or less articular cartilage will be exposed on the base of the bursa, and that the cartilage at this point would be subject to contact with the acromion when the arm is elevated. In old cases at operation or in specimens of extensive tears found at autopsy, one frequently sees a superficial erosion of the joint cartilage with clearly marked outlines separating it from the undamaged surface. These areas of erosion are consistently limited by the size of the rent. Perhaps it is better to say that these areas of erosion are always somewhat larger than the rent, because in different degrees of rotation of the humerus different parts of the articular surface can be exposed through the same rent to pressure on the acromion as the arm is elevated. In practically all the cases where an extensive rupture exists, there is some osteitis on the edge of the acromion, which would increase the wear and tear made by the articular surface touching the acromion through the gap. This erosion of the joint surface is always superficial. It is possible that in some cases the process is reversed. It may be that the rough acromial edges wear through the tendon. (3) Is the stub of tendon which remains on the tuberosity for some weeks or months after the injury, but since it is functionless, eventually disappears. (4) Represents the dotted line which limits the recession of the tuberosity. (5) Is the fluid in the dependent axillary portion of the capsule.
In the above description of the pathologic changes which I have observed in this region, I have endeavored to confine my remarks to the essential features which I am sure that any one who is earnestly studying these joints will be able to verify. Such a student may also find many other atypical little irregularities in the tissues close to the lesion in the tendon, which I have not thought it worth while to describe. However, when one has examined a considerable number of joints, these changes will seem relatively unimportant and entirely secondary to the lesions described above. One must not allow one's self to be deceived by these secondary changes, although sometimes the congested, inflamed synovial folds are the most striking lesions visible. Before closing this chapter it is well to add a word about the question previously brought up as to whether some form of necrosis in the tendons themselves, such as age induces in the walls of arteries, is largely responsible for the various lesions or at least for their failure to repair. The facts that most of my cases are aged, many are bilateral, and that I have observed no cases in young people are strongly suggestive of this idea. Moreover, the traumatic cases as well as the calcified cases show a similar degeneration of the tendons under the microscope, although many of the latter are in somewhat younger people. It seems possible that these lesions may occur merely from gradual deterioration of the musculo-tendinous cuff. The frequency with which they are found at autopsy would suggest this, as well as the reasons spoken of in the last paragraph. When a tendon has disintegrated to a great degree of weakness, even a slight effort might break away the rest of it. However, this is not usually the case, for all but two of my operated cases of complete rupture of the supraspinatus gave a very clear history of serious trauma. Dr. Wilson's cases also had histories of trauma, with one exception. The findings at operation in the three exceptions were similar to those in definitely traumatic cases. Moreover, the results obtained by operation were excellent; in fact, both my cases were demonstrated at a medical meeting as perfect results. How can we account for this combination of a non-traumatic history with typical operative findings and excellent results? If the lesions were caused by a progressive disease we should not expect good results. It happens that in both of my cases I strongly suspect that the injury had occurred when the patients were drunk. Since I believe that the usual cause of this injury is a sudden attempt at elevation of the arm to maintain balance during a fall, I think it is quite likely that such an injury may occur to a reeling drunkard. Therefore, I feel that before we say that these lesions are ever non-traumatic, careful inquiry should be made into the possible chance that the injury occurred while the patient was intoxicated. The early symptoms are not necessarily very marked, and would readily be masked in a case of a steady drinker. Goldthwait has suggested that faulty posture underlies the weakness of the tendons. I am convinced that overuse of the arms in abduction without giving the tendons time to let their circulation do its duty, because they are perpetually stretched, has much to do with these lesions. I have no doubt that trauma may rupture a healthy tendon, but I think rupture from trauma occurs in the great maj ority of cases in aged tendons made weak by overuse, age, or toxic conditions. Dr. Akerson suggests that long-continued disuse might weaken aged tendons to such an extent that they would break under very slight strains and perhaps without much pain. Whether or not injury precedes or follows degeneration in the tendons, it is a fact that complete rupture of the supraspinatus tendon may be diagnosed and even in late cases may sometimes be successfully repaired by surgery.
In studying the lesions that have been discussed, we should first have some idea of the normal microscopic landmarks which may become altered by injury or disease. The diagram (Fig. 37) should be compared with Fig. 9 in Chapter I, which shows an enlargement of the normal insertion of the supraspinatus tendon in the region where pathologic changes usually take place.
FIGURE 37. DIAGRAM OF MICROSCOPIC REGIONAL LANDMARKS The relative sizes of the structures and cells have been altered in order to simplify the figure, which should be compared with a photograph of an actual section of this region (Fig. 9).
1. "The Critical Portion" of the tendon is the half inch proximal to the palisades. It is in this region that calcified deposits gather and where complete rupture frequently occurs, although partial ruptures usually begin at the edge of the cartilage. As has been said, even under the microscope one cannot distinguish, in this part of the tendon, between joint membrane, capsule, tendon substance, and bursal floor, because they are here welded into one single structure. Nor is there a clear line of demarcation on the proximal side of the short tendon, where the muscle begins. 2. "The Torpedo Cells" are so called from their shape. They are probably merely modified cartilage cells which lie in the palisades with their long axes parallel to the columns. They closely resemble the cells of the adjoining articular cartilage, but their intercellular substance is more fibrous. They seem to function in making the columns, or palisades, and also in forming the blue line. 3. "The Palisades," i.e., the portion of the tendon inserted in the tuberosity, is thus named because of its columnar fibers. In cases of complete rupture of the tendon, the stub, which often remains on the tuberosity, represents this structure. It is fibro-cartilaginous in consistency and contains many "torpedo cells." 4. "The Blue Line." With the hematoxylin and eosin stain there is always, in adults, a blue line (of course, really a surface) where the palisades are inserted into the bone. The blue line is not present in infancy and even in a specimen from a girl of eighteen (Plate VI), it is not well developed; i.e., the cells stain blue, but there is little deposit outside the cells as compared to the amount of blue non-cellular material one finds in older patients. The blue line is very close to the surface of the bone, but appears to be fenestrated for the insertion of the tendon. 5. "The Armor of the Sulcus" is the superficial layer of bone on the facets which we find in the dried specimen, and is really the cortical bone beneath the blue line. Like the trabecule it takes a pink stain. The armor in a normal tuberosity should be almost smooth on its surface; i.e., in section it should give a definite regular outline. It is a surprisingly thin layer considering the stress it must bear; beneath it are marrow spaces and cancellated bone. 6. "The Synovial Reflection" is the angle between the edge of the articular cartilage and the palisades. It is described on pages 15-16, Chapter I, and is illustrated in Figs. 9 and 10. In dissecting room subjects this angle is seldom normal; there is almost always evidence of rupture of some of the columnar fibers of the palisades, as in Fig. 9. 7. "The Finger-like Processes" pass through the blue line, and form a singularly strong attachment to the bone beneath. These processes usually contain cells similar to the torpedo cells but apparently charged with calcium, for when close to the bone they take a deep blue stain. 8. "The Articular Cartilage" definitely begins at the very edge of the sulcus where the tendon is inserted. There is a sharp line between it and the "palisades"; i.e., the synovial reflection. 9. "The Cancellated Bone," or Spongiosa, forms the bulk of the head of the humerus. The spaces usually contain fat and scattered marrow cells, and are not normally very vascular. Both the blue line and the armor are continuous with similar but less pronounced structures, beneath the articular cartilage, where there are no finger-like processes and where there appears to be a cleft between the blue line and the bone under the cartilage.
PLATES III AND IV
The cuts in Plates III and IV are made from direct photographs of some of Dr. Akerson's slides of old lesions found at autopsy. Those on the left are enlarged two diameters, and those on the right about four diameters in each case.
Figure 1 shows a beginning tear of the fibers at the synovial reflection, a little more extensive in degree than that shown in Fig. 9 in Chapter I. Figure 2 shows a still more extensive rupture of the deep fibers, i.e., a. " rim rent." More than half of the tendon has been torn away, leaving portions of the columnar fibers (palisades) still attached to the tuberosity. The little hook which is in the center of the small circle is all that remains of the former synovial reflection. One small cavern is present in the tuberosity, which also shows evidence of slight excrescences. Figure 3. A section from the same specimen as that shown in Plate V, Fig. 6, but taken near the edge of the gap, so that there is continuity of some of the superficial portion of the tendon with the external part of the palisades. It would be hard to explain this section or No. 4 by erosion from contact with the acromion process. Figure 4. Another section from the same specimen which shows a partial rupture in the central portion of the tendon, and yet the fibers are continuous with the palisades, superficial to, and also beneath, the torn fibers. Most specimens show, when sectioned, this same irregularity in the extent of rupture in the different layers of the tendons. Compare the frontispiece, and imagine the degree of tearing in each layer which would be shown by a section at the left of the rupture.
Figure 1. A very old complete rupture in which recession has taken place; no evidence of either sulcus or tuberosity left; the whole surface of the tuberosity has become rounded off to avoid friction. It is not enough to say by friction. The process of recession is a response to friction rather than a result of it. The fibrous layer which occupies the place of the tendon is not true tendon substance, but a portion of the roof of the bursa, the entire fioor of which has disappeared. Figure 2. A recessed tuberosity where no sign of sulcus or eminence remains. In the falciform edge of the torn tendon is a small oval speck of bone which formerly was the facet of insertion of the tendon. This is pretty definitely proven, not only by the gross appearance of the specimen, but by the fact that under high magnification one can still see evidence of the blue line on the periphery of the fragment. In this way nature manages to reduce friction even where a fragment of tuberosity is evulsed. Figure 3. Section through an excrescence which has deformed the armor and the blue line in this region; yet under high power there are none of the usual evidences of inflammation, such as lymphocytes or increased fibrosis of the marrow spaces. The synovial reflection is relatively normal and so are the palisades, internal and external to the excrescence. Figure 4. A rim rent where all the tendon is torn away from the sulcus except the superficial portion which extends into the periosteum. Partial recession has occurred. Some of the columnar fibers are still present in the deformed sulcus.
PLATE V. DRAWINGS OF COMMON PATHOLOGIC FINDINGS Figure 1. Section of the greater tuberosity in an old case of rupture of the supraspinatus. It shows the presence of "caverns" containing vascular tissue. The section is taken through an excrescence or "volcano." A section of the same specimen taken in a more transverse plane shows the caverns as rounded, cystlike spaces. Figure 2. High power picture of the lower end of one of these caverns, indicating the vascularity of the tissue within. Figures 3, 4 and 5. Illustrations of a few of the varied appearances presented by villi found in chronic inflammation of the bursa. Fig. 8 shows fibrous, vascular and fatty changes, and Fig. 4 shows richly cellular areas. The section, Fig. 5, showing infiltration with polynuclears was taken from the case reported on page 247. There was no gross evidence of suppuration in this wound, but old silk stitches were causing irritation of the tissues. Figure 6. Section through an old rupture of the supraspinatus tendon. The tuberosity is in process of recession and has become atrophied except for an excrescence at the outer margin. The blue line has almost disappeared. The armor is lacking because for years there has been no functional stimulus. Eventually such a tuberosity would become almost completely rounded off.
PLATE VI. HISTOLOGY OF TENDINOUS INSERTIONS
1. Section .through the attachment of the supraspinatus tendon of an infant. The center of ossification of the articular head is present, but those for the tuberosities have not yet appeared. The tendon takes a bright pink stain, while the cartilage, which is to form both the articular surface and the tuberosity, is purple. 2. Higher magnification of the "synovial reflection" in the same specimen. It shows the line which separates the tendon from the cartilage which is later to form the tuberosity. The coloration of the intercellular substance (i.e., the acidity or alkalinity of the tissue), rather than the morphology of the cells, is the distinguishing feature. Sections of this region from children up to at least the age of twelve show no very definite blue line of demarcation between these two structures, but in sections from a girl of eighteen (Fig. 3) there is the suggestion that the blue line is in process of formation. It therefore probably begins to form somewhere between twelve and eighteen. 3. Section through the cortical (armor) bone of the tuberosities in a girl of eighteen. In this section the blue material appears to be chiefly in and about the cells (bone corpuscles?) in the armor. It suggests that these cells are instrumental in causing the blue deposit. They appear to leave it behind as a kind of shellac for the finished adult surface of the armor of the tuberosity. Whether they die when they have finished this work or whether they leave the deposit behind and proceed upward to become fibrocartilage "torpedo cells" is a matter for histologic research. The present theory is that they do not proceed up into the tendon. In this young girl, the bone below the blue line is rich in cells, but in adult life (Fig. 4) there are relatively few living torpedo cells in the armor. Dr. Wolbach tells me that the formation >of this blue line resembles to some extent histologically the formation of enamel in a tooth. 4. This section shows what is usually found in an adult specimen. The blue line appears to be entirely extracellular and the fibrocartilage cells, which I have called "torpedo cells," in the palisades are very conspicuous. There often occur little masses of purple, crystalline collections, as indicated in this picture, just above the blue line. They are sometimes found even further up in the palisades. Their appearance suggests that they may be somewhat abnormal deposits, due to the failure of the cells to leave their blue staining material in the region of the surface of the bone. It is possible that a knowledge of their formation would throw light on the formation of the peculiar calcified deposits which occur in the tendon at a higher level. In both Figures 3 and 4, notice the finger-like processes which pass down (or it may be pass up?) through foramina in the blue line. Evulsion of these fibers may occur or a portion of the blue line may be retracted with the tendon. 5. A section taken from the supposedly normal adult tendon shown in Figure 9. On study with high power it shows deeply staining areas in the tendon substance which give evidence of abnormality of the collagen. It also shows abnormal changes in the torpedo cells. 6. Early changes in the character of the collagen of the fibrocartilage which composes the palisades. When the collagen is in this condition, the degenerative portions may be indicated by either a bluish or a pinkish stain with H and E.
We may now briefly take up the changes which are often found in these structures. 1. The critical portion of the tendon may show many shades of stain according to the degree of necrosis. It may contain large calcified areas or minute specks or merely necrosed fibers without any deposit. It may show rupture of all the fibers or of only those of the central or peripheral parts. 2. The torpedo cells undergo very interesting alterations. They may become calcified or enlarged into peculiar giant cells, or they may fade. 3. The palisades often show irregular staining qualities indicating necrotic changes; broken fibers, rice bodies, etc. 4. The blue line is a curious structure which is present at most points in the body where cartilage or tendon is attached to bone. It may become irregular on its surface or embossed by the formation of bony excrescences beneath it. It may be torn out in patches by the tendons. 5. The armor may become greatly thickened (eburnated) in laboring men from excessive use of the tendon. It may also become thickened from chronic inflammation in the tendon. Where the blue line is destroyed, the armor is thin; e.g., after recession of the tuberosity it is usually quite thin, and the blue line has disappeared. 6. The synovial reflection is almost always changed to some degree as rim rents form. In most elderly patients we find at the angle of reflection that the columns of the palisades are more or less torn. 7. The finger-like processes may also show evidences of necrotic changes if staining reactions may be considered evidence. I strongly suspect that increase of the calcium deposits in the blue line may choke off these fibers so that the tendons may be more easily pulled out. 8. The articular cartilage may show thinning and superficial loss of substance but usually appears unchanged even to the very edge. 9. Vascular caverns may be formed in the spongiosa near the facets. There are many other interesting and suggestive points about the pathologic histology of these lesions, but the above-mentioned changes may be readily confirmed by any one who has access to autopsy material. This is an uncultivated pathologic field except for Dr. Aker-son's work. Correct interpretation of the common findings is greatly needed so that our clinical results may be improved. To my mind one of the most promising leads for the pathologist is that concerned with the extreme sensitiveness which the tendons show to hematoxylin and eosin stains. Sometimes the necrotic portions are pink or red, and sometimes blue or purple. Notice the staining of the section from the infant's humerus. Why should the contrast be so pronounced? In the adult why is the bone red and the blue line blue? What phases of necrosis attract the blue or the red stain? Could these tissues be acidified by either local or general use of drugs? Could the pathologic process in tendinitis be checked by increasing or diminishing the acidity of the blood or in any way by altering its constituents ?
