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The Natural History and Clinical Syndromes Produced by Calcified Deposits in the Rotator Cuff
The Natural History and Clinical Syndromes Produced by Calcified Deposits in the Rotator Cuff H. FRED MOSELEY, D.M., M.CH. (OXON), F.R.C.S. (ENG.), F.R.C.S. (C), F.A.C.S.
CALCIUM salts are precipitated on the living collagen fibers in many sites in the musculoskeletal system. The most common location is the rotator cuff, but other areas may be involved such as the humeral epicondyles (tennis elbow), the collateral ligaments of the wrist, terminal phalanges of the fingers (Heberden's nodes), the vertebral column, around the greater trochanter of the femur, femoral attachment of the medial collateral ligament of the knee (Stieda-Pelligrini syndrome), and the ligamentous and tendinous attachments of the ankle, foot and toes. It is also characteristic that patients with symptoms and signs related to such deposits in the shoulder are prone to have similar syndromes related to other locations at different times. I have also stressed in my writings the association of tendinitis calcarea in the shoulder with similar depositions in the cardiovascular system. It has, therefore, been of the greatest interest to follow the work of Dr. Hans Selye which he has summarized so clearly for us and to note his method of producing an experimental model in the rat for further research. From the clinical point of view, it would appear that the shoulder offers the ideal site for the study of the deposition of the calcium salts in human tissues because of the frequency of such cases, the ease of radiographic and scanning studies, and the safety of exploration when required.
NATURAL HISTORY OF CALCIFIED DEPOSITS IN THE ROTATOR CUFF
Over the course of the past 25 years it has been possible to see a large number of cases which presented for painful shoulder syndromes with radiological evidence of calcified deposits in the cuff. The majority of
1489
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FRED MOSELEY
these cases have been treated conservatively, but approximately 300 cases have been explored and the area of tendinitis calcarea saucerized. The following remarks are based on this experience. At operation I have always noted that the tendon was well vascularized around the area of the deposit and therefore disagreed with the idea that the calcium salts were precipitated in an area of previous disease with resultant ischemia. It has, therefore, been most satisfying to note that recent work has demonstrated the precipitation on living collagen fibers. The necrosis of tendon results from the increasing deposition, with death of the tendon fibers probably due to pressure and tension. On exploration, the calcific material may be a dry powder or may be semi-liquid like toothpaste or grade to the ;liquid consistency of milk. As far as I am aware, there is no biochemical knowledge which would tell us the varying chemical composition of this material in the different phases. However, it is certain that the change is due to the absorption of fluid liquefying the dry powder. This fluid has been brought by the blood stream and the liquid deposits are always associated with a marked hyperemia and an acute clinical syndrome with pai~ a,nd limitation of function. In the dry state the deposit casts a dense x-ray shadow, and as the deposit becomes liquid the shadow will gradually grade into translucency. The calcium salts are originally deposited in the substance of the tendons of the rotator cuff and the tendons involved are the supraspinatus, infraspinatus, teres minor and subscapularis, in that order of frequency. The exact site is in relation to the critical zone of the tendon which, as previously stated, is the area of arterial anastomosis between the tendinous vessels arising from the muscular and osseous vasculature. As the deposit increases in size it destroys the adjacent tendinous tissue and works its way to the floor of the subacromial bursa. The Silent Phase
The first clinical pattern, then, of the calcified deposit is when the deposit is contained within the tendon. Its presence may be discovered on x-ray examination of the shoulder, possibly taken following a minor trauma. This deposit with minimal clinical signs and symptoms can be designated the silent phase. The Mechanical Phase
When the deposit increases in size and produces an elevation under the floor of the bursa, clinical symptoms and signs appear as the elevated deposit will impinge against the coraco-acromial ligament in abduction to 70 degrees and the increased tension in the deposit will cause pain of varying intensity. This painful catch di~appears at 110 to 120 degrees of elevation as the prominent deposit passes the coraco-acromial arch.