CODMAN-, E. A., AND AKERSOH, I. B., The Pathology Associated with Rupture of the Supraspinatus Tendon, Annals of Surgery, Phila., 1931. GHUBER, W., Hygrom der Bursa mucosa subacromialis, Oesterr. Z. f. prakt. Heilk., Wien, 1869, xv, 819; Also: Ein Hygroma retroglenoidale scapula?, Arch. f. path. Anat., etc., Berlin, 1875, lxv, 288-241. MOSCHCOWITZ, E., Histopathology of calcification of the spinatus tendons, as associated with subacromial bursitis, Proc. N. Y. Path. Soc, 1915, n.s., xv, 1-7; Also: Am. J. M. Sc, Phila., 1915, cl, 115-126. SCHWABZ, E., Untersuchungen tiber die Entstehung der Zotten und Reiskorper in Hygromen sowie die sogenannte "fibrinoide Entartung" des Bindegewebes der Schleimbeutelwand, Dtsch. Z. f. Chir., 1931, ccxxxv, 1-3; Also: Dtsch. Z. f. Chir., 1982, ccxxxv, 140-163. (Contains some excellent photomicrographs of the so-called rice-bodies which are often found in bursa? and which are demonstrated again and again in Dr. Akerson's collection; references are given to most of the important articles on the pathology of bursa; in general, but there is no mention of the subacromial bursa.) STIEDA, A., Zur Pathologie der Schultergelenkschleimbeutel, Arch. f. Klin. Chir., Berlin, 1908, lxxxv, 910; Also with BERGEMANN, Ueber die mit Kalkablagerung einhergehende Entziindung der Schulterschleimbeutel, MUnchen med. Wchn-schr., 1908, lv, 2699-2702. Brief references to the pathology of this region are also made in some of the papers listed at the end of Chapter VI.
Calcified deposits in the supraspinatus tendon
As far as I know, the first patient to be operated upon for this -condition was Miss McM., age 24, Massachusetts General Hospital, No. 127430, June, 1902. I assisted Dr. F. B. Harrington to incise and drain what we took to be an abscess of the subacromial bursa. A culture of staphylococcus aureus was obtained, but the wound showed no sign of infection and promptly healed. I believe now that the culture was contaminated, for I have never been able to obtain a culture from one of these cases since. On reading the record now the description seems impossibly stupid, for in spite of the fact that I was even then interested in the anatomy of the bursa, and also had been an enthusiastic pioneer in using the X-ray for six years, I did not put two and two together and realize that the condition was what we now call a "calcified deposit." It was not until May 17, 1905, when Dr. C. F. Painter asked me to see with him another doctor who was in such acute pain that he begged to be operated upon, that we suddenly understood almost as much as we know now about the condition. Yet I think that even then we were the first surgeons to realize what these cases were and how easy it was to relieve them. I mention these experiences to illustrate how blind the human mind may be to facts which are perfectly obvious, and when such facts are clearly demonstrated how difficult it is to diffuse them so that they may be generally applied. Rontgen's discovery had for several years made the lesson we learned from this case plain for any surgeon to read, yet no one had seen it in just the right light. Those who happened to know about the anatomy of the bursa may not have happened to be able to read the X-ray, or to have had an appropriate patient, who, like our friend Dr. D., urged us to "try anyway." We tried and relieved him at once, yet today right in this city there are probably patients with the same condition being treated week after week as "neuritis." Dr. Painter and I have both written about our experience; other surgeons have confirmed what we say; we have continued to get excellent results from this operation; yet twenty-seven years have elapsed and some cases are still treated without even the diagnosis being made or the X-ray even used. Dr. Painter has reported this case in his original article, March 21, 1907; I also reported it in my paper published June 9, 1908, as follows:
"The patient, Dr. D , is a man of 37 years of age, of heavy (200 pounds) physique and plethoric constitution. His previous history is unimportant, except that ten years ago after playing baseball all one summer he used to have a great deal of pain and soreness in his right shoulder joint. Since that time he has had at intervals a great deal of pain and tenderness in the joint. The pain bothered him particularly at night and was at times severe enough to prevent his sleeping well. He stated that until within a few days he had been able to move his arm without any trouble in all directions; for instance, behind his neck, behind his back, and over his head, without especial pain. There have been times, however, when it was difficult for him to raise the hand over his head, but when it was once put in this position it was comfortable for a time. He used to occasionally put it in this position at night; after lying with the hand behind his head for some time, he would then put it down by his side again. In doing this there was always pain during the motion. He recalls at times having his wife wake him just as he was going to sleep with his hand behind his head and tell him to put it down by his side, so that he would not go to sleep in that position and find it stiff on waking. External and internal rotation of the arm could be gone through without giving any trouble whatever. Eight days ago while in New York he suddenly noticed that the point of his shoulder was tender and painful and that the motions were much restricted. He could with difficulty get into his clothes, but could not reach his hip pocket as he had been accustomed to. During these days the soreness had persisted and there had been great pain, sufficient to prevent sleep at night and to require large doses of morphine; the only comfortable position was sitting with the elbow supported. The pain was so great as to make him desire immediate operation. Examination showed that the external and internal rotation of the humerus on its long axis is restricted about one-half the normal arc. Abduction or elevation of the arm is impossible on account of the pain caused in the neighborhood of the greater tuberosity. Attempts at passive elevation of the arm showed that the scapula moves in conjunction with the humerus. An X-ray from the posterior view shows a pyramidal shadow in the region of the subacromial bursa just above the greater tuberosity and external to the tip of the acromion, the base of the mass being downward and about an inch in length. Between the base and the greater tuberosity is a translucent band about a quarter of an inch wide, occupying the position normally occupied by the tendon of the supraspinatus. The mass is apparently in such a position that the tuberosity could not ride under the acromion without compressing it. Operation, by Dr. C. F. Painter, May 17, 1905. Under the impression that the mass shown in the X-ray was caused by a calcification either of the bursa or its base, a vertical incision of about two inches in length was made through the skin and between the fibers of the deltoid on the point of the shoulder over the greater tuberosity. When the fascia beneath the deltoid was reached a small opening was made in the subdeltoid bursa, and this was enlarged with scissors to an extent great enough to admit the forefinger. The aspect of the bursa was not abnormal inside except for some firm adhesions anteriorly which made it difficult to separate the plane of the bursa from the neighborhood of the bicipital groove and the anterior part of the greater tuberosity. With the finger in the opening, it was found that during the rotation of the humerus, a mass corresponding to the shadow seen in the X-ray could be felt to pass beneath the finger. This mass evidently lay at the base of the bursa on the top of the greater tuberosity. An incision was made into it permitting the escape of about half a drachm of sebaceous material resembling the contents of a dermoid cyst. The cavity, which resembled a wen or dermoid, was thoroughly curetted and the walls excised. The base of it was evidently the tuberosity and tendon of the supraspinatus; the roof was the base of the bursa. When the sac had been entirely removed, it was found that the motion of the joint under ether was perfectly normal, rotation and abduction being easily performed. The incision in the bursa was not closed and the skin was drawn together with silkworm gut and the arm put in the ordinary sling position. Remarks : The point of particular interest in this case is the persistence of the function of rotation in spite of the limitation by abduction. It is obvious that the position of the cyst allowed rotation with comparative freedom, but that attempts at abduction would crowd the cyst between the greater tuberosity and the acromion process and caused pain and spasmodic rigidity of the joint. The acuteness of the symptoms within the last eight days is explained by an inflammatory condition in the cyst. The previous attacks were probably due also to the same cause. That this inflammation did not involve the bursa to any great extent is shown by the persistence of rotation. Since the bursa was not inflamed it would be readily seen that the symptoms which the patient complained of in regard to going to sleep with the arm behind his head can be explained, for the cyst having once got under the acromion was relieved of pressure. In other words, it was only when the cyst was inflamed by over exercise that its presence was noticeable, unless elevation of the arm crowded it between the acromion and the tuberosity. The relief obtained by this operation was immediate and permanent. It will be seen by comparing these notes with the description of the operation by Dr. Painter that the calcareous deposit seemed to me to lie not in the bursa, but beneath its base, and in or adjacent to the tendon of the supraspinatus."
It was difficult to find a heading for this chapter, and the one chosen is not satisfactory. An explanation of why it is not satisfactory may help the reader to understand the subject the caption is supposed to define. "Calcified subdeltoid bursitis" is a term in common use for the same condition, but this could not be accepted as a title for three reasons. First, the calcified deposits are rarely in the bursa, but lie beneath its base in the substance of the tendon of the supraspinatus or in one of the tendons of the other short rotators. To be sure, occasionally after inflammation has occurred the softened tissue containing a deposit bursts (See Plate II, Fig. 4) and the calcified particles are diffused throughout the bursa, the outlines of which may then be delineated by the X-ray. Fig. 44 shows an instance of this, but Figs. 45 and 46 are instances of the usual condition where the deposit is in its place of origin in the substance of the tendon, entirely beneath the base of the bursa. Therefore, "calcified subdeltoid bursitis" is a misnomer. It is also a wrong term because, as is explained on page 18, subacromial is a better term than subdeltoid. A third reason is the use of the word bursitis, as the noun which "calcified" is used to qualify. The bursitis is secondary to the pathologic process in the tendon. One may find no inflammation of the bursa and yet a large deposit beneath it may be demonstrated by the X-ray. It is only when the deposit is large enough, or the inflammation about it is great enough, to cause interference with the function of the bursa, that the symptoms of "bursitis" appear. Our chosen title is also unsatisfactory because the offending deposit may not be in the supraspinatus tendon but in one of the other tendons underlying the base of the bursa, for instance, in that of the subscapularis. The infraspinatus and teres minor tendons may occasionally be involved. (See Figs. 45 and 46.) Sometimes two, three or even four tendons in the same patient are the seats of deposits. It seems to me highly probable that in most cases which show the deposit in one tendon there may be also a "tendinitis," or at any rate a degenerative change in the other tendons, which is not accompanied by much calcification, and therefore is not demonstrated by the X-ray. Furthermore, I am confident that I have seen instances in which the same tendinitis has produced bursitis by involving the base of the bursa before any calcification dense enough to be demonstrated has taken place. We might change the title to "Calcified and Uncalcified Changes in the Tendons of the Supra-spinatus, of the Subscapularis, of the Infraspinatus and of the Teres Minor; the Secondary Changes they may cause in the Subacromial Bursa overlying them, in some cases producing the Clinical Condition known as 'Subdeltoid Bursitis,' which should be called 'Subacromial Bursitis.'" Even this extensive heading can be criticized, because there are still many cases never diagnosed as bursitis, but which pass as "neuritis." I might head the chapter "The Usual Cause of Neuritis in the Arm and Shoulder." In 1908 I wrote as follows regarding subacromial bursitis: "The cases which are to be discussed in this paper are by far the most common lesions of the shoulder joint. It is the writer's experience that more patients seek hospital treatment for lesions involving the subacromial bursa than for all other lesions of the shoulder joint, including tuberculosis and fractures, added together." "Not only is this true, but it is also true that more cases of subacromial bursitis seek hospital treatment than all the cases of the supposedly more common forms of bursitis such as 'miner's elbow,' 'housemaid's knee,' and 'weaver's bottom.' In those clinics in which these statements are apparently not true it will be found that these cases are passing unrecognized under the diagnoses of brachial neuritis, periarthritis, muscular rheumatism, circumflex paralysis, contusion of the shoulder, fibrous ankylosis, gout, rheumatism and other vague terms." These convictions have gained strength with the years, although I now wish that I had expressed them in better English. It may be almost taken for granted that cases diagnosed as neuritis, rheumatism, and arthritis of the shoulder, are really instances of subacromial bursitis; those with a distinct traumatic history being usually cases of bursitis due to rupture of the supraspinatus, and those of spontaneous origin being instances of the process I have tried to define above. Perhaps this seems a sweeping statement to the many physicians who still believe there is such a thing as brachial neuritis in otherwise healthy people; yet the statements are made in all sincerity by one who has studied the shoulder intensively for twenty-five years.
FIGURE 48. VARIED VIEWS OF A CALCIFIED DEPOSIT IN SUBSCAPULARIS
Tracings from three different films of a case in which a calcified deposit had formed in the subscapularis and had caused acute bursal symptoms. The deposit lying in the substance of the subscapularis tendon of course did not move about in relation to the lesser tuberosity; the apparent change of position is entirely due to changes in the relation of the bones in consequence of rotation of the humerus. The first film was taken in the anatomic position, and the deposit is overshadowed not only by the contours of the humerus but by the acromion. The second film was taken in internal rotation and the deposit appears to have moved over to the top of the glenoid. The third figure shows the deposit when the arm is akimbo; i.e., partly abducted and internally rotated. The deposit appears to have traveled to the lower edge of the glenoid. This patient was operated upon by the writer, and the deposit removed. The incision was the same as in cases in which the deposit is in the supraspinatus; the affected area was just as readily brought under the incision by external rotation of the arm. Deposits in the subscapularis are more frequently horizontal in their long axes than when they are in the other tendons. Compare Plate VI, Fig. 6. Sometimes they are not horizontal as in another case shown in d and e.
In order to make the condition plain the shadow of the deposit has been slightly intensified in these cuts. In the anatomic position (d) the deposit shows as a small speck internal to the bicipital groove, which in most antero-posterior X-rays can be located by the dense line of the outer edge of the lesser tuberosity. This line is an important landmark in X-ray interpretation, for by its position one may determine to a certain extent the degree of rotation of the humerus, and therefore make a reasonable guess at which facet shows on the contour of the greater tuberosity. Figure e is taken with the humerus held nearly horizontally and rotated inwardly as far as possible; i.e., the arm is in a high akimbo position. The deposit now shows in profile on the lower margin of the head of the humerus. Compare this plate with Figure 26, which shows an arm in the hammock position, in which the profile of the lesser tuberosity appears superior to the head of the bone.
The relation of trauma to the calcified cases is not yet clear. Since I first studied the subject I have always felt that it was highly probable that an acute or chronic injury to the tendon must occur long before the deposit appears. The pathologic histology of the lesion itself might be accounted for by faulty repair of an injury in tissue which has little vascularity and would be slow to restore itself. This was J. H. Wright's view from some tissue which I gave him. On the other hand, the fortuitous finding of the specimen shown in Plate VI, Fig. 5, indicates that the first change may be degeneration in the interstitial part of the tendon. Moschcowitz feels that the primary process is a tendinitis. Meyer, investigating from anatomic material, feels that both the biceps tendon and that of the supraspinatus may be attenuated from friction in overuse. I take issue with Meyer on the ground that I believe that destruction by friction per se does not occur in living tissue directly. Friction would first produce inflammation with resulting attenuation and atrophy of the part. I would expect in such tissue, if the local area became sufficiently poor in synovial lubrication, that congestion, tenderness and protective reflex spasm of the adjoining muscles would occur long before friction per se could do any damage. Whether the attrition be directly from friction or indirectly from atrophy following inflammation due to friction, the fact is that we rarely find ruptures of the supraspinatus in any but the aged laboring classes. The calcified cases on the contrary occur in young or middle-aged people, and moreover, they are usually not in people who do heavy laboring work, but in the more highly educated classes who do sedentary work, using the arms in a slightly abducted position for hours (See p. 135, Chap. V). Since the calcified cases are, as a rule, in the middle-aged, and the rupture cases in persons at least elderly, some relation may exist. Perhaps aged cases in which rupture occurs had the tendinitis and calcified deposits in their earlier years, and thus had their tendons weakened and made prone to rupture. Or perhaps in youth strains which would rupture the tendons in older people result in merely the rupture of a few fibers. The capacity for repair is then great and restoration results. The same force in middle life might cause a slightly greater damage with hemorrhage into the tendon followed by faulty repair and calcification. Still later in life the same force might tear the aged tendon hopelessly. A partial parallel to this hypothesis is found at the knee, where the same kind of force in early youth avulses the tibial tubercle; in middle life the patella is the weakest point and gives way transversely, but in the aged the quadriceps extensor tendon yields in many cases. In other words, the relative tensile strength of the tissues has changed with age. Although it is the rule that cases of calcified deposits recover with no known sequelae, I am more and more inclined to think that they must result in some atrophy of the tendon, whether they are absorbed naturally or are removed. I cannot believe that complete and sound repair takes place. This belief arises chiefly from a study of the microscopic changes which consist largely of a necrosis of the fibers. I incline to the belief that these same tendons may be prone to rupture in later years. The Workman's Compensation laws (through the pertinent questions they put into the mouths of the members of Accident Boards and of Insurance lawyers) are sharpening the wits of modern Industrial surgeons in many ways and are having their effect on shoulder surgery also. As these little calcified deposits now cause loss to the insurance companies, they are assuming more importance than when they only bothered the individual patient. We are confronted with cases in which a slight trauma is alleged to have occurred and in which, after a lapse of a few days or weeks, disability has appeared and the X-ray shows the shadow of a deposit. Did the lesion precede the trauma? If so, did the accident aggravate the symptoms enough to make the difference between inability and ability to work? May the occupation which called for unusual or repeated use of the affected tendon have caused the lesion prior to the alleged accident? Since in cases not associated with accident at all the symptoms frequently come on suddenly, might not the association with a trivial accident be merely fortuitous? The answers to these questions can be founded on so little in the way of statistics or demonstrable facts that they come into the realm of expert testimony and are matters of opinion only. I will try to set down my own opinions and what few reasons I have to support them.
Precedence of trauma or lesion (i.e., of a single definite trauma). Since in a general way we know that the process of calcification of dead or injured tissue requires a considerable time, it is pretty clear that the lapse of only a few days after the trauma before the X-ray was taken would indicate that the lesion had existed prior to the trauma. The same would probably be true a week or two after the trauma, but there would be increasing doubt as the interval progressed from weeks into months. I incline in general to think that the lesion precedes the trauma even when the X-ray is taken months later because (1) I have seen no instances where an early X-ray showed no deposit and yet a later film demonstrated one. (2) Because I have seen many cases where the X-ray did show a deposit soon after the trauma. In other words, in my experience the calcification usually preceded the trauma and I have never been able to satisfy myself in any case that it followed the accident. It not infrequently happens that the X-ray will show a quiescent deposit without any symptoms in the supposedly well shoulder, as well as in the traumatized one. In fact, bilateral deposits are so common as to make us doubt whether acute trauma is ever a cause. They suggest that the primary cause is a general one. For instance, a systemic one; an attitudinal one; a congenital morphologic one. Yet in persons who use to excess both arms in their daily work, a chronic traumatic cause might be postulated even in bilateral cases.
Aggravation by trauma. Any one who has seen the bursa opened at operation and beheld the angry, red tumefaction with its white or yellow summit would agree that a blow on the inflamed area or even a sudden excess of tension on the tendon might aggravate the condition. One can readily see that the softened area might burst and spread its contents into the bursa under such circumstances. And it is clear that a trauma need not be very severe to do this. Yet to have the deposit burst into the bursa is in my opinion nature's way of curing it (Fig. 34). The acute symptoms are often soon followed by complete and permanent relief!
Excessive use as a cause. I am inclined to believe that this is the most common contributory cause if not the primary one. There are many instances besides "writer's cramp" and "housemaid's knee" to support the statement that in our division of labor the abuse or overuse of particular organs or tissues results in pathologic changes. Millions of years of heredity have not prepared the modern stenographer or machine operator to keep their supraspinatus tendons stretched and under tension, on the qui vive hour after hour, day after day. While only a few individuals in these employments have a severe tendinitis or bursitis, I believe that could we see the supraspinatus tendons from a series of stenographers who have worked steadily five years or more, some pathologic change would be found in them. Miners do not all have "miner's elbow," but I venture to say that all those who habitually work on their elbows would show hypertrophic and degenerative changes in their olecranon bursas. It is therefore my opinion that when disability arises from these calcified deposits in industry, the presumption should be that they are "Industrial," unless it can be shown that the occupation is not of a nature to demand overuse in this region of the body, or that the patient at home pursues an avocation which causes such abuse. Nevertheless it would require many months or years of such abuse to produce a typical "calcified deposit," for the minute pathology of these lesions is of a chronic type, although the inflammation about them may be very acute.
Coincidence of onset with trauma. It is certainly true that many cases have a sudden onset of acute symptoms with no history of trauma. It is easy to suspect in any given case that trauma was only an afterthought to get compensation. I have suspected this was so in some cases, but in others there was a clear history of accident, leaving little room for doubt that the accident precipitated the symptoms. It seems to me that no rule can yet be formulated and each case must be decided on its own merits; the more vague the story, the less likelihood that the course of the trouble was influenced by the trauma. The character of the occupation, the condition of the other shoulder, the duration of the kind of work, and other circumstances should be taken into account. At present my tendency is to consider such cases as instances of coincidence, even when the symptoms followed soon after the accident and the X-ray was taken weeks later. It is so easy to hit any sore spot in the body and to attribute the soreness to the blow which drew attention to it! Add to this the incentive to obtain compensation and the psychologic fact that it is human nature to influence one's self into any belief in which one's fancied interest lies. Nevertheless I would not deny that a single trauma (if well proved and of sufficient force) could be the direct cause of the onset of disabling symptoms. Furthermore, in doubtful cases it is only just to remember that it is likely that the occupation itself may have been the underlying factor.
Symptoms. Symptoms may be absent entirely and yet the X-ray may show a large deposit. This fact is particularly striking in the bilateral cases, for one side may be symptomless and the other the cause of agony. Radiologists not infrequently find these symptomless deposits accidentally. Yet these facts do not prove that the disease may run its entire course without symptoms. On the contrary, since we often see a large deposit in a case which has had symptoms for only a day or two, it is clear that a symptomless case may at any time present symptoms. Therefore, we doubt whether any case ever runs its whole course without symptoms. Most of the bilateral cases I have seen had one symptomless shoulder at first, but perhaps a year or two later had typical symptoms come on in the other. I have yet to see a case in which a good-sized deposit disappeared without ever causing pain or restriction. Beyond question the X-ray demonstrates that spontaneous absorption takes place in most cases, although some such instances may be errors of X-ray interpretation. Some certainly discharge into the bursa and are absorbed from there. Whether there are actually cases which never give symptoms and run their whole course without complications, I do not know. Many never give severe symptoms. Most cases run a subacute course, a few are exceedingly acute, and a few are truly chronic. An attempt to classify cases strictly in this way results in confusion, for we find many cases which are borderline and others which in their course pass through all three stages. The usual history is not of acute pain at the beginning. The first symptom noticed is a slight, painful "hitch" during certain movements of the arm, such as in raising one's arm to put on a coat or in placing an object on a shelf. Sometimes reaching across a table for some object, as a pen or a salt cellar, causes this feeling. Women complain that they cannot do their hair. Little attention is paid to this until it becomes associated with every such motion. The slight pain becomes expected and eventually dreaded before such motions are performed, so that the patient corkscrews his arm in a peculiar way to avoid the "hitch." Instinctively he learns to rotate outwardly as he abducts and thus avoids pinching the inflamed point under the coraco-acromial ligament as the arm is raised. Presently the sensitiveness reaches such a point that involuntary scapulo-humeral spasm is produced, and the normal, smooth division of motion between the movement of the scapula on the chest wall and the elevation of the humerus on the scapula is destroyed.
Loss of Scapulo-humeral Rhythm. Normally when one raises the arm to a position pointing straight toward the ceiling, much of the motion is performed by rotation and elevation of the scapula on the chest wall, while the remainder is performed by the true joint. (See Fig. 25.) The two motions go on pari passu, so that as one watches from behind it is impossible to say that either motion proceeds faster than the other. In nearly all affections of the joint or bursa, this even distribution of motion is destroyed, because the sensitive point, unwilling to move, sends its reflex telegram to the short rotators to lock the joint in a fixed position and to hold it there by spastic tension. This phenomenon is one of the most important for the student of shoulder conditions to learn, and its behavior in these cases of calcified deposit is very characteristic. At first it is not complete, the spasm being semi-voluntary in the sense that the individual can control the inhibition of it to a certain extent. For instance, in mild cases the spasm holds the joint fixed as the arm makes its upward journey for about ninety degrees. Then the individual semi-consciously relaxes it and the joint surfaces themselves carry out the remaining ninety degrees to complete elevation. When the sensitiveness is still greater, even a strong effort of will cannot relax the spasm and the arm only ascends so far as it can through the scapular motion—almost straight out from the shoulder laterally. Later the spasm holds continuously night and day until firm adhesions form, producing a fibrous ankylosis which effectually splints the inflamed parts until they heal. When healing has taken place the adhesions gradually stretch and motion of the joint slowly returns. The course of this whole process in the most severe case is about two years. The fixation is never permanent. The great majority of cases do not have this severe course. Probably none would unless delayed by injudicious treatment.
The cardinal symptoms of the whole picture are pain, spasm, limitation and atrophy. These four symptoms may make a variety of complexes according to their relative severity. In one case pain may be the predominant one; in another, spasm; in a third, adhesion. I have seen cases which ran an almost painless course as if the spasm was started at once without the sensation of pain being experienced. The painful stage when the spasm is intermittent or semi-voluntary was absent; spasm from the early days was complete and adhesions took place before pain was felt in any considerable amount. The ankylosis stage persisted for months, the patient's chief complaint being from the limitation of movement. Some cases have relatively little spasm, no adhesions and constant pain. As a rule the amount of pain is inverse to the amount of restriction. The physician may relieve the pain by fixation of the arm and allow the adhesions to occur at once, but as I shall show later this is bad practice, unless the patient is one who can afford to avoid using the arm for many months. In most cases the "hitch" stage persists for many weeks with gradually increasing pain until past the stage of semi-voluntary spasm when restriction dominates the picture.
Pseudo-neuritis. If there has been a long, painful stage all the adjoining nerves become sensitized and the phenomena we call "neuritis " supervene even when fixation has occurred. The pain or hyperesthesia, originally mainly felt in the circumflex distribution about the shoulder and near the insertion of the deltoid halfway down the arm, becomes more diffused. It shoots up into the neck, on to the back of the shoulder blade and down the distribution of the radial nerve to the thumb and forefinger. Even the ulnar and median nerves may become sensitized, the hand and fingers swell and the skin over them becomes glossy. The picture is that of "brachial neuritis," but removal of the calcified deposits relieves it! When the patient has hugged this painful, tender, useless arm to his side for weeks it presents a most unnatural, misshapen appearance. The back of the hand and upper flexor region of the forearm are swollen, while the anterior portion of the wrist is not. The fingers are partially flexed and cannot be extended even passively. Meantime the sleepless nights, incessant pain, and the dread of incapacity and uselessness have had their dismal effect on the patient, who may reach a very pitiable condition. Drugs have only too often added to the unhappiness of the individual—the family has a querulous invalid to care for. Fortunately this picture is not the usual one nor is it frequent at present in this community, for nowadays the X-ray is sought for most joint conditions and locates the deposit; the condition is treated more hopefully and intelligently than when the diagnosis of "neuritis" was more common. Mild cases are far more frequently seen today. Pain at night and inability to get into a comfortable position is the most uniform and constant complaint in all stages of this disease whether in acute or chronic form. Even the adherent cases cannot sleep for long on the affected side. The average patient tells you that he could put up with the pain in the day if he could only get a good night's sleep. In the early stages before there is much spasm, relief may be obtained by sleeping with the hand behind the head. In this position the tender point lies beneath the acromion, where it has plenty of room and where the supraspinatus tendon is relaxed. It is probably the most favorable position for the blood supply to repair damages. Women seem to assume this position more readily than do men. If a patient told me that she had pain in doing her hair and could not get her arm comfortable at night without putting her hand behind her head, I should be pretty certain that she had a calcified deposit in her shoulder. If she added that there was pain in the lower fibers of the deltoid near its insertion in the humerus, I should feel still more certain. If I found a raised, tender point about the size of the tip of the finger on the greater tuberosity which moved as the humerus was rotated, I should consider the clinical diagnosis established, although subject to confirmation by the X-ray. The location of pain in the region of the lower fibers of the deltoid six inches or so below the real lesion, is a curious but very constant phenomenon in these cases, in all stages of their course. The complaint of pain in this region is almost diagnostic without other symptoms. I am uncertain whether it is to be explained as reflex pain or as directly due to spasm of the lower deltoid fibers. If one compares the two arms by taking the lower parts of the deltoids between fingers and thumbs of both hands simultaneously, one finds a distinct thickening, and there is often tenderness, too, on the affected side, such as would be produced by a tonic spasm of the fibers. The pain located here may be subordinated in the acute cases to the local pain in the bursa. One can in acute cases mark out the exact limits of the inflamed bursa by carefully pressing with a pencil tip and obtaining the patient's cooperation in locating the line of transition to acute tenderness. This is a very definite line and it may sometimes be vaguely seen when the bursa is distended with fluid and fibrin. Even when the bursa is the maximum tender point, the lower deltoid region may be the seat of maximum pain. There may be no local tenderness over the bursa and yet much pain and some tenderness in the lower deltoid.
Acute cases are characterized not only by the above-mentioned, distinct, local tenderness, but by excessive spasm and pain on the slightest motion of the joint. An acute attack may at any time appear in the course of a subacute or chronic case, but the most severe attacks usually appear without warning or known cause, though sometimes following a slight trauma. They represent the onset of bursitis from extension of the inflammation about the deposit in the tendon beneath the bursa. The symptoms are those of an acute bursitis and are homologous with similar acute inflammations in other serous cavities, i.e., congestion, friction, pain, protective spasm, fibrinous exudate, adhesion, cicatrization, partial absorption. The acute stage is therefore brief, lasting a week or two. It is during this period when the bursa is full of fibrin that it may be outlined as described above. The patient may wake at night with agonizing pain in the shoulder and be unable to move the shoulder joint more than a few degrees. Tenderness over the bursa is exquisite. Spasm has fixed the joint rigidly so that the arm is held in the sling position and the patient cannot be persuaded to move it in the least. One can take the patient lightly by the thumb and he will follow submissively where he is led, his whole body on the alert to avoid using the joint in the slightest degree. He cannot by any possibility sleep on the affected side and usually tells you that since the pain began he has "walked the floor" or had to sit up in a chair. For several nights no ordinary remedies give relief and considerable doses of morphine may be required. Exploration of the bursa at this stage usually shows that it contains fluid and fibrinous exudate overlying the boillike elevation on its base with its crimson, turgid periphery and whitish center. Until one has seen this appearance it is hard to realize how much these patients suffer. It is in such cases that the relief by operation is particularly striking, but they often get well promptly without operation or any treatment at all.
FIGURE 44a. BURSA DISTENDED BY FLUID CONTAINING CALCIFIED PARTICLES (Natural size) Case 141
FIGUBE 44b. A DISTENDED BUBSA IS CONCAVO-CONVEX (Size reduced one-half)
a. Shows the greatest distention of the bursa which I have ever seen from this cause. The film was taken by Dr. A. W. George, who referred the patient to me. I have, however, seen many bursse as much distended as this, in cases of rupture of the supraspi-natus, where the constant influx of fluid from the joint during efforts at abduction has dilated the bursa. Notice the gravitation of most of the calcified material to the bottom of the sac, which is bilocular, and yet enough particles have clung to the lining to cause its outline to show in the film. Case 141. b. Schematic drawing to show that a distended bursa is a concavo-convex cap beneath the deltoid and placed in an antero-lateral position over the insertions of the short rotators.