Natural History of Calcified Deposits in the Rotator Cuff
1491
Should repetitive motion be carried out either in elevation or in rotation in this range, 70 to 110 degrees, an irritative phenomenon will result with the development of a bursitis due to hyperemia of the subbursal vessels, liquefaction and increased tension in the deposit. On rest, the inflammatory process will subside and this will be aided by cold therapy. These are the cases which tend to have a painful arc of motion and recurrent attacks of so-called "bursitis" on overuse. This phase can be designated the mechanical phase. Subbursal Rupture
With time, the deposit tends to increase in size and finally, during one of the hyperemic stages, the liquid deposit bursts out of the tendon under the floor of the bursa. Usually only a partial evacuation occurs and with rest the attack will settle down and the deposit gradually change again from the liquid to the inspissated state. This phase is referred to as the mechanical deposit with subbursal rupture. This process of partial evacuation may recur on several occasions and finally the complete deposit is eliminated. In such cases there often remains a tendency to recurrent rheumatic pains in the shoulder in the spring and fall and pain on overuse. This has been found in my explorations to be due to chronic bursal thickening and adhesions which can be relieved, when indicated, by resection of the bursa. A more extensive evacuation of the deposit may occur beneath the floor of the bursa, and x-ray examination will show the small, dense deposit in the tendon and a linear extension along the tendon deep to the bursal floor. In some cases a tear-drop appearance may be seen caused by the pocketing of liquid deposit in this location and this appearance is similar to that seen on the x-ray when the deposit ruptures into the bursa. Intrabursal Rupture
Nature's most radical method of evacuating the whole deposit is by rupture under the floor of the bursa and secondarily into the bursa. In these cases the attack is most severe, and after rupture the point of acute tenderness previously palpable on the cuff has changed to acute tenderness one-third down the deltoid at the inferior reflection of the bursal wall. The rupture usually occurs after the fourth day, and the acute pain is replaced by a more continuous dull pain and absolute immobility of the glenohumeral articulation. This phase can be termed the mechanical deposit with intrabursal rupture. In both phases, with loculation of the liquid deposit under the bursal floor and within the bursa, a foreign body granulomatous tissue may be formed around this material. This may lead to marked stiffness if adequate therapy including heat and motion is not organized at this time.
1492
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FRED MOSELEY
Phase of Adhesive Periarthritis
Probably one of the most common operative patterns seen today is the case with a large multiloculated deposit which has had many forms of therapy including diathermy, deep x-ray and injections of all types of materials extending over some years. The patient comes for consultation in a state of general debility and frustration. Examination of the local condition shows a stiff and painful shoulder with an adduction and internal rotation contracture. The x-ray shows a deposit of variable size, and exploration discloses an adhesive bursitis with single or multiple deposits in the cuff. The Intra-osseous Loculation
Another operative finding which I am perCeIvmg with increasing frequency is the extension of the deposit into cavities in the adjacent greater tuberosity. Such cavities may contain large deposits of the dry type and the cavities measure up to 1 by 0.5 cm. It is my belief that the constant boring pain noted in some cases is due to this localization of the material, which is not usually visualized on the x-ray picture. The Dumbbell Loculation
An interesting rarity of the ruptured subbursal deposit is when the deposit is straddled in dumbbell-shaped loculation by the coraco-acromial ligament. In these cases the arm is held abducted 30 to 40 degrees and movement into either further abduction or adduction is resisted by pain. Evacuation of the deposit by needle or operation is dramatic in such cases. Certain other points should be mentioned from the operative findings. 1. The larger the deposit the more the destruction of the tendinous tissue and the larger the residual defect in the tendon after resection. With time and conservative treatment the deposits may disappear, and the residual defects account for some cases of degenerative periarthritis. 2. Gross destruction may occur if injections are made directly into the deposits, increasing the tension within the tendinous tissue. 3. The deposits are often multiple and should all be evacuated. Socalled postoperative recurrences are usually due to increased precipitation on deposits present at operation but not resected. The best time for evacuation of the large deposit is in the acute phase of the process before rupture when the minimum of tendinous tissue need be resected. 4. Many deposits are not diagnosed on x-ray examination as the shadows are superimposed on that of the humeral head. When severe pain is present it may be impossible to position the humerus so that the deposit is clear of the bone. Further, five or six days after the onset of the acute attack the deposit may be radiolucent and not visualized on x-ray examination.