Such acute symptoms subside in one to two weeks, some cases being followed by adhesions of the bursal surfaces which last many months. More often, especially if the physician has not tried to help, the patient by binding up the arm, the spasm subsides, the soreness disappears, normal motion returns, the "hitch" reappears and the condition is the same or better than before the attack. There are various stages between these two extremes; in some cases the attack seems to clear up the whole trouble, but often more or less spasm and restriction remain for months. I am quite positive that in the cases which clear up, the soft material has perforated into the bursa and been absorbed there. In those cases which have been through an acute attack and on which I have operated long after, I have found the deposit drier and firmer and more crystalline in composition and more intimately combined with the fibers of the tendon than those operated on in the acute stage. The deposit is likely to be firmer in chronic cases which have never had an acute attack. Apparently in acute attacks invasion of leucocytes about the deposit produces a sterile pus which mixes with the finely divided calcareous matter and softens it to the consistency of cream or butter. This creates tension in the substance of the tendon and tends to make the softened matter point into the base of the bursa. For some unknown reason perforation does not occur into the joint. It is the inflammation of the synovial base of the bursa which produces the symptoms so suddenly and starts the sequence of friction, pain, spasm, exudate, etc. At operation one usually finds the softened material under tension, so that when the white or yellow head of the boil-like center is nicked with the knife the material is squeezed out, as if it had been pent up. The operation gives relief to the tension and is effective in the same manner as in opening a boil. It is an interesting fact that under local anaesthesia the patient may express relief as soon as the tension is lessened. It seems that in these acute cases there are two kinds of pain, a deep, severe ache due to tension in the tendon, and the friction pain of the inflamed bursa. I hesitate to describe a chronic form of this condition, since I have seldom known of an instance of more than three years' duration. Nor do I know how long symptomless deposits may exist. What I mean when I speak of a chronic case is one which lasts many months without going through an acute or adherent or neuritic stage. A case in which throughout its course the symptoms are confined to the painful "hitch," pain in the lower deltoid and a distinct rotating sensitive point, I should call chronic. In such cases the amount of the deposit as shown in the X-ray is usually small, perhaps minute, or even not demonstrable. Probably many such patients never consult a doctor. I see them more often among my friends who tell me casually about their symptoms, having heard that I am "interested in shoulders." Patients who consult me and have X-ray proof of the diagnosis and are told that the deposits are no harm in themselves, and that no operation is necessary unless the pain is severe, seldom come back to report when they are well. So that I can only give my impression that mild chronic cases do exist and that their duration, like the subacute ones, is seldom more than three years. As this was being written a patient on whom I had operated for a severe acute attack in his right shoulder, nearly eleven years ago, called to see me about his left shoulder. The right had remained well. Reference to my old notes showed that X-rays had revealed a deposit in his left shoulder at that time. He had been conscious that the left shoulder was not well, but it gave him no real bother until about six weeks ago, when mild symptoms began. They are still mild and he is taking diathermy. X-rays show that there is no deposit at present and there is a slight roughening of the tuberosity at the facet of the supraspinatus tendon, but there is no such roughening on the right side, which was operated upon. Evidently in this case the left ran a truly chronic course without complications. This one case, so far as it goes, indicates that the ultimate damage to the tendon may be greater if the deposit is not removed.
Atrophy of the spinati is found in all cases which have had severe symptoms for more than a few weeks. I have observed it in acute cases as soon as three weeks after the onset, and it doubtless may occur even earlier than this. Looking at the patient from behind one sees the spine of the scapula on the affected side more distinctly. In adherent cases this appearance is very pronounced and the shrinkage of the muscles may be so great that complete paralysis is suggested. I am inclined to think that in the worst cases the muscular bellies are in a condition resembling that of the muscles of the forearm in Volkmann's paralysis, which in fact is an ischaemia. However, they regenerate better under appropriate treatment. In such cases I am satisfied that rough manipulation under ether may rupture the muscles themselves rather than the adhesions in the bursa and joint. Atrophy of the deltoid is also usual; I have known of cases being mistaken for circumflex paralysis. The biceps also is as a rule more or less weak, and in long-standing cases all the rest of the muscles of the arm show the result of lack of use. The teres group is usually found in spasm and it is difficult to tell the amount of atrophy, for they are contracted in contrast to the spinati which atrophy in a stretched position. When one stands back of the patient and with forefingers in the axillae and thumbs behind the posterior axillary folds, and one palpates the muscles near the border of the scapula, one finds that those of the affected side are thicker and firmer than those of the normal side. Nevertheless, there may be atrophy of these muscles. The fact is that the spastic teres muscles are shortened by adduction of the arm and thus appear thick on palpation. Yet they may be shrunken as a whole although short and thick from constant spasm. These spastic muscles are always somewhat tender. This thickening and local tenderness of the teres group should not mislead us, for the cause of their sensitiveness and spasm is. not local in these muscles. In examining for shoulder lesions of any sort it is important to note the condition of the spinati. Atrophy of these muscles is an accompaniment of all lesions of the shoulder joint of a serious inflammatory nature. I do not find it in cases of malingering and of hysteria. Furthermore, its degree is a fair gauge of the gravity of the lesion, and also serves to gauge the prognosis. It may be seen from what I have said about the symptoms caused by calcified deposits in the tendons, that a strict division of cases into acute, subacute and chronic cannot be made. I cannot take my own series and pile them in three groups of records after this manner. Neither can I separate them into adherent and non-adherent cases satisfactorily". Restriction of motion may be slight or complete and of all degrees between. Yet these divisions are all clinically useful, though ill-defined, and mean something, at least for a time, in individual cases. A corollary can be drawn from this that prognosis is uncertain. One cannot tell in a given case exactly what its course is to be. This makes advice as to treatment and comparison of results very difficult.
Restriction of motion is usually in one or both of two different arcs of motion, i.e., in external rotation and in elevation. When elevation is restricted and external rotation is free, one should suspect at once a condition in which the inflammation about the calcified deposit is great enough to make a mound in the base of the bursa, but has not yet created irritation of the synovial lining of the bursa. Rotation is painless because the inflamed, raised spot can rotate under the deltoid without striking any hard or any firm tissue. On the contrary, when abduction or elevation is performed, the inflamed mound is pinched between the tuberosity and the acromion or coraco-acromial ligament. The pain thus caused instantaneously produces scapulo-humeral spasm and the upward movement is restricted. Let this patient stoop over as far as possible with his shoulder muscles relaxed and the arm abducts on the body by gravity. The tender point rides easily under the acromion in this position because the supraspinatus is not acting to produce tension about the deposit, nor is the deltoid pulling the humerus vertically upward against the acromion. If the patient then fixes his shoulder voluntarily, he can stand upright with the arm elevated. Such cases as I have just described can usually be separated from malingerers, because one can always find the rotating tender point where the deposit is, for it is easily felt as it passes beneath the deltoid fibers. Furthermore, having made the patient stand with the elevated arm, he will be seen to have a "hitch" or a period of scapulo-humeral spasm as he lowers it from the vertical position, and the tender point in its downward journey again passes the narrows under the acromion. This sign is also a sine qua non of complete rupture of the supraspinatus, but in the latter no calcified deposit is shown by the X-ray. A symptom which is occasionally seen in these cases is what I call the "down-it-will-go" symptom. It is rather infrequently complained of, but often acknowledged if asked for. Patients with complete rupture also show it. A patient will say that the arm is paralyzed or that he is afraid it is going to be paralyzed. He reaches for some small object or is carrying one, and "down-it-will-go." It seems to be an involuntary sudden relaxation of the grasp. It frightens the patient, although it is usually spoken of diffidently or with an apologetic laugh. It is irregular in its occurrence. I cannot explain it, but my theory is that it is a phenomenon associated with position sense. I have already stated that in some cases spasm starts without pain. In a case of circumflex paralysis which I observed, and on which I operated under local anaesthesia to see whether the supraspinatus was torn, I found that the interior of the bursa and the joint were completely insensitive although the skin sensation was present. In a doctor on whom I was operating under local anaesthesia for a calcified deposit I could at will start spasm without pain by touching the base of the bursa. These observations indicate that the bursa and joint are supplied by nerves which do not transmit ordinary tactile pain but serve to excite the scapulo-humeral reflex. It may be that this "down-it-will-go" symptom is something caused by this set of nerves, when, in reaching for the object, the sensitive point comes against the acromion. Without consciousness the grasp relaxes in order to get rid of the weight which, by leverage, increases the pressure on the tender point. In this connection we also have the phenomenon that the pain in these cases is as a rule attributed to a point near the lower insertion of the deltoid.
FIGURE 45. CALCIFIED DEPOSIT IN THE TERES MINOR In interpreting X-rays of calcined deposits one must be sure of the position in which the film is taken in order to say positively that the calcified material has escaped from a tendon into the bursa. This is particularly true in cases where the deposit is in the teres minor, as in this picture. The insertion of the teres is very low and if, as in this case, the view is taken with the head of the bone in inward rotation, the deposit appears to lie in the bursa, when in reality it is still confined within the tendon substance
FIGURE 46. CALCIFIED DEPOSIT IN THE INFRASPINATUS Figure 46 was taken with the plate on top of the shoulder and the rays nearly parallel with the long axis of the humerus, in order to bring out the bicipital groove. The prominent deposit in this case was in the infraspinatus, as is shown by the fact that it is about one-half inch exterior to the bicipital groove. There is also some deposit in the supraspinatus which shows poorly in this picture, for it is overshadowed by the tuberosity.
There should be some differences between the symptoms of cases of deposit in the subscapularis and in the supraspinatus. The location of the tender point, whether inside or outside of the bicipital groove as shown by the maximum spot of tenderness, is my usual way of differentiating. Careful study of the X-ray is confirmatory. Whether the symptoms themselves differ I am not sure. One would think that external rotation would be limited in subscapularis cases, but I have not found this true enough to rely on. A recent quite acute case had no such limitation. Another case of bilateral subscapularis deposit which occurred in my own household had symptoms quite like those in a supraspinatus case except in the location of the tender spot. My series of cases is not large enough to make comparison, but the point is important because it helps in performing the operation. The X-ray should confirm a diagnosis of calcified deposit, but one should be very exacting in demanding excellent technique and films made from several angles before making a negative diagnosis when the clinical picture is typical. This is particularly important in ruling out a deposit in the subscapularis tendon. A recent instance was only positively diagnosed by a fourth film which showed the deposit in profile. The deposit was large, but in the first three positions the shadow overlaid the bone in such a manner as to elude experienced eyes, although after the fourth film it could be identified in each picture. A very slight rotation of the humerus may throw the shadow over the bony outline, especially if, as often happens, there is only a mere fleck of calcareous material. Even a large recent deposit of little density is easily overlooked. The Rontgenologist must learn to take pains to get each facet of insertion in profile. Even before calcareous material is demonstrated by the X-ray, the diagnosis on clinical signs alone may be made with a considerable degree of certainty.
Since the prognosis of these cases is always eventually a good one, and since in any given case the probable course cannot be foretold with certainty, no treatment of a dangerous nature can be considered. Even a risk of any permanent minor damage would be unwise. All cases, whether treated or not, in which I have known the late result, have recovered without permanent complications of any kind. Recovery is only a question of time. The object of treatment is purely one of the relief of symptoms. Any one who wishes may endure the whole course of the trouble without other treatment than palliative remedies such as occasional doses of aspirin or the application of an ice bag or a hot water bottle. Many acute cases following perforation recover in a few weeks. Some persons prefer to endure daily pain month after month rather than to submit to a minor operation or go to the trouble and expense of prolonged treatment by physiotherapy. My personal opinion is that surgical removal of the deposit is practically free from danger, sure to relieve the severe symptoms at once, and, in fact, that it generally will relieve all really troublesome symptoms within a few weeks. It is not a painful operation; it can be done with local anaesthesia; it requires only a few days of hospitalization, and there is very little postoperative pain as a rule. It seems to me that the patients whom I have followed through an acute attack suffer more in forty-eight hours than does a patient who has been operated upon in his whole convalescence. I have performed the operation on a number of doctors, who have previously had acute attacks, and they have been of the same opinion. Furthermore I have seen, in subacute and chronic cases, the constant neuritic type of pain with consequent loss of sleep, reduce patients to a very serious physical condition, the relief of which would justify a much more dangerous operation. It therefore seems to me that it is better to have the deposit, if large, removed as a routine, than to run the risk of either an acute attack or of severe chronic pain. It is quite reasonable for a patient to say, "But I may never have any severe pain, and then the operation will have been unnecessary." This is quite true and the answer is that there is little objection to waiting until the actual pain makes the prospect of operation more welcome. It would be hard to say for another individual how much annoyance and loss of sleep is equivalent to the operative pain and discomfort. Certainly pain sufficient to prevent work is enough to demand an operation of the trivial character of this one. Statistics as yet cannot show in a given case what the chances are that serious pain will ensue. I think it is fair to say that the severe pain is relieved at once by the operation and that the patient may expect the return of full use of his shoulder in from three to six weeks, although he may feel twinges of pain in extreme positions of the arm for several months. In general my attitude is: "If I had your trouble I would prefer operation as the best way to avoid pain and disability. You will get well anyway, but your total pain and discomfort is pretty sure to be worse and likely to be much worse, if you are not operated upon. I advise you, but I do not urge you, to have this deposit removed. There is no danger of your having a crippled arm or any permanent trouble, whether treated or untreated." Many patients, on receiving this advice and reassurance that they will not lose the use of their arm, prefer to endure the pain, annoyance and discomfort. Others ask what other treatment there is apart from surgery. The answer is that aspirin and similar drugs will help them bear the pain, particularly at night. Morphine will relieve the pain, but its use for more than a few nights is of real danger, for the pain may last many months and a pitiable habit result. No drugs are known which will cause absorption of the deposit when taken internally. Since the deposit is deep in the tissues and covered by skin, fat, fascia, muscles and blood vessels, in which the blood is circulating, no local applications as ointments, linaments, iodine, etc., can reach the lesion and do good. The most that can be expected would be slight, temporary relief from counter irritation, such as is gained by hot or cold applications. Massage and manipulation and active or passive exercises might be harmful unless most judiciously performed. After the acute symptoms are gone these agents may be helpful in restoring motion if it has become restricted. Very acute cases are apt to be very brief cases, and their spontaneous recovery may be coincident with surgical or other therapy. I know of no form of electrical treatment which might be expected to remove the lesion except diathermy. It is rational to hope that the use of this form of physiotherapy might help nature to absorb the deposit and resolve the exudate about it. It is held that diathermy heats living tissues through and through, and the effect of this heat on such deposits has been claimed to cause absorption. Since these deposits are naturally absorbed in varying periods, it is difficult to be sure that their disappearance under treatment by diathermy is not a coincidence. No attempt so far as I know has been made to check up a series of cases so treated with an untreated series. The same criticism applies to the results of surgical removal, but we know then, that the deposits, and symptoms as well, are removed. In some cases I have operated after the patient had been treated with a course of diathermy, and yet found a large deposit. In others so treated the X-ray has continued to show the deposit for some months after the symptoms were relieved. However, it makes little difference whether or not the deposit is removed, if the pain disappears. I have known of a few cases in which this has happened after a few weeks or months of treatment by diathermy. They were relatively mild cases. In others I have operated when diathermy failed to remove either deposit or pain. Furthermore, after perforation in the bursa has occurred the deposit absorbs spontaneously within a few weeks. Yet if a patient wishes some treatment other than operative, I advise diathermy. I do not use it in my own work for two reasons. First, being inexperienced with its use, I should fear the danger of burning the patient more than I would the danger of surgery. Second, I know that operation permanently cures; I have some faith that diathermy will assist the natural process of repair. Dr. E. B. Mumford of Indianapolis, who is a prominent orthopedic surgeon, believes that diathermy is the treatment of choice (Jour. A. M. A., Vol. 97, No. 10, 1931, pp. 690-694). He gives details of his technique. "All of our cases became well by this conservative form of treatment and in all cases with a deposit shadow, the deposit either entirely disappeared or became much smaller in size and less dense in the X-ray. In none was surgery necessary. The average number of treatments was twenty-one, given daily for the first two weeks and then twice a week. Relief from pain was obtained in from three to ten days. The end result was complete restoration of function without pain. Ten cases have been checked at the end of one or more years and no recurrence noted." I am far from denying that diathermy is effective. It is too bad that comparative tests of different forms of treatment cannot be made. One thing is greatly in favor of diathermy, and that is that it is necessary for a surgeon to know the anatomy and pathology of this particular region if he is to obtain uniformly excellent results by operating. There is one form of treatment not uncommonly given, which I believe is to be heartily condemned, i.e., fixation by strapping or bandage. In my opinion many of these cases are made worse by this treatment, which encourages adhesion of the roof of the bursa to the inflamed tendon. All the periarticular structures become fixed, the muscles atrophy and become ischemic and contracted. Many months may pass before the joint moves again, although ultimately it always does become mobile. The neuritic symptoms are particularly troublesome in such cases, although sometimes the ankylosis is entirely painless and the patients are only inconvenienced by the restriction. Spontaneous scapulo-humeral spasm is a sufficient guard for the inflamed joint and we should neither add to it with straps and bandages nor fight it with forced motions. Active "swinging exercises," with the patient in a stooping position, should be used in most cases. When the patient stoops the strain is taken off the supraspinatus and it is far easier to move the joint. I regard it as very unwise, until the convalescence is well advanced, to allow the patient to exercise the arm in a standing position because this forces the supraspinatus to cooperate with the deltoid in supporting the weight of the arm. The pain caused by this at once starts scapulohumeral spasm and the joint ceases to move. It is better to let the patient stoop with the arm hanging relaxed. If the patient straightens up again as soon as spasm begins, he will in fact adduct the arm. In other words, when one stoops with the arm relaxed one abducts (elevates) the arm on the body; when one straightens up with the arm relaxed, one brings the arm into the anatomic position.
FIGURE 47. STOOPING EXERCISES
The principle of the stooping exercises is that they permit the patient to abduct the arm by gravity and therefore no fulcrum is needed. If a patient elevates the arm in the standing position, the humerus obviously must obtain a fulcrum on either the glenoid or on the acromion or on both, while in the stooping position no fulcrum is necessary. In the standing position the little supraspinatus must pull the tuberosity firmly to keep the latter from touching the acromion. In the stooping posture it may remain relaxed. Since the sore point in most lame shoulders is on the tuberosity at just the region where it tends to obtain a fulcrum on the acromion, it is highly important that the patient with a damaged supraspinatus should not delay his recovery by frequently raising his arms. The exquisite tenderness which arises in these cases is nature's defensive effort to warn the patient not to use the arm in this way. When the patient with the sore shoulder is in the stooping posture he can much more readily brush his hair, button the back of his collar or perform any other motions. He can, for instance, learn to put on his shirt and coat over the lame arm when stooping, and then after he has risen to the erect position put on the other sleeve. When in the stooping position, either lateral or antero-posterior motions can be done with a pendulum-like movement without great muscular effort. In this position the humerus not only tends to avoid a fulcrum, but actually the weight of the arm helps to stretch the contracted tissue of the joint.
The principle of "stooping exercises" is useful in many ways. Gentle exercises of this kind prevent adhesions following the acute or subacute attack. Vigorous exercises loosen up adhesions already formed. Gentle postoperative exercises hasten convalescence; too vigorous ones start scapulo-humeral spasm and delay recovery. It is unwise to give passive exercise or permit active exercise which causes even moderate pain. Yet to fix the arm in bandages to relieve pain is also unwise. When one has seen the inside of these inflamed bursas one can readily understand the danger of either fixation or over exercise. Gentle motion, unhampered by bandages or spastic muscles, is indicated to prevent adhesions. The patient should be allowed to change the position of the arm as freely as he cares to. He should be instructed to keep it in external rotation as much as possible, because an arm held in the sling position is in internal rotation, and if it adheres in this position, it requires a long time to gain normal external rotation. We should avoid scapulo-humeral spasm not only because it promotes adhesions, but because much of the actual pain due to the spasm pressing the inflamed parts together. Spastic muscles are not only painful but tender. In two early cases with very small deposits and mild symptoms I have tried the experiment of keeping the patient in bed with the arm abducted, in the way in which I treat cases in the non-calcified type. (See p. 218.) This treatment seemed desirable for several reasons. It is the natural position assumed by many patients to obtain ease; i.e., they sleep with the hand behind the head. In this position the supraspinatus is relaxed and its tendon is not stretched; this would permit an active blood supply to promote repair. This position would bring the inflamed portion of the tendon wholly under the acromion, where it could not adhere readily, and if it did adhere would tend to loosen from mere gravity. Both cases were soon relieved. Another form of treatment remains to be mentioned—aspiration as suggested by Flint. After Flint's publication I tried this once with some success. I am satisfied that in this case I actually punctured the deposit and allowed it to leak into the bursa and thus relieved the pain. This was not exactly Flint's plan, but may also have been his achievement in his cases. I have opened so many bursas without finding much fluid that I doubt the wisdom of trying this procedure. Like most needling in other tissues, it seems to me to carry all of the disadvantages of an exploratory incision and some serious ones of its own. It would be rational to thrust a large aspirating needle into the deposit under guidance of the fluoroscope, but I would prefer to be operated upon were I the patient. As in the case of many other ailments which affect the human body, there is great variation in the degree and duration of the pain it produces. Even very acute cases may recover completely in a few weeks with the simplest palliative treatment. Therefore any form of therapy is deceptive in its results. I have often had a patient postpone accepting my advice for operation and seen recovery promptly ensue! No surgeon should feel as did Jack Horner and say, "What a big boy am I!" after removing one of these deposits. These rapid cures occasionally occur after any of the other forms of therapy, for nature does the work in spite of what we do at the same time. Yet at the present date, I can unhesitatingly say that unless there is some good reason to the contrary I should advise operation in all painful cases, and in all cases where the deposit is as large as a lima bean, even if there is no pain. I sincerely believe that operation is a far less serious matter than fixation, and no more dangerous than diathermy or intravenous therapy.
END RESULTS IN CASES OP CALCIFIED DEPOSITS
The following study is based on an analysis of twenty-nine replies to a questionnaire recently sent to patients on whom I had operated for this condition long enough ago to indicate whether there have been any unpleasant after effects, due to the operation, recurrence of the lesion or other complications. The period elapsed since the operation was ten to twenty-four years in nine cases, five to ten years in eight cases, and one to five years in eleven cases. All these patients stated that they had had no further trouble of any kind with the shoulder which had been operated upon, but ten had had similar trouble of minor degree in the other shoulder. In most of these cases there had been evidence of deposits in the other shoulder at the time of operation. These data confirm my impression that when these patients have been operated upon their symptoms do not return in the same shoulder. Furthermore I have not known of any late complication which followed about forty other similar operations on patients who did not reply to this particular inquiry. Two patients whose deposits were in the subscapularis, will be given separate consideration later, and are not included in the following resume of the replies to the questionnaire. As in the case of most questionnaires, some of the answers were not satisfactory. For the sake of brevity, doubtful replies to individual questions will be omitted without making such notes as "answer equivocal," or "not stated." Consequently in the following analyses the sum of numbers in each statement will not always be twenty-nine. Antecedent Trauma. Twelve stated that the attack followed a definite injury; thirteen stated that there had been no injury; three were uncertain. These figures are also in accord with my whole experience, which is that the injuries are usually trivial, and often uncertain. In compensation cases one is tempted to think that the history of injury may be purely an afterthought, although about half the cases may be said to give a definite enough history of trauma to account for rupture into the bursa. For instance, the twelve injuries were:
No. 79, business man, "Throwing baseball"; No. 81, iron worker, " Pulling on heavy bar"; No. 103, osteopath, "Fall"; No. 105, no occupation, "A bad fall down stone steps, and a sudden wrench later on"; No. 113, physician, "Fell on elbow with arm held rigidly against chest"; No. 121, surgeon, "Fall on stairs with violent swing of arms in attempt to preserve balance unsuccessfully"; No. 122, housework, "Wrenched shoulder in effort to avoid fall on staircase"; No. 138, osteopath, "Fall" ; No. 140, business man, "Fall from a horse"; No. 142, a business man, "In making motion of throwing spear felt a severe pain and was unable to raise the arm."; No. 143, waitress, "Raising tray."
The duration of symptoms prior to operation varied from a few days to ten years in one case. One man even stated twenty years, but the continuity was somewhat doubtful. There were eleven cases who stated that symptoms had existed from six months to five years, and two from one to six months. Ten were acute, that is, there had been no pain until within two weeks.
Relief of Pain. In acute cases pain was at once relieved by the operation and in chronic cases there was very little pain after the first few days. Eight patients reported no pain or actual relief from pain immediately after the operation. In other words, a really acute case is so much relieved by the incision that he may ignore the postoperative pain, but a chronic case, who has had no previous acute pain, is more aware of any later discomfort from the wound itself. Only seven mentioned pain after the first day and only one after the fourth day. The subacute, annoying symptoms in convalescence varied from one to four weeks in most cases, but one case complained of some pain for seven weeks.
Use of Arm. Most patients began to use their arms within a few days and used them with more and more freedom from day to day. As a rule it took from one to three months before perfectly free use returned. By the end of three months all but two patients had ceased to be even annoyed by the shoulder. The symptoms of these two cleared up within seven months. One of these was an iron worker who continued to have pain on using a sledge hammer when he returned to work fourteen weeks after the operation.
Return to Work. In most cases the patients returned to work or to their regular avocations after a month or less, only three cases requiring more time, the longest being the above-mentioned iron worker. (An industrial case.)
Hospital Days. The time spent in bed averaged three and a half days. None were absolutely confined to bed. The time in the hospital averaged five and a half days; three patients remained only three hours; six remained ten days for convenience, not from necessity. All wounds united by first intention.
From the point of view of the operator, who does not endure the pain, the results of this study may be summarized as follows: In acute cases the severe pain is relieved at once by the operation, and even in chronic cases the postoperative pain lasts only a few days. Within a few weeks the patient is about his usual pursuits, although he still has transient pain in extreme motions and cannot lie comfortably on the operated side. Then follows a period of a few months during which certain motions may cause annoying, sharp, brief twinges, and at night the arm may still cause a minor amount of discomfort. These symptoms become less obvious, and presently days together pass without a thought of the shoulder. This period is indefinite, but is to be measured in months, not in years. In order to get the patients' points of view I included in the questionnaire a request for a statement on their general impression about the efficacy of the operation. The following answers were given:
Case No. 51, a physician, "Operation entirely relieved my acute pain which had been present for several weeks. The other shoulder has been involved since, and has cleared up with no treatment. It was never as acute as the operated one"; Case No. 55, a physician, "... as I suffered so intensely for so many months and was entirely relieved within a few days after the operation. If you remember my operation was performed under local anaesthesia. My recovery was a very quick one and as nearly as I can remember I was able to do my regular work in a very short time. In April (2 and a half mos.) I was playing golf with no discomfort whatsoever"; Case No. 56 (from patient's physician), "I feel quite sure he thought it a success. Patient died of angina" (9 yrs. after op.) ; No. 62, "To me the desirability of the operation is unquestioned, in competent hands, however. The pain is so wearing and causes such nerve irritability that the sooner it is over the better. I consider my operation a great success, and would advise any one to put up with the temporary inconvenience"; No. 63, "Grand in every way"; No. 65, "Am pleased to say that I have no pain whatsoever and have perfect use of my arm; in fact, I have had since about two weeks after the operation"; No. 66, "I have never been quite able to make up my mind as to the efficacy of the operation. On the one hand I have had no discomfort in that shoulder; on the other hand, the ease with which I am able to control any kick up in the other shoulder by avoiding gouty foods and drinks leads me to believe that it might have been possible to cure it without an operation"; No. 68 (See Plate II, Fig. 8), "Extremely successful, has never bothered me since"; No. 72, a surgeon, "I obtained immediate relief at the time of operation and aside from some soreness of the wound, I was perfectly well, and as I remember it, I was operating within six or seven days of operation, the exact date I do not remember"; No. 73, "85-90% improvement" (This patient, a physician, had had symptoms for ten years) ; No. 79, "100% successful"; No. 81, "To secure any lasting benefit, I think that an operation is the only thing"; No. 85, "Similar to the removal of an aching tooth, pain all gone, only the soreness which would follow any deep gash in the body, would say no operation could be more efficacious"; No. 93, "Excellent"; No. 103, a physician, "Decided success"; No. 105, "Unqualified approval. The X-ray showed a quiescent bursa in the other shoulder. I have been a bit careful and when there has been the least twinge, have rested it. But even that has only happened three or four times in these years "; No. 113, a physician, "Absolutely perfect. The relief from pain and the conviction that there will be no recurrence are beyond price. Personally, I believe that any other procedure is a waste of time"; No. 114, "A wonderful operation. I walked home from the hospital three hours afterwards, and never had any pain or discomfort at any time except for a month when trying to use arm too strenuously. I recommend it heartily "; No. 121, a surgeon, " I was strong for it! At the end of one week I deliberately broke up adhesions by playing golf. After this the soreness subsided rapidly. The right shoulder bothered three months ago, no known trauma. Symptoms have now all subsided"; No. 122, "My impression is that the operation was very successful, and at times when my other shoulder troubles me I often wish I had both shoulders operated on"; No. 133, "Excellent results. I do not recall that I had any pain following my operation, with the exception of the few days I was in the hospital, and this was more from the soreness of the incision rather than actual pain from the shoulder. It was quite some time before I had the absolute free use of my arm, but I should say this was due to my lack of exercising it. However, it is absolutely perfect and I have used it a great deal"; No. 134, "I consider the operation entirely successful"; No. 140 (See Plate II, Figs. 1 and 2), "No question but that the operation, immediately, and apparently permanently, removes the trouble"; No. 141 (See Fig. 44), "Operation afforded me a very welcome relief after about four weeks of almost steady pain, and, although even now I do not put any more strain on my shoulder than I can help, it feels as strong as it ever did. I would not hesitate to undergo a like operation again to relieve like pain"; No. 142, "The result was most satisfactory. On only three or four occasions have I realized I had a shoulder and then only a slight soreness for a day or two after having used it perhaps a little too strenuously"; No. 143, "Good."
I am quite certain that most of my other patients to whom this questionnaire was not sent, or who did not reply to it, had as favorable results, because I have heard from most of them occasionally for many years after my operations. Details of some of these cases may be found in the Table on pp. 255-260. I also have notes on about an equal number of cases who were not operated upon, usually because I thought the symptoms too trivial, but in some cases, because the patient refused operative treatment after having my assurance that in time they would recover at any rate. In most of these cases, especially in those in whom perforation had already occurred, the results have been as good as in those operated upon, although it seemed to me the patients suffered more. Many have recovered as promptly under some form of palliative treatment, as if I had operated upon them, but a few have had prolonged convalescences and suffered a great deal. My brother, a business man, had acute attacks in both shoulders for several months each, at different times. He would not sacrifice the time to be operated upon, but obtained some relief from diathermy. On the whole it seemed to me he suffered more than any case has suffered after the operation, but he did not lose a day. This was a subacute case with no restriction. As a rule I have operated on only the worst cases. In fact, I seldom advise operation unless the pain is severe. The unoperated series is, therefore, in the main composed of much milder cases, for those with severe pain welcomed operation. For the sake of my argument that operation is wise in those cases where the pain is hard to bear, it is not necessary to attempt to contrast the periods of disability in an unoperated series with those that were operated upon, because the operated series shows many cases where the symptoms prior to the operation had existed much longer than they persisted in any case after it. It does not seem to me worth while at the present time to go into this question in greater detail, because it is evident to me from a study of the unoperated cases that these patients eventually recover under any form of treatment which is not actually detrimental. The question is wholly one of relief of symptoms, not of the removal of a condition which is in itself dangerous or likely to lead to permanent disability. Although I am inclined to think that those cases which are not operated upon may ultimately have weaker tendons than those in whom the deposit is removed, I have no statistical proof of this, nor have I ever known of complete rupture of the supraspinatus occurring as an aftermath of this lesion. My reason for thinking that the tendons are weakened is more on account of the frequency of finding, at autopsy, defects which might be accounted for on this hypothesis.