Natural History of Calcified Deposits in the Rotator Cuff
1493
THE CLINICAL SYNDROMES
Some aspects of the clinical syndromes have been covered in the previous remarks on the natural history of these deposits. This information should be correlated with my previous work on the reproduction of the related pain syndromes using the Lewis and Kellgren method of injection of 5 per cent saline into the common sites for calcium deposition. In my early work, I found that injection of 0.5 ce. of 5 per cent saline into the supraspinatus tendon gave referred pain at the insertion of the deltoid. Further injection could cause the radiation down the arm, forearm to the hand and up the cervical area to the occiput. If operative exploration under local anesthesia is carried out on a large, acute deposit, the pain syndrome with corresponding distal radiation can be reproduced by digital pressure on the exposed deposit; the pain will be immediately relieved by diminishing the tension in the deposit by evacuation. SUMMARY
1. The various states, phases and unusualloculations of the deposits
have been described. 2. The pain syndromes are of four types: first, the elevated deposit which produces a mechanical block with the coraco-acromial ligament over the range 70 to 110 degrees; second, the subacute and acute deposit with increasing tension, which tension causes the referred somatic pain; third, the deposit with bursal irritation with pain localized in the bursa itself; and fourth, the dull, boring pain due to the intra-osseous loculation. Royal Victoria Hospital Montreal, Quebec
CALCIUM salts are precipitated on the living collagen fibers in many sites in the musculoskeletal system. The most common location is the rotator cuff, but other areas may be involved such as the humeral epicondyles (tennis elbow), the collateral ligaments of the wrist, terminal phalanges of the fingers (Heberden's nodes), the vertebral column, around the greater trochanter of the femur, femoral attachment of the medial collateral ligament of the knee (Stieda-Pelligrini syndrome), and the ligamentous and tendinous attachments of the ankle, foot and toes. It is also characteristic that patients with symptoms and signs related to such deposits in the shoulder are prone to have similar syndromes related to other locations at different times. I have also stressed in my writings the association of tendinitis calcarea in the shoulder with similar depositions in the cardiovascular system. It has, therefore, been of the greatest interest to follow the work of Dr. Hans Selye which he has summarized so clearly for us and to note his method of producing an experimental model in the rat for further research. From the clinical point of view, it would appear that the shoulder offers the ideal site for the study of the deposition of the calcium salts in human tissues because of the frequency of such cases, the ease of radiographic and scanning studies, and the safety of exploration when required.
NATURAL HISTORY OF CALCIFIED DEPOSITS IN THE ROTATOR CUFF
Over the course of the past 25 years it has been possible to see a large number of cases which presented for painful shoulder syndromes with radiological evidence of calcified deposits in the cuff. The majority of
1489
1490
H.
FRED MOSELEY
these cases have been treated conservatively, but approximately 300 cases have been explored and the area of tendinitis calcarea saucerized. The following remarks are based on this experience. At operation I have always noted that the tendon was well vascularized around the area of the deposit and therefore disagreed with the idea that the calcium salts were precipitated in an area of previous disease with resultant ischemia. It has, therefore, been most satisfying to note that recent work has demonstrated the precipitation on living collagen fibers. The necrosis of tendon results from the increasing deposition, with death of the tendon fibers probably due to pressure and tension. On exploration, the calcific material may be a dry powder or may be semi-liquid like toothpaste or grade to the ;liquid consistency of milk. As far as I am aware, there is no biochemical knowledge which would tell us the varying chemical composition of this material in the different phases. However, it is certain that the change is due to the absorption of fluid liquefying the dry powder. This fluid has been brought by the blood stream and the liquid deposits are always associated with a marked hyperemia and an acute clinical syndrome with pai~ a,nd limitation of function. In the dry state the deposit casts a dense x-ray shadow, and as the deposit becomes liquid the shadow will gradually grade into translucency. The calcium salts are originally deposited in the substance of the tendons of the rotator cuff and the tendons involved are the supraspinatus, infraspinatus, teres minor and subscapularis, in that order of frequency. The exact site is in relation to the critical zone of the tendon which, as previously stated, is the area of arterial anastomosis between the tendinous vessels arising from the muscular and osseous vasculature. As the deposit increases in size it destroys the adjacent tendinous tissue and works its way to the floor of the subacromial bursa. The Silent Phase
The first clinical pattern, then, of the calcified deposit is when the deposit is contained within the tendon. Its presence may be discovered on x-ray examination of the shoulder, possibly taken following a minor trauma. This deposit with minimal clinical signs and symptoms can be designated the silent phase. The Mechanical Phase
When the deposit increases in size and produces an elevation under the floor of the bursa, clinical symptoms and signs appear as the elevated deposit will impinge against the coraco-acromial ligament in abduction to 70 degrees and the increased tension in the deposit will cause pain of varying intensity. This painful catch di~appears at 110 to 120 degrees of elevation as the prominent deposit passes the coraco-acromial arch.