Deposits in the Subscapularis. It may be that deposits in the subscapulars are less responsive to surgery than when they occur in the other tendons. I have had experience with only two cases, but they were both instructive to me, for I criticize myself for being content with removing one large deposit and making no effort to be sure there was no deposit in the other tendons.
Case No. 84. This was an acute case of two weeks' duration in a single woman of 46. I operated February 2nd, 1926, and removed a deposit from the supraspinatus. The result was satisfactory. However, about two years later, very acute symptoms returned in the same shoulder. This time the X-ray clearly showed a large deposit in the subscapulars and the remains of a smaller one in the supraspinatus. (Plate II, Fig. 6.) I operated again and removed the subscapularis deposit. The immediate result was as good as before, but the convalescence was more protracted in the subacute stage. She was an accountant and used the typewriter a good deal. She states that she went back to work two weeks after the first operation and four weeks after the second one, but her reply indicates some residual trouble: "Always occasional twinges since. Always 'cranky' as to normal use—have to turn certain way to put arm over and upward."
I am inclined to think that I might have saved this patient the second operation by a more careful X-ray study at the time of the first operation, for evidence of the other deposit may have been present at that time.
Case No. 117. A maiden lady of 64, who had a large calcified deposit in the subscapularis. (See Fig. 43.) She had had subacute symptoms for four weeks before the operation. According to her reply she had a longer and more stormy convalescence than any of my other cases have had; i.e., the acute pain after the operation lasted six days; the subacute pain three and a half months, and the occasional twinges ten months. It was a year before she forgot about the arm entirely. There have been no after effects.
This patient did not answer the question about the general impression of the efficacy of the operation, but it is clear that she suffered somewhat more after the operation than she did before it. She was operated upon in another city, and I did not have direct care of her convalescence, as I have in almost all the other cases. I was, however, in telephone communication with her doctor, and saw her from time to time during the year following. There seemed to be no very distinct reason why she should have had a longer convalescence than the other cases, but there were several possible reasons, which it seems worth while to discuss because they may have some future importance. In the first place, the deposit was in the subscapularis, a rather unusual situation. The operation was not difficult, because outward rotation of the arm easily brought the deposit under the wound which was made in the usual situation in the deltoid. I did not, in her case, incise any of the other tendons, and there may have been a tendinitis in those tendons which was the cause of the delay. Also, she did have some haematoma in the wound, which might have accounted for the postoperative pain being longer than usual. It is my usual custom to lightly bandage the arm to the side for the first night, and next morning to remove the bandage and allow the patient to place the arm in any position he chooses. There was some delay in removing the bandage in this case, I am told, because the patient seemed to have so much pain. It is possible, also, that the patient was one who, in her anxiety to be conscientious in her statements, has given an impression in the answer that her pain was greater than it was.
As these two cases were the only unsatisfactory ones I have had, and as they were the only ones in which there were large deposits in the subscapularis, it would be logical to attribute the slow convalescences to the location of the deposit. Two cases do not give much opportunity for logic when complicated by the factors of the personalities of doctors and patients. It may be that I could have saved both patients a considerable amount of pain by more thoroughness, and it may be that the two ladies were not of a satisfactory type for surgery, and would have been better satisfied with diathermy. At any rate, they represent my two worst results from operations for calcified deposits. In spite of the somewhat stormy convalescences I believe both patients were saved much suffering, for they seemed to me to be cases of severe type. The operation is a trivial one from a surgical standpoint, but to some people an operation is an operation, and those who would be inclined to take a surgical experience too seriously may well be treated with palliative measures.
BIBLIOGRAPHY FOR CHAPTER VI
ALLEN, A. R., Penn. M. J., 1911, xiv, 843; Therap. Gaz., 1911, 3, s., xxvii, 546. BAER, W. S., Johns Hopkins Hosp. Bull., 1907, xviii, 282-284. BERGEMANN and STIEDA, A., MUnchen med. Woch., 1908, lv, 2699-2702. BERRY, J. McW., Am. J. Orthop. Surg., 1916, xiv, 476-483. BETAGH, G-, Policlin., Roma, 1904, xi, sez, chir., 1930. BLANCHARD, W., J. Orthop. Surg., 1920, ii, 466. BOCK-OVEN, S., U. S. Vet. Bur. M. Bull., 1930, vi, 549-550. - BOU PUJOL, A., Arch, de ginecop., Barcelona, 1909, xxii, 99-104. BRENCKMANN, E., and NADAUD, P., Arch, d'elec. med., 1932, xl, 27-29. BRICKNER, W. M., Intern, clin., 1911, 1929; Am. J. Surg., 1912, xxvi, 196-204; Med. Rec, 1915, lxxxvii, 121 and 498; Am. J. M. Sc, 1916, cxlix, 351-864; Interstate M. J., 1915, xxii, 331-343; J. A. M. A., 1916, lxvi, 912; Am. Atlas Stereoroentgenol., 1916, i, 34-36; Am. J. Surg., 1916, xxx, 108-110; Am. J. Orthop. Surg., 1916, xiv, 231; J. A. M. A., 1917, lxix, 1237-1248; Midland M. J., 1918, xvii, 33-37. BROWN, A. J., Surg. Gyn. and Obs., 1919, xxix, 381-386. BUCHOLZ, C. H., J. A. M. A., 1917, lxix, 968; book, Lea and Febiger, 1917, Arch. f. klin. Chir., Berlin, 1922, cxxi, 255-264. BUCKLEY, C. W., Pract., 1914, xcii, 777-787; Proc. Roy. Soc. Med., London, 1913-14, vii, 59-70. BUTLER, P. F., and ELWARD, J. F., Am. J. Roent., 1925, xiii, 536-541. CALATUYAD, C, and ESTOPINA, L., Rev. espanol, de electrol y radiol. med., Valencia, 1912, i, 325-383. CAMPBELL, W. F., Med. Times, 1916, xliv, 244. CARNETT, J. B., and CASE, E. A., S. Clin. N. Am., 1929, ix, 1107-1126. CARNETT, J. B., S. Gyn. and Obs., 1925, 404-121; S. Clin. N. Am., 1930, x, 1309-1817; Radiology, 1931, xvii, SOS-SIS. CODMAN, E. A., Boston Med. and Surg. Jour., cl, 14, 371-374, 1904; Boston Med. and Surg. Jour., cliv, 22, 613-620, 1906; Records of the Massachusetts Medical Society, June 9, 1908; Boston Med. and Surg. Jour., Oct. 22, 29; Nov. 6, 12, 19, 26; Dec. 8, 1908. COLE, W. H., Surg. Clin. N. Am., 1923, iii, 1361-1363. COLLEY, F., Dtsch. Z. f. Chir., 1899, liii, 563-574. COMBEAU, Gaz. d. hdp., Paris, 1868, xli, 207. CONLOMB, Rev. d'orth., Paris, 1922, 3, s., ix, 251-253. COOPER-MAN, M. B., N. Y. State J. M., 1926, xxvi, 807-814. COUES, W. P., Boston M. and S. J., 1921, clxxxiv, 176-179. CUMSTON, C. G., Ann. Surg., 1913, lvii, 143. DAWBARN, R. H. M., Boston M. and S. J., 1906, cliv, 691. DAY, H. F., Boston M. and S. J., 1918, clxxviii, 389-392. DEERING, G. E., Phys. Therap., 1930, xlviii, 362-366; Am. J. Electrotherap. and Radiol., 1917, xxxv, 170-176. DESPLATS, H., J. d. sc. med. de Little, 1891, i, 265-271; Bull. off. Soc. franc, d'electro-ther., Paris, 1904, xi, 289-301; Ann. d'electrobiol., Paris, 1904, vii, 674-685. DIALTI, G., Cesalpino, Arezzo, 1908, iv, 169-176. DICKSON, J. A., S. Clin. N. Am., 1924, iv, 1053-1063. DOLLINGER, G., Orvosi hetil., 1932, lxxvi, 27-29; Zentrbl. f. Chir., 1982, lix, 579-583. DONLEY, J. E., Boston M. and S. J., 1911, clxv, 273. DOUGLAS, J., Ann. Surg., 1917, lxvi, 230. DUNLOP, J., Am. J. Orth. Surg., 1916, xiv, 102. DUPLAY, Rev. part. d. trav. de med., Paris, 1896, liii, 226; Semaine med., Paris, 1896, xvi, 193-194; Med. Week, Paris, 1896, iv, 258; Med. Press & Circ, London, 1900, n.s., lxix, 571-573. ECCLES, McA., West London Med. J., London, 1920, xxv, 87. ELMSLIE, R. C, Br. J. of Surg., 1932, xx, 78, 190-196. ELY, L. W., Am. J. Orth. Surg., 1914-15, xii, 447-450. ERB, K. H., and FRIEDRISZIK, W., Dtsch. med. Woch., 1982, lviii, 1004-1005. FALTA, Wien, med. Woch., 1920, lxx, 1414-1416. FIELDS, S. O., N. Y. M. J., 1915, ci, 163. FISHER, C. F., West Virginia M. J., 1927, xxiii, 250-252. FLINT, J. M., J. A. M. A., 1913, lx, 1224. FORT, F. T., Kentucky M. J., 1911, ix, 897-899; Railway Surg. J., 1912-13, xix, 8-14. FOWLER, E. B., Illinois M. J., 1932, lxi, 332-334. FRAUENTHAL, H. W., Internat. Clin., 1918, 28 s., iv, 60. FREUND, L., Wien klin. Woch., 1917, xxx, 665; Munch, med. Woch., 1917, lxiv, 784; Med. klin., Berlin, 1909, v, 387-390. FRIEDRISZIK, W., Rbnt. Med. Woch., 1982, Iviii, 1004. GALLOWAY, H. P. H., Canadian J. M. and S., Toronto, 1909, xxvi, 277-284. GARIBDJANJAN, G. A., Z. f. Orth. Chir., 1932, lviii, 48-53. GERSTER, A. G., Med. News, 1884, xliv, 428. GIBNEY, H., Am. J. Orth. Surg., 1906-7, iv, 91-93. GIBSON, A., Canadian M. A. J., Toronto, 1928, xviii, 80-34; J. Bone and Joint Surg., 1922, iv, 552-559. GIBSON, H., Am. J. Orth. Surg., 1906-7, iv, 91-93. GILCREEST, E. L., S. Surg. Transact., 1981, xliv, 522-545. GONTIER, A., Union med., Paris, 1869, vii, 6-8. GRACE, J. J., British M. J., London, 1914, i, 1012. GRANGER, L. B., Internat. Clin., 1926, 36, s., iv, 265-268. GROSSMAN, J., M. Times, 1928, lvi, 131-134. GUIBE, M., Rev. gen. de clin. et de therap., Paris, 1919, xxxiii, 408. GUNZ-BURG, J., Geneesk. Tijdschr. v. Belgie, Amsterdam, 1910, i, 36-39. HAENISCH, G. F., Fortschr. a.d. Geb. d. Roentg., Hamburg, 1910, xv, 293-300. HAMMER, A. W., Am. J. Surg., 1921, xxxv, 29-31. HAMMOND, R., Rhode Island M. J., 1917, i, 223. HARBIN, M., Arch. Surg., 1929, xviii, 1491-1512. HARRIS, J. F., J. A. M. A., 1923, lxxxi, 98; J. A. M. A., 1925, lxxxv, 1134. HARSHA, W. M., Internat. Clin., 1919, 29, s., ii, 66-69. HAUSSLING, F. R., S. Clin. N. Am., 1926, vi, 1508-1528. HAYDEN, J. G., Railway Surg. J., 1917-18, xxiv, 8-11. VON HEDRY, N., Beitr. z. klin. Chir., Tubing., 1924, cxxxii, 244-247. HELLFORS, A., Med. Klin., 1930, xxvi, 309-311. HIRTZ, Soc. de med. mil. franc. BuU., Paris, 1912, vi, 277- 284. HITZROT, J. M., Min. Med. Cornell U. Med. Bull., 1928. HOGLER, F., Ars. med., Vienna, 1931, ix, 547-552; Arch. Innere Med., Vienna, obstr. J. A. M. A., 1928. HODGES, F. M., Virginia M. Month., 1925, lii, 155-156. HOLZKNECHT, G., Wien med. Wochr., 1911, lxi, 2757-2760. HOWARD, A. G., and HARVEY, C. D., Hahneman Month., 1915, 1, 323-833. HANCREDE, C. B., Internat. Encycl.Surg., 1895, vii, 395-402; 1882, ii, 691-733; 1884, iii, 105-147. ISRAEL, J. G., Internat. J. Surg., 1921, xxxiv, 8-14. JARJAVAY, J. F., Gaz. hebd. de med. et de chir., Paris, 1867, iv, 325-327, 357-359, 387-391. JONES, H. W., and ALLISON, N., N. Y. M. J., 1904, Ixxx, 930-934. JUNG, A., and BRUNSCHWIG, A., Rev. de chir., Paris, 1931, 1, 611-616. KAMMERER, F., Ann. Surg., 1917, lxvi, 112-115. KIENBOCK, R., Arch. f. phys. med. u. med. Tech., Leipzig, 1910, v, 98-99. KLEINBERG, S., Med. Rec, 1915, lxxxvii, 870-873. KOVACS, R., Phys. Therap., 1926, xliv, 90-109; 1927, xxxxvi, 181. KUSTER, E., Verhandl. d. dtsch. Gesell. f. Chir., Berl., 1902, xxxi, 364-372; Archiv. f. Klin. Chir., 1902, lxvii, 1018. KREUTER, E., Dtsch. Z. f. Chir., Leipzig, 1904, lxxii, 136-152. LAMY, L., and P^RES, P., Presse med., Paris, 1926, xxxiv, 739-740. LAVRAND, H., J. d. sc. med. de Lille, 1896, ii, 25-34. LEMONIE, Presse med. beige., Brux., 1904, Ivi, 660. LEONARD, T. B., Virginia M. Semi-Month., 1916, xxi, 349-350. LERICHE, R., and BRENCK-MANN, E., Lyon chir., 1931, xxviii, 281-285. LERICHE, R., and POLICARD, A., Masson et Cie., Paris, 1930, 69. VON LIEBERMANN, A., Med. Klin., 1930, xxvi, 1073; Munch, med. Woch., 1928, lxxv, 605. LITTIG, L. W., J. Iowa State M. Soc, 1913-14, iii, 625-630; Tr. West. Surg. Ass., 1913, 1914, 107-113, 117-124. LOTSY, G. O., Fortschr. a. d. Geb. d. Roentgenstrahlen, 1910, xvi, 158. LOVETT, R. W., Surg., Gyn. and Obst., 1922, xxxiv, 437-444. LOZANO, R., Clin, med., Zaragoza, 1914, xiii, 487-440. McGAULEY, F. F., N. Y. State Med. J., 1925, xxv, 472-474. MAGNUS0N, P. B., and COULTER, J. S., Intemat. Clin., 1920, iv, 203. MAIR, R., Ztschr. f. d. Ges. Avat., 1927, vxxxiv, 203. MARSHALL, H. W., Med. Rec, 1914, lxxxv, 280-289. MARTIN, P. F., J. Indiana M. Ass., 1910, iii, 109-117. MAUCLAIRE, Ann. de med. leg., 1932, xii, 471-472. MIGLIEWITCH, Arch, gen. de Kinestherapie, Paris, 1909, xi, 224-228. MONTGOMERY, A. H., J. Am. M. Ass., 1916, lxvi, 264. MOREN, J. J., Kentucky M. J., 1911-12, ix, 881-884; Louisville Month. J. M. and S., 1914-15, xxi, 68-75. MORRIS, J. M., M. J. Australia, 1926, i, 432-437. MOSCHCOWITZ, E., Am. Jour. Med. Sc., 1915, xv, 1-7. MU'LLER, A., Zentralbl. f. Chir., 1932, lix, 1810. MUMFORD, E. B., and MARTIN, F. J., J. A. M. A., 1931, xcvii, 690-694. MURPHY, J. B., Surg. Clin., 1915, iv, 661. NANCREDE, C. B., Internat. Encycl. Surg., 1882, ii, 691-733; Transl. Encycl. Internat. de chir., Paris, 1884, iii, 105-147; Internat. Encycl. Surg., 1895, vii, 395-402. NICHOLIS, S., Radiol, med. Milano, 1924, xi, 638-640. O'FERRALL, J. T., M. and S. J., 1925, lxxviii, 259-267. O'REILLY, A., and EWERHARDT, F. H., J. Missouri M. A., 1919, xvi, 149. ORR, T. G., J. A. M. A., 1923, lxxx, 1434-1436. PAAL, E., Arch. f. Orth. und Unfall Chir., 1932, xxxii, 100-106. PACKARD, G. B., Colorado Med., 1908, v, 5-9. PANNER, H. J., Hosp., Tid., Kobenh., 1912, v, R., v, 561-567. PAINTER, C. F., Boston Med. and Surg. J., 1907, clvi, 345-849. PAUS, M. Forh. med. Selsk. i. Kristiania, 1914, 135-138. PLUMMER, W. W., N. Y. State J. M., 1916, xvi, 203-208. POHL, R., Wiener Klin. Woch., 1930, xliii, 397-398. POPE, S. T., California State J. M., 1917, xv, 268. PUTNAM, J. J., Boston M. and S. J., 1882, cvii, 509, 536. RABINERSON, A. B., Vestnik khir., 1929, xvi, 100-103. RAMIREZ, Y. S., New Orleans M. and J., 1927, Ixxx, 324. RESNIK, J., Physical Therap., 1929, xlvii, 322-329. RICHARDS, T. K., New England J. of Med., 1931, ccv, 812-813. RUGH, J. T., Penn. M. J., 1911, xiv, 845-850. SADOLIN, F., Hosp. Ted., Kobenh., 1902, 4, R., x, 225-231. SCHLESINGER, A., Berlin Klin.Woch., 1908, xvi, 249-252. SCHREIBER, A., and HOFMEISTER, F., Syst. Pract.Surg., 1904, iii, 17-160. SCHWARZ, A., Wien, med. Woch., 1913, Ixiii, 1858-1857.SCHWARZ, E., Dtsch. Z. f. Chir., 1931, ccxxxv, 1-3; Dtsch. Z. f. Chir., 1932, ccxxxv, 140-163. SCHWYZER, A., St. Paul M. J., 1908, v, 45-48. SEGOND, Rev. gen. de clin. et de therap., Paris, 1910, xxiv, 785. SIEBERT, K., Fortschr. d.Med., Berlin, 1926, xliv, 509-515. SIEVERS, R., Dtsch. Z. f. Chir., Leipzig, 1914, cxxix, 583-653; Verhandl d. dtsch. Gesell. f. Chir., Berlin, 1914, xliii, 243-253. SIMON, S., Ztschr. f. d. Ges. Anat., 1926, lxxxi, 389. SKILLERN, P. G., JR., Internat. Clin., 1914, 24, s., ii, 233; Internat. Clin., 1913, 23, s., iii, 205. SMITH, M. K., Med. Rec, 1917, xci, 406-408. SMYTH, W. J., Practitioner, London, 1917, xcviii, 575-576. STEINDLER, A., J. Orth. Surg., 1921, iii, 652. STERN, W. G., Surg. Gyne. and Obst., 1925, xl, 92-94. STEWART, J. E., South. M. J., 1928, xxi, 280-283. STULZ, E., and BRENCKMANN, E., Rev. d'orth., 1929, xvi, 481-489. SWETT, P. P., Yale M. J., 1910-11, xvii, 154-167. SZUBINSKI, A., Zentralbl. f. Chir., 1932, lix, 1638-1644. TAKAHAYASHI, K. A., Geibi Iji, Tokyo, 1900, xlix, 4-6. TAVERNIER, L., Bull, et mem. Soc. nat. de chir., 1932, lviii, 956-960. THOMAS, T. T., Am. J. M. Sc., 1911, xcli, 515-534; Therap. Gaz., 1912, 3, s., xxviii, 88-95; Therap. Gaz., 1913, 3, s., xxix, 229-247; J. A. M. A., 1914, lxiii, 1018-1025. TITUS, N. E., Am. J. Siirg., 1929, vi, 318-321; Brit. J. Actino-therap., 1930, v, 36. TUSZEWSKI, F., 8°, Greifswald, 1878. USLAND, O.,Norsk. Mag. f. Laegevidensk., Kristiania, 1920, lxxxi, 980. VADON, H., 4°, Mont-pellier, 1880. VALENTIN, B., Ztschr. Orth. Chir., 1931, lv, 229-240. VAN ASSEN, J., Nederl. Tijdschr. v. Geneesk., Amst., 1912, ii, 1517-1519. WALDEN-STROEM, J. A., Dtsch. Klin., Berlin, 1874, xxvi, 172. WATKINS, J. T., J. Bone and Joint Surg., 1925, vii, 787-789. WEISSENBACH, J. R., and FRANCON, F., Bull, et mem. Soc. med. d. hop. de Paris, 1930, liv, 1733-1738. WEISSENBACH, R. J., and TRUCHOT, P., Bull, et mem. Soc. med. d. hop. de Paris, 1931, xlvii, 1790-1793. WILSON, P. D., J. A. M. A., 1931, xcvi, 438-439. WILCOX, A. E., Minn. Med., 1928, vi, 245-247. WOJCIECHOWSKA, H., Lausanne, 1907, Ixxii, 8°. WOLF, H. F., A. J. Surg., 1923, xxxvii, 59-62; N. Y. M. J., 1916, civ, 217. WORMS, G., Soc. de med. mil. franc. Bull., Paris, 1912, vi, 202-209. WREDE, Arch. f. Klin. Chir., 1912, xcix, 259. YOUNG, J. K., Therap. Gaz., 1917, 3, s., xxxiii, 1-4; Ann. Surg., 1916, lxiv, 368-871. ZOLLINGER, F., Arch. f. Orth., Munchen and Berlin, 1927, xxiv, 456-467.
Almost all of the above articles are brief reports of the first few cases of calcified deposit which were observed in each locality, and give illustrations of the X-ray findings. In my opinion the articles by Brickner, Carnett, Harbin and Stieda are the most instructive. The article by Kiister in 1902 did not mention calcified deposits, but I am quite sure that the cases which he observed were such cases. His excellent and brief article was, so far as I know, the first rational description of subacromial bursitis. It was called to my attention some years after I had written my first paper, but was in fact written before mine. Duplay's first article appeared in the Archives General de Medecin, Nov., 1872, but it apparently was not at first appreciated. Another paper in 1896 received more notice and literal translations were at once printed in two English Journals (see ref. above). Most European authors credit to him the introduction of the term "Periarthritis of the Shoulder" (periarthrite scapulo-humerale, periarthritis humero-scapularis). The chief advances in our knowledge of the subject since Duplay's contribution have been due to the use of the X-ray (discovered in Dec, 1895), so that we have been able to study separately the cases in which there is a calcified deposit or in which a fracture of the tuberosity had taken place. Except for that of Dickson and Crosby, quoted on page 224,1 have found no important study of the type of cases to be considered in the next chapter in which little if any calcification is found. The articles by Baer and Painter both appeared in 1907 and I think were the first articles in this country to recommend surgical removal of the deposits. Bergemann and Stieda recommended surgery in Germany in 1908. Most of the articles advise some form of physiotherapy. It has seemed unnecessary to me to print the titles of all these papers on account of the large amount of space that this would require. Doubtless most of these authors would today be able to give as detailed a study as I have given in this chapter, but many of the articles show a lack of knowledge of minor points which have probably become plain to most of them during the intervening years. For instance, none of the articles seem to give proper consideration to the fact that nature's method of cure is by evacuation of the calcified material into the bursa. Many of the authors seem to think that the origin of the particles is in the bursa, and hence use the term "calcified bursitis." A good many attribute the onset of the trouble to recent trauma. Most striking is the length of the bibliography of this chapter as compared to that of the last one on complete rupture of the supra-spinatus, which, to my mind, is so much more important and disabling a lesion than that caused by calcified deposits. The reader should refer to the comparison of costs on the scheme on page 124. Even the brief bibliography that I have given at the end of that chapter is partly composed of articles which really do not refer to the subject, and are only related to it. In fact, my papers and that of Wilson are really the only ones devoted to the subject. It seems to me most important for the profession to learn to differentiate between these two common causes of shoulder disability. As a matter of fact it is essential on the patient's account that rupture of the supraspinatus tendon should be recognized and operated upon promptly, whereas, the treatment of calcified deposits is a matter of choice, although my personal opinion is in favor of prompt surgical removal of the deposit. There is so little difference between the results of surgery and the results of any form of palliative treatment that I do not feel in these cases, as I do in those of ruptured supraspinatus, that their treatment is essentially surgical.
My own articles have been extensively quoted (often incorrectly) in American and English literature. This has been one reason why I have taken so much pains in this chapter to enter into the minor details of this comparatively insignificant lesion, cases of which recover in due time by nature's own methods. This chapter may also be of some importance because I am able to report the results of many cases which were operated on a long time ago. However, I feel that in some of these patients, whether or not operated upon, the tendons have probably been weakened through destruction of the tendon fibers so that had they been subjected to unusual trauma they might have ruptured more easily than normal ones. As stated in the chapter on Pathology, there is some doubt as to whether the defects so frequently found by Dr. Akerson may not have been sometimes due to destruction of the tendon by these calcified deposits years before autopsy. In the cases which I have reported as operated on for complete rupture, there was no doubt in my mind from the pathology found that the lesion was purely traumatic, although I could not, of course, determine whether there may not have been a weakened tendon before the actual rupture. In no case did I get a definite history of a calcified deposit in years previous to the rupture. Autopsy specimens from cases known to have had these calcified deposits in earlier years, and in whom there had been no operation or history of later trouble, might clear up this point.
THE TECHNIQUE OF THE OPERATION FOR REMOVAL OF CALCIFIED DEPOSITS
In most cases this operation can be done through an incision about one-half inch in length, but it will be perhaps safer for both patient and surgeon if an incision an inch and one-half is made to allow ample room to identify the anatomic landmarks. I will assume that the incision is of this size, although I have developed a technique of doing it through an incision just large enough to admit a nasal speculum with recurved tips. The only objects of this modification are to have less scar and less chance of intrabursal adhesions and perhaps less postoperative pain. Since even with the larger wound, i.e., one inch and one-half, opening the bursa as widely as possible, the scar is small and postoperative pain slight, and adhesions more of theoretic than practical importance, one should not hesitate at any time to enlarge a half-inch wound.
FIGURE 49 On the left is a figure showing the size of the open exploratory incision, which is also sufficiently large for the removal of most calcined deposits. The figure on the right shows the size to which it is necessary to enlarge the incision in order to suture a rupture of the supraspinatus by the author's method. Both figures depict a normal bursa with the edges of the roof caught with sutures and held apart to show the smooth, white, convex base which covers the tuberosity and insertions of the tendons. In the lower portion of both figures a nictitating fold is represented. By rotation of the humerus, the whole base of the bursa may be inspected through the small left-hand incision. Lesions are seldom found at any other situation than on that part of this base which is just above the greater tuberosity. The writer believes that the little exploratory incision is almost harmless, provided the surgeon understands what he is looking for and does not attempt to explore further if the pathology is not at once evident when the bursa is opened.
Anaesthesia. I prefer to do this operation under local anaesthesia in suitable cases, because it is easier for the patient. However, it is easier for the surgeon to have the patient under general anaesthesia, because local anaesthesia does not relax the spasm, and renders it necessary to be more accurate in cutting down directly on the lesion. Even if no spasm is present before making the incision, it may be started up by touching the inflamed region with a retractor or other instrument. In a recent case the reflex spasm could be produced at will by touching the surface near the lesion, yet the touch of the instrument caused no sensation of pain. The patient was an intelligent doctor, and could describe his sensations accurately. When the retractors were out of the wound he could rotate the arm, but when they were in the wound he found himself unable to overcome the spasm by force of will, although he felt no pain except when I endeavored to force the rotation. Although the operation can be done under such circumstances, it is unsatisfactory. I have found it so difficult to anaesthetize the base of the bursa where the deposit is, that now I do not attempt to do so. The tendon near its insertion is so dense that it is difficult to inject the novocaine, and this is as painful as incising the tendon; possibly more so. Local anaesthesia does not permit a thorough exploration of the bursa, but when one is familiar with the local anatomy one does not need to see the whole bursa. When the patient is under ether, by a certain maneuver the arm can be pulled downward and forward, and the surgeon's forefinger introduced between the tuberosities and the acromion. When air once gets into this opening the atmospheric pressure is overcome, and the subacromial space remains open, permitting inspection and palpation of the whole bursa. This maneuver is more especially useful in cases of rupture of the tendon. In this case the joint is not held together either by atmospheric pressure or by the tension of muscles. Manipulation of this type is not necessary, and cannot, of course, often be done under local anaesthesia, but probably might be done under regional anaesthesia. I regard the latter as too serious a procedure, and would prefer a general anaesthetic. From the patient's point of view, in spite of these drawbacks I favor a local anaesthetic, provided the surgeon knows where the deposit is, and can go directly to it through a small incision. It is then a trivial operation. But if the deposit cannot be accurately localized, and the anatomy is not clear in the surgeon's mind, general anaesthesia would be preferable in order to allow for some unnecessary manipulation and rough handling. I have operated on many doctors, and had a chance to hear their commendations or objections. I am told that the actual curetting of the lesion is painful, but not more than can be readily borne. The incision of the skin and muscle, and of the bursal roof, is not felt at all. Some patients are obviously poor subjects for local, and others for general anaesthesia. Surgical judgment on general principles is needed. I should advise any surgeon to do his first few cases under ether, for in spite of all the directions I can give, the anatomy is difficult to describe, and one is easily confused unless very familiar with it. The facts that the structures to the right or left of this small wound are reversed in relation to the surgeon's position as to whether he stands on the acromial or axillary side of the wound, and are also reversed in right and left shoulders, add to the puzzle.
FIGURE 50. OPERATIVE POSITION This is an important figure. The writer did not realize the advantage of placing the patient in this position, until he had done many of these operations, which had been attempted with the patient either in recumbency or in a sitting posture, strapped in a chair. The latter was a very satisfactory position after the strapping had been adjusted if the assistants could be trained to work in this unusual attitude. However, the cases were too infrequent for any routine to be established. Until one operates on these cases one does not realize how elusive is the shoulder on the operating table, and, since the field is entirely controlled by the position of the humerus in relation to the scapula, how any minute change in the position of either the arm or of the body is at once transmitted to the tiny wound. Gradually I worked out this position, and find that it gives the best possible exposure, and enables one, if the assistant is attentive, to perform a very satisfactory suture through the very small incision.