Natural History of Calcified Deposits in the Rotator Cuff
1491
Should repetitive motion be carried out either in elevation or in rotation in this range, 70 to 110 degrees, an irritative phenomenon will result with the development of a bursitis due to hyperemia of the subbursal vessels, liquefaction and increased tension in the deposit. On rest, the inflammatory process will subside and this will be aided by cold therapy. These are the cases which tend to have a painful arc of motion and recurrent attacks of so-called "bursitis" on overuse. This phase can be designated the mechanical phase. Subbursal Rupture
With time, the deposit tends to increase in size and finally, during one of the hyperemic stages, the liquid deposit bursts out of the tendon under the floor of the bursa. Usually only a partial evacuation occurs and with rest the attack will settle down and the deposit gradually change again from the liquid to the inspissated state. This phase is referred to as the mechanical deposit with subbursal rupture. This process of partial evacuation may recur on several occasions and finally the complete deposit is eliminated. In such cases there often remains a tendency to recurrent rheumatic pains in the shoulder in the spring and fall and pain on overuse. This has been found in my explorations to be due to chronic bursal thickening and adhesions which can be relieved, when indicated, by resection of the bursa. A more extensive evacuation of the deposit may occur beneath the floor of the bursa, and x-ray examination will show the small, dense deposit in the tendon and a linear extension along the tendon deep to the bursal floor. In some cases a tear-drop appearance may be seen caused by the pocketing of liquid deposit in this location and this appearance is similar to that seen on the x-ray when the deposit ruptures into the bursa. Intrabursal Rupture
Nature's most radical method of evacuating the whole deposit is by rupture under the floor of the bursa and secondarily into the bursa. In these cases the attack is most severe, and after rupture the point of acute tenderness previously palpable on the cuff has changed to acute tenderness one-third down the deltoid at the inferior reflection of the bursal wall. The rupture usually occurs after the fourth day, and the acute pain is replaced by a more continuous dull pain and absolute immobility of the glenohumeral articulation. This phase can be termed the mechanical deposit with intrabursal rupture. In both phases, with loculation of the liquid deposit under the bursal floor and within the bursa, a foreign body granulomatous tissue may be formed around this material. This may lead to marked stiffness if adequate therapy including heat and motion is not organized at this time.
1492
H.
FRED MOSELEY
Phase of Adhesive Periarthritis
Probably one of the most common operative patterns seen today is the case with a large multiloculated deposit which has had many forms of therapy including diathermy, deep x-ray and injections of all types of materials extending over some years. The patient comes for consultation in a state of general debility and frustration. Examination of the local condition shows a stiff and painful shoulder with an adduction and internal rotation contracture. The x-ray shows a deposit of variable size, and exploration discloses an adhesive bursitis with single or multiple deposits in the cuff. The Intra-osseous Loculation
Another operative finding which I am perCeIvmg with increasing frequency is the extension of the deposit into cavities in the adjacent greater tuberosity. Such cavities may contain large deposits of the dry type and the cavities measure up to 1 by 0.5 cm. It is my belief that the constant boring pain noted in some cases is due to this localization of the material, which is not usually visualized on the x-ray picture. The Dumbbell Loculation
An interesting rarity of the ruptured subbursal deposit is when the deposit is straddled in dumbbell-shaped loculation by the coraco-acromial ligament. In these cases the arm is held abducted 30 to 40 degrees and movement into either further abduction or adduction is resisted by pain. Evacuation of the deposit by needle or operation is dramatic in such cases. Certain other points should be mentioned from the operative findings. 1. The larger the deposit the more the destruction of the tendinous tissue and the larger the residual defect in the tendon after resection. With time and conservative treatment the deposits may disappear, and the residual defects account for some cases of degenerative periarthritis. 2. Gross destruction may occur if injections are made directly into the deposits, increasing the tension within the tendinous tissue. 3. The deposits are often multiple and should all be evacuated. Socalled postoperative recurrences are usually due to increased precipitation on deposits present at operation but not resected. The best time for evacuation of the large deposit is in the acute phase of the process before rupture when the minimum of tendinous tissue need be resected. 4. Many deposits are not diagnosed on x-ray examination as the shadows are superimposed on that of the humeral head. When severe pain is present it may be impossible to position the humerus so that the deposit is clear of the bone. Further, five or six days after the onset of the acute attack the deposit may be radiolucent and not visualized on x-ray examination.
Natural History of Calcified Deposits in the Rotator Cuff
1493
THE CLINICAL SYNDROMES
Some aspects of the clinical syndromes have been covered in the previous remarks on the natural history of these deposits. This information should be correlated with my previous work on the reproduction of the related pain syndromes using the Lewis and Kellgren method of injection of 5 per cent saline into the common sites for calcium deposition. In my early work, I found that injection of 0.5 ce. of 5 per cent saline into the supraspinatus tendon gave referred pain at the insertion of the deltoid. Further injection could cause the radiation down the arm, forearm to the hand and up the cervical area to the occiput. If operative exploration under local anesthesia is carried out on a large, acute deposit, the pain syndrome with corresponding distal radiation can be reproduced by digital pressure on the exposed deposit; the pain will be immediately relieved by diminishing the tension in the deposit by evacuation. SUMMARY
1. The various states, phases and unusualloculations of the deposits
have been described. 2. The pain syndromes are of four types: first, the elevated deposit which produces a mechanical block with the coraco-acromial ligament over the range 70 to 110 degrees; second, the subacute and acute deposit with increasing tension, which tension causes the referred somatic pain; third, the deposit with bursal irritation with pain localized in the bursa itself; and fourth, the dull, boring pain due to the intra-osseous loculation. Royal Victoria Hospital Montreal, Quebec