Preparation. The patient is placed on his back on the table, and small sand bags or folded sheets are put under the shoulder blade and corresponding hip. This slightly raises the shoulder. It is well to draw the patient as close to the edge of the table as may be, so that when desired the elbow can be pushed backwards below the plane of the table—a maneuver which may be needed to expose the upper part of the bursa. The patient's face should be turned toward the opposite shoulder, and the anaesthetist and patient's head protected with a "goiter apron" tied around the patient's neck. I always arrange a sterile dressing over the hand and forearm, so that during the operation the arm may be manipulated by the operator or assistants. A convenient way is to sterilize the shoulder and arm to below the elbow, and then to draw a sterile pillow slip over the hand, forearm and elbow, and attach it with sterile bandages as high on the upper arm as desired. The arm may then be drawn through the hole in a laparotomy sheet, and moved about at any stage of the operation.
Position of Incision. In deciding on the point at which to incise, one must Temember that the skin incision will remain stationary, and that by rotation of the humerus the point at which the calcified deposit lies may be brought beneath the incision. The deltoid muscle, which forms the bulk of the tissue which must be cut through, also remains nearly completely fixed. It moves a negligible amount when the humerus is rotated. One must remember also that the sides of the subdeltoid portion of the bursa move considerably in rotation of the humerus. For instance, having incised the skin and muscle, it is possible to continue the incision in such a manner that it would be entirely outside of the bursa; i.e., it might not penetrate the bursa at all when the arm is in extreme internal rotation, but if the cut were made with the arm in external rotation, the bursa would be opened. To make the operation easy, one would desire to have the skin incision as nearly opposite the calcified deposit in the base of the bursa as possible. I have found that the incision best on the average is directly anterior to the head of the humerus, with its upper end near the acromio-clavicular joint, and its lower end at about the level of the top of the bicipital groove. In thin subjects one can feel the bicipital groove through the deltoid, and it is always well to do this if possible, because the acutely tender point will lie external or internal to the groove, according to whether the deposit is in the supraspinatus or subscapularis. The expansions of these two tendons bridge the bicipital groove, but their real attachments are to the greater and lesser tuberosities on each side of the groove. I have sometimes seen the deposit apparently over the groove, but it had probably extended from the tendon on one side or the other. If one cannot feel the groove before making the incision, one can always determine its position by palpation in the wound after the deltoid has been incised. It is well to do this in every case, for often the exact location of the deposit can be made previously by X-ray, and one can readily locate the subscapularis and supraspinatus if the groove is determined. Sometimes the floor of the bursa does not show sufficient indication of the deposit to guide the surgeon. In such a case the tip of either tuberosity may be readily determined with the point of the knife, and the tendon incised just above it. When a little of the white deposit appears, the incision can be enlarged in the line of the fibers of the supraspinatus or subscapularis, as the case may be. In order to determine the position of the bicipital groove, one may take it as a good rule that when the elbow is flexed at a right angle, and the posterior part of the elbow put down on the table at the side of the patient so that the axis of the forearm stands directly vertical to the table, the bicipital groove will be at the most anterior portion of the prominence caused by the head of the humerus. From this point, rotation of the forearm either way brings the tendons into view according to the obvious anatomical arrangement. (Pigs. 6 and 51.)
Incising the Deltoid Muscle. Separating the fibers of the deltoid muscle is a little more difficult than parting those of the rectus in abdominal incisions, owing to the fact that the fibers of the deltoid are more or less "herringbone" in arrangement. The incision seems to close right up on withdrawal of the knife, so that it is difficult to find the line again. I therefore usually put another instrument, as the point of a hemostat, in along the knife before withdrawing it, so that with my knife in my right hand and the hemostat in my left, I push the fibers apart as the assistant places two aneurism needles as retractors to take the places of my two instruments. These hold the line of incision, and the fibers of the deltoid are cut upward and downward to equal the length of the skin incision. Small, broader retractors are then introduced, exposing the upper surface of the roof of the bursa.
If the above has been understood, it will be seen that the skin incision and the deltoid incision are simple and standard. If correctly placed they would lie over the very top of the bicipital groove in the above-mentioned position, with the forearm vertical to the table. It is by no means necessary to hold the arm in this position while the skin and muscle are incised, but when the bursa is to be opened, the arm should be held in this position, the assistant being ready to rotate it one way or the other as the surgeon desires. Make sure that this point is understood.
This figure should be studied with the last one, although for convenience the patient is here represented as standing up while the operator looks downward from above, and the assistant, holding the elbow at the side, rotates the forearm and consequently the humerus beneath the wound. The figures below represent the incision and its relation to the bicipital groove as the humerus is rotated. The Incision remains stationary while the facets of insertion pass beneath the incision. A thorough understanding of these two diagrams is most important.
Incising the Bursa. The incision in the deltoid having been made, and the fibers retracted, it is well for the assistant to rotate the arm, and in most cases the roof of the bursa is so transparent that the base beneath it can be seen to move as the arm is rotated. In cases in which the bursal wall is thickened from old inflammation, one cannot see through it, but one can palpate the tuberosities moving beneath it. Since it is important not to allow any blood to enter the bursa, small sponges should be ready. It is well to tie up vessels before making the incision into the bursa, for if blood fills it, it is harder to determine the appearance of the base. At this stage the roof of the bursa is picked up with two pairs of forceps, as is customary when incising the peritoneum. A cut is made between the two forceps, and the air rushes into the bursa, so that the incision can then be enlarged upward and downward as desired. A normal bursa has a white, shiny floor, but a circular zone of deep red injected tissue is usually the guide to the area where a deposit lies. This deep red tissue, resembling that of a bloodshot eye, surrounds a white or pale area about one-half the size of a ten cent piece. Sometimes this area is obviously under tension and mounded up like a boil. At other times when the inflammation is less, the affected area is not raised, and there is only a barely perceptible whitening where the calcium deposit shows through the synovial floor of the bursa. Before incising this area it is well to look the rest of the bursa over, to make sure that there are no other lesions. The X-ray will probably have already determined whether there is more than one deposit, but even if the X-ray does not show more than one deposit, there may be a second one, so that in case of doubt, I believe it is better to prick any suspected area with the point of a knife. I have done this many times, and have seen no variation which could be attributed to this practice in the convalescence of these patients. Sometimes such exploratory punctures of the tendons have fortunately led to the finding of a second deposit, for the patient may suffer an attack of inflammation about one deposit, and then later have another attack due to inflammation about another deposit. While immediate attention to the inflamed deposit is the most important thing, it is desirable when possible to remove or free any other deposit. I recall few cases of deposits which were not surrounded by red zones. Experience has shown that we rarely find any lesion of the bursa except at the points close to the attachments of the tendons, and these points may all be inspected by simply rotating the arm through its full arc while the wound is held open. It is a little harder to see the extreme edges upward and downward, but practically the whole bursa may be inspected by merely rotating the arm. Pushing the elbow backward (dorsal flexion) tends to demonstrate the upper edge, and pushing it forward reveals the lower limits of the bursa. I have never recognized any lesion of the roof of the bursa. Lesions at the attachment of the supraspinatus are the most common, those at the attachment of the infraspinatus next, and those of the attachment of the subscapularis perhaps a little less common. This relative frequency also holds good in regard to traumatic rupture of these tendons. One must remember that the three tendons are closely incorporated at their attachments, and that these attachments to some extent overlap.
Removing the Deposit. To return to the operative technique—we may assume that we have reached the point of incising a calcified deposit which we have found in the supraspinatus tendon. According to the stage of the pathologic process, whether acute or chronic, the calcified mass will be softer or harder; in the earlier stages it is little more than a milky fluid; in the older stages it is hard and gritty, coherent and sometimes encapsulated. In most cases it is of the consistency of ointment; often it resembles the contents of a wen. On incision this material usually escapes as if under tension. Sometimes this is very striking. A little nick is made, and there emerges a ribbon of whitish material just as one sees when a tube of zinc oxide ointment is squeezed. Sometimes, however, there is not much tension, particularly in the old cases, and the particles of calcareous matter seem to be incorporated in the substance of the tendon so that they cannot be curetted out without removing shreds of tendon with them. Occasionally the material occupies a well-formed pocket, and one gets the impression that it is wholly removed with the curette. I have oftentimes been content with merely incising one of these pockets, making no effort to curette out all of the material. The symptoms have disappeared quite as satisfactorily as in cases where a thorough curetting was done. Some surgeons, notably Brickner and Harbin, have stated that they excised all the calcified material. I am sure that if they do this, they will remove a considerable amount of tendinous substance which will be replaced with very little scar tissue, so that the tendon will be much weaker. I have sometimes thought that possibly cases of rupture of the supraspinatus tendon from trauma may be particularly common in cases which have had previous attacks of this so-called calcified bursitis, which has weakened the tendon. At any rate, I feel that it is well to do as little damage to the tendons as possible. Attempts to "excise the bursa" are absurd and indicate an entire lack of knowledge of the local anatomy, physiology and pathology.
Closing Incision. Having removed with the curette the major portion of the deposit, I wipe the cavity out, but do not attempt to sew up the incision in the tendon or in the bursa. Most other writers have recommended that the roof of the bursa be sutured. I have rarely done this, believing that it is better to allow the fluid formed by the synovial secretion of the bursal walls to seep into the areolar tissue. This would naturally wash out any particles of calcium and blood which remained in the bursa. If the bursa is closed these particles might cause adhesions, and perpetuate inflammation. Then, too, in a few cases in which I have closed the bursa, I think there has been more postoperative pain, due to distention of the bursa with blood and serum. I have not found that the adhesions due to the incision healing down to the tuberosity cause any permanent restriction of motion. It appears that the bursa itself reforms as a rule, perhaps not as a simple space, but as several small spaces. I close the muscle with a few loose catgut stitches, because I have found that unless I do so the wound eventually heals with a depression between the fibers of the deltoid. Therefore, it is better to see that the deltoid muscle returns to its normal contour. Perhaps it is better to close the roof of the bursa, but it would need a considerable number of cases to prove it, for my experience is sufficient to show that it is certainly not necessary. It may add some slight shred of advantage, but I think not. The skin is closed as in any other surgical wound.
Postoperative Treatment. After the operation I treat the patient just as I would a normal person who had a similar wound caused by an accident. The arm is carried in a sling most of the time for a few days. In about a week or ten days the patient can use the arm in a gingerly way, and can manage to dress himself, and use a knife and fork. Discarding the sling, I then encourage "swinging exercises" in a stooping position. When these become free the "standing exercises" are prescribed. In from three to six weeks the patient should be well, except for occasional twinges of pain and soreness and slight restriction in extreme degrees of motion. These twinges of pain are not severe or incapacitating, and I suppose are due to the irregular contours of the bursal surfaces after the incision. They slowly disappear. My tendency is to allow any free use which does not cause pain.
Finer Points and Occasional Obstacles in the Operation. In ladies it is well to have the patient try on a low-neclced dress, and to make the incision at a point where the scar will be concealed by the shoulder strap. Since rotation of the humerus covers a considerable arc, the site of the skin incision can be varied a good deal. I have tried a horizontal incision once, but the scar seemed to have a tendency to stretch more than does a vertical one. I want to repeat that it is important to tie all bleeding vessels before opening the bursa. The blood supply of the skin on the point of the shoulder is very active, and this is increased in cases of longstanding inflammation. Many small vessels sometimes have to be clamped to obtain a dry field. At the extreme upper angle of the wound there is one which is especially annoying, for it retracts into the muscle and readily drips into the open bursa, obscuring the field. As the wound is deep and small, even a little blood causes delay. Incising the bursa itself may prove confusing, especially where there are adhesions. Normally the roof of the bursa is even thinner and more delicate than the normal peritoneum, but where there has been inflammation in the bursa, it may be as thick as blotting paper, and quite opaque, so that it is hard to see the floor rotate beneath it as the arm is moved. In such cases one usually finds straw-colored fluid in the bursa. In some cases where the deposit has broken through into the bursa, flecks of deposit in sheets of fibrin or milky fluid will be found in the bursa. Such cases would probably get well without operating. It is not easy to open the bursa in some cases or even to know when your knife has passed through it into the areolar tissue in the nictitating folds. In case confusion arises, keep the arm in the position advised with the forearm vertical to the table, and cut down on the outer lip of the bicipital groove at its upper extremity. Do not cut directly on the bicipital groove, for you might unnecessarily open the sac about the tendon, if the bursal surfaces were adherent. This would probably do no harm, for in the cases of exploration for a ruptured biceps tendon I do not hesitate to do this and have had no unpleasant results. However, it does not help to locate the bursa, so it is best to recognize the groove by palpation before incising. Adhesions of the surfaces of the bursa may make it difficult to open. In two cases I have opened directly into the space containing the deposit, passing through the two adherent surfaces of the bursa without separating them. Such an experience might give the impression that the deposit was in the bursa. In my experience adhesions are not the rule. They vary, when present, from recent film-like strands hardly more solid than fibrin to dense scar tissue which effectually prevents rotation. As a rule, one readily opens into a good, large bursa, and the white or yellowish deposit surrounded by the turgid, red zone is as conspicuous as it well can be. The confusion comes in long-standing cases when the acute inflammation has subsided, and is replaced by firm, relatively bloodless adhesions about a very small deposit. It is quite possible that in cases where the deposit is in the subscapulars, a quicker and smoother convalescence might be obtained by pushing the bursa up from below, or from the inner side, and removing the deposit from beneath it without opening the bursa at all. This would leave a smooth bursa, and avoid the twinges of pain which the roughened surfaces produce if the bursa has been opened. I have done this in one case. However, it is surer and safer in most cases to incise directly into the bursa, and be guided by the red zone. Remember that when the incision is once made, only gentle retraction is necessary. Rotation of the humerus, by using the forearm flexed at a right angle, should take the place of retraction of the lips of the wound. It would be unfair to a patient to attempt to open his bursa unless the meaning of the above sentence was clearly understood. (Fig. 516.) I have operated on a few cases after the calcified material has perforated into the bursa, but I think now that these operations were probably unnecessary. So many similar cases have promptly got well without any treatment, that I suspect that although my operated cases also promptly got well, the operations had little to do with the recovery. In opening the bursa in these cases a few days after the perforation, I have found a film of whitish fibrin between the two bursal surfaces. Under the microscope little particles of calcium were found thickly scattered through the fibrin, accounting for its whitish look. Recently I have seen two such cases demonstrated by X-ray, on which I did not operate, and the symptoms cleared up as promptly as if I had removed the fibrin. It seems to me that the time when operation is most indicated is when the deposit has begun to cause subacute symptoms and has not yet perforated. It is in such cases that the mound on the base of the bursa is found, and from which the white material exudes as soon as it is punctured. I am inclined to think that spontaneous perforation will by nature relieve the symptoms in a few weeks, although it brings on the acute symptoms during the first few days. Operation, diathermy, puncture, injection of proteids, violet light or other treatment may easily get the credit for the good result. It seems a pity that comparative series of such cases treated by different methods cannot be arranged and controlled by a series of untreated cases. It is at least a comfort to know that all the cases under any treatment get well. The object of treatment is only to find the easiest, quickest, and most comfortable way. My feeling at present is that when the X-ray shows that the deposit has become diffused in the bursa it is unnecessary to operate, unless the quantity is great, as in Fig. 44. One can tell that it has become diffused if the film shows that the deposit lies outside of the tuberosity and, vice versa, if it lies within the contour of one of the tendons it cannot be in the bursa. (See Plate II.) Sometimes after perforation a portion of the deposit remains in the pocket in the tendon, and this gives a "shirt-stud" shadow in the X-ray. Be on your guard in interpreting the shadow cast by the bursa with a film of fibrin in it containing the diffused particles. Remember that the bursa is a very thin concavo-convex space, and therefore the mass of material in a lateral view seems greater than it really is. (See Fig. 45.)